A. Introduction. Unstable angina, non–ST segment elevation myocardial infarction (NSTEMI) and ST segment elevation myocardial infarction (STEMI) constitute acute coronary syndrome (ACS). The term encompasses the entire range of presentations associated with a common pathophysiology along a continuum of severity of acute ischemic heart disease. ACS is a leading cause of death in the United States. Many therapies have a proven mortality benefit in the treatment of ACS; therefore, the failure to recognize ACS can lead to delayed and suboptimal therapy.
B. Pathophysiology of Acute Coronary Syndrome. ACS usually results from the rupture of an unstable atherosclerotic plaque with subsequent thrombosis within the lumen of a coronary artery. This leads to inadequate blood flow and oxygen delivery, which in turn results in myocardial cell injury and necrosis. It is important to recognize that the underlying biology of the plaque rendering it unstable is more important than the severity of angiographic stenosis that it creates. This is why some patients can have a true negative stress test a short period of time before presenting with ACS. Less common causes of ACS without plaque rupture include coronary vasospasm (usually associated with coronary artery disease), coronary artery dissection, coronary emboli (e.g., atrial fibrillation with left atrial appendage thrombus, left atrial myxoma, paradoxical emboli), aortic dissection (usually with right coronary artery involvement), vasculitis, and cocaine use (atherosclerosis, vasospasm, and platelet aggregation are presumed etiologies).
Recognized triggers of plaque rupture include but are not limited to exertion, sexual activity, anger, mental stress, cocaine use, tobacco use, fevers, and specific infections (influenza).
C. Clinical Manifestations of Myocardial Infarction. Typical symptoms and signs associated with cardiac ischemia are discussed in Chapters 9 and 10. The chest pain associated with ACS differs from that of stable angina in that it can occur while the patient is at rest or with minimal exertion, lasts more than 20 minutes, is more severe, and is unrelieved with rest or sublingual nitroglycerin; however, these findings are variable. Pain that lasts for more than 20 minutes should be considered due to myocardial infarction (MI) (either NSTEMI or STEMI) until proven otherwise.
D. Diagnosis. Because unstable angina and MI share similar pathophysiology, it is not surprising that they frequently cannot be distinguished by clinical criteria alone. When ACS is suspected, patients are usually referred for emergent evaluation including serial electrocardiograms (EKGs) and cardiac biomarker studies, which are helpful to establish a definitive diagnosis. The diagnosis of MI is made by the presence of cardiac biomarker elevation in the setting of typical symptoms and signs of MI, EKG changes consistent with an MI, or both. However, lack of EKG changes or cardiac biomarker elevation does not rule out ACS in the form of unstable angina defined as (1) ischemic cardiac symptoms at rest typically lasting 20 minutes or longer, (2) new/recent onset (4–6 weeks) of exertional ischemic symptoms with low level of exertion, or (3) rapid progression of preexisting exertional angina.
The diagnosis of MI is made by the presence of cardiac biomarker elevation in the setting of typical symptoms and signs of MI, or EKG changes consistent with an MI, or both.
a. Patient history and physical examination. Chest pain is the most common symptom of ACS, but other signs and symptoms may also be present (e.g., flash pulmonary edema, hypotension, dyspnea, ischemic mitral regurgitation). Atypical presentations can include dyspnea, fatigue, epigastric pain, or pleuritic pain and are more likely to occur in older adult patients, women, diabetic patients, or patients with dementia.
b. Electrocardiography. An initial EKG is the key to triaging patients with ACS and should be performed within 10 minutes of arriving at the emergency department. Following admission of the patient, EKGs are usually obtained on a serial basis until resolution of symptoms occurs and/or the EKG changes stabilize. For example, if the initial EKG is normal in a patient who has symptoms with high level of suspicion for ACS, serial EKGs should be repeated every 15–30 minutes within the first hour to help detect ischemic changes. A daily EKG and an EKG following reports of any symptoms are usually obtained thereafter. Specific EKG findings for MI or ischemia include hyperacute (peaked) T waves, ST elevations, ST depressions, Q waves, or inverted T waves. Comparison to prior EKG (obtained when the patient was not symptomatic) can be very helpful.
