It is essential that all individuals involved in the assessment and management of patients with cardiac surgical disease have a basic understanding of the disease processes that are being treated. This chapter presents the spectrum of adult cardiac surgical disease that is encountered in most cardiac surgical practices. The pathophysiology, indications for surgery, specific preoperative considerations, and surgical options for various diseases are presented. Diagnostic techniques and general preoperative considerations are presented in the next two chapters. Issues related to cardiac anesthesia and postoperative care specific to most of the surgical procedures presented in this chapter are discussed in Chapters 4 and 8, respectively. The most current guidelines for the evaluation and management of patients with cardiac disease can be obtained from the American College of Cardiology website (www.acc.org).

I. Coronary Artery Disease

1. Pathophysiology. Coronary artery disease (CAD) results from the progressive blockage of the coronary arteries by atherothrombotic disease. Significant risk factors include hypertension, dyslipidemia (especially high LDL, low HDL, elevated Lp(a) or apoB, or triglycerides), diabetes mellitus, obesity (a combination of the above being termed metabolic syndrome), cigarette smoking, and a family history of premature CAD. Clinical syndromes result from an imbalance of oxygen supply and demand resulting in inadequate myocardial perfusion to meet metabolic demand (ischemia). Progressive compromise in luminal diameter producing supply/demand imbalance usually produces a pattern of chronic stable angina, commonly referred to as “stable ischemic heart disease (SIHD). Plaque rupture with superimposed thrombosis is responsible for most acute coronary syndromes (ACS), which include classic “unstable angina”, non‐ST‐elevation myocardial infarctions (non‐STEMI), and ST‐elevation infarctions (STEMI). Paradoxically, plaque rupture more commonly occurs in coronary segments that are not severely stenotic. Endothelial dysfunction has become increasingly recognized as a contributing factor to worsening ischemic syndromes. Generalized systemic inflammation, indicated by elevated C‐reactive protein levels, is usually noted in patients with ACS, and appears to be associated with adverse outcomes.
   
2. Primary prevention of cardiovascular disease entails control of modifiable risk factors. Notably, statins are generally not recommended for patients with normal cholesterol levels (unless there is a family history of premature CAD) or for patients at low risk for atherosclerotic cardiovascular disease (ASCVD) based on the ASCVD risk calculator (available at https://clincalc.com/cardiology/ascvd/pooledcohort.aspx). Furthermore, aspirin, which had been widely utilized for primary prevention in the past, has received only a level IIb recommendation for patients age 40–70 with higher ASCVD risk, but not at increased bleeding risk, and was considered contraindicated on a routine basis in patients >age 70 or in any patient with an increased risk of bleeding, according to a 2019 ACC report.¹
   
3. Management strategies in stable ischemic heart disease (SIHD)
   
   
   
   1. Symptomatic coronary disease is initially treated with medical therapy, including aspirin, nitrates, ß‐adrenergic blockers, and calcium‐channel blockers (CCBs). Ranolazine may be added as a second‐line drug for symptomatic relief in patients with refractory angina. It inhibits inward sodium currents in the heart muscle, leading to a reduction in intracellular calcium levels, which reduces myocardial wall tension and oxygen requirements. It does not cause bradycardia and hypotension, which occasionally are limiting factors with the use of other antianginal drugs. Statins should be given to control dyslipidemias and are effective for plaque stabilization. Angiotensin‐converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are given to patients with depressed left ventricular (LV) function (ejection fraction [EF] <40%) and to those with hypertension and diabetes. P2Y12 inhibitors (clopidogrel, ticagrelor) generally do not provide benefit to patients with SIHD.
      
   2. Optimal medical therapy should be the initial management strategy for patients with SIHD, since studies have not shown that proceeding to percutaneous coronary intervention (PCI) reduces the risk of death, infarction or other major adverse cardiovascular events.² Thus, the decision to proceed with cardiac catheterization should be based on the rationale that the patient’s symptoms are disabling enough or the degree of ischemia is significant enough to warrant an intervention to revascularize the heart. Risk stratification with noninvasive functional testing is important to provide objective evidence of inducible ischemia, using exercise stress testing, nuclear imaging, or dobutamine stress echocardiography.
      
   3. The decision to proceed with an intervention must then take into consideration an angiographic assessment of the extent of coronary disease and an invasive assessment of its physiologic significance by fractional flow reserve (FFR)³ or instantaneous flow reserve (iFR)⁴, which is not dependent on the administration of adenosine. Additional critical information when considering PCI or coronary artery bypass grafting (CABG) includes the patient’s comorbidities, particularly diabetes mellitus, and an assessment of LV function. Multiple studies comparing medical therapy with PCI for patients with SIHD have shown that PCI reduces the incidence of angina, may increase the short‐term risk of myocardial infarction (MI), but does not lower the long‐term risk of MI or improve survival.⁵ However, PCI does reduce the need for urgent revascularization and may reduce the risk of MI in patients with a large ischemic burden. Superior clinical outcomes are achieved with complete revascularization, which in many patients is better accomplished with CABG than PCI.⁶ Use of systematic anatomic assessments, such as with the SYNTAX score (see section C.4.a), has been accepted as an adjunct to this decision‐making process.
      
   4. Appropriate use criteria (AUC) with complex matrices have been set forth for coronary revascularization strategies in patients with SIHD.⁷ These are subdivided by the number of diseased vessels (1–2–3), the presence of symptoms, the use of antianginal therapy, and whether noninvasive testing indicates the patient is at low, intermediate, or high risk for a cardiac event, or in the absence of testing, by the results of FFR/iFr studies.
      
      
      
      1. The SYNTAX score (http://www.syntaxscore.com) is also incorporated into the AUC guidelines and can be used to determine whether PCI or CABG is preferable for multivessel or left main (LM) disease. This provides an angiographic assessment of coronary disease with an additive score that evaluates the location and degree of stenosis in each vessel, the angiographic complexity of the lesion, vessel diameter and calcification. The SYNTAX trial divided patients into low risk (score of 0–22), intermediate risk (score of 23–32), and high risk (score >32) categories and used a primary end point of major adverse cardiac and cerebrovascular events (MACCE), which includes mortality, myocardial infarction (MI), stroke, and the need for repeat revascularization.
         
      2. Five‐year follow‐up data from the SYNTAX trial showed that patients in the low‐risk category had similar MACCE rates with PCI or CABG. However, CABG produced superior results in intermediate‐ to high‐risk patients with three‐vessel disease (score >22), and those at high risk with LM disease. In these cohorts, CABG was associated with less MACCE, more complete revascularization, reduced need for repeat revascularization, and improved long‐term benefit.^8,9
         
      3. The FREEDOM trial showed that CABG was superior to PCI in diabetic patients with multivessel disease,^10,11 and the presence or absence of diabetes is specifically incorporated into the AUC guidelines for multivessel and LM disease. In these diabetic patients, the SYNTAX score was found to be a predictor of MACCE only with PCI, and therefore was not recommended to guide therapy.¹²
         
      4. A “residual SYNTAX” score >8 after PCI for patients in the moderate‐ to high‐risk cohorts, indicative of incomplete revascularization, had worse 30‐day and one‐year survival.¹³ In fact, in the entire SYNTAX study, PCI resulted in a 10‐fold increase in MI‐related death compared with CABG, but this was mostly accounted for in patients with diabetes, multivessel disease, and high SYNTAX scores.¹⁴
         
      5. One shortcoming of the SYNTAX score was that it correlated only an angiographic assessment with the best revascularization strategy. Because surgery might provide more benefit to patients with significant clinical comorbidities in addition to the anatomical complexity of disease, the SYNTAX II scoring system was devised. This included eight predictors – two anatomic (SYNTAX score and unprotected LM disease), and six clinical predictors (age, creatinine clearance, ejection fraction, female gender, peripheral vascular disease, and chronic obstructive pulmonary disease [COPD]). The SYNTAX II study used second‐generation drug‐eluting stents and intravascular ultrasound imaging with PCI. It showed that some patients with low SYNTAX scores had higher mortality rates with PCI and some with higher SYNTAX scores did better with PCI. Generally, the SYNTAX II score was a better predictor of four‐year mortality rates than the original score.¹⁵ To achieve similar four‐year survival rates with PCI or CABG, it was found that young patients, females, and patients with reduced LVEF required lower SYNTAX scores, while older patients, those with COPD, and those with unprotected LM disease did well with PCI despite higher anatomical SYNTAX scores. The SYNTAX II score can be accessed at www.syntaxscore.com and it calculates the comparative four‐year survival rates for PCI and CABG.
         
      6. Although diabetes was not a discriminator using SYNTAX II scoring, other studies, including a subanalysis from the FREEDOM trial of diabetic patients with multivessel disease, found CABG superior to PCI in both insulin‐treated and noninsulin‐treated diabetics, but results were generally worse after either procedure in insulin‐treated diabetics.¹⁶
         
      7. Thus, the SYNTAX or SYNTAX II score might be used as part of the decision‐making process for the preferable mode of revascularization, since, along with older age, female gender, smoking, and diabetes, it appears to be a strong predictor of mortality and MACCE in patients undergoing PCI for multivessel disease and unprotected left main stenosis. These scoring systems provide an evidence‐based justification for selecting CABG as the treatment of choice for many patients with more complex multivessel disease.
      
      
   5. Indications for surgery in SIHD – symptom relief. The primary indication for surgical revascularization is to improve symptoms. PCI is applicable to many of these patients, but CABG must be considered for diabetic patients and those with high SYNTAX scores and when satisfactory PCI cannot be accomplished.⁵
      
      
      
      1. Class I indications
         
         
         
         • ≥1 significant stenoses with unacceptable angina despite guideline‐directed medical therapy (GDMT)
         
         
      2. Class IIa indications
         
         
         
         • ≥1 significant stenoses in patients who cannot implement GDMT
           
         • Complex three‐vessel disease (SYNTAX score >22) with/without proximal left anterior descending (LAD) artery stenosis
         
         
      3. Class IIb indications
         
         
         
         • Redo CABG with ≥1 significant stenoses with ischemia and unacceptable angina despite GDMT
      
      
   6. Indications for surgery in SIHD – improvement in survival. Although symptom relief is one objective of any revascularization procedure, an additional important benefit is an improvement in long‐term survival compared with medical therapy. For example, CABG for LM disease >50% or for multivessel disease with extensive ischemia and/or impaired LV function can accomplish this, but there are limited data showing that PCI can do the same. It is also likely that CABG can prolong life by preventing MI, whereas the same may not be true for PCI.¹⁷ The following recommendations for surgery represent slight modification from the randomized controlled trials of patients with primarily chronic stable angina in the early 1980s and were incorporated into the 2011 guidelines for CABG.⁵ These are the anatomic subsets for which improved survival has been noted compared with medical therapy. Thus, for these patients, surgery can be justified even in the absence of disabling symptoms. PCI is often utilized for many of these indications, although a survival benefit has not necessarily been demonstrated.
      
      
      
      1. Class I indications
         
         
         
         • Unprotected left main stenosis >50%
           
         • Three‐vessel disease with/without proximal LAD disease
           
         • Two‐vessel disease with proximal LAD disease
           
         • Survivors of sudden death with presumed ischemic‐mediated ventricular tachycardia (VT)
         
         
      2. Class IIa indications
         
         
         
         • Two‐vessel disease without proximal LAD disease with a large area of ischemic myocardium
           
         • One‐vessel disease with proximal LAD disease (with a left internal thoracic artery [LITA] graft)
           
         • Proximal LAD or multivessel disease with EF 35–50% if viable myocardium in the region of intended revascularization
         
         
      3. Class IIb indications
         
         
         
         • One‐, two‐ or three‐vessel disease except left main with EF <35%
      
      
   7. The optimal strategy in patients with severe ischemic LV dysfunction is somewhat controversial. The STICH (Surgical Treatment for Ischemic Heart Failure) trial comparing CABG with optimal medical therapy in patients with ischemic LV dysfunction found an increased 30‐day mortality but better 10‐year survival with CABG, the crossover occurring at two years.¹⁸
      
      
      
      1. There was no correlation of survival with the presence or absence of angina in the intention‐to‐treat analysis, but there was a prognostic benefit when cross-overs were included. Either way, angina relief was superior with surgery.¹⁹
         
      2. Worse outcomes with medical management were noted with more extensive CAD, more LV dysfunction (EF <27%) and larger ventricles (LV end‐systolic volume index >79 mL/m²), but these risk factors were not predictive of CABG mortality – thus a greater benefit with CABG was noted in these patients.
         
