Acute ST-Elevation Myocardial Infarction
Brahmajee K. Nallamothu
Debabrata Mukherjee
Eric R. Bates
Acute ST-elevation myocardial infarction (STEMI) remains a major public health issue and is a leading cause of death in the United States. The American Heart Association estimated that in the year 2003, 946,000 Americans would sustain an acute myocardial infarction (MI) (1) and that approximately 30% to 45% of these are STEMI.
Although substantial overlap exists in diagnostic and therapeutic approaches, the other acute coronary syndromes, unstable angina and non-STEMI, are addressed in Chapter 10.
USUAL CAUSES
Atherosclerotic coronary artery disease and plaque rupture with resultant thrombosis remain the most common causes of MI (2). Other, less common causes include arteritis, trauma, embolization, congenital anomalies, hypercoagulable states, and substance abuse. Table 11.1 lists a number of pathologic processes other than atherosclerosis that may cause MI (3).
PRESENTING SYMPTOMS AND SIGNS
History
A thorough history is extremely important in establishing the diagnosis of STEMI. The classic symptom is crushing retrosternal chest discomfort with radiation to the left arm (4). Some individuals may have epigastric pain, which can lead to the misdiagnosis of heartburn or another abdominal disorder. Elderly individuals may not have any chest discomfort but may have symptoms of left ventricular failure, marked weakness, or syncope (5). Postoperative patients and diabetic patients are other subgroups that may not experience classic symptoms. Patients may also have neck, jaw, back, shoulder, or right arm pain as the sole manifestation. Other associated symptoms include diaphoresis, dyspnea, fatigue, weakness, dizziness, palpitations, acute confusion, nausea, or emesis. Nausea and emesis are seen more frequently with inferior-wall MI.
Physical Examination
The physical examination is more important in excluding other life-threatening diagnoses and in risk-stratifying patients than in establishing the diagnosis of MI. Patients with STEMI often appear anxious and in distress. A fourth heart sound is frequently present in patients who are in sinus rhythm. All patients should have a thorough cardiovascular examination as a baseline to monitor for complications that may develop, such as ventricular septal defect or acute mitral regurgitation. Systolic blood pressure, heart rate, rales, and a third heart sound are important prognostic determinants that are obtainable from the physical examination (6,7). A baseline neurologic examination also is important, particularly before fibrinolytic therapy is instituted.
TABLE 11.1. Nonatherosclerotic causes of acute myocardial infarction | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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HELPFUL TESTS
Electrocardiography
The diagnosis of STEMI requires at least 1 mm of acute ST-segment elevation in two or more contiguous leads on the electrocardiogram (ECG). The presence of prior left bundle-branch block may confound the diagnosis, but striking ST-segment deviation that cannot be explained merely by conduction abnormality is suggestive of STEMI. Sgarbossa et al. (8) validated three electrocardiographic criteria with independent value in the diagnosis of STEMI in patients with left bundle-branch block: (a) ST-segment elevation of 1 mm or more that was concordant with (in the same direction as) the QRS complex; (b) ST-segment depression of 1 mm or more in lead V1, V2, or V3; and (c) ST-segment elevation of 5 mm or more that was discordant with (in the opposite direction from) the QRS complex. The ECG also remains a valuable clinical tool for determining infarct location and estimating potential infarct size (9).
Cardiac Markers
The World Health Organization (WHO) criteria for the diagnosis of MI require at least two of the following three elements: (a) history of typical chest discomfort, (b) electrocardiographic changes consistent with MI, and (c) rise and fall in serum cardiac markers (10). The serum cardiac markers that are used in the diagnosis of MI include creatine kinase (CK), creatine kinase-myocardial band fraction isoenzyme (CK-MB), cardiac-specific troponins, and myoglobin. The American College of Cardiology, the American Heart Association, the European Society of Cardiology, and the World Heart Federation recently redefined the diagnosis of MI to include any elevation of serum cardiac markers (preferably cardiac troponins) combined with symptoms, ECG signs, or imaging evidence of new myocardial ischemia. The new definition goes on to classify myocardial infarction further into five different categories based on its pathophysiology and clinical presentation (Table 11.2) (11).