The EKG is normal in up to 10% of patients with documented MI.
i. ST segment depressions and elevations may reflect both MI and injury.
1. The subendocardial region of the myocardium is the most susceptible to ischemia because it is perfused “last” (i.e., the coronary arteries course from the outer epicardial surface inward). Because the subendocardium is on the inner surface of the heart away from the EKG leads on the chest wall, subendocardial injury may be seen as ST segment depression. Epicardial injury, in contrast, is closer to the surface EKG leads and typically occurs with transmural ischemia; it most often results in a larger amount of myocardial damage and is evident as ST segment elevation on EKG. ST segment elevations also may occur with transient ischemia (e.g., from vasospasm).
2. Traditional terminology that identifies ST segment depressions as “ischemia” and ST segment elevations as “infarct” is an oversimplification. ST depressions may occur with infarction, and ST segment elevations may occur with transient epicardial ischemia (e.g., from coronary vasospasm). ST segment changes in ACS are more accurately thought of as representing myocardial “injury.”
ii. Q waves signify electrical activity moving away from the area of the heart where they are seen; they usually indicate dead muscle (previous MI) in that region. Q wave MIs may occasionally disappear on EKG over years.
iii. T wave abnormalities including peaked, tall T waves (can precede ST elevations in STEMI), T wave inversion, or pseudo-normalization can be markers of ischemia in the appropriate clinical setting.
iv. A right-sided EKG (leads V1 and V2 reversed, with the other leads placed in corresponding positions on the right side of the chest) should be obtained in all patients with an acute inferior wall MI. Right ventricular infarction may complicate the clinical course of an MI and is associated with a higher in-hospital mortality rate. ST segment elevation in leads RV4 or RV3 on a right-sided EKG indicates right ventricular infarction. Likewise, in patients with high suspicion for ACS with active symptoms and nondiagnostic EKG, it is reasonable to perform an EKG with posterior leads (V7–V9) because it can help uncover ischemic changes in an otherwise EKG-silent ACS.
v. Some baseline EKG abnormalities such as left bundle branch block or ventricular pacing can reduce the utility of EKGs in identifying ischemia. The Sgarbossa criteria may be helpful in identifying ischemia with these EKG abnormalities but have a low sensitivity.
c. Cardiac biomarker studies
i. MI is usually associated with an elevation in the level of cardiac biomarkers. Cardiac biomarkers should be checked at presentation and 3–6 hours after symptom onset in all patients with suspected ACS. Serial measurement of cardiac biomarkers should be obtained every 6–8 hours for 24 hours or until a trend is established. Currently, clinically used cardiac biomarkers include:
1. Cardiac troponins (troponin I and troponin T): Troponins are currently considered the gold standard biomarker given their high specificity and sensitivity compared with creatine kinase. Troponin levels usually rise within 2–4 hours of cell injury, peak at 18–24 hours, and may remain elevated for several days (up to 2 weeks). Newer high-sensitivity troponin assays can help rule in or rule out myocardial infarction more rapidly than older generation assays.
2. Creatine kinase (CK) and CK-myocardial band (CK-MB) have lower sensitivity and specificity compared with cardiac troponins. Their levels usually peak in 16–18 hours. Because of the different kinetics of CK-MB release, CK-MB could still have a role in the detection of early recurrent MI (although troponins have proven to be just as useful).
3. Myoglobin levels are nonspecific to cardiac injury and therefore are no longer used.
Causes of troponin elevation other than ACS:
Cardiac: type 2 MI (demand ischemia), myocarditis, myocardial injury (contusion), post- cardioversion/ablation, infiltrative diseases (amyloidosis), cardiomyopathy (hypertrophic cardiomyopathy), Takotsubo cardiomyopathy, drug-induced cardiomyopathy (chemotherapy), sustained arrhythmias, coronary vasospasm, and hypertensive emergency
Noncardiac: pulmonary embolism, sepsis, acute neurologic disease, acute blood loss anemia, and decreased clearance in renal failure
d. Additional testing. Bedside resting echocardiogram can be helpful in some patients with clinically suspected ACS without EKG changes or biomarker elevation. New wall-motion abnormalities in a specific coronary territory in the setting of active symptoms could be highly suggestive of ACS. Other information about global left ventricular function and valve abnormalities could also be helpful.