      3. Another interesting finding of the STICH trial was that there was no difference in surgical outcomes whether viability was present or not, and in fact, this observation was irrespective of treatment strategy.²⁰ This seemed to contradict multiple studies and meta‐analyses that have shown that viability testing is helpful in assessing which patients may benefit from surgery.²¹ One potential limitation of this trial was the use of thallium stress imaging, which is not as discriminatory as PET (positron emission tomography) scanning in differentiating viable from nonviable myocardium. It was concluded that viability was predictive of a survival benefit in patients with moderate LV dysfunction, but lost its prognostic benefit when LV dysfunction became severe.¹⁹
         
      4. Other studies comparing PCI with CABG in diabetic patients with LV dysfunction have confirmed that CABG is associated with a lower risk of death, MI, MACE, and repeat revascularization.²²
   
   
4. Management strategies in acute coronary syndromes
   
   
   
   1. Non‐STEMI patients or those with unstable angina without a troponin leak usually have the substrate for recurrent ischemia and infarction. They should be treated with aspirin (162–325 mg) and unfractionated or low‐molecular‐weight heparin (LMWH), as well as standard therapies (e.g. nitrates, β‐blockers, statins, ACE inhibitors).^23,24 A P2Y12 inhibitor, usually clopidogrel or ticagrelor, should be given in addition to aspirin to patients with non‐STEMIs, but it is not necessarily indicated in patients with normal troponin levels. Initiation of dual antiplatelet therapy will provide a clinical benefit and will also provide adequate platelet inhibition for a PCI which is feasible in most patients to relieve ischemia and prevent infarction. In patients who are considered intermediate–high risk for a clinical event or exhibit a large thrombus burden, the addition of a glycoprotein (GP) IIb/IIIa inhibitor may be considered (class IIb indication). If PCI is not feasible or is unsuccessful, a CABG is indicated for the anatomic findings listed in section C.6.
      
      
      
      1. Low‐risk patients may stabilize on medical therapy and can undergo risk stratification by noninvasive testing to assess the extent of inducible ischemia (the “ischemia‐guided strategy”). Various scoring systems (GRACE or TIMI score for UA/NSTEMI) can be used to quantitate the patient’s short‐term risk of an ischemic event. The GRACE score provides estimates of in‐hospital and six‐month mortality and the TIMI score provides the 14‐day risk of mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent revascularization. Both of these scoring systems are available at a variety of sites on‐line, including www.mdcal.com (search “GRACE” or “TIMI”).²⁴
         
      2. In patients at intermediate–high risk, an “early invasive strategy” is used, which triages the patient to early catheterization. Although this strategy is considered to lead to improved outcomes compared with the ischemia‐guided approach, some studies show that 10‐year outcomes are comparable.²⁵ This approach provides an early definition of the patient’s coronary anatomy and allows for early intervention to prevent myocardial damage. This strategy has been subdivided into immediate (<2 hours), early (<24 hours), or delayed (25–72 hours) catheterizations, depending on the patient’s presentation. The immediate approach is applicable to patients with recurrent or refractory angina, ECG changes at rest, new‐onset heart failure (HF), new‐onset mitral regurgitation (MR), or hemodynamic instability. New ST depressions with rising troponins or a GRACE score >140 are an indication for an early approach, and patients with diabetes, chronic kidney disease, EF <40%, a GRACE score of 109–140, or a TIMI score ≥2 can have a delayed invasive approach.^24,26
         
      3. Since most patients are given a P2Y12 inhibitor upon hospital admission, when the extent of their coronary disease is not known, there will be patients undergoing catheterization in whom PCI is not feasible or in whom the benefits of CABG outweigh those of PCI (i.e. most diabetic patients with multivessel disease and patients with distal LM disease). An urgent CABG may then be recommended. A lower risk of renal dysfunction is noted for patients having on‐pump CABG if surgery can be delayed for 24 hours after catheterization.²⁷ However, the timing of surgery must primarily balance the risk of a recurrent ischemic event vs. the risk of excessive bleeding. For patients requiring urgent, but not emergent, surgery who receive a P2Y12 inhibitor, surgery should be delayed at least 24 hours, if possible, and platelet aggregation testing obtained to elucidate whether the patient is sensitive or not to the P2Y12 inhibitor.^28,29 If inhibition is <30%, surgery can usually be done safely without resorting to platelet transfusions to control mediastinal bleeding.
      
      
   2. ST elevation infarctions (STEMIs) are usually associated with coronary occlusions, and are preferentially treated by primary PCI, although thrombolytic therapy may be considered when PCI cannot be performed within a few hours. Clinical benefit is time‐related (“time is myocardium”), and the best results are obtained with a “door to balloon” time of less than 90 minutes. However, PCI should still be considered up to 12 hours after the onset of symptoms, at 12–24 hours if the patient has HF, persistent ischemic symptoms, or hemodynamic or electrical instability, or at any time if cardiogenic shock is present.²⁴ For the latter, emerging data suggest that improved survival may be achieved using mechanical circulatory support (MCS), such as an Impella (Abiomed, Danvers, MA) device, prior to PCI.^30,31 All patients presenting with a STEMI and with no contraindications to antiplatelet treatment should be given one dose of aspirin 325 mg, a load of either clopidogrel 600 mg or ticagrelor 180 mg, and either unfractionated heparin or bivalirudin upon presentation to the emergency room, if not sooner (i.e. in the ambulance).
      
      
      
      1. If PCI of the culprit vessel can be accomplished in a patient with multivessel disease, it remains controversial as to whether stenting of other nonculprit stenotic vessels should be performed at the same time, even in patients with cardiogenic shock, although some observational studies do suggest a benefit.^32,33 However, if it is concluded that the other vessels would be better revascularized by surgery, the patient may be referred for CABG having received a P2Y12 inhibitor to prevent stent thrombosis. Once the culprit vessel has been opened, surgery is rarely required emergently. Thus, the oral P2Y12 inhibitor may be stopped and the patient given either a short‐acting P2Y12 inhibitor (IV cangrelor) or a GP IIb/IIIa inhibitor as a bridge to surgery.
         
      2. If PCI cannot be accomplished or is considered inadvisable due to extensive LM or multivessel disease, emergency surgery should be performed. Early surgical studies showed little myocardial salvage if CABG was not performed within six hours, with a significant increase in mortality for surgery performed between 7 and 24 hours, and then a lower mortality thereafter.³⁴ Thus, beyond six hours, surgery may be delayed in the absence of cardiogenic shock, active ischemia, or a significant area of myocardium at risk, although the latter is usually present. However, active ischemia with or without cardiogenic shock should usually be treated urgently by CABG, independent of the time since presentation. In a report from the STS database, the operative mortality rate for patients in cardiogenic shock was about 20%, but it was 37% in patients requiring intraoperative MCS and 58% in patients requiring postoperative MCS support.³⁵ Thus, if cardiogenic shock is present without active ischemia or with end‐organ dysfunction, consideration might be given to use of MCS alone.²⁴
         
      3. If PCI cannot be performed or has failed, the ACC guidelines recommend emergency surgery for the following:
         
         
         
         1. Class I
            
            
            
            • Persistent ischemia or hemodynamic instability refractory to nonsurgical therapy (it is not stated if that includes an intra‐aortic balloon pump [IABP])
              
            • Cardiogenic shock irrespective of the time from MI to the onset of shock and the time from MI to CABG
              
            • Mechanical complications of MI
              
            • Life‐threatening ventricular arrhythmias with LM or three‐vessel disease
            
            
         2. Class IIb
            
            
            
            • Multivessel disease with recurrent angina or MI within 48 hours of presentation
              
            • Patients >age 75 with ST elevation or left bundle branch block (LBBB) regardless of time since presentation if in cardiogenic shock
   
   
5. CABG vs. PCI as a revascularization strategy – other comments
   
   
   
   1. The ongoing debate about the relative merits and advantages of CABG or PCI has spawned innumerable studies, publications, and controversies. PCI is generally utilized for patients with a lesser extent of disease, as noted in the appropriate use criteria (AUC) guidelines, and should incorporate SYNTAX scores in the decision. However, PCI is also useful in patients at very high risk for surgery due to either very advanced “nonbypassable” coronary disease or significant comorbidities that make surgery a prohibitive risk. Mechanical circulatory‐supported PCI procedures, primarily using the Impella devices, have been performed successfully in high‐risk cases.³⁶
      
   2. Studies have shown that FFR‐guided, rather than anatomy‐guided, PCI produces superior outcomes in patients with SIHD, reducing the need for urgent revascularization.³⁷ In the 2011 ACC guidelines for CABG, there is no mention of using an FFR‐guided approach to surgical revascularization. Some studies have shown that this approach results in less grafting, a higher graft patency rate, a lower rate of angina, and a significant reduction in MI and mortality out to six years.^38–40 Such information could be helpful in deciding which patients should undergo surgery and in fact which vessels need to be bypassed.
      
   3. Second‐generation drug‐eluting stents (DES) have been associated with a lower risk of restenosis requiring repeat revascularization, lower rates of stent thrombosis, and fewer MIs than bare‐metal stents (BMS), without a significant impact on mortality.⁴¹ Although the risk of stent thrombosis may be greater in patients who are resistant to the antiplatelet effects of aspirin and/or a P2Y12 inhibitor, platelet function testing has not been that useful in adjusting treatment and influencing outcomes.⁴² To minimize the risk of stent thrombosis, it is recommended that patients receiving a BMS take aspirin and a P2Y12 inhibitor for at least one month, and those receiving a DES take these medications for at least six months to one year.⁴³
      
   4. One should not consider either PCI or CABG an exclusive approach to a patient’s CAD. For example, one hybrid approach is to perform a PCI of the culprit lesion causing a STEMI to achieve prompt myocardial salvage and then refer the patient for surgical revascularization of other lesions. If a patient does undergo PCI and urgent surgery is then recommended, a strategy must be devised to minimize the risk of stent thrombosis while minimizing the risk of perioperative bleeding. It has even been proposed that placing a LITA to the LAD in a patient with three‐vessel disease provides the essential long‐term benefit of a CABG and converts the patient’s anatomy to two‐vessel disease which can be managed medically or with PCI.^44,45 However, one study did suggest that the rate of mid‐term reinterventions rates was higher using a hybrid approach.⁴⁶
   
   
6. Preoperative considerations
   
   
   
   1. A thorough history and physical examination is imperative when cardiac surgery is being contemplated. Whereas PCI specifically addresses the patient’s cardiac issues with minimal impact on other organ systems except the kidneys, open‐heart surgery can produce a significant number of potential morbidities, especially in patients with pre‐existing problems, such as COPD, hepatic or renal dysfunction, cerebrovascular disease, diabetes, etc. Careful attention to and management of such issues prior to surgery may optimize surgical outcomes. These issues are discussed in detail in Chapter 3.
      
   2. Myocardial ischemia. Aggressive management of ongoing or potential ischemia is indicated in patients with critical coronary disease to reduce surgical risk. This may include adequate sedation and analgesia, anti‐ischemic medications to control heart rate and blood pressure (IV nitrates and β‐blockers), antiplatelet and anticoagulant medications (aspirin, P2Y12 inhibitors, heparin, GP IIb/IIIa inhibitors), and/or placement of an IABP for refractory ischemia. It cannot be overemphasized that just because a patient has been catheterized and accepted for surgery does not mean that medical care should not be aggressive up to the time of surgery! If the patient has persistent ischemia despite all of these measures, emergency surgery is mandatory.
      