Echocardiography
The portability of echocardiography makes it a valuable clinical tool in the rapid assessment of patients with STEMI, particularly in the emergency department. This technique can be useful to confirm or exclude the diagnosis (12) and to help with risk
stratification (13). The echocardiogram is very helpful in diagnosing the mechanical complications of STEMI.
stratification (13). The echocardiogram is very helpful in diagnosing the mechanical complications of STEMI.
TABLE 11.2. Biochemical markers for detecting myocardial necrosis | ||||||||||||||||||||||||||||
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DIFFERENTIAL DIAGNOSIS
Pericarditis
Pericardial pain is usually aggravated by inspiration and lying supine. It is important to distinguish pericarditis from STEMI because fibrinolytic therapy in patients with pericarditis may lead to hemopericardium. The ST-segment changes in pericarditis are diffuse, with a concave upward slope. Other important diagnostic features include PR-segment depression and absence of reciprocal ST-segment depression.
Myocarditis
Symptoms and signs of myocarditis may closely mimic those of STEMI. A thorough history may be helpful if it reveals a more gradual onset of symptoms and prior upper respiratory tract symptoms in a relatively young patient. Serum cardiac markers usually remain elevated rather than peaking and returning to baseline levels. A recently described syndrome known as “takotsubo” cardiomyopathy has been linked to transient left ventricular apical ballooning and may closely mimic myocarditis or STEMI on the ECG, despite a lack of epicardial coronary artery disease. This syndrome appears predominantly to affect postmenopausal women with an episode of emotional or physical stress preceding their presentation (14).
Aortic Dissection
The pain due to an acute aortic dissection is typically central, extremely severe, and often described by the patient as a tearing sensation. The pain is maximal at onset and persists for many hours. It is extremely important to diagnose this condition because fibrinolytic therapy usually results in death. Chest radiography may show a widened mediastinum. A transthoracic echocardiogram may show an intimal flap in the proximal aorta. If the echocardiogram is nondiagnostic and dissection is still a clinical possibility, the patient should undergo more definitive testing in the form of computed tomography, magnetic resonance imaging, or transesophageal echocardiography.
Hypertrophic Cardiomyopathy
Patients with hypertrophic cardiomyopathy may initially have chest discomfort similar to angina, related to increased
myocardial oxygen demand. Transthoracic echocardiography is a useful test for diagnosing this condition. Use of nitroglycerin or dobutamine may precipitate hypotension and syncope in affected patients.
myocardial oxygen demand. Transthoracic echocardiography is a useful test for diagnosing this condition. Use of nitroglycerin or dobutamine may precipitate hypotension and syncope in affected patients.
Pulmonary Embolism
Chest pain associated with severe shortness of breath without clinical or radiographic evidence of pulmonary edema should suggest pulmonary embolism. Echocardiography may be useful by demonstrating normal left ventricular wall motion and right ventricular dilatation and strain. Patients with pneumothorax and pleuritis may also have substernal chest discomfort, but the character of the pain is different, and the pain is often worse with inspiration.
Cholecystitis
Patients with inferior MI may initially have epigastric or right upper quadrant pain that may mimic acute cholecystitis. Conversely, patients with acute cholecystitis may have symptoms and occasionally ECG findings suggestive of inferior MI. The presence of fever, marked leukocytosis, and right upper quadrant tenderness favor the diagnosis of cholecystitis. Esophageal and other upper gastrointestinal symptoms may also mimic ischemic chest discomfort.
Costochondritis
Costochondritis pain is usually associated with localized swelling and redness, and the character of the pain is usually sharp with marked focal tenderness.
Hyperventilation
Patients with panic attacks may have chest discomfort that closely simulates angina. A thorough history is very useful for diagnosing this condition.
