Approach to Percutaneous Coronary Intervention in Myocardial Infarction




Introduction


Percutaneous coronary intervention (PCI) is the dominant strategy used for coronary revascularization in acute myocardial infarction (MI). In the United States, approximately 600,000 patients are discharged from the hospital with a principal diagnosis of acute MI (see Chapter 2 ), which includes a substantial percentage of the primary indications for PCI of the estimated 954,000 PCIs performed annually. This chapter reviews the evidence and practical considerations for PCI in patients with acute MI, including both ST-elevation MI (STEMI) and non–ST-elevation MI (NSTEMI). Selection among the options for reperfusion therapy for STEMI is addressed in Chapter 14 , and selection among strategies for management of NSTEMI is discussed in Chapter 16 . Antiplatelet therapy is discussed in Chapter 19 , and anticoagulant therapy is discussed in Chapter 18 .




Timing of Percutaneous Coronary Intervention


ST-Elevation Myocardial Infarction Strategies for Reducing Time to Treatment


If performed in a timely fashion by experienced operators, primary PCI is the recommended method for reperfusion in patients presenting with STEMI. The benefit of reperfusion therapy is greatest in the first 3 hours after symptom onset (see Chapter 13 ). The development of regional systems for STEMI care and reperfusion therapy to limit the total ischemic time and meet time-to-treatment goals is detailed in Chapter 5 . Regardless of the recommended time-to-treatment goals, reperfusion should always be established as rapidly as possible for any individual patient. It is estimated that 90% of STEMI patients presenting to a PCI-capable hospital achieve the door-to-device time goal of ≤90 minutes in the absence of a clinical reason for delay. A checklist ( Table 17-1 ) was developed by the American College of Cardiology (ACC)/American Heart Association (AHA) with practical system strategies to minimize door-to-device time.



TABLE 17-1

Checklist for Reducing Door-to-Device Times in ST-Elevation Myocardial Infarction

Adapted from O’Gara PT, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 127:e362, 2013.

















Time-to-Treatment Goals
PCI-Capable Hospital



  • Goal: FMC-to-device time <90 min

Non–PCI-Capable Hospital



  • Goal: Transfer to PCI-capable hospital with FMC-to-device time of <120 min (door-in-door-out <30 min)



  • If anticipated FMC-to-device is >120 min, administer fibrinolytic within 30 minutes of arrival.

Checklist for Reducing Door-to-Device Times



  • Pre-hospital ECG to diagnose STEMI and activate PCI team



  • Emergency room physicians activate the PCI team



  • A single call to a central paging system activates the PCI team



  • PCI team arrival to the catheterization laboratory within 20 min



  • Timely analysis and feedback of time-to-treatment metrics by the STEMI care team


ECG , Electrocardiogram; FMC, first medical contact; PCI , percutaneous coronary intervention; STEMI , ST-elevation myocardial infarction.


Non–ST-Elevation Myocardial Infarction: Timing of Angiography


In patients with NSTEMI, the timing of diagnostic angiography with intent to perform PCI is driven by risk stratification, clinical stability, and patient preferences (see Chapter 16 ). Patients treated using an early invasive strategy will undergo angiography, whereas those managed with the ischemia-guided strategy will typically receive angiography after medical treatment has failed, with objective evidence of ischemia on noninvasive stress testing or with a very high risk for mortality or morbidity. The timing of angiography in the invasive strategy is stratified based on clinical risk assessment ( Table 17-2 ) into urgent (<2 hours), early (<24 hours), and delayed (25 to 72 hours). Patients with refractory symptoms, severe heart failure, or electrical and/or hemodynamic instability should undergo immediate invasive evaluation (see Chapter 16 ).



TABLE 17-2

Timing of Angiography in the Early Invasive Strategy or Ischemia-Guided Strategy in Patients with Non–ST-Elevation Myocardial Infarction

Adapted from Amsterdam EA, et al: 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 130:e344, 2014.



















