NAMED VESSELS	BRANCHES
Left main coronary artery	Left anterior descending Circumflex coronary Ramus intermedius
Left anterior descending	Diagonal arteries Septal perforators
Circumflex coronary artery	Obtuse marginal branches Left posterolateral artery
Right coronary artery	Acute marginal artery Posterior descending artery Right posterolateral artery

All the epicardial conductance vessels and septal perforators from the LAD give rise to a multitude of branches, termed resistance vessels, which traverse perpendicularly into the ventricular wall. These vessels play a crucial role in oxygen and nutrient exchange with the myocardium by forming a rich plexus capillary network. The rich capillary plexus offers a low-resistance sink to allow for unimpeded increase of arterial blood flow when oxygen demand rises. This is important because the myocardial vascular bed extracts oxygen at its full capacity, even in low-demand circumstances, thereby allowing no margin for further oxygen extraction when demand is high.

An intricate network of veins drains the coronary circulation and the venous circulation can be divided into three systems—the coronary sinus and its tributaries, the anterior right ventricular veins, and the thebesian veins. The coronary sinus predominantly drains the left ventricle and receives 85% of coronary venous blood. It lies within the posterior AV groove and empties into the right atrium. The anterior right ventricular veins travel across the right ventricular surface to the right AV groove, where they enter directly into the right atrium or form the small cardiac vein, which enters into the right atrium directly or joins the coronary sinus just proximal to its orifice. The thebesian veins are small venous tributaries that drain directly into the cardiac chambers and exit primarily into the right atrium and right ventricle. Understanding the anatomy of the coronary sinus is essential for placing the retrograde cardioplegia cannula during cardiopulmonary bypass.

Physiology and Regulation of Coronary Blood Flow

Aortic pressure is a driving force in the maintenance of myocardial perfusion. During resting conditions, coronary blood flow is maintained at a fairly constant level over a wide range of aortic perfusion pressures (70 to 180 mm Hg) through the process of autoregulation.

Because the myocardium has a high rate of energy use, normal coronary blood flow averages 225 mL/min (0.7 to 0.9 mL/g of myocardium/min) and delivers 0.1 mL/g/min of oxygen to the myocardium. Under normal conditions, more than 75% of the delivered oxygen is extracted in the coronary capillary bed, so any additional oxygen demand can only be met by increasing the flow rate. This highlights the importance of unobstructed coronary blood flow for proper myocardial function. Box 60-1 summarizes the unique features of coronary blood flow.

In response to increased load, such as that caused by strenuous exercise, the healthy heart can increase myocardial blood flow fourfold to sevenfold. Increased blood flow occurs through several mechanisms. Local metabolic neurohumoral factors cause coronary vasodilation when stress and metabolic demand increase, thereby lowering the coronary vascular resistance. This results in increased delivery of oxygen-rich blood, mimicking the phenomenon of reactive hyperemia. When a transient occlusion to the coronary artery is released (e.g., during the performance of a beating heart operation), blood flow immediately rises to exceed the normal baseline flow and then gradually returns to its baseline level. The autoregulatory mechanism responsible is guided by several metabolic factors, including CO₂, O₂ tension, hydrogen ions, lactate, potassium ions, and adenosine. Of these, adenosine is one of the leading candidates in the autoregulatory mechanism. Adenosine, a potent vasodilator and a degradation product of adenosine triphosphate (ATP), accumulates in the interstitial space and relaxes vascular smooth muscle. This results in vasomotor relaxation, coronary vasodilation, and increased blood flow. Another substance that plays an important role is nitric oxide (NO), which is produced by the endothelium. Without the endothelium, coronary arteries do not autoregulate, suggesting that the mechanism for vasodilation and reactive hyperemia is endothelium-dependent.