COMPLICATIONS
Sudden cardiac death before hospital admission is the most common cause of mortality in STEMI. In-hospital mortality is primarily due to circulatory failure resulting from either severe left ventricular dysfunction or one of the mechanical complications (see later). The complications of STEMI may be broadly classified as mechanical, electrical, ischemic, embolic, and pericardial.
Mechanical Complications
Cardiac rupture
Ventricular septal rupture, papillary muscle rupture, and free-wall rupture are serious, life-threatening mechanical complications. Reperfusion therapy has reduced the overall incidence of cardiac rupture and shifted its occurrence to an earlier point in time.
Ventricular septal rupture occurs in 0.5% to 2% of patients (15). The diagnosis should be suspected when a pansystolic murmur develops that was not present initially. Echocardiography with color-flow imaging is the test of choice for diagnosing a ventricular septal rupture. Pulmonary artery catheterization with oximetry is also a useful diagnostic aid. This involves measuring oxygen saturations in the right atrium, right ventricle, and pulmonary artery under fluoroscopy. An intraaortic balloon pump (IABP) should be inserted as early as possible as a bridge to surgery, unless significant aortic regurgitation is present. This decreases systemic vascular resistance, decreases shunt fraction, increases coronary perfusion, and maintains blood pressure. After insertion of the IABP, vasodilators can be used with close hemodynamic monitoring. Surgical repair is the treatment of choice.
Most mitral regurgitation associated with STEMI is transient, asymptomatic, and benign. However, severe mitral regurgitation due to papillary muscle rupture is a life-threatening, but treatable, complication that contributes to 5% of the deaths after STEMI. The overall incidence of papillary muscle rupture is 1%. Papillary muscle rupture is more common with inferior MI that involves the posteromedial papillary muscle, because its blood supply is solely via the posterior descending artery. In contrast, the anterolateral papillary muscle is perfused by
both the left anterior descending and the left circumflex arteries. Complete transection of the papillary muscle is rare and usually results in immediate shock and death. Patients with rupture of one or more papillary muscle heads typically have sudden severe respiratory distress from development of pulmonary edema, and cardiogenic shock may rapidly develop. A new pansystolic murmur is audible at the cardiac apex with radiation to the axilla or to the base of the heart. In posterior papillary muscle rupture, the murmur radiates up the left sternal border and may be confused with the murmur of ventricular septal rupture or aortic stenosis. Two-dimensional echocardiography, with Doppler and color-flow imaging, is the diagnostic modality of choice. Hemodynamic monitoring with a pulmonary artery catheter may reveal large V waves in the pulmonary capillary wedge pressure (PCWP) tracing. Vasodilator and IABP therapy are very important in patients with acute severe mitral regurgitation. IABP decreases left ventricular afterload, improves coronary perfusion, and increases forward cardiac output. The prognosis is very poor in patients treated medically, and even though perioperative mortality (20% to 25%) is higher than that for elective surgery, immediate surgical repair should be considered in every patient.
both the left anterior descending and the left circumflex arteries. Complete transection of the papillary muscle is rare and usually results in immediate shock and death. Patients with rupture of one or more papillary muscle heads typically have sudden severe respiratory distress from development of pulmonary edema, and cardiogenic shock may rapidly develop. A new pansystolic murmur is audible at the cardiac apex with radiation to the axilla or to the base of the heart. In posterior papillary muscle rupture, the murmur radiates up the left sternal border and may be confused with the murmur of ventricular septal rupture or aortic stenosis. Two-dimensional echocardiography, with Doppler and color-flow imaging, is the diagnostic modality of choice. Hemodynamic monitoring with a pulmonary artery catheter may reveal large V waves in the pulmonary capillary wedge pressure (PCWP) tracing. Vasodilator and IABP therapy are very important in patients with acute severe mitral regurgitation. IABP decreases left ventricular afterload, improves coronary perfusion, and increases forward cardiac output. The prognosis is very poor in patients treated medically, and even though perioperative mortality (20% to 25%) is higher than that for elective surgery, immediate surgical repair should be considered in every patient.