Ischemia-Guided Strategy



  • Low-risk score (e.g., TIMI [0 or 1], GRACE [<109])



  • Low-risk troponin-negative female patients



  • Patient or clinician preference in the absence of high-risk features

Immediate Invasive (within 2 h)



  • Refractory angina



  • Signs or symptoms of heart failure



  • New or worsening mitral regurgitation



  • Hemodynamic instability



  • Recurrent angina or ischemia at rest or with low-level activities despite intensive medical therapy



  • Sustained VT or VF

Early Invasive (within 24 h)



  • None of the above, but GRACE risk score >140



  • Temporal change in troponin



  • New or presumably new ST depression

Delayed Invasive (within 25–72 h)



  • None of the above, but diabetes mellitus



  • Renal insufficiency (GFR <60 mL/min/1.73 m 2 )



  • Reduced LV systolic function (EF <0.40)



  • Early postinfarction angina



  • PCI within 6 months



  • Previous CABG



  • GRACE risk score 109–140; TIMI score >2


CABG , Coronary artery bypass graft; EF , ejection fraction; GFR , glomerular

filtration rate; LV , left ventricular; PCI , percutaneous coronary intervention; VF, ventricular fibrillation; VT , ventricular tachycardia.


An early invasive strategy did not improve survival or reduce recurrent MI compared with a delayed invasive strategy in a meta-analysis of seven randomized trials and four observational studies that included 82,869 patients with non–ST-elevation acute coronary syndrome (NSTE-ACS). In the TIMACS (Timing of Intervention in Patients with Acute Coronary Syndromes) trial, high-risk patients (GRACE [Global Registry of Acute Coronary Events] risk score >140) who underwent an early invasive strategy had a 38% reduction in death, MI, and stroke at 6 months compared with a delayed invasive strategy. An early invasive strategy is advocated in patients at higher risk for adverse clinical events (see Table 17-2 ).




Vascular Access


Vascular access is vitally important for the success of PCI. Femoral access is the most common approach used for PCI in the United States. Radial access has gained significant popularity and is preferred by many patients and operators. Importantly, bleeding is the most common PCI-related complication, and it is also associated with higher rates of mortality.


Performing Vascular Access


Femoral


Retrograde puncture of the femoral artery ( Figure 17-1 ) is required for femoral access during diagnostic coronary angiography and PCI. The common femoral artery is used because of its larger size and its ability to compress against the femoral head during manual compression. Patients should receive sedation and a local anesthetic before arterial cannulation. Because of the variability in body habitus, several landmarks should be noted before choosing an arteriotomy site. A line drawn between the anterior superior iliac spine and pubis demarcates the inguinal ligament. The inguinal crease should not be used to approximate the inguinal ligament, especially in obese patients. Fluoroscopy should be used to mark the femoral head. The common femoral should be entered at a 30- to 45-degree angle approximately 1 to 2 cm below the inguinal ligament, which is typically at the center of the femoral head. A “low stick” can result in cannulation of the superficial femoral artery, which increases the risk of hematoma, dissection, arterial occlusion, or formation of a pseudoaneurysm or arteriovenous fistula. Conversely, a “high stick” above the inguinal ligament or above the inferior epigastric artery on angiography does not allow for effective manual compression against the femoral head, and significantly increases the risk for retroperitoneal hemorrhage. Before administering therapeutic anticoagulation for PCI, limited angiography through the femoral sheath at an oblique ipsilateral angle should be performed to determine the arteriotomy site in relationship to the femoral head, inferior epigastric artery, and femoral bifurcation, which could modify the timing of PCI and/or choice to use a vascular access closure device.




FIGURE 17-1


Anatomy of the femoral artery.

Femoral angiography of the right femoral artery in a right anterior oblique view. The common femoral artery should be entered below the inguinal ligament in the middle one-third of the femoral head to avoid a low (i.e., at or below the femoral bifurcation) or high stick (i.e., above the inferior epigastric artery). CFA , Common femoral artery; PFA , profunda femoris artery; SFA , superficial femoral artery.

(From Bangalore S, Bhatt DL: Femoral arterial access and closure. Circulation 124:e147–156, 2011.)