E. Approach to the Patient. The treatment of ACS requires both precision and speed. The following stepwise approach allows you to make critical treatment decisions immediately, followed by those that are less urgent. Whenever a patient is admitted with ACS, it is helpful to answer three questions: (1) What is the patient’s hemodynamic status? (2) Is reperfusion (i.e., thrombolysis or primary percutaneous coronary intervention [PCI]) indicated? (3) What other treatments may benefit the patient?
a. What is the patient’s hemodynamic status?
i. Assessment. Hemodynamic status can be approximated by examination of the volume status (e.g., jugular venous pressure [JVP] and lungs) and end-organ perfusion (e.g., extremities examination, mental status, and urine output).
1. Low-risk patients (as determined by hemodynamic status) have normal JVP, clear lungs, and warm extremities associated with normal peripheral pulses and no findings of end-organ hypoperfusion. The presence of clear lungs usually indicates normal left ventricular filling pressures (i.e., a normal pulmonary capillary wedge pressure [PCWP]), and normal findings on examination of the extremities imply adequate cardiac output.
2. Intermediate-risk patients have a normal extremity examination, but elevated JVP and/or pulmonary rales are found on examination. In these patients, elevated right-sided and left-sided filling pressures (i.e., right atrial pressure [RAP] >10 mm Hg and PCWP >18 mm Hg) are suspected.
3. High-risk patients (as determined by hemodynamic status) have pulmonary rales and cool extremities (due to vasoconstriction and decreased cardiac output) with diminished peripheral pulses. These patients are in cardiogenic shock. The presence of pulmonary edema suggests that the PCWP, an estimate of end-diastolic volume, is elevated. Normally, according to the Starling curve, a high end-diastolic volume ensures that the stroke volume will be maximized. If the heart is unable to adequately perfuse the end organs despite adequate filling (i.e., a high PCWP), cardiogenic shock is diagnosed. Urine output and mental status can be very helpful in assessing adequate end-organ perfusion.
1. Low-risk patients are by definition hemodynamically stable and have a low mortality rate. Management of these patients entails deciding whether reperfusion therapy (i.e., thrombolysis or primary PCI) is indicated and what other forms of medical therapy might benefit the patient.
2. Intermediate-risk patients have evidence of pulmonary edema, which may decrease oxygenation while increasing oxygen demand (increased sympathetic tone increases the heart rate and myocardial contractility).
a. Agents frequently used in the treatment of MI (e.g., nitrates, morphine) may also treat pulmonary edema by decreasing preload.
b. Intravenous diuretics could be given as needed.
3. High-risk patients have cardiogenic shock.
a. Early/emergent percutaneous intervention (PCI) is the only therapy that has been reliably shown to decrease mortality rates in patients with cardiogenic shock from ACS and is clearly the treatment of choice.
b. Pharmacologic therapy is dictated by the patient’s blood pressure. Although cardiogenic shock is often accompanied by hypotension, blood pressure may still be normal with low-flow states because of a significant increase in systemic resistance.
Do not assume that normal blood pressure indicates adequate end-organ flow.
i. Systolic blood pressure >90–100 mm Hg
1. Dobutamine is often started intravenously at a dose of 2.5 mcg/kg/min. The dose may be increased gradually (up to 15–20 mcg/kg/min) until the cardiac output rises and the PCWP falls. Dobutamine raises cardiac output by increasing myocardial contractility and by decreasing systemic vascular resistance. Because blood pressure is the product of cardiac output and systemic vascular resistance, it may remain stable, increase, or decrease depending on how much the cardiac output increases in comparison with the decrease in systemic vascular resistance. A decrease in blood pressure could occur with dobutamine therapy, so the systolic blood pressure should be greater than 90 mm Hg (and preferably greater than 100 mm Hg) before the initiation of therapy.
