35. Acute Myocardial Infarction/Unstable Angina-Clinical Scenarios

Basil S. Nasir, MBBCh, and James E. Davies, Jr., MD

Concept

• Initial management of patients with acute myocardial infarction (MI)/unstable angina (UA) with a focus on patients in cardiogenic shock
• Define roles for percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG)
• Perioperative anticoagulation strategies
• Critical steps for CABG
• Potential pitfalls and alternate scenarios

Chief complaint

“A 63-year-old woman presents with acute onset crushing, substernal chest pain and dyspnea at rest lasting 1 hour. Her past medical history is significant for insulin-dependent diabetes mellitus, hypertension, and hyperlipidemia.”

Differential

The initial distinction to make in these patients is stable angina versus acute coronary syndrome (ACS). The later includes unstable angina (UA) or non-ST elevation MI (NSTEMI) [often grouped together for management purposes] and ST elevation MI (STEMI). This further distinction is made on the basis of EKG tracing and cardiac markers. Symptoms occurring at rest rule out stable angina. Other potential diagnoses include acute aortic dissection and pulmonary embolism. In the event that all the above are ruled out, other pulmonary or gastrointestinal causes for the pain may be sought, including cholecystitis, pneumonia, peptic ulcer disease, etc. The initial management, including confirmation of the diagnosis as well as ruling out other pathology will be reviewed below.

History and physical

A full history should be undertaken with a focus on symptoms of chest pain, dyspnea or heart failure, and the chronicity of these symptoms. Assessment of past medical and social history to illicit risk factors for cardiac ischemia should also be performed. A full physical examination should be performed with attention to vital signs, neurological, cardiovascular and respiratory systems to help support the diagnosis and identify potential complications of MI or UA.

Differential

• Laboratory studies. Cardiac biomarkers are used to confirm the diagnosis of myocardial infarction. Complete blood count (CBC), coags, LFTs, blood gas, lactate and electrolyte panel including creatinine level should be obtained.
• EKG. EKG leads are placed in all 4 extremities with the ground typically in the right leg. Six precordial leads wrap around left thorax. Assessment for EKG abnormalities including ST changes, Q waves or T wave inversions may help delineate the myocardium at risk and the culprit vessel. EKG abnormalities in the inferior leads (II, III, aVf) and posterior findings (reciprocal changes in V1-2) suggest RV or RCA territory ischemia (or left dominant PDA disease). EKG abnormalities in the antero septal (V1-2), anteroapical (V3-4) or anterolateral (V5-6, I, aVL) suggest LV or LAD/LCx territory ischemia. Categorization of the myocardial infarction is based on ST changes and the initial clinical evaluation. Patients who present with angina-type symptoms for greater than 20 minutes with ST elevation > 1 mm in 2 contiguous leads or a new left bundle-branch block are diagnosed with an ST elevation myocardial infarction (STEMI). These patients are at greatest risk of transmural ischemia and are most often approached with PCI initially rather than CABG. Patients presenting with chest pain at rest lasting at least 10 minutes with elevated cardiac biomarkers or ST elevation of 0.5 to 1 mm or ST depression greater than 0.5 mm or T wave inversion greater than 1 mm are categorized as having non-ST elevation myocardial infarction (NSTEMI). These patients are more likely to have subendocardial ischemia rather than transmural. NSTEMI and UA patients are often grouped together for management purposes. The goal of management in UA/NSTEMI is prevention of a transmural MI (ST elevations +/- Q waves). The EKG is also helpful in assessment of arrhythmias.
• CXR. Evaluate for pulmonary edema, congestive heart failure, or other pulmonary pathology. A widened mediastinum may be a clue to a diagnosis of aortic dissection/aneurysm. Look for calcification of the aorta which should then prompt a CT for further evaluation.
• Transthoracic echo. Evaluate global LV and RV function (EF%), regional wall motion abnormalities, valvular dysfunction, septum (VSD), and pericardium (effusions). Regional wall motion abnormalities may reveal the coronary territories involved in the infarct (i.e., posteroseptal/posterior/inferior/diaphragmatic free RV wall – RCA or left dominant PDA; anteroseptal/apical – LAD; lateral wall – LCx). Type of wall motion abnormality may suggest the stage of infarction (i.e., hypokinetic – early, akinetic – old, dyskinetic – could be either).
• Myocardial viability studies. These will rarely be obtained in a patient with STEMI but may be useful in patients with chronic stable angina or history of prior infarct. A reasonable indication for a viability study would be a history of ischemia with low ejection fraction (< 50%) and extensive akinesis on echo. This is especially true in a high-risk patient when it is unclear if revascularization will improve function or symptoms. Positron emission tomography (PET) scanning is the most common method used for this. If the PET shows decreased perfusion with preserved F-fluorodeoxyglucose (FDG) uptake, then this patient has viable myocardium that will benefit from revascularization. If there is extensive scar tissue as evidenced by decreased perfusion and decreased uptake, then the benefits of revascularization are questionable. MRI is another viability study that is being used.
• Computed tomography (CT). If the initial work-up for cardiac ischemia is negative, CT angio can be used to rule out pulmonary embolism, aortic dissection or other intra-abdominal pathology. CT is useful for ruling out ascending calcification if the CXR suggests excessive calcium.
• Coronary angiogram: gold standard for evaluating coronary lesions. Any lesion ≥ 70% is significant and thus a candidate for revascularization. Concomitant lesions > 50% may be reasonable to revascularize during open heart surgery for other issues. LM lesions ≥ 50% are significant. Physiologic studies may be used for questionable lesions. Fractional Flow Reserve (FFR) ≤ 0.8 is considered “significant.”