      
      
      1. All antianginal medications should be continued up to and including the morning of surgery. Studies have demonstrated the benefit of preoperative β‐blocker therapy in lowering perioperative mortality in elective cardiac surgery patients, although this is probably limited to patients sustaining a remote infarction.^47,48 Patients being admitted the morning of surgery should be reminded to take their medications before coming to the hospital.
         
      2. Unfractionated heparin (UFH) is often used in patients with an ACS, left main coronary disease, or a preoperative IABP. The heparin may be stopped about four hours prior to surgery, but in patients at higher risk for ischemia, it may be continued up to the time of surgery without causing problems with central line insertion. Patients receiving heparin should have their platelet count rechecked daily to be vigilant for the development of heparin‐induced thrombocytopenia (HIT). Note that preoperative assessment for HIT antibodies is not indicated in the absence of a clinical indication.
         
      3. Low‐molecular‐weight heparin (LMWH) is often used in patients presenting with an ACS and may be used in the cath lab as well. It must be stopped at least 24 hours prior to surgery to minimize the risk of perioperative bleeding. The non‐vitamin K antagonist oral anticoagulants (NOACs) (dabigatran, apixaban, rivaroxaban, edoxaban) should be stopped 48 hours prior to surgery and probably longer in patients with renal dysfunction.^49–51 Fondaparinux, occasionally used for venous thromboembolism prophylaxis, has a half‐life of 17–21 hours and must be stopped at least 60 hours prior to surgery.
         
      4. Aspirin is routinely used in patients with known coronary disease or is given upon presentation to the hospital. Aspirin 81 mg should be continued up to the time of surgery for virtually all patients undergoing CABG, since most studies have demonstrated improved outcomes without a significant increase in the risk of bleeding.^52–55
         
      5. Preoperative use of P2Y12 inhibitors within a few days of surgery has been shown to significantly increase the risk of bleeding and re‐exploration for bleeding. Thus, it has been recommended that clopidogrel and ticagrelor be stopped for five days and prasugrel for seven days before elective surgery.⁵⁵ Stopping the medication for only three days may be acceptable prior to off‐pump surgery.⁵⁶ Platelet aggregation testing, more so than the duration of cessation prior to surgery, may dictate when surgery can be performed with a lower risk of bleeding.^28,29
         
         
         
         1. In some cases, emergency balloon angioplasty and potential stenting of a culprit lesion causing an evolving infarction may be performed, with subsequent referral for urgent surgery to achieve complete revascularization. In this situation, it is preferable to use a short‐acting platelet inhibitor as a bridge to surgery to minimize the risk of stent thrombosis. IV cangrelor is preferable as it has a half‐life of 3–6 minutes and need be stopped only 1–2 hours before surgery.⁵⁷ Alternatively, a GP IIb/IIIa inhibitor can be used and should be stopped four hours prior to surgery so that by the time surgery starts, 80% of platelet activity will have recovered.
            
         2. In patients requiring surgery who have had prior stenting (<1 month for a BMS and 6–12 months for a DES), there is an increased risk of stent thrombosis if the P2Y12 inhibitor is stopped. P2Y12 reaction units (PRU) testing may indicate the patient’s sensitivity to the drug. It is best to avoid operating if the PRU suggests >30% inhibition. In the absence of such testing, stopping the medication for three days may leave some residual protective antiplatelet activity, yet hopefully cause less intraoperative bleeding.
         
         
      6. Anemia is associated with worse clinical outcomes after surgery, but this may be related to its association with other risk factors, such as HF or chronic kidney disease. In fact, it has been reported that blood transfusions have a greater impact on risk‐adjusted morbidity and mortality than the anemia itself.^58–61
         
         
         
         1. Most hospitalized patients suffer from hospital‐acquired anemia, which results from repeated blood withdrawal for lab tests as well as the blood loss and hydration during a catheterization procedure. Guidelines recommend transfusion for a hemoglobin (Hb) <8 g/dL in patients with an ACS, although hemodynamically unstable patients may benefit from a Hb level between 8 and 10 g/dL.^58,61
            
         2. Even in the stable patient awaiting surgery, it is not unreasonable to give a blood transfusion prior to surgery if the anticipated hematocrit (HCT) on pump will be <20%. Low hematocrits on pump will lower oncotic pressure and viscosity, increase fluid requirements, which contributes to extracellular edema, and make it more difficult to maintain an adequate blood pressure during and after cardiopulmonary bypass (CPB). A HCT below 20% has been associated with an increased risk of renal dysfunction, stroke, ischemic optic neuropathy, and mortality. Patients with profound anemia during surgery also tend to bleed more and require more blood component transfusions. Thus, preoperative transfusion to an adequate level may be considered to reduce patient morbidity, possibly reduce the overall number of transfusions required intra‐ and postoperatively, and potentially decrease mortality.
      
      
   3. Other preoperative medications to be considered include the following:
      
      
      
      1. Amiodarone is beneficial in reducing the incidence of postoperative atrial fibrillation (AF). Protocols that initiate amiodarone prior to or during surgery have been utilized successfully (see pages 623–624 in Chapter 11).⁶²
         
      2. Statins have been demonstrated to reduce operative mortality, the risks of stroke, delirium, AF, and arguably the risk of acute kidney injury.^63–66
         
      3. Steroids have been evaluated as a means of reducing the systemic inflammatory response to surgery and have been shown to improve myocardial function and possibly reduce the incidence of AF.⁶⁷ However, improvement in pulmonary function has not been clearly shown, and steroids do worsen postoperative hyperglycemia. Since the benefits are controversial, steroids have not seen widespread usage.
   
   
7. Surgical procedures
   
   
   
   1. Traditional coronary artery bypass grafting is performed through a median sternotomy incision with use of CPB. Myocardial preservation is provided by cardioplegic arrest. The procedure involves bypassing the coronary blockages with a variety of conduits. The left internal thoracic (or mammary) artery (ITA) is usually used as a pedicled graft to the LAD and is supplemented by either a second ITA graft or radial artery graft to the left system and/or saphenous vein grafts interposed between the aorta and the coronary arteries (Figure 1.1).
      
      
      
      1. The saphenous vein should be harvested endoscopically to minimize patient discomfort, reduce the incidence of leg edema and wound healing problems, and optimize cosmesis. There are some concerns that endoscopic harvesting could produce endothelial damage that might compromise long‐term patency and reduce long‐term survival, but with more experience, this has not been found to be an issue.^68–70
         
      2. Use of additional arterial conduits (bilateral ITAs, radial artery) can be recommended to improve event‐free survival.^71–73 The radial artery can be harvested endoscopically using a tourniquet to minimize bleeding during the harvest with placement of a drain afterward to prevent blood accumulation within the tract. With radial artery grafting, use of a topical vasodilator, such as a combination of verapamil‐nitroglycerin, is useful in minimizing spasm.⁷⁴ The STS guidelines suggest use of a systemic vasodilator during surgery, and IV diltiazem 0.1 mg/kg/h (usually 5–10 mg/h) or IV nitroglycerin 10–20 μg/min (0.1–0.2 μg/kg/min) are commonly used.⁷¹ This is continued in the intensive care unit and then converted to either amlodipine 5 mg po qd or Imdur 20 mg po qd for several months. The purported benefit of such pharmacologic management to prevent spasm has been universally accepted, although not rigorously studied, and routine use may not be indicated.⁷⁵
      
      
   2. Concerns about the adverse effects of CPB spurred the development of “off‐pump” coronary surgery (OPCAB), during which complete revascularization should be achieved with the avoidance of CPB. Deep pericardial sutures and various retraction devices are used to position the heart for grafting without hemodynamic compromise. A stabilizing platform minimizes movement at the site of the arteriotomy (Figure 1.2). Intracoronary or aortocoronary shunting can minimize ischemia after an arteriotomy is performed.
      
      
      
      1. Conversion to on‐pump surgery may be necessary in the following circumstances:
         
         
         
         1. Coronary arteries are very small, severely diseased, or intramyocardial.
            
         2. LV function is very poor, or there is severe cardiomegaly or hypertrophy that precludes adequate cardiac translocation without hemodynamic compromise or arrhythmias.
            
         3. The heart is extremely small and vertical in orientation.
            
         4. Uncontrollable ischemia or arrhythmias develop with vessel occlusion that persists despite distal shunting.
            
         5. Intractable bleeding occurs that cannot be controlled with vessel loops or an intracoronary shunt.
         
         
      2. OPCABs reduce transfusion requirements and the incidence of AF, but whether there is a reduction in the risk of stroke and renal dysfunction remains controversial.⁷⁶ OPCABs generally result in fewer grafts being placed, resulting in more incomplete revascularization and more repeat revascularization. Numerous long‐term follow‐up studies have shown inferior survival to on‐pump surgery.^77–79 Enthusiasm for this technique is modest, and it is estimated that less than 20% of CABGs are performed off‐pump. One randomized trial did show better outcomes with OPCABs when performed for a STEMI within six hours from the onset of symptoms or for patients in cardiogenic shock,⁸⁰ but most surgeons reserve its use for patients with limited disease. Its major advantage may be in the very high‐risk patient with multiple comorbidities in whom it is critical to avoid CPB.
         
      3. In some patients with severe ventricular dysfunction, the heart will not tolerate the manipulation required during off‐pump surgery. In this circumstance, right ventricular (RV) assist devices can be used to improve hemodynamics. Alternatively, surgery can be done on‐pump on an empty beating heart to avoid the period of cardioplegic arrest. This technique may be beneficial in patients with ascending aortic disease that prevents safe aortic cross‐clamping, but does allow for safe cannulation and use of an aortic punch, such as the Heartstring proximal seal system (MAQUET Cardiovascular), to perform the proximal anastomoses.
      
      
   3. Minimally invasive direct coronary artery bypass (MIDCAB) involves bypassing the LAD with the LITA without use of CPB via a short left anterior thoracotomy incision. Bilateral ITAs can be harvested under direct vision and an additional incision is made in the right chest to bypass the right coronary artery.^81,82 Combining a LITA to the LAD with stenting of other vessels (“hybrid” procedure) has also been described. A meta‐analysis of the MIDCAB procedure found a lower risk of repeat revascularization compared with PCI of the LAD.⁸³
      
   4. Robotic or totally endoscopic coronary artery bypass (TECAB) can be used to minimize the extent of the surgical incisions and reduce trauma to the patient. Robotics can be used for both ITA takedown and grafting to selected vessels through small ports.⁸⁴ These procedures can be done without CPB or using CPB with femoral cannulation. Generally, TECAB is used for limited grafting, but wider applicability is certainly feasible. Anesthetic concerns during this procedure are discussed in Chapter 4, pages 265–266.
      
   5. Transmyocardial revascularization (TMR) is a technique in which laser channels are drilled in the heart with CO₂ or holmium‐YAG lasers to improve myocardial perfusion. Although the channels occlude within a few days, the inflammatory reaction created induces neoangiogenesis that may be associated with upregulation of various growth factors, such as vascular endothelial growth factor. This procedure is most commonly used as adjunct to CABG in viable regions of the heart where bypass grafts cannot be placed.^85,86 It can also be used as a sole procedure performed through a left thoracotomy or thoracoscopically for patients with inoperable CAD in regions of viable myocardium.⁸⁷ TMR has a level IIb indication to improve symptoms and may be reasonable to consider in patients with viable ischemic myocardium in areas that cannot be grafted.⁵

II. Left Ventricular Aneurysm

1. Pathophysiology. Occlusion of a major coronary artery may produce extensive transmural necrosis, which converts muscle into thin scar tissue. This results in formation of a left ventricular aneurysm (LVA) which exhibits dyskinesia during ventricular systole. Most LVAs occur in the anteroapical region due to occlusion of the LAD without collateralization, and are more likely to form in the absence of a patent infarct‐related vessel. In contrast, early reperfusion of an occluded vessel by PCI or thrombolytic therapy may limit the extent of myocardial damage with preservation of epicardial viability, resulting in an area of akinesia. This will result in an ischemic cardiomyopathy with a dilated ventricle that remodels with altered spherical geometry but does not produce an aneurysm.
   