Two commonly used techniques to reduce vascular complications during femoral access include use of a micropuncture needle (Cook Medical, Bloomington, Ind.) or guidance using ultrasound. Traditionally, an 18-gauge wide open-bore needle has been used for arterial cannulation. A smaller micropuncture 21-gauge needle can be used to access the common femoral artery. After placement of a 0.018-inch wire into the artery, limited angiography can be used to localize the site of cannulation through the needle or inner dilator, and if acceptable, the 4F micropuncture sheath can be advanced over the wire. If the arteriotomy site is too low or high, then femoral access at an alternative site can be reattempted, and the needle or inner dilator removed, with minimal risks of bleeding. Real-time ultrasound guidance has also been used for femoral access and allows for visualization of needle entrance into the femoral artery. It can also determine the femoral bifurcation to facilitate cannulation of the common femoral artery above the bifurcation.


Radial


The learning curve for radial access is typically longer compared with femoral access. It should not be used in patients with forearm arteriovenous fistulas. Assessment for collateral ulnar circulation via the ulno-palmar arterial arch is advocated. However, failure to demonstrate dual circulation to the hand (i.e., incomplete palmar arch) is not an absolute contraindication. Assessment is performed using either the modified Allen’s or plethysmo-oxymetric test, the latter of which has a higher specificity. Any abnormal Allen’s test should be confirmed by plethysmo-oxymetric testing. When attempting radial access, a smaller amount of lidocaine (1 to 2 mL) should be administered to minimize the risk of local vasospasm or obscuring the radial pulse. A micropuncture needle is used to access the radial artery and for placement of a hydrophilic radial arterial sheath over a 0.021- to 0.025-inch guidewire ( ). Ultrasound can also be used to minimize the number of attempts needed for arterial cannulation. Vasospasm can be a significant limitation in radial access. Intra-arterial administration of an antispasmolytic drug (e.g., nitrogylcerin, diltiazem, verapamil) is mandatory. A number of single agents or “cocktail” regimens have been used to prevent vasospasm. Most operators use verapamil (2.5 to 5 mg) and/or nitroglycerin (100 to 200 μg). Anticoagulation should be initiated after radial artery cannulation to minimize the risk for radial artery occlusion. Low-dose unfractionated heparin (e.g., 2000 to 3000 IU or 50 IU/kg) can be administered and converted to therapeutic dosing upon placement of the guide catheters in the ascending aorta or with coronary cannulation. Access via the left radial may be advantageous over the right radial because of the higher prevalence of right-handed individuals; the aortic path approximates a transfemoral approach, which allows for easier coronary cannulation with standard Judkin’s guide catheters and easier access to the left internal mammary artery in coronary artery bypass graft (CABG) patients.


Advantages and Disadvantages of Radial versus Femoral Access


When considering vascular access, operators should consider important differences between femoral and radial access ( Table 17-3 ). In the United States, rates of radial access for PCI had been less than 2% because of unfamiliarity with the radial approach and a concern for increased procedure length and radiation exposure. However, rates in the United States have increased to approximately 15% to 20% and are expected to increase over the next decade.



TABLE 17-3

Comparison of Femoral and Radial Access for Percutaneous Coronary Intervention

Adapted from Byrne RA, et al: Vascular access and closure in coronary angiography and percutaneous intervention. Nat Rev Cardiol 10:27–40, 2013.


















































































Femoral Radial
Anatomic
Vessel size 6–10 mm 2–3 mm
Vascular course Less variable Highly variable
Vessel location Variable because of body habitus Superficial
Nearby neurovascular Yes No
Procedural
Procedural success Marginally higher Marginally lower
Procedural time Comparable Comparable
Contrast load Comparable Comparable
Fluroscopy time Marginally lower Marginally higher
Choice of sheath size Unrestricted Restricted (typically 6F)
Learning curve Shorter Longer (typically 50 cases)
Patient Care
Preference Lower Higher
Time to ambulation Typically 2–6 h Immediate
Length of stay Longer Shorter
Complications
Access site bleeding Higher Lower
Vessel occlusion Rare 0–10%
Pseudoaneurysm 1–5% Rare