Index scenario (additional information)

“History reveals similar episodes of chest pain in the past but lasting less than 10 minutes. Physical exam shows a diaphoretic woman with cool, clammy peripheries. Her heart rate is 120 beats per minute and blood pressure is 80/40 mmHg. The rest of the exam is unremarkable. Serum troponin levels are shown to be 10.2 µg/L (normal is < 0.1) and EKG shows ST elevation (> 1 mm) in leads V2 – V5. CXR is unremarkable.”

Treatment/management

The diagnosis is cardiogenic shock secondary to an acute anterior STEMI. Initial medical therapy includes aspirin, nitroglycerin, morphine and supplemental oxygen. Heparin is often used as well especially in UA/NSTEMI patients awaiting surgery. Plavix is used if it is likely that a percutaneous intervention will be performed. If Plavix is given it is advisable to wait 5 days prior to CABG when possible (most applicable to UA/NSTEMI or stable angina). Ask about any other GPIIb/IIIa receptor blockers. Beta blockers, although indicated in patients with coronary ischemia, are contraindicated in this case due to hypotension. Appropriate venous access, with a central line if needed, is established. Invasive arterial monitoring and pulmonary artery catheters are helpful in guiding resuscitation.

Optimizing cardiac filling pressures should be undertaken by using fluid resuscitation or diuretics depending on the situation. Pulmonary capillary wedge pressures (PCWP) should be kept in the 16-22 mmHg range. Additional medical therapy includes use of inotropic agents such as milrinone, dobutamine or epinephrine to augment cardiac contractility once filling pressures are optimized. Vasopressors, such as phenylephrine or vasopressin, may be indicated, but they should be used with caution as they can cause an increase in afterload and other negative effects.

Intra-aortic counterpulsation

Use of an intra-aortic balloon pump (IABP) is helpful in cases of refractory shock despite initial medical management or in patients with major complications of myocardial infarction such as postinfarction ventricular septal defect (VSD) or acute papillary muscle rupture. It is also helpful for patients with UA/NSTEMI awaiting surgery.

The IABP is inserted via the femoral artery. The tip of the balloon should be positioned in the descending thoracic aorta just distal to the left subclavian artery. The position could be estimated at the time of insertion using the manubriosternal junction (angle of Louis) as an external landmark. Position could be confirmed by CXR, echocardiography or by fluoroscopy if placed at the time of catheterization. The IABP is set to inflate during diastole, just after the aortic valve closes, which is signified by the dicrotic notch on the arterial blood pressure tracing. The balloon deflates as late as possible during diastole, just before the aortic valve opens, which is marked by the onset of the R wave on the EKG tracing. By increasing coronary flow during diastole and decreasing afterload during systole the IABP improves myocardial oxygen supply and demand. Severe aortic insufficiency and peripheral vascular disease are contraindications for IABP.

Reperfusion strategies

Despite initial medical therapy and stabilization of the patient, establishing reperfusion of the ischemic myocardium is most important. Options include thrombolysis, PCI and CABG. In the setting of an STEMI, PCI is first line therapy. The goal should be door-to-balloon time of 90 minutes or less. In hospitals with limited access to interventional cardiology expertise, thrombolysis is a reasonable alternative. CABG has a limited role and has largely been replaced by PCI as first line therapy.

Once the culprit lesion is identified and treated with a balloon angioplasty, the decision must be made to proceed with PCI and intracoronary stenting or CABG for definitive revascularization. Emergency CABG is indicated in the following situation:

• Patients in whom primary PCI has failed or cannot be performed, AND…
• Coronary anatomy is suitable for CABG, AND…
• Persistent ischemia of a significant area of myocardium at rest and/or hemodynamic instability refractory to nonsurgical therapyis present.

OR…

• Patients with mechanical complication of MI including papillary muscle rupture, post-infarction VSD or left ventricular rupture. Note that these are late complications which typically occur 5 to 7 days following MI.

There are situations where emergency CABG may be preferred over PCI even in the setting of an acute STEMI and they generally revolve around scenarios where the lesions are not favorable for complete revascularization with PCI:

• Left main disease > 50% → PCI has become a reasonable alternative in the setting of an STEMI according to most experts although surgery is still the default option. If the patient’s lesion is such that the anatomy is favorable for PCI, with a low syntax score, low chance of periprocedural complications and the patient is at high risk for CABG then PCI is the intervention of choice. Otherwise go to CABG.
• Left main equivalent (> 70% stenosis in the proximal left anterior descending (LAD) and circumflex arteries). Similar considerations to that discussed for LM (high risk patient, good anatomy, low syntax – consider PCI if its faster).
• Severe 3-vessel disease → CABG, especially if diabetic, reduced ejection fraction (EF) < 50%, high syntax score (> 32).

Operative steps

Coronary artery bypass grafting in the setting of acute MI and cardiogenic shock.   

Note: Preoperatively, have a sense of the degree of end organ damage that has already occurred. Check lactate, LFTs, creatinine. If the patient has already suffered a significant amount of end organ injury, then stabilizing the patient with mechanical support (IABP versus ECMO versus VAD) may be reasonable until some reversal of end organ effects has occurred prior to surgery. If you decide to go to surgery, bear in mind that there is data suggesting waiting for at least 24 hours after the infarct has occurred prior to CABG unless you can revascularize within 6 hours of the infarct. There is some conflicting evidence regarding this issue and thus, the most prudent decision would be revascularize as soon as possible unless there is severe end organ dysfunction. The official ACC/AHA 2011 guidelines support emergent revascularization “irrespective” of the time from MI to CABG.

• Large bore peripheral intravenous access, radial arterial line, central venous line, pulmonary artery catheter, urinary catheter.
• General endotracheal anesthesia. Pre-induction IABP is recommended, especially in patients with reduced EF. Patients taken directly to surgery from the catheterization lab should have an IABP placed prior to transfer.
• Intraoperative transesophageal echocardiogram. Check for complications including ischemic mitral regurgitation (MR), left ventricular rupture, etc.
• Median sternotomy.
• Choice of conduit: Based on American Heart Association guidelines, use of the left internal mammary artery (LIMA) for LAD bypass is reasonable, even in the urgent setting. If the patient is unstable, and salvage surgery is undertaken, then vein grafts are acceptable because of the reduced time in harvesting the conduit.
• Open the pericardium, check the aorta for plaque and have lines available prior to LIMA harvest.
• Give heparin (400 units/kg).
• Arterial cannulation: Cannulation of the ascending aorta is preferred. Palpate the aorta and look for plaques. Epiaortic ultrasound is an adjunctive measure.
• Venous cannulation: two-stage cannula via the right atrial appendage.
• Myocardial protection. Place antegrade cardioplegia catheter/aortic root vent in the ascending aorta. Place a retrograde catheter in the coronary sinus. Remember to de-air cardioplegia lines prior to connecting them.
• Check activated clotting time (ACT). If ACT > 480 seconds, initiate CPB at normothermia or mild hypothermia.
• It may be helpful to identify targets for the distal anastomoses prior to cross clamping, as that may be difficult in the arrested heart, especially if targets are small.
• Prepare for aortic cross clamp. Reduce arterial flow. Apply cross clamp. Go back up to full flow (2.0-2.5 L/min/m²). Arrest the heart with antegrade cardioplegia followed by retrograde cardioplegia.
• Distal anastomoses. Usually start with the right sided grafts. In the case of vein grafts, instillation of blood cardioplegia down the vein graft after finishing the distal anastomosis is encouraged. In general, 7-0 or 8-0 polypropylene suture is used in a running fashion. For the LIMA graft, make sure the graft is occluded with a bulldog clamp while the heart is arrested to ensure adequate myocardial protection.
• Proximal anastomoses. Make sure that the vein grafts are not twisted and there is enough slack to allow for distension of the heart when it fills. Create aortotomy. In general, 5-0 polypropylene in running fashion is used.
• Remove aortic cross clamp. Consider terminal infusion of warm blood cardioplegia or “hot shot” in patients with left ventricular dysfunction prior to removing cross clamp.
• Check for hemostasis and wean from CPB.
• Give protamine.
• Place temporary atrial and ventricular pacing wires. Place chest tubes and close.

Potential questions/alternative scenarios

“Patient with acute NSTEMI, hemodynamically stable and meets indications for CABG.”