2. Vasodilators (sodium nitroprusside) are alternatives to dobutamine but often require a higher starting blood pressure or the concomitant administration of an inotrope. Sodium nitroprusside is very effective in decreasing systemic vascular resistance, thus increasing cardiac output and end-organ perfusion.
ii. Systolic blood pressure <90 mm Hg
1. Vasopressors and inotropes are often used to maintain a perfusing blood pressure and cardiac output. Norepinephrine has emerged as the vasopressor of choice in cardiogenic shock. Dopamine can be used as an alternative. After hypotension resolves with the use of vasopressors, hemodynamics are usually further optimized using an inotrope (such as dobutamine or milrinone). Because arrhythmias may complicate inotropic (and vasopressor) therapy, patients require careful rhythm monitoring, and electrolytes should be maintained in the normal range (especially potassium and magnesium levels).
2. Temporary mechanical support such as the placement of an intra-aortic balloon pump (IABP) increases cardiac output, reduces systemic resistance, and improves coronary blood flow by improving perfusion pressure during diastole. When available, it should be considered in patients with acute ischemia and cardiogenic shock for hemodynamic stabilization.
c. Pulmonary artery (PA) line placement can be useful for monitoring cardiac output, systemic vascular resistance, and PCWP. In ACS, patients with evidence of cardiogenic shock can be assessed on a case-by-case basis for the need of hemodynamic monitoring with a PA line. Early removal of the pulmonary artery catheter (PAC), after the provided information is no longer necessary to manage the patient, can reduce complications from PAC, including infection and thrombosis.
d. Rule out other causes of shock. Assess for mechanical complications or other factors that could be contributing to noncardiogenic shock (e.g., distributive shock from sepsis).
Several clinical predictor calculators have been developed to risk-stratify and identify high-risk ACS patients. Of these calculators, the GRACE (Global Registry of Acute Coronary Events) is a well-validated predictor of in-hospital and 6-month outcomes (death, MI). The GRACE score is derived from patient characteristics, EKGs, and biochemical findings as well as hemodynamic findings suggestive of heart failure and cardiogenic shock.
b. Is reperfusion therapy with thrombolysis or primary PCI indicated? The initial triage EKG is critical in determining whether patients are appropriate candidates for immediate reperfusion therapy. In patients with ACS symptoms of 12 hours or less duration (and possibly up to 12–24 hours with clinical or EKG evidence of ongoing ischemia) and ST elevations of at least 1 mm in two contiguous EKG leads (i.e., STEMI) or evidence of a new left bundle branch block, immediate coronary reperfusion reduces mortality. Unless contraindicated, all such patients should be considered for emergent primary PCI or fibrinolysis. Importantly, studies in patients with NSTEMI have not shown any benefit with emergent reperfusion strategies. Rather (in the case of thrombolytics), potential harm may result in this situation.
1. Primary PCI for STEMI or STEMI equivalent: emergent primary PCI is the treatment of choice for patients with STEMI in centers that can perform PCI quickly and with expertise. It also may be favored when there are contraindications to thrombolytic therapy, and in select patients who can be transferred to a PCI capable facility with a goal reperfusion time of less than 120 minutes (preferably less than 90 minutes) from the time of first medical contact. More specifically, STEMI patients who should be considered for primary PCI include:
a. STEMI with symptoms onset <12 hours and goal reperfusion within <90 minutes of first medical contact.
b. STEMI with symptoms onset between 12 to 24 hours with clinical or EKG evidence of ongoing ischemia.
c. STEMI with cardiogenic shock, regardless of delay from STEMI onset.
d. STEMI with symptoms onset ≤12 hours and contraindication to fibrinolysis regardless of time delay needed to transfer to PCI-capable facility.
e. STEMI patients who received fibrinolytics with failed reperfusion or reocclusion.
f. Left heart catheterization with intention for revascularization should be considered in late presenting/completed STEMI if predischarge risk stratification is consistent with intermediate-risk or high-risk findings (systolic dysfunction, recurrent symptoms, or stress test with significant ischemia).