Extravascular compression of the coronaries during systole also plays an important role in the regulation of blood flow. During systole, the intracavitary pressures generated in the left ventricular wall exceed intracoronary pressure and blood flow is impeded. Hence, approximately 60% of the coronary blood flow occurs during diastole. During exercise. increased heart rate and reduced diastolic time can compromise flow time but this can be offset by vasodilatory mechanisms of the coronary vessels. Buildup of atherosclerotic plaques and fixed coronary occlusion significantly impair coronary blood compensatory mechanisms during increased heart rates. This forms the basis for exercise-induced stress tests, in which increased activity or exercise unmasks underlying coronary disease.

History of Coronary Artery Bypass Surgery

One of the first attempts at myocardial revascularization was made by Dr. Arthur Vineberg from Canada. He operated on a series of patients who presented with symptoms of myocardial ischemia and implanted the left internal mammary artery into the myocardium by creating a pocket. The operation did not entail a direct anastomosis to any coronary vessel and was performed on a beating heart through a left anterolateral thoracotomy. Dr. Michael DeBakey performed a successful aortocoronary saphenous vein graft in 1964. Dr. Mason Sones, who is credited with inventing cardiac catheterization, helped establish coronary artery bypass surgery as a planned and consistent therapy in patients with angiographically documented coronary artery disease.

The development of the heart-lung machine and demonstration of successful clinical use by Dr. John Heysham Gibbon in the 1950s and the advancement of cardioplegia techniques in later years by Dr. Gerald Buckberg allowed surgeons to perform coronary anastomosis on an arrested (nonbeating) heart with a relatively bloodless field, thus increasing the safety and accuracy of the coronary bypass. In the 1990s, the advent of devices that could atraumatically stabilize the heart provided another pathway for the development of off-pump techniques of myocardial revascularization. Today, an armamentarium of techniques, ranging from conventional on-pump CABG to minimally invasive robotic and percutaneous approaches, is available to manage coronary artery disease. Table 60-2 summarizes the timeline of major historical events in the development of surgery for myocardial revascularization.

Table 60-2 Evolution of Surgical Coronary Artery Interventions: Timeline

1950	A. Vineberg	Direct implantation of mammary artery into myocardium
1953	J. H. Gibbon	First successful use of cardiopulmonary bypass machine
1962	F. M. Sones	Successful cine-angiography
1964	M. E. DeBakey	First successful coronary artery bypass grafting
1964	T. Sondergaard	Introduced routine use of cardioplegia for myocardial protection
1964	D. A. Cooley	Routine use of normothermic arrest for all cardiac cases
1968	R. Favoloro	First large series demonstrating success of CABG
1973	V. Subramanian	Beating heart coronary artery bypass graft
1979	G. Buckberg	Introduced the use of blood cardioplegia as preferred method for to arrested myocardial protection

Atherosclerotic Coronary Artery Disease

Coronary atherosclerosis is a process that begins early in the patient’s life. Epicardial conductance vessels are the most susceptible and intramyocardial arteries, the least. Risk factors for atherosclerosis include elevated plasma levels of total cholesterol and low-density lipoprotein cholesterol (LDLc), cigarette smoking, hypertension, diabetes mellitus, advanced age, low plasma levels of high-density lipoprotein cholesterol (HDLc), and a family history of premature coronary artery disease.

Epidemiologic evidence suggests that coronary artery atherosclerosis is closely linked to the metabolism of lipids, specifically LDLc. The development of lipid-lowering drugs has resulted in a significant reduction in mortality. In one observational study of patients who received statin therapy and were known to have coronary artery disease (CAD), statin treatment was associated with improved survival in all age groups.¹ The greatest survival benefit was found in those patients in the highest quartile of plasma levels of high-sensitivity C-reactive protein (hs-CRP), a biomarker of inflammation and CAD.² Animal and human studies have demonstrated that statin therapy also modifies the lipid composition within plaques by lowering the amount of LDLc and stabilizing the plaque through various mechanisms, including reduction in macrophage accumulation, collagen degradation, reduction in smooth muscle cell protease expression, and decrease in tissue factor expression.