Maximize the patient medically with heparin, ASA, oxygen, and IABP if refractory angina or low EF. Plan for urgent CABG. As mentioned above for revascularization in the setting of acute STEMI, some studies recommend waiting 1-3 days but ACC/AHA 2011 guidelines recommend revascularization irrespective of the timing between MI and CABG. Thus, in general proceed to the OR ASAP although you can afford a short delay of 24 hrs if the patient remains exceedingly stable. Outcomes may be better with the later approach.

“A 70 M patient is resuscitated from a witnessed cardiac arrest. Coronary angiography shows 3 V disease.”

Urgent CABG is indicated for patients who have suffered a sudden cardiac arrest or life-threatening arrhythmia due to ischemic disease.

“Patient with inferior infarction and right ventricular involvement.”

In general, similar considerations regarding timing of OR apply here as well. The assumption is that PCI has failed, or the patient has severe three vessel disease that is more amenable to CABG. Thus, CABG should be considered in an urgent fashion. The one caveat is that outcomes are poor in the setting of severe right heart failure, despite adequate revascularization and myocardial protection. In this setting, it may be preferred to delay CABG until the RV is optimized with inotropes, diuretics, or even mechanical support as needed depending on the degree of shock.

“Patient with recent MI and drug-eluting stent (DES), now presents for CABG.”

The question of what do with a recently stented artery is controversial. If the stent is compromised, then it is reasonable to place a vein graft distal to the stent. If the stent is wide open without stenosis, any graft placed distal to it is likely to fail due to competitive flow. It is reasonable to leave that vessel alone, and just graft other compromised vessels.

“The above alternative patient is less than 1 year out from his DES placement. He is currently on clopidogrel and presents for urgent CABG 2 days after a NSTEMI.”

Stopping the clopidogrel for 7 days carries a high risk for in-stent thrombosis since the DES is less than 1 year old (30 days in the setting of a bare metal stent). Performing surgery < 24 hrs after stoping plavix increases the risk of bleeding. The best scenario is to discontinue the plavix for 5 days in the elective setting or at least 24 hrs in the urgent setting. Short-acting antiplatelet agents, such as eptifibatide or tirofiban should be discontinued for at least 2 to 4 hours before surgery and abciximab for at least 12 hours before surgery. Clopidogrel is resumed shortly after surgery (usually the next day). If there is concern about in stent thrombosis due to an inability to resume plavix for any reason then it may be reasonable to place a vein graft distal to the stented vessel, regardless of patency. If you find yourself operating emergently on clopidogrel, there are no good options to reduce the risk of bleeding. Antifibrinolytic agents, such as aminocaproic acid, should be used. There is a higher risk of postoperative bleeding and increased transfusion requirements. Platelet transfusion is helpful in this setting, even if the platelet count appears adequate, as native platelets are dysfunctional.

“Patient with history of MI. Echocardiogram shows akinetic myocardium.”

In this setting dobutamine echocardiography, thallium imaging or positron emission tomography (PET) are useful. If hibernating myocardium is identified, then that region will benefit from revascularization. Infarcted myocardium will not.

“Seven days post-CABG, a patient complains of pleuritic chest pain and a fever. There is an associated lymphocytosis.”

This likely represents postpericardiotomy syndrome, or if following an AMI, Dressler’s syndrome. A pericardial rub may be present. The associated leukocytosis is predominated by lymphocytes or eosinophils. It is important to rule out other infectious complications, especially pneumonia. The diagnosis is one of exclusion. The treatment includes non-steroidal anti-inflammatory agents for 1 to 3 months. If this fails, then a course of steroids should be started. Colchicine has also been described in cases with persistent symptoms.

Pearls/pitfalls

• Distinguish between STEMI and NSTEMI/UA. The former is almost always treated with PCI while the later is more likely to be considered for CABG if anatomy is suitable (LM, 3V Dz).
• CABG is indicated in STEMI for failed PCI, mechanical complications of MI and cardiogenic shock if anatomy is unfavorable for PCI.
• If urgent CABG is indicated and the patient can be stabilized medically, it may be beneficial to delay surgery for 1-3 days.
• Pre-induction IABP placement is recommended for emergency CABG.
• If possible, stop plavix at least 24 hours prior to surgery and preferably 5 days before surgery.

Suggested readings

• Geroge I and Oz MC. Myocardial revascularization after acute myocardial infarction. Cohen LH (ed). Cardiac Surgery in the Adult. 2008;669-697.
• Hillis LD, et al. 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: Executive Summary. Circulation. 2011;124:2610-2642.
• Antman EM, et al. ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction. Circulation. 2004;110:e82-e292.
• Jneid H, et al. 2012 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction (Updating the 2007 Guideline and Replacing the 2011 Focused Update). Circulation. 2012;126:875-910.