2. PCI for non–ST Elevation ACS (NSTE-ACS). In the absence of STEMI, revascularization remains a cornerstone in the management of NSTE-ACS with either an early invasive approach or a conservation approach.
a. Early invasive approach. In addition to optimal medical and antiischemic therapy, patients triaged to this strategy undergo diagnostic coronary angiography within 24–48 hours with the intent to revascularize. Patients with hemodynamic or electrical instability, refractory symptoms despite medical therapy, dynamic EKG changes, elevated troponins, new left ventricular systolic dysfunction (ejection fraction <40%), new significant mitral regurgitation, estimated high-risk patients (GRACE score >140 or TIMI score greater than or equal to 2) or patients with prior PCI within 6 months or prior coronary bypass surgery should be selected for this approach.
b. Conservative approach (ischemia-guided strategy) is reserved for low-risk patient (e.g., GRACE score <109, particularly in women) and focuses on intensification of antithrombotic and antiischemic treatment followed by further risk stratification based on results of noninvasive testing.
ii. Fibrinolysis should be considered for patients presenting with STEMI at a non-PCI capable facility within 12 hours of symptom onset (12–24 hours if active ischemia or hemodynamic/electrical instability) if there are no contraindications to fibrinolysis and the anticipated delay in reperfusion due to transferring to a PCI capable facility exceeds 120 minutes. Fibrinolysis should not be used to treat patients with NSTE-ACS (unless true posterior transmural injury/infarct is suspected with ST depressions in two or more precordial leads of V1–V3).
a. Absolute contraindications to fibrinolysis generally include the presence of:
i. Central nervous system (CNS) disease. A history of intracranial hemorrhage at any time or nonhemorrhagic stroke within 3 months, known structural cerebral vascular lesions (arteriovenous malformations or aneurysms), known malignant intracranial neoplasm, significant closed-head or facial trauma within 3 months, and recent intracranial surgery within 2–3 months are usually considered contraindications.
ii. Active bleeding (excluding menses)
iii. Suspected aortic dissection
b. Relative contraindications generally include:
i. Traumatic or prolonged cardiopulmonary resuscitation (>10 minutes).
ii. Recent non-cranial trauma or surgery (within 2–3 weeks).
iii. History of ischemic stroke more than 3 months prior.
iv. Sustained hypertension on presentation (e.g., blood pressure >180/110 mm Hg after appropriate treatment).
v. Recent internal bleeding (2–4 weeks).
vi. Noncompressible arterial or venous puncture sites during access attempts.
vii. Active peptic ulcer disease.
ix. Coagulopathy, thrombocytopenia, or current oral anticoagulation therapy.
2. Agents. The commonly used thrombolytic agents include streptokinase (non–fibrin specific) with preference for fibrin-specific agents including reteplase, tenecteplase, and alteplase. There may be slight advantages to one or the other agent, depending on the clinical situation.
3. General recommendations. The mortality benefit decreases drastically with delay in therapy, so speed is of the essence. Make sure a large-bore peripheral intravenous catheter (usually 16-gauge) is in place before therapy and limit venous and arterial blood draws. It is clear that the type of agent used is less important than ensuring that all patients who meet appropriate criteria receive thrombolytic therapy as rapidly as possible.
Time elapsed = myocardium lost.
4. Signs of successful reperfusion include a prompt decrease in chest pain, normalization of the ST segment (or at least 70% improvement), an accelerated idioventricular rhythm, or an early peak of the CK enzymes (within 12 hours).
c. What other treatments may benefit patients with ACS? Specific forms of therapy with nitrates, β-blockers, and CCBs as well as potential contraindications are outlined in Chapter 10. The coronary care unit (CCU) or specialized telemetry cardiac units are the best places to manage patients with ACS, given the need for frequent vital sign checks and continuous rhythm monitoring.
i. Acute medical therapy and early hospital care
1. Bed rest in the first 12–24 hours is recommended.
2. Analgesia. Nitrates are given initially to relieve pain, but morphine sulfate (2–4 mg intravenously) may be used for persistent pain (careful titration of dose may be needed in patients who have borderline low blood pressure.