Cardiac free-wall rupture occurs in 3% of patients and accounts for about 10% of deaths from STEMI. Advanced age, female gender, hypertension, first MI, and poor coronary collateral vessels are risk factors for free-wall rupture. Free-wall rupture constitutes part of the “early hazard” in patients treated with fibrinolytics (the mortality rate among patients who receive fibrinolytics is actually higher for the first 24 hours and is attributable partially to cardiac rupture). Emergency thoracotomy with surgical repair is the definitive therapy and may save a few patients who can be taken to surgery immediately. Pseudoaneurysm results from a contained rupture of the left ventricular free wall by the pericardium and mural thrombus. Pseudoaneurysms communicate with the body of the left ventricle through a narrow neck, the diameter of the neck being less than 50% of the diameter of the fundus. Spontaneous rupture occurs without warning in approximately one third of these patients; therefore surgical resection is recommended for both symptomatic and asymptomatic patients, irrespective of the size of the pseudoaneurysm.
Left ventricular failure and cardiogenic shock
The severity of left ventricular dysfunction correlates with the extent of myocardial injury. Patients with a small MI may have regional wall-motion abnormalities but overall normal left ventricular function because of compensatory hyperkinesia of the nonaffected segments. Killip and Kimball (6) classified four subsets of patients on the basis of clinical presentation and physical findings at the onset of STEMI (Table 11.3). More recently, in comparison with the 81% mortality with cardiogenic shock in their original article (6), the 30-day mortality rate was 58% among patients in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) I trial (16) who were first seen with cardiogenic shock and who were treated with fibrinolytics. An IABP should be inserted as soon as possible in a patient with cardiogenic shock. In the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) trial (17), patients with cardiogenic shock were randomly assigned to undergo emergency
revascularization (n = 152) or initial medical stabilization (n = 150). The rates of overall mortality at 30 days did not differ significantly between the revascularization and medical-therapy groups because of sample size (46.7% vs. 56.0%; difference, 9.3%; 95% confidence interval, 20.5% to 1.9%; p = 0.11). However, the 6-month mortality rate was significantly lower among the patients who underwent revascularization than in those receiving medical therapy (50.3% vs. 63.1%; p = 0.027). Therefore emergency revascularization should be strongly considered for patients with STEMI complicated by cardiogenic shock.
revascularization (n = 152) or initial medical stabilization (n = 150). The rates of overall mortality at 30 days did not differ significantly between the revascularization and medical-therapy groups because of sample size (46.7% vs. 56.0%; difference, 9.3%; 95% confidence interval, 20.5% to 1.9%; p = 0.11). However, the 6-month mortality rate was significantly lower among the patients who underwent revascularization than in those receiving medical therapy (50.3% vs. 63.1%; p = 0.027). Therefore emergency revascularization should be strongly considered for patients with STEMI complicated by cardiogenic shock.
TABLE 11.3. Mortality based on Killip class | ||||||||||||||||||
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Right ventricular failure
Mild right ventricular dysfunction is common after inferior MI, but hemodynamically significant right ventricular impairment is seen in only 10% of patients. Right ventricular involvement depends on the location of the right coronary artery occlusion; significant dysfunction is noted only if occlusion is proximal to a large acute marginal branch. The triad of hypotension, jugular venous distention, and clear lungs is very specific but has poor sensitivity for right ventricular infarction. Patients with severe right ventricular failure have symptoms of low cardiac output. These include diaphoresis, clammy extremities, and altered mental status. Patients are often oliguric and hypotensive. The ECG usually shows an inferior injury. Current. ST elevation in V4R in the setting of suspected right ventricular infarction has a positive predictive value of 80%. Hemodynamic monitoring with a pulmonary artery catheter usually reveals high right atrial (RA) pressures relative to the PCWP. Acute right ventricular failure results in underfilling of the left ventricle and a low-cardiac-output state. A RA pressure higher than 10 mm Hg and a RA/PCWP ratio of 0.8 or higher are strongly suggestive of right ventricular infarction (18). Treatment of right ventricular infarction involves volume loading, inotropic support with dobutamine, and maintenance of atrioventricular synchrony. Patients who undergo successful reperfusion of the right coronary artery and the right ventricular branches have improved right ventricular function and decreased 30-day mortality rates (19).
Left ventricular aneurysm
An acute aneurysmal segment expands in systole, wasting contractile energy generated by the normal myocardium. Chronic true aneurysms develop in 10% of patients without reperfusion therapy and are more commonly seen after anterior MI. Chronic aneurysms are defined as those persisting more than 6 weeks after MI. Patients with acute aneurysms may first be seen with heart failure and even cardiogenic shock. Patients with chronic aneurysms may have heart failure, ventricular arrhythmias, and systemic embolism, or they may be asymptomatic. Heart failure with acute aneurysm is treated with intravenous vasodilators and IABP. Anticoagulation with warfarin is indicated for patients with mural thrombus. In patients with refractory heart failure or ventricular arrhythmias, surgical resection of the aneurysm should be considered. Revascularization may be beneficial in patients with a large amount of viable myocardium in the aneurysmal segment.
Electrical Complications
Arrhythmias are the most common complications after STEMI, affecting approximately 90% of patients. Conduction abnormalities causing hypotension may necessitate temporary or permanent pacemaker therapy. These are briefly summarized in Table 11.4. An implantable cardioverter defibrillator (ICD) is indicated in patients with sustained ventricular fibrillation (VF) or ventricular tachycardia (VT) more than 2 days after the AMI if recurrent ischemia or transient causes have been excluded.
Ischemic Complications
Infarct extension is a progressive increase in the amount of myocardial necrosis within the same arterial territory as the original MI. This may manifest as a subendocardial MI
extending to a transmural MI or as an MI that extends and involves the adjacent myocardium. Recurrent angina within a few hours to 30 days after MI is defined as postinfarction angina. The incidence is between 23% and 60%. The frequency of postinfarction angina is higher after non-Q-wave MI and fibrinolytic therapy than after primary PCI. Patients with postinfarction angina have an increased incidence of sudden death, reinfarction, and acute cardiac events. Either percutaneous or surgical revascularization improves prognosis in these patients. Infarction in a separate territory may be difficult to diagnose in the first 24 to 48 hours after the initial event. It may be very difficult to differentiate ECG changes of reinfarction from the evolving ECG changes of the index MI. Recurrent elevations in CK-MB after normalization or to more than 50% of the prior value are diagnostic of reinfarction. Echocardiography may also be useful in revealing a wall-motion abnormality in a new area.
extending to a transmural MI or as an MI that extends and involves the adjacent myocardium. Recurrent angina within a few hours to 30 days after MI is defined as postinfarction angina. The incidence is between 23% and 60%. The frequency of postinfarction angina is higher after non-Q-wave MI and fibrinolytic therapy than after primary PCI. Patients with postinfarction angina have an increased incidence of sudden death, reinfarction, and acute cardiac events. Either percutaneous or surgical revascularization improves prognosis in these patients. Infarction in a separate territory may be difficult to diagnose in the first 24 to 48 hours after the initial event. It may be very difficult to differentiate ECG changes of reinfarction from the evolving ECG changes of the index MI. Recurrent elevations in CK-MB after normalization or to more than 50% of the prior value are diagnostic of reinfarction. Echocardiography may also be useful in revealing a wall-motion abnormality in a new area.
TABLE 11.4. Electrical complications of acute myocardial infarction and their management | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Embolic Complications
The incidence of clinically evident systemic embolism after MI is approximately 2%; the incidence is higher in patients with anterior MI. The overall incidence of mural thrombus after MI is approximately 20%. Large anterior MIs may be accompanied by associated mural thrombus in 60% of patients. Patients with large anterior MI or mural thrombi should be treated with intravenous heparin for 3 to 4 days with a target partial thromboplastin time of 50 to 70 seconds. Oral therapy with warfarin should be continued for at least 3 months in patients with mural thrombi and in those with large akinetic areas detected by echocardiography.
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