Pathogenesis

The primary cause of atherosclerotic coronary disease is endothelial injury induced by an inflammatory wall response and lipid deposition. There is evidence that an inflammatory response is involved in all stages of the disease, from early lipid deposition to plaque formation, plaque rupture, and coronary artery thrombosis. Vulnerable or high-risk plaques that are prone to rupture are characterized by the following:

1 A large, eccentric, soft lipid core

2 A thin fibrous cap

3 Inflammation within the cap and adventitia

4 Increased plaque neovascularity

5 Evidence of outward or positive vessel remodeling

Thinner fibrous caps are at a higher risk for rupture, probably because of an imbalance between the synthesis and degradation of the extracellular matrix in the fibrous cap that results in an overall decrease in the collagen and matrix components (Fig. 60-2). Increased matrix breakdown caused by matrix degradation by an inflammatory cell-mediated metalloproteinase or reduced production of extracellular matrix results in thinner fibrous caps. Not all plaque ruptures are symptomatic; whether they are is dependent on the thrombogenicity of the plaque’s components. Tissue factor within the lipid core of the plaque, secreted by activated macrophages, is one of the most potent thrombogenic stimuli. Rupture of a vulnerable plaque may be spontaneous or caused by extreme physical activity, severe emotional distress, exposure to drugs, cold exposure, or acute infection.

FIGURE 60-2 Components of atherosclerotic plaque. Thinning of the fibrous cap eventually results in plaque rupture with extrusion of highly thrombogenic lipid laden material into the coronary artery. This causes an acute occlusion of the coronary artery resulting in myocardial infarction.

(Adapted from Choudhury RP, Fuster V, Fayad ZA. Molecular, cellular and functional imaging of atherothrombosis. Nature Rev Drug Discov 3:913–925, 2004.)

Fixed Coronary Obstructions

More than 90% of patients with symptomatic ischemic heart disease have advanced coronary atherosclerosis caused by a fixed obstruction. Atherosclerotic plaques of the coronary arteries are concentric (25%) or eccentric (75%). Eccentric lesions compromise only a portion of the lumen; through vascular remodeling, the arterial lumen may remain patent until late in the disease process. The impact of an arterial stenosis on coronary blood flow can be appreciated in the context of Poiseuille’s law. Reductions in luminal diameter up to 60% have minimal impact on flow but when the cross-sectional area of the vessel has decreased by 75% or more, coronary blood flow is significantly compromised. Clinically, this loss of flow often coincides with the onset of exertional angina. A 90% reduction in luminal diameter results in resting angina.

Clinical Manifestations and Diagnosis of Coronary Artery Disease

Clinical Presentation

The most common presenting symptom of CAD is angina. It may be accompanied by dyspnea or mistaken for a gastrointestinal disturbance. The symptoms typically are exacerbated or incited by effort but subsequently resolve with rest. Unstable angina encompasses resting angina, new-onset angina, and accelerated angina and is usually indicative of severe ischemia and impending MI. However, not all cases of angina are necessarily indicative of CAD, because disease processes from other systems can closely mimic those of angina. Approximately 15% of patients with CAD do not present with angina.

The term acute coronary syndrome (ACS) has evolved to refer to a constellation of clinical symptoms that represent myocardial ischemia. It encompasses both ST-segment elevation MI (STEMI) and non–ST-segment elevation MI (NSTEMI). MI often presents as crushing chest pain that may be associated with nausea, diaphoresis, anxiety, and dyspnea. Symptoms of hypoperfusion may also include dizziness, fatigue, and vomiting. Heart rate and blood pressure may be initially normal, but both increase in response to the duration and severity of pain. Loss of blood pressure is indicative of cardiogenic shock and indicates a poorer prognosis. At least 40% of the ventricular mass must be involved for cardiogenic shock to occur. The first manifestation of CAD in 40% of patients is sudden onset of a nonperfusing ventricular rhythm, such as ventricular tachycardia or fibrillation.

The prehospital mortality rate for an acute MI (AMI) is approximately 50%. Of those patients who reach the hospital, another 25% die during the hospital stay and another 25% die in the first year afterward.^3,⁴ Mechanical complications of MI include acute ventricular septal defect (VSD), papillary muscle rupture, and free ventricular rupture. They usually occur approximately 7 to 10 days after the initial MI.

Physical Examination

Some clinical findings are generic and are related to the systemic manifestations of atherosclerosis. Eye examination may reveal a copper wire sign, retinal hematoma or thrombosis secondary to vascular occlusive disease, and hypertension. Corneal arcus and xanthelasma are features noticed in cases of hypercholesterolemia. Other clinical manifestations are caused by sequelae of CAD, as noted in Box 60-2.

Box 60-2 Sequelae of Coronary Artery Disease: Clinical Manifestations

Abnormal neck vein pulsations, which may be seen in patients with second- or third-degree heart block or CHF:

• Bradycardia—a subtle presentation of ischemia involving the right coronary territories and a possible sign of heart block

• Weak or thready pulse suggestive of ectopic or premature ventricular beats

• Third heart sound that is noted with elevated left ventricular filling pressures/CHF

• Fourth heart sound, which is commonly heard in patients with acute and chronic CAD

• Mitral regurgitant heart murmurs caused by ischemic papillary muscles

• Ejection systolic murmur indicative of aortic stenosis, which can contribute to coronary ischemia

• Holosystolic murmurs caused by ventricular septal rupture

• Manifestations of CHF, such as rales, hepatomegaly, right upper abdominal quadrant tenderness, ascites, and marked peripheral and presacral edema

A thorough vascular evaluation is essential for any patient who presents with coronary disease because atherosclerosis is a systemic process. In addition, if surgery is being planned, the extremities should be evaluated for any previous surgical scars or fractures that could potentially preclude vein harvest.

Diagnostic Testing

BOX 60-3 Stress Tests to Identify Coronary Artery Disease

^* Commonly known as the treadmill test.

Conditions that preclude accurate interpretation of the stress ECG include digoxin therapy, widespread resting ST-segment depression (≥1 mm), left ventricular hypertrophy, left bundle branch block, and other conduction abnormalities. For patients with these conditions and those unable to exercise, a pharmacologic stress test with an imaging modality using a radionuclide agent such as thallium or sestamibi, multiple-gated acquisition [MUGA] scanning, or positron emission tomography (PET) should be considered. Echocardiography may be considered as an alternative. Pharmacologic stress agents include adenosine, dobutamine, and dipyridamole.

Echocardiography

Many patients undergoing CABG also undergo transthoracic echocardiography by the evaluating cardiology team to estimate ventricular wall abnormalities and the ejection fraction. Common indications for a resting echocardiogram include heart murmurs and a suspicion of a structural problem, such as aortic stenosis or insufficiency, hypertrophic cardiomyopathy, mitral valve stenosis or regurgitation, and congestive heart failure. Ventricular dilation and wall thinning are other features noted on the echocardiogram in patients with chronic ischemic CAD or prior infarcts.

Multidetector Computed Tomography

Multidetector computed tomography (MDCT), one of the most recent imaging modalities, allows imaging of the coronary arteries, especially of coronary artery bypass grafts. Studies have indicated that the sensitivity and specificity MDCT approach or exceed those of other noninvasive methods of visualizing the coronary artery anatomy.⁵ MDCT is especially useful for imaging proximal CAD and coronary artery bypass grafts. More recent technology improves on conventional MDCT by adding more arrays to the imaging process; 128-slice MDCT arrays are currently available. These scanners can acquire myocardial images within 1 second while exposing the patient to less radiation than traditional scanners. Although it is still preferable that patients have relatively low heart rates during imaging (to reduce artifact), the technology has significantly advanced and produces images on par with those generated by the gold standard, conventional angiography.⁶

Magnetic Resonance Imaging and Gadolinium Magnetic Resonance Imaging

Myocardial first-pass perfusion magnetic resonance imaging (MRI) has been considered a good alternative to nuclear cardiac ischemia and viability testing. However, the procedure has not gained widespread popularity because special training and expertise are required to perform this type of imaging and interpret the results.

Cardiac Catheterization and Intervention

Cardiac catheterization remains the gold standard for evaluating the anatomy of the coronary arteries. High-quality coronary angiography is essential for identifying CAD and assessing its extent and severity.

Cardiac catheterization is commonly performed by inserting a short, self-sealing vascular sheath into either femoral artery. Vascular access may also be obtained via a brachial or radial artery. Angiography is done by using hollow preshaped catheters (5 or 6 Fr), which are placed under fluoroscopic guidance retrograde through the aorta into the ostia of the coronary arteries and coronary bypass grafts. A solution of radiographic contrast material is injected through the catheter to opacify the lumen. Images are recorded in rapid succession onto film or in a digital format. The surgeon typically uses the coronary angiography images to determine the number and location of coronary targets where bypass anastomoses are to be constructed (Figs. 60-3, 60-4, and 60-5).

FIGURE 60-3 Left coronary angiogram demonstrating hemodynamically severe lesions in the left anterior descending artery (small arrow) and the circumflex artery (large arrow).

FIGURE 60-4 Right coronary angiogram demonstrating hemodynamically significant lesions (arrow). The right coronary artery terminates as a posterior descending artery in the right dominant system.

FIGURE 60-5 Coronary angiogram demonstrating critical left main coronary artery stenosis (arrow).

Other information obtained from cardiac catheterization includes coronary and aortic calcification, ventricular function, and, if ventriculography is performed, mitral regurgitation. Injection of contrast into the aortic root provides useful root and ascending aortic images when indicated.

Right heart catheterization is used to measure central venous, right atrial, right ventricular, pulmonary artery, and pulmonary wedge pressures, as well as cardiac output. It can also be used to identify intracardiac shunts, assess arrhythmias, and initiate temporary cardiac pacing. Preoperative right heart catheterization is used selectively and is generally not necessary unless right ventricular dysfunction or pulmonary vascular disease is suspected.

Percutaneous coronary intervention (PCI) techniques in current use include balloon dilation, stent-supported dilation, atherectomy, and plaque ablation with a variety of devices, thrombectomy with aspiration devices, specialized imaging, and physiologic assessment with intracoronary devices.

Coronary artery stents were the first substantial breakthrough in the prevention of restenosis after angioplasty. Although stent recoil or compression are not completely insignificant problems, the greatest cause of lumen loss in stented coronary arteries is neointimal hyperplasia. This is the principal mechanism of in-stent stenosis and results from inappropriate cell proliferation—hence, the advent of cytotoxic drug-eluting stents.

Indications for Coronary Artery Revascularization

Box 60-4 summarizes the indications for myocardial revascularization. The first four indications are managed preferably by PCI, whereas indications 5 through 7 are managed preferably by surgical revascularization. The last two indications constitute surgical emergency. Although this stratification is broad and provides a bird’s eye view of the management approach, each patient should be risk-stratified before an appropriate strategy is initiated. When possible, proper risk stratification is absolutely essential to determine the balance of risks and benefits of medical management, PCI, and CABG.

Chronic Stable Angina

Cardiovascular risk reduction strategy is essential to treating patients with chronic stable angina. In the 2007 focused update of the 2002 American Heart Association (AHA)/American College of Cardiology (ACC) guidelines ⁷ for managing chronic stable angina, cardiovascular risk reduction strategies included smoking cessation, blood pressure control, lipid-lowering regimens, physical activity, antiplatelet agents, angiotensin-converting enzyme (ACE) inhibitors, weight control, diabetes management, and influenza vaccination. Such risk reduction strategies should be used for all patients, irrespective of the type of intervention planned on the coronary artery.

Coronary Artery Bypass Grafting Versus Medical Management

In the 1970s and 1980s, several prospective randomized clinical trials evaluated the survival benefit of CABG in patients with chronic stable angina. The most influential of these trials were the Veterans Administration Study of Chronic Stable Angina (VA Study), European Coronary Surgery Study (ECAS), and Coronary Artery Surgery Study (CASS). These studies have shown that CABG has significant benefits, resulting in the widespread use of CABG to treat patients with CAD. They also helped identify specific categories of patients with angina who were most likely to benefit from CABG—namely, patients with left main CAD, one-, two-, or three-vessel disease with proximal LAD involvement, and three-vessel disease with impaired left ventricular function.

In the current practice of medicine, the results of these trials should be viewed with caution because of advancements in modalities and therapeutics not available at the time. Many patients were not on aspirin or beta blockers, and most patients did not receive an internal thoracic artery (ITA) graft. Calcium channel blockers, ACE inhibitors, and lipid-lowering agents were not available. In addition, women and young patients were excluded from most of the trials. Nonetheless, modern comparative studies have shown a persistent advantage of revascularization over optimal medical management, especially in higher risk patients with more severe coronary disease.

Percutaneous Coronary Intervention Versus Medical Management

In the 1980s, PCI was introduced as an alternative to CABG. Although the short-term symptomatic success rate for PCI approaches 85% to 90%, the usefulness of PCI remains controversial for patients with angina whose symptoms are adequately controlled with medical therapy.^8,⁹ The main results of the VA Clinical Outcomes Utilizing Revascularization and Aggressive druG Evaluation (COURAGE) trial revealed no significant differences in the primary end point of all-cause mortality or nonfatal MI, or in the major secondary end points, during a median 4.6-year follow-up period in patients with stable CAD who were randomly assigned to receive optimal medical therapy (OMT), with or without PCI.¹⁰

Coronary Artery Bypass Grafting Versus Percutaneous Coronary Intervention

Pre–Stent Era

One of the first large-scale, prospective, randomized studies of PCI and CABG was the Bypass Angioplasty Revascularization Investigation (BARI) trial reported in 1996.¹¹ Patients with multivessel disease were randomly assigned to CABG or PCI and followed up for a mean of 5.4 years. In the short term, the incidence of MI was higher in the CABG group (4.6% versus 2.1%), but stroke rates were similar (0.8% versus 0.2%, CABG versus PCI). Five years after treatment, the survival rate was 89.3% for the CABG cohort and 86.3% for the PCI cohort (P = .19). Of the PCI patients, however, 54% required additional revascularization procedures, whereas only 8% of the CABG patients required repeat revascularization. Thus, although PCI did not compromise the 5-year survival rate in patients with multivessel disease, subsequent revascularization, including CABG, was required more often. Among the diabetic patients, the 5-year survival rate for the CABG patients was markedly greater (80.6% versus 65.5%).

Bare Metal Stent Era

In the 1990s, coronary stents were introduced to address the problematic occurrence of restenosis after PCI. Six randomized trials have compared PCI with stenting and CABG.¹²^–¹⁴ Except for the Angina With Extremely Serious Operative Mortality Evaluation (AWESOME) trial, these trials enrolled patients who were relatively low risk and had no serious comorbidities, normal ventricular function, and mostly two-vessel CAD that was amenable to both PCI and CABG. All these trials showed similar survival rates but there were higher revascularization rates in patients with bare metal stents. A meta-analysis of four randomized trials has shown that PCI with stenting is associated with a long-term safety profile similar to that of CABG. However, as a result of persistently lower repeat revascularization rates in the CABG patients, overall major adverse cardiac and cerebrovascular event rates were significantly lower in the CABG group at 5 years.¹⁵ Although these randomized studies are often used to demonstrate survival equivalence of CABG and PCI in patients with multivessel CAD, the studies were underpowered, the patients were low-risk, and the follow-up was too short. In contradistinction, a large New York State registry study has demonstrated that patients with double- or triple-vessel disease derive a greater survival benefit from CABG than from PCI with stenting.¹⁶ Analysis of this large database of more than 50,000 patients found that during the 3-year follow-up, repeat revascularization was 11 times higher in the percutaneous transluminal coronary angioplasty (PTCA) group (37% versus 3.3% CABG). Furthermore, 3-year mortality was significantly higher in the PTCA group.

Drug-Eluting Stent Era

The proponents of drug-eluting stent (DES) implantation claim that improved technology has made the results of randomized controlled trials (RCTs) favoring CABG obsolete. However, in patients with multivessel disease, PCI with DES can produce survival rates equivalent to those associated with CABG only if the reduction in restenosis rate translates into reduced mortality. Additionally, no mortality benefit of DES compared with bare metal stents has been demonstrated; in a meta-analysis of 11 RCTs of PCI with DES versus bare metal stents, none of the trials found a mortality benefit for DES.¹⁷

The Synergy between PCI with Taxus and Cardiac Surgery (SYNTAX) trial compared PCI and CABG for patients with previously untreated three-vessel or left main CAD. At 12 months, major adverse cardiac or cerebrovascular events were significantly more frequent in the PCI group (17.8% versus 12.4%). This finding was attributed primarily to the greater use of imaging surveillance in the CABG group (13.5% versus 5.9%). Although the trial found similar rates of death and MI, stroke was significantly more likely to occur in CABG patients (2.2% versus 0.6%). Nevertheless, the study findings suggested that CABG remains a favorable option in the care of patients with three-vessel or left main CAD.

It is likely that the use of a DES, or any stent, does not confer a mortality benefit because subsequent coronary events are often related to the progression of disease in arteries other than the stented artery or in other segments of the stented artery. In contrast, CABG treats the stenosis present at the time of surgery and any additional stenoses that develop proximal to the bypass graft in the future.

Finally, one must remember that CABG has a long track record, with studies reporting over 2 decades of follow-up, whereas reports on DES performance are short- to midterm studies. This is an important limitation on comparisons of the durability and cost-effectiveness of the two procedures. Reports of early thrombosis of a DES have dictated the use of a dual antiplatelet regimen for at least 1 year after stent deployment. Clopidogrel is usually used in conjunction with aspirin, but there are other more potent antiplatelet agents on the horizon. The increased risk of bleeding and additional cost of dual antiplatelet therapy are important limitations of treatment with DES.

In summary, compared with PCI, CABG confers superior long-term survival in patients with specific anatomic lesions (e.g., multivessel disease, left main CAD, one- and two-vessel disease with proximal LAD obstruction) and is associated with fewer subsequent interventions.

Acute Coronary Syndrome

Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction

Patients who present with unstable angina (UA) or NSTEMI may have associated symptoms that confer a high short-term risk of death that necessitates invasive intervention. Two treatment pathways are used for treating UA-NSTEMI patients: the early invasive strategy and an initial conservative strategy. Patients treated with an invasive strategy generally undergo coronary angiography within 4 to 24 hours of admission.² Estimating the risk of an adverse outcome is paramount for determining which strategy is best for an individual patient. High-risk patients who benefit from invasive therapy include those with recurrent angina, ischemia at rest, low-level activity despite intensive medical therapy, elevated levels of cardiac biomarkers (troponins), new ST-segment depression, signs or symptoms of congestive heart failure or of new or worsening mitral regurgitation, findings from noninvasive testing that suggest high risk, hemodynamic instability, sustained ventricular tachycardia, PCI within the previous 6 months, prior CABG, and reduced left ventricular function (<40%).

According to the AHA/ACC/American Association for Thoracic Surgery (AATS) guidelines, UA-NSTEMI and features associated with high short-term risk of death or nonfatal MI indicate revascularization of the presumed culprit artery. These indications are similar to those for coronary revascularization in patients with chronic stable angina.¹⁸