3. Oxygen should be used for all ACS patients with Spo2 <90% or other high-risk features of ischemia.
ii. Antiplatelet therapy
1. Aspirin. A one-time dose of chewable aspirin (325 mg) should be given as soon as possible to all patients with ACS unless there is an absolute contraindication. Maintenance-dose aspirin (usually 81 mg daily) should be continued indefinitely regardless of treatment strategy.
2. P2Y12 inhibitor antiplatelet agents. All ACS patients should receive a loading dose followed by maintenance therapy with a P2Y12 inhibitor in addition to aspirin for up to 12 months if there is no contraindication. Oral P2Y12 inhibitors include clopidogrel, prasugrel, and ticagrelor. Prasugrel should be reserved for patients undergoing PCI or coronary stenting and is contraindicated in patients with a history of prior cerebrovascular accident or transient ischemic attack.
3. Glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors, including abciximab, eptifibatide, or tirofiban, could be considered as part of antiplatelet therapy in select patients (high-risk patients, particularly those with marked troponin elevation).
iii. β-Blockers have been shown to decrease mortality rates in patients with ACS. Oral β-blockers should be started within 24 hours in all ACS patients unless there is a contraindication (evidence of low cardiac output, signs of heart failure, bradyarrhythmias including high-grade atrioventricular (AV) block, findings suggestive of high risk for cardiogenic shock or active bronchospastic pulmonary disease). If left ventricular systolic function is reduced (<40%), β-blockers specific for heart failure (e.g., carvedilol) should be used. Intravenous β-blockers should be avoided due to potential harm (occasionally needed for patients in atrial fibrillation with rapid ventricular response and necessary in the setting of acute aortic syndrome).
iv. Nitrates are usually helpful for ACS patients with persistent ischemic symptoms, heart failure symptoms, or hypertension. Nitrates should be avoided in patients with hypotension, marked bradycardia, or right ventricular infarction given their dependence on preload. Nitrates are contraindicated in patients who recently received phosphodiesterase inhibitors (within 24 hours for sildenafil and 48 hours for tadalafil).
v. Angiotensin-converting enzyme (ACE) inhibitors (or the alternative angiotensin receptor blockers) should be considered within 24 hours for all STEMI patients (especially those with anterior MI, heart failure symptoms) or all ACS patients with left ventricular ejection fraction <40%, hypertension, diabetes mellitus, or chronic kidney disease if there are no contraindications. Angiotensin receptor blockers can be used to replace ACE inhibitors in patients who cannot tolerate these agents.
vi. CCBs have not been shown to have a mortality benefit or an effect on infarct size in patients with ACS. Nondihydropyridine CCBs can be used if there are persistent/recurrent ischemic symptoms after optimization of β-blocker therapy or if β-blockers are contraindicated in the absence of heart failure symptoms, left ventricular systolic dysfunction, risk for cardiogenic shock or bradycardia/high-grade AV block. Immediate-release nifedipine has been associated with worse outcomes (possibly owing to reflex sympathetic activation and tachycardia) and is contraindicated in the setting of ACS.
vii. Mineralocorticoid receptor antagonist. Aldosterone antagonist (spironolactone or eplerenone) treatment is recommended after ACS in patients who can tolerate therapeutic doses of β-blockers and ACE inhibitors and who have a left ventricular ejection fraction <40% with symptoms/signs of heart failure or history of diabetes mellitus, so long as there are no contraindications of significant renal dysfunction or hyperkalemia.
viii. Anticoagulation therapy. Currently available anticoagulants used in patients with ACS include heparin, low-molecular-weight heparin (LMWH), and the direct thrombin inhibitor bivalirudin. Fondaparinux is less commonly used. These agents are usually started on presentation and are often used until PCI is performed. If the patient is being medically treated without PCI, heparin is usually discontinued after 48 hours, whereas LMWH is used for up to 7 days or until discharge (whichever happens first).
ix. Statins. High-intensity statin therapy should be started or continued in all patients with ACS.
Nonsteroidal antiinflammatory drugs (NSAIDs) and nifedipine are contraindicated in ACS.