2. Presentation. The most common presentation of an LVA associated with an ischemic cardiomyopathy is heart failure (HF) due to systolic dysfunction. With LVAs, there is a reduction of forward stroke volume caused by geometric remodeling of the aneurysmal segment due to loss of contractile tissue and an increase in ventricular dimensions. This results in an increase in wall stiffness and an increase in the LV end‐diastolic pressures. Angina may also occur due to the increased systolic wall stress of a dilated ventricle and the presence of multivessel CAD. Systemic thromboembolism may result from thrombus formation within the dyskinetic or akinetic segment, with thrombus being noted in over 50% of cases. Malignant ventricular arrhythmias or sudden death may result from either enhanced automaticity or triggered activity related to myocardial ischemia and increased myocardial stretch, or to the development of a macroreentry circuit at the border zone between scar tissue and viable myocardium.
   
3. Indications for surgery. Surgery is usually not indicated for the patient with an asymptomatic aneurysm, because of its favorable natural history. This is in contrast to the unpredictable prognosis and absolute indication for surgery in a patient with a false aneurysm, which is caused by a contained rupture of the ventricular muscle. Surgery may be beneficial in the asymptomatic or mildly symptomatic patient with significant volume overload causing LV dilatation and reduced ventricular function prior to the development of advanced HF symptoms. It may also be considered where there is extensive clot formation present within the aneurysm. However, surgery is most commonly indicated to improve symptoms and prolong survival when one of the four clinical syndromes (angina, HF, embolization, or arrhythmias) is present. Arrhythmias may be treated by a nonguided endocardial resection through the aneurysm with/without cryosurgery along with subsequent placement of a transvenous implantable cardioverter‐defibrillator (ICD).
   
4. Preoperative considerations
   
   
   
   1. Echocardiography is best for assessing ventricular size and dimensions, wall motion of the noninfarcted segments, the presence of thrombus, and mitral valve function, which is often abnormal with dilated cardiomyopathies. Biplane left ventriculography is helpful in identifying regions of akinesia and dyskinesia and assessing the function of noninfarcted segments. Cardiac CT angiography or cardiovascular magnetic resonance imaging (CT‐MRI) are also helpful in making the diagnosis, and the latter can also be used to assess myocardial viability.⁸⁸
      
   2. Patients with LVAs with LV dysfunction are usually managed with an ACE inhibitor and ß‐blocker. Anticoagulation may also be given during the early postinfarction period, but may not be necessary in chronic aneurysms with thrombus due to the low risk of embolism.⁸⁹ If the patient remains on warfarin, bridging to surgery with heparin can be recommended.
   
   
5. Surgical procedures
   
   
   
   1. Standard aneurysmectomy (“linear repair“) entails a ventriculotomy through the aneurysm, resection of the aneurysm wall, including part of the septum if involved, and linear closure over felt strips (Figure 1.3).^90,91
      
   2. Endoventricular reconstruction techniques are applicable to large aneurysms or akinetic segments with the intent of reducing ventricular volume and restoring an elliptical shape.
      
      
      
      1. The “endoaneurysmorrhaphy” technique is used for large aneurysms. A pericardial or Dacron patch is sewn to the edges of viable myocardium at the base of the aneurysm and the aneurysm wall is reapproximated over the patch (Figure 1.4). This preserves LV geometry and improves ventricular function to a greater degree than the linear closure method.
         
      2. A slightly more elaborate endoventricular reconstruction involves the endoventricular circular patch plasty technique of Dor, which is termed “surgical ventricular restoration” (SVR). This can be applied to LVAs as well as cases of ischemic cardiomyopathy with anterior akinesis (Figure 1.4D).^92,93 The procedure involves placement of an encircling suture at the junction of the contracting and noncontracting segments, and then exclusion of the noncontracting segment with a patch. This produces an elliptical contour of the heart and results in significant improvement in ventricular size and function. This procedure is generally done on a beating heart to allow for better differentiation of akinetic and normal segments of the heart.
         
      3. Although SVR is associated with a reduction in LV volume, clinical improvement is not uniform. Several studies have suggested that the addition of SVR to a CABG improves clinical status and long‐term survival.^94–96 However, the STICH trial of patients with CAD‐related anterior akinesia or dyskinesia with an EF <35% was unable to demonstrate that reduction in LV size was associated with an improvement in symptoms or a reduction in mortality after four years.⁹⁷
      
      
   3. For patients with recurrent ventricular tachycardia, an endocardial resection with or without endocardial mapping may be performed with good results.^98,99
      
   4. Coronary bypass grafting of critically diseased vessels should be performed. Bypass of the LAD and diagonal arteries should be considered if septal reperfusion can be accomplished.
      
   5. A mitral valve procedure is also indicated if the severity of MR is 2+ or greater. MR is usually related to apical tethering of the leaflets due to ventricular dilatation or may result from annular dilatation. Mitral valve repair with a complete annuloplasty ring may be successful when performed with ventricular restoration.

III. Ventricular Septal Rupture

1. Pathophysiology. Extensive myocardial damage subsequent to occlusion of a major coronary vessel may result in septal necrosis and rupture. This usually occurs within the first week of an infarction, more commonly in the anteroapical region (from occlusion of the LAD artery), and less commonly in the inferior wall (usually from occlusion of the right coronary artery). It is noted in less than 1% of acute MIs, and the incidence has declined because of early reperfusion therapy for STEMIs. The presence of a ventricular septal defect (VSD) is suggested by the presence of a loud holosystolic murmur that reflects the left‐to‐right shunting across the ruptured septum. The patient usually develops acute pulmonary edema and cardiogenic shock from the left‐to‐right shunt.¹⁰⁰
   
2. Indications for surgery. Surgery is indicated on an emergency basis for nearly all postinfarction VSDs to prevent the development of progressive multisystem organ failure. A report from the STS database in 2012 noted an operative mortality rate of 54% if surgery was performed within seven days of an infarction, usually because the patient was hemodynamically unstable and often in cardiogenic shock. For surgery performed after seven days, the mortality rate decreased to 18.4%, most likely because these patients were more hemodynamically stable, had smaller VSDs and <2:1 shunts, and were naturally selected to have survived long enough to survive subsequent lower‐risk surgery.¹⁰¹ Risk factors for operative mortality included preoperative dialysis, older age, female gender, cardiogenic shock, use of an IABP, moderate–severe MR, redo operation, and emergency status.¹⁰²
   
3. Preoperative considerations
   
   
   
   1. Prompt diagnosis can be made using a Swan‐Ganz catheter, which detects a step‐up of oxygen saturation in the RV. Two‐dimensional (2D) echocardiography can confirm the diagnosis of a VSD and differentiate it from acute MR, which can produce a similar clinical scenario.
      
   2. Inotropic support and reduction of afterload, usually with an IABP, are indicated in virtually all patients with VSDs in anticipation of emergent cardiac catheterization and surgery.
      
   3. Cardiac catheterization with coronary angiography should be performed to confirm the severity of the shunt and to identify associated CAD.
   
   
4. Surgical procedures
   
   
   
   1. The traditional surgical treatment for postinfarct VSDs had been the performance of a ventriculotomy through the infarcted zone, resection of the area of septal necrosis, and Teflon felt or pericardial patching of the septum and free wall. This technique required transmural suturing and was prone to recurrence.
      
   2. The preferred approach is to perform circumferential pericardial patching around the border of the infarcted ventricular muscle. This technique excludes the infarcted septum to eliminate the shunt and reduces recurrence rates, because suturing is performed to viable myocardium away from the area of necrosis (Figure 1.5).¹⁰³
      
   3. Coronary bypass grafting of critically diseased vessels should be performed. Early studies suggested this improved short‐ and long‐term survival after surgery, but more recent data from the STS database did not corroborate this.^101,104
      
   4. Consideration may be given to percutaneous VSD closure with the Amplatzer VSD closure device in patients with smaller VSDs or prohibitive surgical risks.¹⁰⁵ Use of MCS may also be considered in patients in cardiogenic shock to improve hemodynamics and organ system function, allowing for a lower‐risk nonemergency procedure at a future date.

IV. Aortic Stenosis

1. Pathophysiology. Aortic stenosis (AS) results from thickening, calcification, and/or fusion of the aortic valve leaflets, which produce an obstruction to LV outflow.^106,107 In younger patients, AS usually develops on congenitally bicuspid valves, whereas in older patients, degenerative change in trileaflet valves is more common. Aortic sclerosis is a very common finding in elderly patients, and may be a manifestation of atherosclerosis, but usually does not progress to AS. Progression of AS may be related to endothelial cell activation and atherogenesis, as it is associated with the presence of cardiac risk factors, including hypertension, hyperlipidemia, and diabetes, but it has not been shown that statins or other medical therapy will slow the progression of degenerative AS.^108,109
   
   
   
   1. The impairment to cusp opening leads to pressure overload, compensatory left ventricular hypertrophy (LVH), and reduced ventricular compliance. The development of LVH maintains normal wall stress and a normal EF.
      
   2. If the increase in wall thickness does not increase in proportion to the rise in intraventricular pressure, wall stress will increase and EF will fall. It is important to assess whether a reduced EF in patients with severe AS is the result of excessive afterload (i.e. inadequate hypertrophy to overcome the obstruction) or depressed contractility. If the latter is present, surgical risk is higher.
      
   3. In patients with excessive and inappropriate degrees of LVH, wall stress is low and the heart will become hyperdynamic with a very high EF. This finding portends a worse prognosis after surgical correction.¹¹⁰
   
   
2. Symptoms. The classic symptoms associated with AS are angina, shortness of breath, and syncope. However, fatigue with limited activity appears to be one of the first symptoms described by most patients.
   
   
   
   1. Angina may result from the increased myocardial oxygen demand caused by increased wall stress, from reduction in blood supply per gram of hypertrophied tissue, and/or from limited coronary vasodilator reserve. Hypertrophied hearts are more sensitive to ischemic injury, and exercise may induce subendocardial ischemia, inducing systolic or diastolic dysfunction. Thus, angina may occur with or without concomitant epicardial CAD.
      
   2. Congestive HF results from elevation of filling pressures (LV end‐diastolic pressure) with diastolic dysfunction and eventually by progressive decline in LV systolic function. This results in progressively worsening dyspnea on exertion.
      
   3. Cardiac output is relatively fixed across the valve orifice and can lead to faintness, dizziness, or frank syncope in the face of peripheral vasodilation.
      
   4. Palpitations may occur with the occurrence of AF, which, if persistent, leads to clinical deterioration, because the hypertrophied ventricle relies on atrial contraction to maintain a satisfactory stroke volume.
   
   
3. Diagnosis. Most patients do not become symptomatic until the degree of AS becomes severe (Table 1.1). The severity of AS is preferentially assessed by Doppler echocardiography, with evaluation by cardiac catheterization only indicated in equivocal cases. Performing a left heart catheterization and crossing the valve to measure gradients in a patient with known severe AS is considered a contraindication by the ACC guidelines (Level III indication) because of the increased risk of embolic stroke.¹¹¹ Coronary angiography is indicated before surgery to identify whether CAD is present.
   