Current Evidence: Radial versus Femoral


Radial access is associated with a lower rate of vascular complications and major bleeding in comparison to femoral access, and in some studies, a lower rate of adverse cardiac events. In the RIVAL (Radial vs. Femoral Access for Coronary Intervention) trial, no difference was observed in the composite rate of death, MI, stroke, or non-CABG major bleeding in patients who presented with ACS without ST-segment elevation and who were randomized to femoral versus radial access. However, vascular complications were significantly lower with radial access. Patients who presented with STEMI in the RIFLE-STEACS (Radial Versus Femoral Randomized Investigation in ST-Elevation Acute Coronary Syndrome) and STEMI-RADIAL (ST Elevation Myocardial Infarction Treated by Radial or Femoral Approach) trials demonstrated a significant reduction in bleeding and vascular complications, which translated into shorter hospital stays and lower mortality compared with the femoral approach. The lower mortality in STEMI with radial catheterization was also demonstrated in a meta-analysis and observational data from the National Cardiovascular Data Registry. More recently, the MATRIX (Minimizing Adverse Haemorrhagic Events by Transradial Access Site and Systemic Implementation of AngioX) trial also showed fewer major bleeding complications with a radial versus a femoral approach and lower mortality in ACS patients with or without STEMI.


Considerations for Radial Approach in ST-Elevation Myocardial Infarction


Despite evidence that the radial approach reduces vascular complications, major bleeding, and mortality in STEMI patients, its use is paradoxically lower in this population than in patients with NSTEMI. One concern is that the increased time required for the radial approach may prolong the time-to-treatment goal in STEMI. However, a door-to-device delay of 83 minutes would be required to offset the mortality benefit of radial PCI over femoral PCI in STEMI. Because of the higher risk for cardiogenic shock, the groin of a patient with STEMI should always be prepped for immediate venous access or additional arterial access for hemodynamic support.


Vascular Closure Devices: When to Consider Use


Vascular closure devices were initially designed to improve safety of PCI by reducing access site bleeding and vascular complications. However, clinical trials and meta-analyses have demonstrated that vascular closure devices do not lower bleeding or vascular complications compared with manual compression. To this end, current ACC/AHA guidelines do not recommend routine use of vascular closure.


When manual compression (i.e., 3 minutes per sheath French size [e.g., 6F = 18 minutes]) is used, femoral arterial sheaths can typically be pulled when the activated clotting time (ACT) is less than 160 to 180 seconds with heparin use or 2 hours after bivalirudin is stopped without checking the ACT. Manual compression can be performed digitally or using a manual compression assist device (e.g., FemoStop, St. Jude Medical, St. Paul, Minnesota). Vascular closure devices achieve faster hemostasis, which allows for earlier ambulation, improved patient satisfaction, and possibly shorter hospital length of stay. In the absence of a radial approach, obese patients, whose body habitus may limit effective manual compression, or individuals who cannot tolerate prolonged periods in a supine position, should undergo closure using a vascular closure device. Arteriotomy sites at the femoral bifurcation, in the superficial femoral artery, or in a smaller femoral artery (<5 mm) are associated with a higher risk for device failure, and potentially, arterial occlusion; thus, in general, vascular closure devices would not be recommended. A number of devices are currently approved and available with different mechanisms used for closure. No sizeable randomized trial comparing the safety and efficacy of each device has been conducted.


Management of Vascular Complications


Vascular complications are the most common adverse event following PCI and are associated with an increase in cost, length of stay, morbidity, and mortality. The two most common complications are hematoma and pseudoaneurysm, whereas less common complications include dissection, arteriovenous fistula, arterial occlusion, retroperitoneal hemorrhage, femoral nerve damage, and infection. A hematoma is typically managed conservatively with local compression and rarely requires blood transfusion. The presence of a palpable bruit or pulsatile mass should prompt evaluation with an ultrasound. Small pseudoaneurysms (<3 cm) can be followed with serial ultrasounds. Pseudoaneurysms larger than 3 cm can be treated with ultrasound-guided thrombin injection. Retroperitoneal hemorrhage (RPH) should be suspected in any patient with a sudden onset of hypotension and flank pain ipsilateral to the vascular access site. Prompt recognition with concomitant volume and blood support is essential for the management of a suspected RPH. Anticoagulation reversal or platelet infusion may also be necessary, despite the theoretical risks for stent thrombosis. Early computed tomography may be useful, but should not delay aggressive supportive measures or involve transport of an unstable patient. Most RPHs can be managed conservatively, and endovascular or open surgical treatment should only be considered in patients who cannot be stabilized hemodynamically. Arterial occlusion should be suspected in any patient with sudden onset of leg pain, paresthesia, decreased or absent pulses, and a cool and/or cyanotic limb. Suspected arterial occlusion is a vascular emergency and should be treated with intravenous (IV) anticoagulation and emergent endovascular or surgical repair.




Interventional Pharmacotherapy


Procedural Sedation


PCI is typically performed under minimal to moderate sedation. The usual goal is for patients to be comfortable with depressed consciousness and the ability to follow verbal commands. Patients should receive supplemental oxygen during PCI as needed. Because of the potential risk for respiratory depression leading to hypoxia and/or hypercarbia, all patients should be assessed for a history of or clinical predictors for difficult intubation (e.g., obesity). If present, anesthesiology can be consulted to consider the need for monitored anesthesia care. Typically, an IV sedative and analgesic are administered in small incremental dosages during PCI. The two most common agents used are midazolam (0.5 to 1 mg IV boluses) as a sedative and fentanyl (25 to 50 μg IV bolus) as an analgesic. Both have a rapid onset of action (2 to 5 minutes), are rapidly metabolized within 30 to 60 minutes after administration, and are reversible with flumazenil and naloxone, respectively.


Oral Antiplatelet Therapy


Antiplatelet therapy is essential for PCI in acute MI (see Chapter 19 and Chapter 20 ). In this section, we focus on the practical aspects of oral antiplatelet therapy for operators performing PCI. All patients should receive a loading dose of aspirin (i.e., 325 mg) or a 600-mg rectal suppository if unable to swallow or if they are vomiting. Most patients with STEMI and NSTEMI should receive a loading dose of an adenosine diphosphate (ADP) P2Y 12 inhibitor (although the exact timing of administration is a matter of debate, especially in NSTEMI).


When to Preload with Oral Adenosine Diphosphate P2Y 12 Inhibitors


When possible, pretreatment with a loading dose of an oral ADP P2Y 12 inhibitor in patients with acute MI is recommended, with administration as early as possible after a diagnosis of STEMI. In a meta-analysis, clopidogrel pretreatment reduced mortality in STEMI and major coronary events in both STEMI and NSTE-ACS compared with no pretreatment. The PLATO (Study of Platelet Inhibition and Patient Outcomes Clopidogrel) trial led to the approval of ticagrelor for patients with ACS. All the patients in PLATO were pretreated with ticagrelor before PCI. Delayed administration of ticagrelor has not been formally tested against pretreatment in NSTEMI. Prasugrel is not currently recommended for use as upstream therapy in NSTEMI. In the TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in MI) trial, prasugrel was administered at the time of PCI after coronary angiography. However, current ACC/AHA guidelines do advocate for prasugrel pretreatment when possible in STEMI.


Anticoagulation Strategies


Anticoagulant therapy must be administered to all patients undergoing PCI. Selecting an initial agent will be discussed in detail in a subsequent chapter (see Chapter 18 ). In STEMI, unfractionated heparin or bivalirudin are the two agents recommended for anticoagulation; most operators will also use either agent for PCI in NSTEMI. Fondaparinux should never be used alone as an anticoagulant because of the risk of catheter thrombosis. In patients on therapeutic enoxaparin (i.e., 1 mg/kg every 12 hours), unfractionated heparin or bivalirudin is not recommended during PCI. If the last dose of enoxaparin was more than 8 to 12 hours before PCI or if the dosage was subtherapeutic, an IV dose of 0.3 mg/kg should be administered.


Practical Aspects of Monitoring Anticoagulation


ACTs are the standard method used to monitor the therapeutic effect of anticoagulation during PCI. In the balloon angioplasty era, higher levels of ACTs were associated with lower rates of periprocedural ischemic events, but also increased the risk of bleeding. However, this association has not been consistent in coronary stent trials. ACTs are routinely checked throughout the PCI procedure after administration of unfractionated heparin. A bolus of unfractionated heparin (70 to 100 U/kg) is administered, and the ACT is checked approximately 5 minutes later. Traditionally, a minimum therapeutic ACT level is more than 250 seconds without a glycoprotein IIb/IIIa inhibitor (GPI). If a GPI is also administered, an ACT level should be more than 200 seconds. The range of ACT levels may vary based on the complexity of the PCI, but typically should not exceed 350 seconds. If bivalirudin (0.75 mg/kg followed by a 1.75 mg/kg per hour IV infusion) is used, monitoring of ACT levels is not required. However, most operators will check one ACT level to determine that bivalirudin has been administered through a “working” peripheral IV line. In addition, low-molecular-weight heparin does not require any monitoring during PCI. Fondaparinux requires co-administration of heparin during PCI, for which an ACT can be checked to ensure therapeutic levels of anti-IIa activity.


Current Evidence: Bivalirudin versus Heparin in ST-Elevation Myocardial Infarction


Significant controversy has arisen about the safety and efficacy of bivalirudin in primary PCI during STEMI. The HORIZONS-AMI (Harmonizing Outcomes with Revascularization and Stents in Acute MI) trial showed that bivalirudin lowered mortality (all-cause and cardiac) in STEMI compared with heparin plus a GPI. Bivalirudin was associated with a significantly higher rate of acute (i.e., <24 hours of primary PCI) stent thrombosis in the HORIZONS-AMI trial. It was theorized that the risk of stent thrombosis surrounding PCI may be caused by discontinuation of bivalirudin after PCI, with clopidogrel (i.e., a less potent and slower onset ADP P2Y 12 agent) as the predominant antiplatelet therapy.


In the EUROMAX (European Ambulance ACS Angiography) trial, bivalirudin lowered net adverse events and major bleeding compared with unfractionated or low-molecular-weight heparin plus provisional GPI at 30 days. This trial was designed to overcome the limitations of HORIZONS-AMI by using more potent oral ADP P2Y 12 inhibitors (i.e., prasugrel and ticagrelor). In addition, a reduced dose of bivalirudin (0.25 mg/kg per hour) was continued for several hours after PCI. Despite these differences, a higher rate of acute stent thrombosis was still observed in EUROMAX with bivalirudin. A subsequent open-label trial in consecutive STEMI patients who underwent primary PCI (HEAT-PPCI [How Effective are Antithrombotic Therapies in Primary PCI]) demonstrated that heparin with the use of bailout GPIs reduced all-cause mortality, stroke, reinfarction, or unplanned revascularization and stent thrombosis without any differences in the rates of major bleeding compared with bivalirudin.


The BRIGHT (Bivalirudin in Acute Myocardial Infarction vs. Heparin and GPI Plus Heparin Trial) study was designed to overcome the limitations of HORIZONS-AMI by continuing bivalirudin at the standard dose (1.75 mg/kg per hour) for a median of 3 hours after PCI in acute MI patients, of whom 88% presented with STEMI. In BRIGHT, a significant reduction in bleeding was seen in patients treated with clopidogrel and bivalirudin compared with heparin, with and without a GPI. No differences were observed between the groups in the rates of major adverse cardiac or cerebral events, including acute stent thrombosis. It is postulated that a prolonged infusion of standard dose bivalirudin abrogated the risk of acute stent thrombosis seen in the HORIZONS-AMI and EUROMAX trials. A meta-analysis comparing bivalirudin and heparin confirmed the higher rate of acute stent thrombosis with bivalirudin compared with heparin. Prolonged infusion of bivalirudin may eliminate this risk, but this strategy should be confirmed in additional studies. Bleeding is lower with bivalirudin compared with heparin and GPI; yet, in the absence of routine GPIs and with radial access, the benefit appears to be less striking.