F. Complications of Acute Coronary Syndromes
a. Arrhythmias are most common during the initial 12–24 hours.
i. Tachyarrhythmias are evaluated and treated as discussed in Chapter 7. Of note, prophylactic lidocaine is no longer recommended in ACS. Rather, lidocaine is reserved for patients with sustained or nonsustained ventricular tachycardia. Patients with life-threatening tachyarrhythmias (ventricular tachycardia/fibrillation or nonsustained ventricular tachycardia [NSVT]) occurring 48 hours after presentation and without reversible causes (active reversible ischemia or reinfarction, metabolic derangements) are considered to be at high risk for sudden cardiac death. These patients should be evaluated for the placement of an implantable cardiac defibrillator (ICD) for secondary prevention. For patients with significant left ventricular systolic dysfunction, but no evidence of late (>48 hours) ventricular arrhythmias, left ventricular function should be reassessed after discharge to reevaluate the need for ICD for primary prevention of sudden cardiac death. Patients with nonsustained ventricular tachycardia occurring as early as 2–4 days after MI and in the setting of left ventricular systolic dysfunction should be appropriately assessed for ICD placement.
Therapeutic hypothermia should be considered and initiated as soon as possible in neurologically compromised or comatose patients following ventricular fibrillation or pulseless ventricular tachycardia arrest in the setting of ACS.
ii. Bradyarrhythmias are relatively common after STEMI and relate to an increase in vagal tone or hypoperfusion of the sinoatrial (SA) and AV nodes. They commonly occur in inferior wall or right coronary artery territory infarctions. High-grade AV block (Mobitz type 2 or complete heart block) is associated with worse prognosis in the setting of anterior/lateral wall infarcts. High-grade AV blocks in the setting of inferior/posterior infarcts are more likely to be transient and reversible.
1. Intravenous atropine (0.5–1 mg every 3–5 minutes, up to 3 mg) is usually effective for sinus bradycardia and symptomatic Wenckebach (Mobitz type 1) second-degree AV block.
2. Temporary pacing is generally recommended for patients with acute MI and:
a. Symptomatic sinus bradycardia and Wenckebach block that is unresponsive to medical therapy.
b. Mobitz type 2 second-degree AV block or third-degree AV block.
c. New bifascicular block, including alternating left and right bundle branch block, right bundle branch block with left anterior or posterior fascicular block, and left bundle branch block with first-degree AV block (particularly in patients with anterior/lateral MI).
b. Recurrent ischemia or chest pain following MI that is not responsive to medical management is usually an urgent indication for coronary angiography and revascularization.
c. Cardiogenic shock could be related to severe left ventricular failure or due to mechanical complications. In severe cases, intra-aortic balloon pump (IABP) and left ventricular assist devices may be necessary for patients who cannot be quickly stabilized with pharmacologic therapy. Revascularization or correction of mechanical complications in a timely manner is the most important intervention.
d. Right ventricular infarction should always be suspected when hypotension accompanies an inferior MI. Treatment involves large fluid boluses to increase right-sided cardiac output and left ventricular filling. Inotropic agents (i.e., dobutamine) with hemodynamic monitoring may also be required. Nitrates should be avoided because these patients are preload dependent.
e. Mechanical complications can have bimodal timing of presentation occurring within the first 24 hours or the first week after MI.
i. Free wall rupture and cardiac tamponade usually lead to abrupt hypotension, electromechanical dissociation, and death. When a rupture is contained, a pseudoaneurysm may form and can be visualized on echocardiography. Emergency surgery should be considered for this event.
ii. Ventricular septal defect or acute mitral regurgitation (papillary muscle rupture of dysfunction)
1. Clinical signs and symptoms
a. These disorders are often heralded by hemodynamic instability, pulmonary edema, or both. Any abrupt change in hemodynamics should increase clinical suspicion of one of these mechanical complications.
b. A holosystolic murmur may be present in both conditions, but the location is usually at the left sternal border in ventricular septal defect and at the apex in papillary muscle rupture.