   
   
   1. Doppler echocardiography assesses the severity of AS by measuring the maximum instantaneous jet velocity and the mean transvalvular gradient, and allows for calculation of the aortic valve area (AVA) using the continuity equation (Tables 1.2 and 1.3, Figure 1.6). Because this calculation also includes the cross‐sectional area of the left ventricular outflow tract (LVOT), it may indicate a very small valve area in a very small patient when severe stenosis may not be present. Using the ratio of the velocity time integral (VTI) of the LVOT to the aorta to eliminate the LVOT measurement provides a “dimensionless index”. Echo imaging in the short‐axis view can also measure the valve area directly by planimetry and can give an appreciation of the degree of calcification and cusp separation during systole.

2. Since the pressure gradient is related to both the orifice area and the transvalvular flow, low gradients may be noted with low stroke volumes despite an AVA of <1 cm². This issue of AVA‐gradient discordance might create confusion as to which patients actually have severe AS and would benefit from an intervention versus those who might not.^112–114 Therefore, a critical measurement during echocardiography is calculation of the stroke volume index (SVI). A low‐flow state (SVI <35 mL/m²) can be seen in patients with reduced or preserved EF. This concept has led to a classification system incorporating SVI and EF.¹¹⁵
   
   
   
   1. Normal‐flow, high gradient (NF/HG), which fits the classic definition of severe AS (i.e. AVA <1 cm², peak velocity (Vmax) >4 m/s, or a mean gradient >40 mm Hg).
      
   2. Normal‐flow, low gradient (NF/LG), which in most cases is not severe AS. However, some studies have shown that NF/LG patients with an indexed AVA <0.6 cm²/m² have improved survival with aortic valve replacement (AVR).^113,114
      
   3. Low‐flow, high gradient (LF/HG), which by virtue of gradient and AVA would be severe AS.
      
   4. Low‐flow, low‐gradient (LF/LG), which can be seen with a normal EF, termed “paradoxical LF/LG” AS (stage D3 if symptomatic) or with a reduced EF (stage D2 if symptomatic). In the LF/LG patient, survival without surgery appears to be worse than in the other groups, and survival is markedly improved by AVR.¹¹⁶
   
   
3. Dobutamine stress echocardiography (DSE) is an important test in patients with LF/LG as well as NF/LG AS to corroborate the severity of AS. In patients with normal LV function, it has limited value except to indicate that the patient might have pseudo‐severe AS. However, in patients with impaired LV function, it can be used to determine contractile reserve and assess whether the patient has true or pseudo‐severe AS. The latter is present if dobutamine increases cardiac output without a concomitant increase in gradient, so the AVA increases to >1 cm². About one‐third of patients with LF/LG, both with normal and reduced EF, are felt to have pseudo‐severe AS.¹¹³
   
4. Quantification of aortic valve calcium has been recommended as a means of identifying severe AS in patients with LF/LG and NF/LG and has correlated with clinical outcomes.^117–119
   
5. Assessment of the degree of AS is generally not indicated at the time of catheterization, except in equivocal cases. The AVA is calculated by most cath lab software programs and is derived from a measurement of transvalvular flow (essentially the cardiac output or stroke volume) and the peak and mean pressure gradients across the valve calculated from pressures obtained on a catheter pull‐back from the LV into the aorta (Figure 2.4, page 136). The AVA may be manually calculated using the Gorlin formula:
   
   
   
   

   where:

   
   
   
   
   
   
   

   Alternatively, the simplified Hakki formula calculates the AVA as follows:

   
   
   
   
   
6. If the above tests confirm the presence of severe AS, yet the patient is asymptomatic, exercise testing may be used to assess whether AVR may be indicated.^120,121 A meta‐analysis reported that adverse cardiac events were three times more likely to occur in patients with an abnormal stress test, which was defined as the development of symptoms, a decrease in blood pressure or an increase in systolic pressure of <20%, <80% of normal exercise tolerance, ≥2 mm ST depression during exercise, or the development of complex ventricular arrhythmias. Thus, these findings were incorporated into the 2014 indications for AVR, such that a positive stress test was a level I indication for AVR.
   
7. Virtually all of the indications for AVR in the guidelines are for patients with severe AS, whether symptomatic or not. However, some patients with moderate AS and LV systolic dysfunction are symptomatic and at risk for adverse clinical events. It is not clear if earlier AVR may be beneficial to these patients.¹²²

4. Natural history
   
   
   
   1. It is estimated that approximately 40% of patients with asymptomatic severe AS will become symptomatic within two years and about 67% will be symptomatic by five years.^123,124 The rate of progression of AS is variable, and serial echocardiograms should be performed to assess for the rate of hemodynamic progression, which is predictive of clinical outcome. Patients with high jet velocities, LV hypertrophy, or severe valve calcification have a faster rate of progression of valve stenosis and a shorter symptom‐free interval.
      
   2. The presence of LV systolic dysfunction is an uncommon but ominous prognostic sign, as the long‐term outlook is dismal. Although survival is generally improved by AVR for patients with LV dysfunction caused by afterload mismatch, a study from the Mayo Clinic reported a nearly 50% five‐year mortality for asymptomatic patients with severe AS with an EF <50% with no survival benefit noted for AVR.¹²⁵ Another study of patients with moderate AS yet LV dysfunction found that most patients were symptomatic and were at high risk for clinical events.¹²²
      
   3. BNP (brain natriuretic peptide) levels in asymptomatic patients correlate with adverse events, including aortic valve‐related deaths and HF admissions, so BNP or pro‐BNP levels can serve as markers supporting early AVR.¹²⁶
      
   4. Once symptoms of AS are present, the prognosis for untreated AS is very poor with an average survival of one to two years and a less than 20% chance of surviving five years.¹²⁷ These data have been confirmed in the era of transcatheter aortic valve replacement (TAVR), with the PARTNER B cohort of “inoperable” patients having a 50% one‐year mortality without AVR.¹²⁸ Patients with symptoms of heart failure (HF) have the worst survival, averaging only one year, whereas average survival is two years for patients with syncope and four years for patients with angina.
      
   5. AVR has unequivocally been shown to improve survival, and in elderly patients has been found to restore a normal life expectancy. However, in younger patients (age <50), one study found a substantial loss in life expectancy.¹²⁹ It can be theorized that intervention prior to the development of myocardial fibrosis might improve long‐term results, thus justifying early intervention in asymptomatic patients with severe aortic stenosis.¹³⁰
   
   
5. Indications for AVR per 2014 ACC 2014 Guidelines¹³¹
   
   
   
   1. Class I indications (“AVR is recommended”)
      
      
      
      • Stage D1 – symptomatic patients with a peak velocity ≥4 m/s or a mean gradient >40 mm Hg; this also includes patients who may be asymptomatic at rest but have symptoms during an exercise tolerance test (ETT).
        
      • Stage C2 – patients who are asymptomatic but have high gradients and depressed LV function (EF <50%). As noted above, the Mayo Clinic study showed that these patients have a poor prognosis even with AVR.¹²²
        
      • Severe AS (any stage C or D) in a patient undergoing other cardiac surgery with a peak velocity ≥4 m/s or a mean gradient ≥40 mm Hg.
        
      • Stage D2 – symptomatic patients with an AVA <1 cm2 but a mean gradient <40 mm Hg with reduced EF. Since the gradient is conditional upon transvalvular flow, these patients are considered to have “low flow, low gradient” severe AS. A DSE should be performed to determine whether poor ventricular function with a low stroke volume is primarily related to afterload mismatch from true severe AS or is due to contractile dysfunction.
        
        
        
        1. If dobutamine produces an increase in stroke volume (or cardiac output) with little increase in gradient, the valve area may increase to >1 cm², suggesting this may be pseudo‐severe AS. However, if both the gradient and cardiac output increase in tandem, the AVA will remain <1 cm², confirming severe AS. Patients in this category achieve a significant benefit from AVR.¹³²
           
        2. Confirmation of stage D2 generally requires an increase in the peak velocity to >4 m/s or a mean gradient to >40 mm Hg with dobutamine. However, the validity of the DSE may be limited if dobutamine fails to increase the stroke volume more than 20%. These patients have poor contractile reserve, suggesting that afterload mismatch is not the problem and inferentially that AVR may not improve LV function. However, studies have shown that both surgical aortic valve replacement (SAVR) and TAVR improve LV function independent of contractile reserve and improve long‐term survival.^133,134 Interestingly, an elevated BNP level (>550) has been shown to be a very strong predictor of operative mortality, even more important than lack of contractile reserve documented by DSE.¹³⁵ Some studies have suggested that DSE has limited value in predicting the severity of AS and outcomes of AVR.¹³⁶ Use of the projected AVA (which estimates the AVA at a standardized normal flow rate) can better distinguish pseudo‐severe from severe AS and correlates better with observed mortality in patients managed conservatively.^137,138
        
        
      • Stage D3 – symptomatic patients with an AVA <1 cm² (indexed AVA ≤0.6 cm²/m²), a low gradient, normotension, but a normal EF. In addition, a calcified valve with significantly reduced leaflet motion should be present. These patients are considered to have “paradoxical low flow/low gradient” severe AS if the SVI is <35 mL/m².¹³⁸ Reduced transvalvular flow may produce lower gradients despite the presence of a severely stenotic valve. This may be noted in patients with AF, concomitant MR, and impaired diastolic filling, and may be exacerbated in hypertensive patients with reduced arterial compliance or increased vascular resistance.¹¹² The prognosis is poor with medical therapy, and both SAVR and TAVR have been shown to improve survival in these patients.^114,139,140 Nonetheless, one study found that the survival of LF/LG patients with normal EF was fairly similar to that of patients with mild–moderate AS and was not influenced by performing an AVR.¹⁴³
        
      • When the indication for AVR is met, the ascending aorta should be resected if ≥4.5 cm, whether with bicuspid or trileaflet valves.
      
      
   2. Class IIa indications (“AVR is reasonable”)
      
      
      
      • Stage C1 – asymptomatic low-risk patients in whom exercise testing shows decreased exercise tolerance or a fall in systolic BP ≥10 mm Hg.
        
      • Stage C1 – asymptomatic patients with very severe AS with a peak velocity ≥5 m/s. Nearly 50% of these patients will become symptomatic within 2 years and AVR has been shown to produce a significant survival benefit.¹⁴²
        
      • Stage C1 – asymptomatic patients with a BNP level > 3 times normal.
        
      • Stage C1 – asymptomatic, high gradient patients in whom serial testing shows an increase in aortic velocity >0.3 m/s/yr.
      
      
   3. Class IIb indications (“AVR is reasonable”)
      
      
      
      • Stage C1 – asymptomatic patients with severe high-gradient AS with a progressive decrease in LVEF on 3 serial imaging studies to <60%.
        
      • Stage B – asymptomatic patients with moderate AS undergoing other cardiac surgery. Most surgeons would consider performing an AVR with a cutoff around an AVA < 1.4 cm² to avoid another operation in the next few years. However, with the applicability of TAVR, the surgeon may consider not replacing the valve with an AVA >1.2 cm² with a mean gradient in the teens.
   
   
6. Indications for AVR per 2017 appropriate use criteria.¹⁴¹ A 2017 publication from multiple societies reviewed the 2014 criteria noted above as well as the 2017 focused update and assessed the appropriateness of AVR for severe AS (AVA <1 cm²) in 95 different clinical scenarios, coding them as “appropriate”, “may be appropriate”, or “rarely appropriate”. Assessments were made for patients corresponding to stages C1–2 and D1–3, those with comorbidities or frailty that might alter the procedural approach, and for patients requiring additional surgery (ascending aorta, valve, CABG) or undergoing reoperations. For certain categories, recommendations for surgical AVR (SAVR) or TAVR were made. Some differences from the 2014 criteria noted above include the following:
   
   
   
   1. AVR “may be appropriate” for asymptomatic patients with high gradient AS (Vmax 4–4.9 m/s), a negative stress test, and no predictors of symptom onset or rapid progression, such as Vmax >0.3 m/s/yr, severe valve calcification, elevated BNP, or excessive LVH in the absence of hypertension. These stage C1 patients would not be candidates for AVR per the 2014 criteria unless the peak velocity was >5 m/s. However, AVR would be appropriate for these patients in the 2014 and AUC guidelines if the stress test were positive or these predictors were present.
      
   2. AVR “may be appropriate” for asymptomatic patients with LF/LG severe AS with normal EF with a heavily calcified valve. As these patients would be stage C, not stage D3, AVR per the 2014 criteria would only be indicated if these patients were symptomatic and had an SVI <35 mL/m².
      
   3. AVR is “appropriate” for symptomatic patients with preserved EF, NF/LG and an AVA <1 cm² if they have a heavily calcified valve, the latter being referred to as “a calcified valve with significantly reduced leaflet motion” in the 2014 guidelines. However these guidelines also required a low SVI to qualify for an AVR.
      
   4. AVR was “inappropriate” for patients with an EF of 20–49%, and LF/LG severe AS with no flow reserve on low‐dose DSE. Although not specifically addressed in the 2014 guidelines, the literature does suggest that, despite the increased risk, SAVR or preferably TAVR may provide a hemodynamic and clinical benefit to these patients.^133,134
      
   5. AVR was “inappropriate” for patients with an EF <20% with a mean gradient <20 at rest and no flow reserve. The issue for these patients is whether there might be any clinical improvement after AVR despite lack of contractile reserve if the valve appeared severely stenotic on echo. Surgery would probably be contraindicated due to the high risk, but high risk “salvage” TAVR might be considered if the patient were severely symptomatic, had normal mental status, no other major comorbidities, and understood that the procedure might not provide any benefit.
   
   
7. Selection of procedure: TAVR vs. SAVR
   
   
   
   1. The clinical trials of TAVR vs. medical therapy and TAVR vs. SAVR have confirmed excellent clinical outcomes for patients with progressively lower STS risk profiles, such that in 2019, TAVR was approved in the United States for use in low‐risk patients.¹⁴⁴ Comparable results have been noted with the balloon‐expandable valves (primarily the Edwards SAPIEN series) and self‐expanding valves (primarily the Medtronic CoreValve/Evolut series). Consequently, calculation of the predicted operative risk using the STS risk model, which has been updated to reflect more comorbidities including frailty, has become less important in the selection of the appropriate procedure.
      
   2. Not only have the hemodynamics of TAVR valves proven to be superior to surgically implanted valves with lower transvalvular gradients,¹⁴⁵ but the risk of mortality and morbidity with transfemoral TAVR procedures has been equivalent to if not better than SAVR. The risk of stroke is approximately 2% with the latest generation TAVR valves, and the need for a permanent pacemaker has gradually been declining, now estimated at around 5%, comparable to or perhaps slightly greater than SAVR. Patient recovery is expedited by the less‐invasive nature of the procedure, and improvement in the quality of life is better as well. Remaining issues are those of long‐term durability of the transcatheter valves if they are to be used in younger patients,¹⁴⁶ successful implantation within bicuspid valves, and use in patients with pure aortic regurgitation, which most likely will be feasible with newer valve designs.
      
   3. AUC for TAVR continue to evolve, so any published recommendation is outdated. The STS‐TVT registry tracks implantation data, and TAVR volumes have exceeded SAVRs for several years, and will only increase with the inclusion of more low‐risk patients. TAVRs are indicated for the same reasons as SAVRs, but are preferable when the risk is high and the benefit is uncertain.
   
   
8. Preoperative considerations
   
   
   
   1. Prior to SAVR or TAVR, coronary angiography should be performed in any patient over the age of 40 or in a younger patient with coronary risk factors, angina, or a positive stress test. TAVR can generally be performed in patients without an extensive ischemic burden, but preliminary or simultaneous PCI can be considered if TAVR is selected over SAVR + CABG.
      
   2. Ischemic syndromes in patients with AS require judicious management. Medications that must be used very cautiously are those that can reduce preload (nitroglycerin), afterload (calcium channel blockers), or heart rate (β‐blockers), because they may lower cardiac output and precipitate cardiac arrest in a patient with critical AS. The ventricular response to AF must be controlled.
      
   3. Some patients with AS have a history of gastrointestinal bleeding ascribed to colonic angiodysplasia (Heyde’s syndrome). This has been associated with acquired type 2A von Willebrand syndrome.^147,148 This develops due to proteolysis of the largest multimers of von Willebrand factor by shear stress on the blood as it passes through the stenotic valve. Understandably, this is also noted with dysfunctional prosthetic valves.¹⁴⁹ These multimers are important for platelet‐mediated hemostasis, so when reduced, they can cause bleeding. Use of preoperative desmopressin (0.3 μg/kg) given after the induction of anesthesia in patients with abnormal platelet function associated with this syndrome has been shown to significantly reduce perioperative blood loss.¹⁵⁰ AVR generally will resolve this hemostatic problem.
      
   4. Dental work should be performed before surgery to minimize the risk of prosthetic valve endocarditis (PVE), unless it is felt to be a prohibitive risk. A study from the Mayo Clinic reported a 3% risk of death within 30 days after dental extraction in patients awaiting surgery.¹⁵¹
      
   5. Selection of the appropriate procedure and valve type for surgical AVR depends on a number of factors, including the patient’s age, contraindications to long‐term anticoagulation, and the patient’s desire to avoid anticoagulation. All mechanical valves require lifelong warfarin, as the NOACs do not appear to suffice. Structural valve deterioration of tissue valves is inversely related to patient age and is worse in the presence of renal failure (Figure 1.7). Improvements in valve preservation techniques may improve valve longevity, supporting the use of tissue valves in younger patients. When either severe bioprosthetic stenosis or regurgitation occurs, it may be treated by reoperation or a valve‐in‐valve TAVR. The latter can often provide superior hemodynamics to even the original valve replacement because many tissue valve frames can be fractured allowing for better expansion of the transcatheter valve within the valve orifice.¹⁵²
      
   6. Selection of valve product for TAVRs is a matter of preference and experience, with potentially lower gradients in the small aortic root with the Medtronic CoreValve Evolut valves, which are constructed of porcine pericardium within a nitinol frame and lie more supra‐annular than the Edwards valves.
   
   
9. Surgical procedures
   
   
   
   1. Aortic valve procedures may be performed through a full median sternotomy incision or through a minimally invasive incision. These include an upper or lower sternotomy with a “J” or “T” incision into the third or fourth intercostal space, or an anterior right second or third interspace incision.^153–155 Cannulation for CPB for minimally invasive approaches can be performed either through the incision or using the femoral vessels. If the latter is planned, a preliminary abdominal‐pelvic CT scan should be performed to assess for iliofemoral artery size, tortuosity, and calcification.
      
   2. SAVR with either a tissue or mechanical valve has been the standard treatment for AS (Figure 1.8), but has been superseded by the use of transcatheter valves in most patients.
      
      
      
      1. Mechanical valves of bileaflet tilting disk design have virtually completely replaced single‐leaflet tilting disk valves. They require lifelong anticoagulation with warfarin. Valve longevity is contingent on the development of complications such as thrombus formation or pannus ingrowth that impairs leaflet function, or the development of endocarditis.
         
      2. Tissue valves include porcine and bovine pericardial valves, all of which have various heat or chemical treatments to improve longevity. Rapid deployment valves are often considered to reduce cross‐clamp times during complex operations or in older patients. These include the Sorin Perceval valve and the Edwards Intuity valves. They have similar valve leaflets but are designed for implantation with few sutures to expedite implantation. The lower segment of the valve frame may predispose to bundle branch blocks and complete heart block, the latter being noted in about 10% of patients.^156,157
         
      3. A stentless valve may be selected to provide a larger effective orifice area and may be placed in the subcoronary position or as a root replacement. Its primary benefit may be noted in the small aortic root (Figure 1.9).^158,159
         
      4. The Ross procedure, in which the patient’s own pulmonary valve is used to replace the aortic root, with the pulmonary valve being replaced with a homograft (basically a double‐valve operation for single‐valve disease), is an even more complicated procedure generally reserved for patients younger than age 50 who wish to avoid anticoagulation (Figure 1.10).^160,161
         
      5. Homografts are usually reserved for patients with aortic valve endocarditis, although other types of prostheses arguably provide comparable results.^162,163
         
      6. An aortic root replacement, usually as a valved conduit, is indicated when the ascending aorta must also be replaced (Figure 1.11). If the sinuses of Valsalva are not dilated, replacing the aortic valve and using a supracoronary graft simplifies the procedure. In younger patients, a commercially available mechanical valved conduit is selected. In older patients, a “bioroot” may be used to avoid anticoagulation. This is constructed by sewing a tissue valve into the proximal end of the Dacron graft.¹⁶⁴
      
      
   3. Transcatheter aortic valve replacement (TAVR) involves the endovascular placement of a tissue valve mounted on a catheter delivery system. Although numerous valves have been designed and are being evaluated, the two most popular ones are the Edwards SAPIEN series, which is a balloon‐expandable bovine pericardial valve (Figure 1.12), and the Medtronic CoreValve/Evolut series, which has a porcine pericardial valve within a nitinol self‐expanding valve frame delivered within a sheath (Figure 1.13). Both of these systems can be used for stenotic native valves as well as stenotic or regurgitant bioprosthetic valves (“valve‐in‐valve” procedure).
      
      
      
      1. A CT scan is an essential component of the preoperative evaluation. The chest imaging will assess the aortic annular area and perimeter to determine the appropriate‐sized transcatheter heart valve. The distance from the annulus to the coronary ostia is measured to ensure that native valve displacement does not obstruct the coronary ostia. This is especially important in valve‐in‐valve procedures. A BASILICA (Bioprosthetic Aortic Scallop Intentional Laceration to prevent Iatrogenic Coronary Artery obstruction) may be necessary in these procedures to avoid coronary ostial obstruction in patients with low coronary ostia. The abdominal‐pelvic imaging assesses the size, tortuosity, and calcification of the iliofemoral vessels to determine whether a transfemoral approach is feasible (Figure 2.37, page 163).
         
      2. The procedural risk is lower with a transfemoral approach. If not feasible, subclavian imaging should be evaluated to assess for axillary/subclavian access which can be achieved via cutdown or percutaneously. Additional alternative access sites include transcaval, transaortic through a limited upper sternotomy, transcarotid, and transapical approaches.^163–165 The latter was initially the approach of second choice, but was fraught with more complications, especially in elderly patients.
         
      3. Transcatheter valves have less stent frame width than surgical valves and are designed for optimal opening of the leaflets. This produces superior hemodynamics to surgical valves, especially in the small aortic annulus. Clinical outcomes in patients at high, intermediate, and low surgical risk are equivalent, if not superior, to SAVR. The major risks are those of stroke, estimated at around 2%, which might be reduced by use of a cerebral protection device (SENTINEL cerebral protection systems [Boston Scientific Sentinel device]),^166–168 and the necessity for a permanent pacemaker for complete heart block. With less deployment in the LVOT, this risk has been substantially reduced to less than 5%. This risk is greater in patients with a pre‐existing right bundle branch block and a left anterior hemiblock.
      
      
   4. Reparative procedures, such as commissurotomy or debridement, have little role in the management of critical AS. However, debridement may be considered in the patient with moderate AS in whom the valve disease is not severe enough to warrant valve replacement, but in whom decalcification may delay surgery for a number of years.

V. Aortic Regurgitation

1. Pathophysiology. Aortic regurgitation (AR) results from abnormalities in the aortic valve leaflets (calcific degeneration, bicuspid valves, destruction from endocarditis) or from aortic root dilatation that prevents leaflet coaptation (idiopathic root dilatation causing annuloaortic ectasia, aortic dissection with cusp prolapse).¹⁰⁶
   
   
   
   1. Acute AR usually results from endocarditis or a type A dissection. The ventricle is unable to dilate acutely to handle the sudden increase in regurgitant volume, which increases the LV end‐diastolic volume (LVEDV) and pressure (LVEDP), resulting in acute LV failure, cardiogenic shock, and pulmonary edema. Dramatic elevations in filling pressures may occur if acute AR is superimposed on a hypertrophied ventricle. Acute myocardial ischemia may result from increased afterload (LV dilatation), compensatory tachycardia, and a reduction in perfusion pressure as the LVEDP approaches the aortic diastolic pressure. As a result, sudden death may occur.
      
   2. Chronic AR produces pressure and volume overload of the LV, resulting in progressive LV dilatation (increase in LVEDV) with an increase in wall stress, an increase in ventricular compliance, and progressive hypertrophy. Most patients remain asymptomatic for years, even with severe AR, because recruitment of preload reserve and compensatory hypertrophy maintain a normal EF despite the increased afterload. The increased stroke volume maintains forward output and is manifest by an increase in pulse pressure with bounding peripheral pulses. Eventually, increased afterload and impaired contractility lead to LV systolic dysfunction and a fall in EF. Usually at this point, the patient becomes symptomatic with dyspnea. Impairment of coronary flow reserve may cause angina (Table 1.4).
      
   3. Generally, patients with advanced HF symptoms (NYHA class III–IV) or systolic dysfunction with a decreased EF and/or increased LV end‐systolic dimension (LVESD) have a higher perioperative mortality rate and compromised long‐term survival. Normalization of a depressed EF may occur after surgery when afterload excess is the cause of LV systolic dysfunction and when LV dysfunction is not long‐standing. However, patients with prolonged LV dysfunction usually have depressed myocardial contractility and will have a suboptimal result from surgery with persistent LV dysfunction.

2. Diagnosis. Careful monitoring is essential to identify when patients become symptomatic, develop severe AR, and/or have evidence of incipient LV dysfunction. Echocardiography and aortic root aortography at the time of catheterization can delineate the degree of AR (Figure 2.8, page 138). Echo is valuable in assessing valve morphology, aortic root size, LV cavity dimensions, wall thickness, and systolic function. Color and pulsed wave Doppler findings can be used to assess the degree of AR (Table 1.5).

	Moderate	Severe
Doppler jet width	25–64% of LVOT	≥65% of LVOT
Vena contracta	0.3–0.6 cm	>0.6 cm
Diastolic flow reversal	no	yes
Regurgitant volume	0–59 mL/beat	≥60 mL/beat
Regurgitant fraction	30–49%	≥50%
ERO	0.1–0.29 cm2	≥0.3 cm2
LV dilatation	no	yes
Pressure half‐time	200–500 ms	<200 ms

ERO, effective regurgitant orifice

3. Indications for surgery (based on 2020 ACC guidelines)¹³¹
   
   
   
   1. Class I Indication (“Surgery is recommended”)
      
      
      
      1. Stage D – symptomatic severe AR, irrespective of LV systolic function. Once the heart becomes severely dilated, irreversible myocardial damage may already have occurred and the long‐term results of surgery are suboptimal. The estimated mortality rate is >10%/year for patients with angina and >20%/year for patients with CHF without surgery.¹⁰⁶ Some patients are symptomatic with moderate AR when there is a reduced EF, LV dilatation, and a markedly elevated LVEDP.
         
      2. Stage C2 – asymptomatic severe AR with LVEF ≤55% at rest unless there is another cause for the decreased LVEF. These patients are already in a decompensated phase and develop symptoms at a rate of 25%/year. Prompt surgical intervention is indicated because long‐term survival is compromised with a lower EF and LV dilatation (LVESD ≥40mm) due to more advanced remodeling.¹⁷¹ If the etiology of the decreased EF is unrelated to the AR (i.e. a prior infarction, infiltrative disease, dilated cardiomyopathy), LV function may not improve and surgery may not be indicated.
         
      3. AVR is indicated for severe AR if cardiac surgery is being performed for another indication.
      
      
   2. Class IIa indication (“Surgery is reasonable”)
      
      
      
      1. Asymptomatic severe AR with an EF >50 mm or indexed LVESD >25 mm/m². Evidence of LV dilatation also indicates a decompensated phase with a nearly 20% annual risk of developing systolic dysfunction once the LVESD exceeds 50 mm and a 25% risk once it exceeds 55 mm.
         
      2. AVR is reasonable with moderate AR if other cardiac surgery is being performed for another indication.
      
      
   3. Class IIb indication (“Surgery may be considered”)
      
      
      
      1. Stage C1 – Asymptomatic severe AR with normal EF (EF >55%), but with progressive severe LV dilatation (left ventricular end‐diastolic dimension [LVEDD] >65 mm) or progressive decline in EF to the low‐normal range (55-60%). These patients are at high risk for sudden death.
      
      
   4. Other comments
      
      
      
      1. Serial echocardiograms are important to identify early evidence of ventricular decompensation, since survival without surgery and the long‐term prognosis after surgery are influenced by the degree of LV systolic dysfunction. Asymptomatic patients in stage C1 with an LVESD of 40–49 mm have about a 4% annual risk of developing symptoms, LV dysfunction or death, yet about 25% of patients may develop LV dysfunction or die before they become symptomatic. Thus, surgery is indicated at the first sign of ventricular decompensation, which is generally when the LVEF falls below 55% or the LVESD exceeds 50 mm.
         
      2. The utility of stress testing in asymptomatic patients is not well defined. High‐risk findings include development of symptoms, exercise capacity <85% of predicted, absence of contractile reserve with borderline hemodynamic indications for surgery (LVEF 50–55% or LVESD approaching 50 mm), and tricuspid valve annular plane systolic excursion <21 mm (a sign of RV dysfunction). These findings may identify patients who are truly not asymptomatic and those with subclinical LV dysfunction who might benefit from earlier surgery. A fall in ejection fraction during stress testing has unclear prognostic significance. None of these considerations was included in the 2014 guidelines.
         
      3. Aortic valve endocarditis producing acute AR and hemodynamic compromise, or the presence of an annular abscess or conduction abnormalities are indications for urgent, if not emergent surgery (see section IX, pages 61–62). The presence of residual vegetations after an embolic event, large mobile vegetations, or persistent bacteremia are other indications for early surgery.
   
   
4. Preoperative considerations
   
   
   
   1. Systemic hypertension may be treated with ACE inhibitors, ARBs, amlodipine, β‐blockers, diuretics, and aldosterone receptor antagonists (spironolactone, eplerenone). Reducing the blood pressure may increase forward flow and reduce the degree of regurgitation, but excessive afterload reduction may reduce diastolic coronary perfusion pressure and exacerbate ischemia. β‐blockers for control of ischemia must be used cautiously because a slow heart rate increases the amount of regurgitation. They are contraindicated in acute AR because they will block the compensatory tachycardia. ACE inhibitors and ARBs are usually held the morning of surgery to prevent vasoplegia, although this remains controversial.
      
   2. Coronary angiography is indicated before surgery for virtually all patients to identify coronary dominance and potential stenoses that may need to be addressed.
      
   3. Placement of an IABP for control of anginal symptoms is contraindicated.
      
   4. As for all non‐emergent valve patients, dental work should be completed before surgery.
      
   5. Contraindications to warfarin should be identified so that the appropriate valve can be selected.
   
   
5. Surgical procedures
   
   
   
   1. AVR has traditionally been the procedure of choice for adults with AR. This may involve use of a tissue or mechanical valve, the Ross procedure, or a cryopreserved homograft. Studies are underway to determine the feasibility of TAVR for pure AR.¹⁷²
      
   2. Aortic valve repair, involving resection of portions of the valve leaflets and re‐approximation to improve leaflet coaptation (especially for bicuspid valves), often with a suture annuloplasty, has been performed successfully. This is valuable in the younger patient in whom any valve‐sparing procedure is preferable to valve replacement.¹⁷³
      
   3. A valved conduit (Bentall procedure) is placed if an ascending aortic aneurysm (“annuloaortic ectasia”) is also present (Figure 1.11). In younger patients, manufactured mechanical valved conduits are preferable, but if there is a strong indication for avoiding anticoagulation, a “bioroot” created by sewing a tissue valve into a graft can easily be accomplished.¹⁷⁴ Alternatively, a Medtronic Freestyle stentless valve can be placed with distal graft extension to replace an aortic aneurysm.¹⁷⁵
      
   4. Aortic valve‐sparing root replacement is feasible in some patients with significant AR if adequate remodeling of the root can be accomplished, and it can be used successfully even in patients with bicuspid valves or Marfan syndrome (Figure 1.14). The aorta is resected, sparing the commissural pillars. A graft is then sewn at the subannular level, the aortic valve is resuspended within the graft, and the aortic remnants are sewn to the graft. Coronary ostial buttons are then sewn to the graft.^176–178

VI. Mitral Stenosis

1. Pathophysiology.¹⁰⁶ Mitral stenosis (MS) occurs nearly exclusively as a consequence of rheumatic fever. Thickening of the valve leaflets with commissural fusion and thickening and shortening of the chordae tendineae gradually reduce the size of the mitral valve orifice and the efficiency of LV filling. The increase in the diastolic transmitral gradient increases the left atrial and pulmonary venous pressures. Initially, left atrial size and compliance increase, and symptoms may be brought on by exercise or rapid heart rates, such as with AF. As the MS becomes severe, the left atrium remodels, and symptoms of heart failure, including dyspnea, orthopnea, and hemoptysis, may occur. An adaptive measure that can minimize symptoms is a decrease in pulmonary microvascular permeability and the development of pulmonary arteriolar vasoconstriction and thickening, which leads to pulmonary hypertension (PH). This may then lead to right‐sided HF and functional tricuspid regurgitation (TR). As the severity of MS and PH worsen, the cardiac output is compromised at rest and fails to increase with exercise. The development of AF further increases LA pressures, decreases ventricular filling, and compromises cardiac output. It may predispose to left atrial thrombus formation and systemic thromboembolism (Table 1.6).
   
2. Natural history. MS is a slowly progressive process which may not produce symptoms for several decades. The minimally symptomatic patient has an 80% 10‐year survival, but once symptoms develop, survival is very poor with a 10‐year survival in some of the early natural history studies of only 33% and 0% for patients in NYHA classes III and IV, respectively.¹⁷⁹ Severe PH (pulmonary artery [PA] pressure >80 mm Hg) is associated with a mean survival of less than three years. Therefore, intervention should be considered when the patient develops class II–III symptoms.

3. Diagnosis. The severity of MS is determined primarily by echocardiography and can also be defined by cardiac catheterization (Table 1.7).
   
   
   
   1. Echocardiography measures the mean diastolic gradient and, by the continuity equation, determines the mitral valve area (MVA). Echo also measures the diastolic pressure half‐time, estimates the PA pressure from the tricuspid velocity jet, and can evaluate valve morphology using an echo score (Table 1.7).¹⁸⁰ This assesses leaflet mobility, thickening, calcification, and subvalvular thickening and can be used to determine whether the valve is amenable to balloon valvuloplasty.
      
   2. Cardiac catheterization allows for calculation of the MVA from the cardiac output and the transvalvular mean gradient (pulmonary capillary wedge pressure [PCWP] minus the LV mean diastolic pressure). The PA pressure is measured by right‐heart catheterization.

where:

MVA = mitral valve area in cm² (normal = 4−6 cm²)

DFP = diastolic filling period/beat

mean gradient = PCWP − LV mean diastolic pressure

3. Exercise stress echocardiography is helpful in assessing the physiologic severity of disease in patients whose symptoms appear inconsistent with the degree of MS.¹⁸¹ Exercise will increase the heart rate and decrease the diastolic filling time. In patients with significant MS, this will increase the mean gradient and/or pulmonary artery pressures. Hemodynamically significant MS, an indication for intervention, includes an exercise‐induced increase in the mean gradient to >15 mm Hg (>18 mm Hg if a dobutamine stress echo is performed), or an increase in the PCWP to >25 mm Hg. Another high‐risk finding is a rise in the RV systolic pressure to >60 mm Hg at peak exercise, although that is not included in the guidelines.

4. Indications for intervention¹⁰⁷,¹³¹
   
   
   
   1. Percutaneous mitral balloon commissurotomy (PMBC) is the procedure of choice for patients with an indication for intervention if valve morphology is favorable by echo score. This procedure generally results in a doubling of the valve area and a 50% reduction in the mean gradient, with excellent long‐term results. Mitral valve surgery is indicated when PMBC is contraindicated or not feasible due to unfavorable valve morphology, left atrial thrombus, or 3−4+ MR.^182,183
      
   2. Class I indications
      
      
      
      1. Stage D – PMBC is recommended for symptomatic patients with severe MS (MVA <1.5 cm²) and favorable anatomy with less than 2+ MR and no LA thrombus.
         
      2. Stage D – mitral valve surgery is indicated in NYHA class III–IV patients with severe MS (MVA <1.5 cm²) who are not candidates for PMBC, have failed a prior PMBC, or require other cardiac procedures.
         
      3. Stage C or D – concomitant mitral valve surgery is indicated for severe MS when cardiac surgery is performed for another indication.
      
      
   3. Class IIa indications
      
      
      
      1. Stage C – PMBC is reasonable for asymptomatic patients with very severe MS (MVA <1.5 cm²), favorable anatomy with less than 2+ MR, no LA thrombus, and a PA systolic pressure > 50 mm Hg).
      
      
   4. Class IIb indications
      
      
      
      1. Stage C – PMBC may be considered for asymptomatic patients with severe MS (MVA <1.5 cm²) and favorable anatomy with new onset of AF.
         
      2. Stage B/D – PMBC may be considered for symptomatic MS with a mitral valve >1.5 cm² if there is hemodynamically significant MS during exercise stress testing (PCWP > 25 mm Hg or mean mitral gradient > 15 mm Hg).
         
      3. Stage D – PMBC may be considered for NYHA class III–IV patients with severe MS with suboptimal anatomy for PMBC when surgery is considered too high risk.
         
      4. Mitral valve surgery with excision of the left atrial appendage may be considered for any patient in stage C or D who has had recurrent embolic events on adequate anticoagulation.
   
   
5. Preoperative considerations
   
   
   
   1. Hemodynamic performance is frequently compromised by a low cardiac output state, which can be worsened by the presence of AF. A rapid ventricular response will shorten the diastolic filling period, reduce LV preload, and elevate LA pressures. Thus, the ventricular response to AF is best controlled in the perioperative period by β‐blockers or calcium channel blockers. There is usually a delicate balance between fluid overload, which can precipitate pulmonary edema, and hypo-volemia from aggressive diuresis, which can compromise renal function when the cardiac output is marginal. Thus, preload must be adjusted judiciously to ensure adequate LV filling across the stenotic valve.
      
   2. Many patients with long‐standing MS are cachectic and at increased risk for developing respiratory failure. Aggressive preoperative diuresis and nutritional supplementation may reduce morbidity in the early postoperative period.
      
   3. Warfarin used for AF, left atrial thrombus, or a history of systemic embolism should be stopped four days before surgery. Since most patients with MS and AF are considered at high risk for embolization, outpatient LMWH may be prescribed as a bridge, but must be stopped 24 hours before surgery. Admission for unfractionated heparin the day before surgery may be considered once the international normalized ratio (INR) falls below the therapeutic range. The NOACs (dabigatran, apixaban, rivaroxaban) should not be used in patients with rheumatic MS.
   
   
6. Surgical procedures
   
   
   
   1. Closed mitral commissurotomy has been supplanted by PMBC, which produces superior results. Either should be considered in the pregnant patient with critical MS in whom CPB should be avoided.
      
   2. Open mitral commissurotomy is performed if PMBC is not considered feasible or there is evidence of left atrial thrombus. It produces better hemodynamics than either a PMBC or a closed commissurotomy and is associated with improved long‐term event‐free survival, especially in patients with high echo scores or AF.^182–185 Although recurrent symptoms are noted in 60% of patients after nine years, most symptoms are related to the development of MR or CAD, and not to recurrent MS.¹⁰⁶
      
   3. Mitral valve replacement (MVR) is indicated if the valve leaflets are calcified and fibrotic or there is significant subvalvular fusion (Figure 1.15).
      
   4. Transcatheter treatment of MS is in its infancy. Transcatheter “valve‐in‐valve” procedures using aortic transcatheter heart valves have been used to treat bioprosthetic MS or regurgitation.^186,187 If imaging suggests that leaflet displacement may produce LVOT obstruction, a LAMPOON procedure (Laceration of the Anterior Mitral leaflet to Prevent lvOt ObstructioN) may be necessary. Use of these valves for MS associated with very heavy mitral annular calcification (“valve‐in‐MAC”) has been performed, but with high mortality rates.¹⁸⁸ Routine transcatheter MVR with specifically designed valves has been accomplished and may eventually see more widespread use.¹⁸⁶
      
   5. Patients with a duration of AF exceeding six months will most likely remain in that rhythm postoperatively. Therefore, a Maze procedure should be considered in a patient with either paroxysmal or persistent AF. This should also include exclusion of the left atrial appendage by various techniques. The “cut and sew” Cox‐Maze procedure has been replaced by use of energy sources (usually radiofrequency and cryoablation) that can be applied to create transmural ablation lines in well‐described patterns to ablate this arrhythmia with fairly good success rates (see section XIII, pages 84–89). It is less likely to be successful when the left atrial dimension exceeds 6 cm.^189,190
      
   6. Functional TR usually improves after left‐sided surgery due to a reduction in pulmonary vascular resistance, but is more likely to persist or progress in patients with AF, large atria, or moderate TR. Since moderate TR often progresses to severe TR, which may compromise long‐term survival, tricuspid valve repair is recommended for patients with moderate or severe TR or tricuspid annular dilatation.^189,190 Further comments on TV repair during surgery for MR are noted on pages 57–58.

VII. Mitral Regurgitation

1. Pathophysiology. Mitral regurgitation (MR) has been classified as primary (degenerative) or secondary (functional) depending on the pathologic changes involved.^106,107,193
   
   
   
   1. Primary MR usually results from myxomatous change or fibroelastic deficiency of the valve leaflets causing redundancy, along with chordal elongation or rupture. This results in leaflet prolapse and flail and is also commonly associated with annular dilatation. Rheumatic changes can cause leaflet distortion and chordal damage. Endocarditis is usually associated with the formation of vegetations, leaflet deformity, or perforation.
      
   2. Secondary or functional MR is associated with LV dysfunction, most commonly following an infarction, but also in association with dilated or hypertrophic cardiomyopathies. LV remodeling with a change in LV geometry and papillary muscle displacement may cause apical leaflet tethering as well as annular dilatation resulting in failure of the mitral leaflets to coapt properly, resulting in MR. The prognosis is worse with secondary MR because the MR is the result of a ventricular problem rather than a primary leaflet or chordal problem.
      
      
      
      1. The term “ischemic MR” has been applied to most cases of secondary MR caused by coronary disease. The spectrum of “ischemic MR” includes acute MR from infarct‐related acute papillary muscle rupture or ischemic dysfunction of the ventricular wall below the papillary muscles as well as chronic secondary MR from prior myocardial damage.
         
      2. Patients with long‐standing AF and those with restrictive cardiomyopathies (amyloid) may develop “atrial functional MR” when severe LA dilatation causes pure annular dilatation.¹⁹¹
   
   
2. Clinical presentation
   
   
   
   1. Acute MR usually results from myocardial ischemia, an acute MI with papillary muscle rupture, endocarditis, or from idiopathic chordal rupture. Acute LV volume overload develops with a reduction in forward output and new‐onset regurgitant flow into a small noncompliant left atrium. This may result in both cardiogenic shock and acute pulmonary edema.
      
   2. Chronic MR is a condition of volume overload that is characterized by a progressive increase in compliance of the left atrium and ventricle, followed by a progressive increase in LVEDV as the LV dilates. Some degree of hypertrophy accompanies LV dilatation to normalize LV systolic wall stress. The increase in preload increases overall stroke volume and maintains forward cardiac output. At the same time, there is a decrease in afterload due to ventricular unloading into the left atrium which will normalize systolic wall stress. In the compensated phase, the ejection fraction will usually increase as contractility is also maintained. Patients are usually asymptomatic at this point and may remain so even as ventricular decompensation occurs. An EF in the low–normal range usually reflects some degree of contractile dysfunction. Eventually, prolonged volume overload causes more LV dilatation, significant contractile dysfunction, and an increase in afterload, which lowers the ejection fraction. This results in an increase in end‐systolic volume with less forward output, and elevated filling pressures which worsen symptoms of HF.
   
   
3. Diagnostic considerations. The progression of MR and assessment of LV dimensions and function should be followed by serial echocardiograms to identify when an intervention should be undertaken to optimize the clinical outcome.
   
   
   
   1. Transesophageal echocardiography (TEE) with 3D imaging is the best technique to quantitate the severity of MR and identify its mechanism, and it also assesses LV function and provides an estimate of PA pressure. It can define whether MR is primary (degenerative) with leaflet prolapse from chordal prolongation or rupture, or secondary (functional) on the basis of a dilated annulus or enlarged LV with apical tethering of the leaflets. Generally, single‐leaflet prolapse or tethering produces eccentric jets (Figures 2.22 and 2.23), whereas annular dilatation causes central MR (Figure 2.24). TEE assessment is invaluable to the surgeon in helping to determine whether a valve can be repaired, what type of repair may be necessary, or whether replacement is indicated from the outset (Tables 1.8 and 1.9).
      
      
      
      1. Both color flow Doppler and quantitative parameters, such as calculation of the effective regurgitant orifice area (EROA), regurgitant fraction (RF), and regurgitant volume (RV) are important to appropriately assess the severity of MR.¹⁹¹
         
      2. The presence of LV or LA dilatation in primary MR is consistent with severe MR, whereas lack of LA or LV dilatation suggests that the MR is not severe.
         
      3. The degree of MR can be difficult to determine in some cases of secondary MR, because findings such as a dilated LA and LV and systolic blunting of pulmonary venous flow may be related to an underlying cardiomyopathy. Furthermore, the shape of the regurgitant orifice in secondary MR is crescentic and may lead to an underestimation of the EROA.¹⁹¹
         
      4. A discrepancy is often noted between the degree of MR identified preoperatively in the awake patient and that assessed under general anesthesia, which alters systemic resistance and loading conditions. Thus, a preoperative TEE is important to quantitate the degree of MR and define the precise anatomic mechanism for the MR. However, the use of sedation for a preoperative TEE may also lessen the degree of MR to some extent.
      
      
   2. Cardiac magnetic resonance (CMR) imaging is helpful in determining the severity of MR when TEE is inconclusive. It is considered more accurate for quantitating the RV and RF as well as LV volumes and LVEF.¹⁹¹
      
   3. Left ventriculography may be used to assess LV function and the degree of MR, but it is frequently insensitive in assessing its severity, which may depend on catheter position, the amount and force of contrast injection, the size of the left atrium or ventricle, and the presence of arrhythmias or ischemia.

4. Indications for intervention for acute MR
   
   
   
   1. Acute MR due to papillary muscle rupture usually produces the picture of HF or cardiogenic shock and mandates emergency surgery prior to the development of multisystem organ failure.
      
   2. Active infective endocarditis producing severe MR with hemodynamic compromise is a class I indication for urgent surgery.
   
   
5. Indications for intervention in chronic primary MR^{107,131,193–195}
   
   
   
   1. Class I indications
      
      
      
      • Stage D – symptomatic, severe MR, irrespective of LVEF
        
      • Stage C2 – asymptomatic, severe MR, LVEF ≤60% and/or LVESD ≥40 mm
        
      • Chronic severe MR if undergoing another cardiac procedure
        
      • Mitral valve repair is preferable to MVR if feasible in both of these categories
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