Intravenous Antiplatelet Therapy


When to Use a Glycoprotein IIb/IIIa Inhibitor?


GPI use was established predominantly in the era that predated the use of oral dual antiplatelet therapy (DAPT). The use of GPIs reduces ischemic events during PCI, but it also increases the risk of bleeding. Currently, GPIs should be used provisionally during PCI for acute MI. Routine use with bivalirudin is not recommended. Provisional GPIs can be considered in patients with a large thrombus burden, patients with stent thrombosis while on DAPT, or patients with an inadequate loading of an ADP P2Y 12 inhibitor (e.g., poor gastrointestinal absorption in the setting of vomiting or cardiogenic shock). If used, abciximab (0.25 mg/kg IV bolus, then 0.125 μg/kg per minute [maximum 10 μg/min]), double-bolus eptifibatide (two 180 μg/kg IV boluses within 10 minutes and 2 μg/kg/min after the first bolus), or high-dose bolus tirofiban (25 μg/kg IV bolus, then 0.15 μg/kg/min) can be used. Intracoronary abciximab bolus (same dosing) may also be considered in patients with a large STEMI or clot burden, although there is no proven benefit over IV abciximab.


Role for Intravenous Adenosine Diphosphate P2Y 12 Inhibitors?


In acute MI, an IV ADP P2Y 12 may be useful in selected patients. Cangrelor is a reversible, IV ADP P2Y 12 receptor antagonist that potently inhibits platelets within 3 to 6 minutes with complete platelet recovery after 60 minutes after discontinuation. Cangrelor was initially studied in the CHAMPION (Cangrelor versus Standard Therapy to Achieve Optimal Management of Platelet Inhibition)-PCI and CHAMPION-PLATFORM trials, which compared cangrelor against a 600-mg loading dose of clopidogrel initiated before or after PCI. Both trials were stopped early because of no differences in the rates of the primary efficacy endpoint at 48 hours. A pooled analysis of these trials, which used the universal definition of MI (removing approximately 60% of clinical endpoints, namely, periprocedural MI), demonstrated a reduction in the composite of death, MI, or ischemia-driven revascularization and stent thrombosis without any increase in severe bleeding in patients randomized to cangrelor compared with clopidogrel. Subsequently, the CHAMPION-PHOENIX trial was conducted; it randomized patients (44% with ACS, including 18% with STEMI) to cangrelor or a clopidogrel loading dose (300 to 600 mg) before elective or urgent PCI, which demonstrated that cangrelor reduced the primary efficacy endpoint (death, MI, ischemia-driven revascularization, or stent thrombosis) and the individual endpoints of stent thrombosis and intraprocedural stent thrombosis without any increase in bleeding. Cangrelor may be useful as an agent to guarantee platelet inhibition in acute clinical situations like STEMI or NSTEMI, in which oral ADP P2Y 12 inhibition is inadequate or cannot be administered.


Practical Considerations for Patients on Oral Anticoagulation


Approximately 5% to 8% of patients are on an oral anticoagulant at admission for conditions such as atrial fibrillation, venous thromboembolism, or mechanical heart valves. Interrupting therapy can lead to a higher rate or thromboembolism ; however, bridging strategies increases the risk of bleeding and adverse ischemic events. If patients are on therapeutic oral anticoagulation and undergoing PCI for acute MI, a radial approach should be used, if possible, to minimize the risks of bleeding. Anticoagulation during PCI with either IV unfractionated heparin (dosed according to baseline ACT) or bivalirudin (without dose adjustment) is needed, regardless of the timing of the last dose of oral anticoagulation. GPIs should be avoided in these patients during PCI because of the higher risk of bleeding, other than for bailout indications.


Following PCI, the optimal antithrombotic regimen is not known. Alternatives are discussed in Chapter 21 . The WOEST (What Is the Optimal Antiplatelet and Anticoagulant Therapy in Patients with OAC and Coronary Stenting) study randomized patients who underwent PCI (n = 573) with an indication for oral anticoagulation to triple antithrombotic therapy (aspirin/clopidogrel/warfarin) or clopidogrel and warfarin. Both groups had similar ischemic event rates at 12 months, but bleeding was significantly higher with the triple antithrombotic therapy. Somewhat analogously, the ISAR-TRIPLE (Intracoronary Stenting and Antithrombotic Regimen–Testing of a 6-Week Versus a 6-Month Clopidogrel Treatment Regimen in Patients With Concomitant Aspirin and Oral Anticoagulant Therapy Following Drug-Eluting Stenting) trial found that 6 months of triple therapy was not superior to 6 weeks of triple therapy, although there was less bleeding with the shorter duration of triple therapy. Expert opinion on the management of patients on oral anticoagulation who are undergoing PCI is suggested in Table 17-4 .



TABLE 17-4

Suggested Management of Patients on Oral Anticoagulation Undergoing Percutaneous Coronary Intervention in Acute Myocardial Infarction

Adapted from Rubboli A, et al: The optimal management of patients on oral anticoagulation undergoing coronary artery stenting. The 10th anniversary overview. Thromb Haemost 112:1080–1087, 2014.




































































































Timing VKA NOAC
Periprocedural Management: STEMI
Anticoagulation Uninterrupted Uninterrupted
Additional IV UFH
(dose)
Yes
(reduced: 50 U/kg)
Yes
(reduced: 50 U/kg)
IV bivalirudin
(no dose adjustment)
May be considered, especially if bleeding risk high May be considered, especially if bleeding risk high
Vascular access site Radial Radial
Type of stent New-generation DES New generation DES
Antiplatelet therapy ASA 325 mg and
clopidogrel LD (300–600 mg)
ASA 325 mg and
clopidogrel LD (300–600 mg)
Adjunct GPI No No
Periprocedural Management: NSTEMI
Anticoagulation Uninterrupted Discontinuation
(24 h in advance without bridging)
Additional IV UFH
(dose)
Yes
(reduced: 50 U/kg)
Yes
(reduced: 50 U/kg or standard 70–100 U/kg, depending on last dose)
IV bivalirudin
(no dose adjustment)
May be considered, especially if bleeding risk high May be considered, especially if bleeding risk high
Vascular access site Radial Radial
Type of stent New-generation DES New-generation DES
Antiplatelet therapy ASA 325 mg and
clopidogrel LD (300–600 mg)
ASA 325 mg and
clopidogrel LD (300–600 mg)
Adjunct GPI No Provisional
Antithrombotic Management: 0–12 mos
Initital therapy Triple therapy
(ASA 81 mg/day, clopidogrel, VKA)
Triple therapy
(ASA 81 mg/day, clopidogrel, NOAC)
Duration of triple therapy 6 mos 6 mos
Intensity of OAC during triple therapy Reduced
(goal INR 2–2.5)
Reduced
(lower dose of NOAC: dabigatran 110 mg bid; rivaroxaban 15 mg/day; apixaban 2.5 mg bid)
Monitoring during triple therapy INR every 2 weeks Hemoglobin and kindey function every 4 wks
Gastric protection Yes (PPI) Yes (PPI)
Antithrombotic management after triple therapy VKA (goal INR 2–3)
+ single antiplatelet therapy (ASA 81 mg/day or clopidogrel)
NOAC (standard dosing)
+ single antiplatelet therapy (ASA 81 mg/day or clopidogrel)
Antithrombotic Management: > 12 mos
Antithrombotic management VKA monotherapy
(+ ASA 81 mg/day or clopidogrel)
NOAC monotherapy
(+ ASA 81 mg/day or clopidogrel)

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Aug 10, 2019 | Posted by in CARDIOLOGY | Comments Off on Approach to Percutaneous Coronary Intervention in Myocardial Infarction
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