2. Diagnosis. An emergent surface echocardiogram is a quick and easy way to make the diagnosis. Hemodynamic monitoring with a PA line is usually necessary for treatment and may also be used diagnostically—an increased oxygen saturation between the right atrium and PA is seen with ventricular septal defect, and both disorders may display prominent v waves.
3. Treatment. Nitroprusside or IABP may be used temporarily to decrease afterload and improve forward cardiac output. Emergent surgical repair is indicated for definitive therapy.
Causes of postinfarct systolic murmur include ventricular septal defect (VSD), acute mitral regurgitation, or dynamic left ventricular outflow obstruction in the setting of a large left anterior descending artery infarct.
iii. Left ventricular aneurysm or pseudoaneurysm
1. Left ventricular aneurysm most often occurs after large anterior wall MI. Warfarin therapy for 3–6 months can be considered in patients with large anterior wall MI and severe left ventricular dysfunction, even in the absence of a left ventricular thrombus. Left ventricular aneurysms may also be associated with refractory heart failure or arrhythmias and may rarely require surgical correction if refractory to medical or procedural therapy.
2. Pseudoaneurysms are contained left ventricular free-wall ruptures distinguished by a relatively narrow neck and a predisposition for an inferior-posterior location. Surgical correction is generally performed to prevent delayed rupture.
f. Pericarditis should be suspected if there is recurrence of chest pain with the character and EKG changes suggestive of pericarditis. It is very important to distinguish pericarditis from chest pain caused by ischemia. Aspirin is recommended for the treatment of pericarditis after an acute MI. Colchicine can be added if aspirin is not effective. NSAIDs and steroids can be potentially harmful in the setting of acute MI and should be avoided.
G. Post-Hospitalization and Long-Term Management
a. Maintenance of optimal medical therapy. Guideline-directed medical therapy after ACS includes dual antiplatelet therapy, β-blockers, high-intensity statin therapy, and ACE inhibitors. Educating the patient about the importance of these medications and potential side effects, as well as appropriate and timely post-hospitalization follow-up, is necessary to ensure compliance and adjustment of therapy.
b. Exercise-based cardiac rehabilitation and secondary prevention programs are recommended after ACS. The benefits include improvement of patient commitment to treatment, improved functional capacity, and reduced risk for rehospitalization because of ischemic symptoms. These programs also provide the opportunity to screen patients for depression, which is not an uncommon event after ACS.
c. Smoking cessation. Counseling and pharmacologic therapy should be discussed with the patient to maximize the chances for successful abstinence from smoking.
e. Indications for ICD placement after MI for primary prevention of sudden cardiac death.
i. Criteria for patients who are >40 days post-MI or >3 months post- PCI or post–coronary artery bypass graft
1. Prior MI with an ejection fraction of ≤30%
2. Ejection fraction of ≤35% and New York Heart Association class II or III heart failure symptoms
3. Patients with prior MI and ejection fraction of ≤40% and evidence of nonsustained ventricular tachycardia on Holter monitor are recommended to have an electrophysiology study. If positive, then ICD is indicated.
Suggested Further Readings
Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes. Executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;130:2354–94.Find this resource:
Anderson JL, Morrow DA. Acute myocardial infarction. N Engl J Med 2017;376:2053–64.Find this resource:
Levine GN, Bates ER, Blankenship JC, et al. 2015 ACC/AHA/SCAI focused update on primary percutaneous coronary intervention for patients with st-elevation myocardial infarction: an update of the 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention and the 2013 ACCF/AHA guideline for the management of st-elevation myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Circulation 2016;133:1135–47.Find this resource:
Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med 2013;368:2004–13.Find this resource:
Panju AA, Hemmelgarn BR, Guyatt GH, Simel DL. The rational clinical examination. Is this patient having a myocardial infarction? JAMA 1998;280:1256–63. (Classic Article.)Find this resource:
Timmis A. Acute coronary syndromes. BMJ 2015;351:h5153.Find this resource:
Wilansky S, Moreno CA, Lester SJ. Complications of myocardial infarction. Crit Care Med 2007;35:S348–54.Find this resource: