Introduction
Acute inferior myocardial infarction on an ECG.
Apical left ventricular (LV) dyskinesis (ventricular aneurysm) after an anterior myocardial infarction.
Background
Acute myocardial infarct (MI), commonly known as a heart attack, is a condition characterized by ischemic injury and necrosis of the cardiac muscle. Ischemic injury occurs when the blood supply is insufficient to meet the tissue demand for metabolism. More than two thirds of myocardial infarctions occur in lesions that are less than 60% severe.
Each year in the United States, approximately 1.5 million persons have an acute MI, and one third die. Although tremendous progress has been made in the diagnosis and management of MI over the past 25 years, MI continues to be a major public health problem, not only in the United States but also throughout most of the industrialized world. Indeed, MI is an increasingly important problem in the developing countries. In the United States, despite a 30% decline in the death rate from MI over the past 3 decades, MI remains one of the most important causes of death. One half of all such deaths occur within an hour of the start of symptoms of acute MI and are generally caused by concomitant arrhythmias, most often ventricular fibrillation (VF).
Almost all MIs are caused by rupture of coronary atherosclerotic plaques with superimposed coronary thrombosis. Patients with MI usually present with signs and symptoms of crushing chest pressure, diaphoresis, malignant ventricular arrhythmias, heart failure (HF), or shock. MI may also manifest itself as sudden cardiac death, which may not be apparent on autopsy (because necrosis takes time to develop). Presentations may be atypical and clinically subtle, especially in women. Findings may include new-onset or accelerated angina; atypical chest discomfort or abdominal discomfort mimicking indigestion; decreased cerebral perfusion with syncope; dizziness; cerebrovascular accident; altered mental status; or nausea and fatigue without chest pain.
Coronary thrombolysis and mechanical revascularization have revolutionized the primary treatment of acute MI, largely because they allow salvage of the myocardium when implemented early after the onset of ischemia. The modest prognostic benefit of an opened infarct-related artery may be realized even when recanalization is induced only 6 hours or later after the onset of symptoms, that is, when the salvaging of substantial amounts of jeopardized ischemic myocardium is no longer likely. The opening of an infarct-related artery may improve ventricular function, collateral blood flow, and ventricular remodeling, and it may decrease infarct expansion, ventricular aneurysm formation, left ventricular (LV) dilatation, late arrhythmia associated with ventricular aneurysms, and mortality.1,2,3,4,5
Evidence suggests a benefit from the use of beta blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARB), and possibly from insulin infusion (with potassium and glucose) to inhibit apoptosis (cell death).
Related eMedicine topics:
Myocardial Infarction (from Cardiology)
Myocardial Infarction (from Emergency Medicine)
Complications of Myocardial Infarction
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Pathophysiology
Right coronary artery occlusion
The right coronary artery (RCA) supplies the right atrium (RA) and at least part of the right ventricle (RV). It commonly also feeds the posterior descending artery (PDA), which supplies the posterior third of the interventricular septum and the rest of the RV, in which case the RCA is described as dominant.
In two thirds of patients, the first branch is the conus artery. The conus artery, which supplies the conus arteriosis (RV outflow tract), occasionally arises from a separate orifice. In 60% of patients, the sinus node artery arises from the proximal RCA, and in 40%, it arises from the left circumflex (LCX) artery. The anterior branches supply the free wall of the RV, and the acute marginal branches supply the RV. When the RCA extends to the crux (the origin of the PDA), it supplies the AV node (90%); otherwise, the AV node is supplied by the LCX. Therefore, obstruction of the RCA commonly affects the sinus node and the atrioventricular (AV) node, resulting in bradycardia, with or without heart block.
In view of these anatomic considerations, it is not surprising that RCA occlusion frequently manifests with sinus bradycardia, AV block, RV MI, and/or inferoposterior MI (of the LV).
Occlusion of the left coronary artery
The left coronary artery system covers more territory than does the right system; therefore, an MI in this system is most likely to produce extensive injury, with impairment of function, pulmonary congestion, and low output. Occlusion of the left coronary artery may also cause a left anterior hemiblock or a left posterosuperior hemiblock conduction abnormality; these effects are evidenced by a change of frontal axis on the ECG.
Inferior-wall MI and RV MI
In patients with acute inferior-wall MI with RV involvement, distention of neck veins is commonly described as a sign of failure of the RV. Central venous pressure (CVP) is most properly estimated independently of venous distention on the basis of the height of the meniscus of venous pulsation above the mid atrium. Dependent edema (in the lower back in a supine patient or else pretibial) and abdominojugular reflux (increased venous filling that occurs with compression of the abdomen by hand) often accompany an elevation in CVP. In severe cases, the forward delivery of blood from the RV to the LV may be insufficient to fill the LV, resulting in low blood pressure even if the LV is intact.
Chemoreceptor activation in the myocardium actuates vagal (parasympathetic) efferent discharge, known as the Bezold-Jarisch reflex, which causes bradycardia and vessel dilation that may further lower blood pressure. Adenosine may accumulate in the infarct zone secondary to a local inhibition of adenosine deaminase, for which aminophylline may act pharmacologically as an antagonist. The hemodynamic changes resemble many of those seen with pericardial constriction or tamponade. Patients with this condition respond well to an infusion of normal sodium chloride solution. Improvement with such infusion compensates for failure of the pumping action of the RV; it reduces vagal tone, and it deactivates the pressure sensors that were sending a hormonal signal to the kidneys to retain salt.
No-reflow phenomenon
If, after medical therapy with fibrinolytic drugs, percutaneous intervention with angioplasty, surgery, or spontaneous resolution, coronary blood flow does not resume relatively promptly, good myocardial perfusion may not be achieved despite restoration of luminal patency.6 This situation is known as the no-reflow phenomenon; it occurs because of swelling of endothelial cells, formation of platelet and leukocyte plugs, or complement-mediated microvascular inflammation.
Arrhythmogenesis
In addition to the direct effects of ischemia and tissue hypoxia, decreased removal of noxious metabolites, including potassium, calcium, amphophilic lipids, and oxygen-centered free radicals, also impair ventricular performance. These abnormalities promote potentially lethal arrhythmias.
Intramural thrombus development
Inflammation of the endocardial surfaces and stasis of blood flow associated with regional akinesis (no wall motion) or dyskinesis (abnormal, passively reversed wall motion) may lead to the formation of ventricular mural thrombi, which have the potential to embolize.
Pericarditis
Epicardial inflammation may initiate pericarditis, which is seen in more than 20% of patients presenting with Q-wave infarctions. Also, a primary inflammatory condition of myopericarditis may resemble an acute MI.
Effect on systolic function
Lack of adequate oxygen and insufficient metabolite delivery to the myocardium diminish the force of muscular contraction and decrease systolic wall motion in the affected territory.
Abnormal regional wall motion
Even brief deprivation of oxygen and the requisite metabolites to the myocardium diminishes diastolic relaxation and causes abnormal regional systolic contractile function, wall thickening, and abnormal wall motion. If the area affected is extensive, diminished stroke volume and cardiac output may result.
Myocardial hibernation and stunning
After the occurrence of one or more ischemic insults, impaired wall motion is often transient (myocardial stunning) or prolonged (myocardial hibernation). These phenomena occur because of the loss of essential metabolites such as adenosine, which is needed for adenosine triphosphate (ATP)–dependent contraction. Hibernation, a persisting wall-motion abnormality curable with revascularization, must be differentiated from permanent irreversible damage or completed infarct.
The differential diagnosis is usually accomplished by performing tests for muscle viability by use of positron-emission tomography (PET), MRI with delayed enhancement, a dobutamine stress nuclear medicine study, or stress echocardiography. Scars involving less than one third of the thickness of the wall, as shown on contrast-enhanced MRI, likely correspond to a recovery of myocardial function. Other findings associated with such recovery are activity on 18[F]-fluoro-deoxyglucose (FDG) PET and a monophasic or biphasic contractile response to dobutamine infusion, caused by the induction of ischemia.
Hypokinesis and akinesis
In general, regions of hypokinesis and akinesis of the ventricular myocardium reflect the location and extent of myocardial injury.
MI expansion
In general, expansion of infarcted myocardium and resultant ventricular dilatation (ie, ventricular remodeling) ensues within a few hours after the onset of an MI. An expanding MI leads to thinning of the infarct zone and realignment of layers of tissue in and adjacent to it, causing ventricular dilatation.
Myocardial rupture
Myocardial rupture was seen in as many as 10% of fatal MIs before the era of thrombolytics but it is now encountered much less often. When rupture occurs, it may be associated with large infarctions; indications include cardiogenic shock or hemodynamically significant arrhythmia. Patients may have a history of hypertension with ventricular hypertrophy.
Ventricular aneurysm
A ventricular aneurysm is an outward bulging of a noncontracting segment. In the early days of cardiac imaging, ventricular aneurysms were seen in as many as 20% of patients with Q-wave MI, but now it is seen in less than 8%. On clinical evaluation, aneurysms may be recognized late, with symptoms and signs of HF, recurrent ventricular arrhythmia, or recurrent embolization.
Cardiogenic shock
In patients with extensive myocardial injury, coronary blood flow diminishes as cardiac output declines and heart rate accelerates. Because coronary artery disease is usually generalized or diffuse, ischemia that occurs at a distance from the infracted segment may result in a vicious cycle in which a stuttering and expanding MI ultimately leads to profound LV failure, hypotension, and cardiogenic shock.
Coronary collateral circulation
The coronary collateral circulation is an important factor in terms of the amount of damage to the myocardium that results from coronary occlusion. Well-developed collaterals may greatly limit or even completely eliminate MI despite complete occlusion of a coronary artery. Reports vary as to the number of patients who have collaterals at the time of an MI; many patients develop collaterals in the hours and days after an occlusion occurs.7 When the patient is at rest, blood flow through collaterals is normal — a fact that accounts for the absence of resting ischemia. However, blood flow through collaterals does not increase with exercise; this inability accounts for the occurrence of ischemia during periods of stress.8
Effect on diastolic function
Immediately after the onset of MI, the ability of ischemic myocardium to relax declines. Relaxation is an active process that uses ATP. Impaired relaxation increases LV end-diastolic volume (LVEDV) and LV end-diastolic pressure (LVEDP).
The increased LVEDP results in ventricular dilation, increased pulmonary venous pressure, decreased pulmonary compliance, and interstitial and (ultimately) alveolar pulmonary edema. These effects lead to increased hypoxemia, which may worsen ischemic injury to the myocardium.
Frequency
United States
Coronary artery disease is diagnosed in approximately 1.5 million Americans per year and results in more than 500,000 deaths annually. Sudden death occurs in more than 350,000 cases of acute MI in the prehospital phase. Even among those who die after they arrive at the emergency department, death is most often sudden. Acute MI accounts for 1 million hospital admissions each year.9
Despite an impressive decline in age-adjusted death rates attributable to acute MI since the mid-1970s, the total number of MI-related deaths in the United States has not declined. This may in part be the result of population growth.
Individuals who survive MIs commonly develop HF or are predisposed to develop HF. Overall, coronary artery disease is responsible for more years of potential life lost before the age of 65 years than any other illness, regardless of sex or race.
International
Acute MI continues to be a major public health problem in the industrialized world, and it is becoming an increasingly important problem in developing countries. Of particular concern are projections from the World Heart Federation that the burden of atherosclerotic cardiovascular disease in developing countries will increasingly become commensurate with that seen in developed countries. With a decline in infectious disease-related deaths, in conjunction with accelerated economic development and life-style changes that promote atherosclerosis, rates of ischemic heart disease and MI are expected to sharply increase in developing countries, especially such countries in Eastern Europe, Asia, and parts of Latin America.
Mortality/Morbidity
- More than 1 million patients with probable MI are admitted to cardiac care units (CCUs) each year.
- Although the death rate from MI has declined by about 30% over the past decade, MI is still the leading cause of fatality.
Race
- Acute MI more often occurs in white men.
- The incidence of MI is increased in Asian Indians.
- The lowest rates are seen in Japanese and French populations — a finding known as the French paradox.
Sex
Men are predominantly affected; however, for women with diabetes and for those in a postmenopausal state, the risk of MI is equal to that in men.
Age
Age is one of the major risk factors for atherosclerosis and MI. MIs may be clinically silent in as many as 25% of elderly patients, a population in whom 50% of MIs occur. Among the elderly, the diagnosis is sometimes established only retrospectively by use of ECG criteria or imaging.
Anatomy
Normal anatomy
The right and left coronary arteries most often arise independently from individual ostia in association with the right and left aortic valve cusps.
The left anterior descending (LAD) and LCX coronary arteries arise at the left main coronary artery bifurcation; they supply the anterior LV, the bulk of the interventricular septum (anterior two thirds), the apex, and the lateral and posterior LV walls. The RCA generally supplies the RV, the posterior third of the interventricular septum, the inferior wall (diaphragmatic surface) of the LV, and a portion of the posterior wall of the LV (by means of the posterior descending branch).
When the posterior descending coronary artery (PDA) that supplies the posterior interventricular septum arises from the LCX artery, the circulation is called left dominant. Most often, the PDA arises from the RCA; this anatomy is called right-dominant circulation.
Pathologic anatomy
Coronary atherosclerosis is especially prominent near branching points of vessels. More than half of all culprit lesions in patients who recently underwent angiography were stenoses of less than 70%. Lipid-rich soft plaques with thinned fibrous caps are particularly prone to rupture and to precipitate an acute coronary event.
The spectrum of myocardial injury depends not only on the intensity of impaired myocardial perfusion but also on the duration and the level of metabolic demand at the time of the event. The damage of the myocardium is essentially a tissue response that includes apoptosis (cell death) and inflammatory changes. Therefore, the hearts of patients who suddenly die from an acute coronary event may show little or no evidence of damage response to the myocardium at autopsy.
The typical MI initially manifests as coagulation necrosis that is ultimately followed by myocardial fibrosis. Contraction-band necrosis is also seen in many patients with ischemia. This is followed by reperfusion, or it is accompanied by massive adrenergic stimulation, often with concomitant myocytolysis.
Presentation
Signs and symptoms of typical Q-wave MI
Patients with typical Q-wave MI may have prodromal symptoms of fatigue, chest discomfort, or malaise in the days preceding the event; alternatively, typical Q-wave MI may occur suddenly, without warning.
MI occurs most often in the early morning hours, perhaps partly because of the increase in catecholamine-induced platelet aggregation and increased serum concentrations of plasminogen activator inhibitor-1 (PAI-1) that occur after awakening. In general, the onset is not directly associated with severe exertion. Instead, it is concomitant with exertion. The immediate risk of MI increases 6-fold on average and by as much as 30-fold in sedentary people.
The typical chest pain of acute MI is intense and unremitting for 30-60 minutes. It is retrosternal and often radiates up to the neck, shoulder, and jaw and down to the ulnar aspect of the left arm. In some patients, the pain is epigastric. The pain is classically described as crushing or squeezing in nature, but it is sometimes described as an ache, a burning pain, a feeling of indigestion, or a feeling of fullness or gas.
Diaphoresis, weakness, a sense of impending doom, profound restlessness, confusion, presyncope, hiccupping (which presumably reflects irritation of the phrenic nerve or diaphragm), nausea and vomiting, and palpitations may be present.
Decreased systolic ventricular performance may lead to impaired perfusion of vital organs and reflex-mediated compensatory responses, such as restlessness, impaired mentation, pallor, peripheral vasoconstriction and sweating, tachycardia, and prerenal failure. By contrast, impaired LV diastolic function leads to pulmonary vascular congestion with shortness of breath and tachypnea and, eventually, pulmonary edema with orthopnea. Impaired RV diastolic function leads to systemic venous hypertension, neck vein distention, edema, and hepatomegaly with abdominojugular reflux, which may result in saline-response underfilling of the LV and a concomitant reduction in cardiac output.
MI is clinically silent in as many as 25% of elderly patients, a population in whom 50% of MIs occur; in such patients, the diagnosis is often established only retrospectively by applying ECG criteria or by performing imaging with 2-dimensional (2D) echocardiography or MRI.
The patient may recall only an episode of indigestion. Patients may not recognize chest pain, for the following reasons: they have a stoic outlook; they have an unusually high pain threshold; they have a disorder that impairs function of the nervous system and that results in a defective anginal warning system (eg, diabetes mellitus); or they have obtundation caused by medication or impaired cerebral perfusion.
Physical examination
General appearance
Patients may appear acutely ill. They often clutch their chest and cannot lie flat or breathe calmly. Pallor, diaphoresis, and restlessness may be observed.
Vital signs
The patient's heart rate is often increased secondary to sympathoadrenal discharge. The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm, ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias. Bradyarrhythmias may be present; bradyarrhythmias may be attributable to impaired function of the sinus node. An AV nodal block or infranodal block may be evident.
In general, the patient's blood pressure is initially elevated because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain and ventricular dysfunction. However, with RV MI or severe LV dysfunction, hypotension is seen.
The respiratory rate may be increased in response to pulmonary congestion or anxiety.
Coughing, wheezing, and the production of frothy sputum may occur.
Fever is usually present within 24-48 hours, with the temperature curve generally parallel to the time course of elevations of creatine kinase (CK) levels in the blood. Body temperature may occasionally exceed 102° F.
Funduscopic examination
Manifestations of atherosclerotic vascular disease include copper wiring, or narrowing, of arterioles. Hypertension may manifest with arteriovenous nicking, which is a pinching of the veins by small arteries where they cross. Extreme hypertension may cause cupping or loss of the margins of the optical disk. Antecedent long-standing hypertension may be reflected by arterial narrowing and hemorrhages.
Arterial pulsations
Arterial pulsations may exhibit pulsus alternans, which reflects impaired LV function and which is characterized by strong and weak alternating pulse waves (the variation in systolic pressure is >20 mm Hg). Carotid pulsation may be thin (pulsus parvus) because of decreased amplitude and length of the pulse secondary to decreased stroke volume.
Pulsus bisferiens consists of 2 systolic peaks; it may be palpated in association with hypertrophic obstructive cardiomyopathy (HOCM) or mixed aortic stenosis and regurgitation. A dicrotic pulse is encountered in cases involving hypovolemic shock, severe HF, or cardiac tamponade. It manifests as a double pulse, produced by a combination of the systolic wave followed by an exaggerated dicrotic (diastolic) wave.
A bigeminal pulse is observed in the presence of ectopic beats or Wenckebach heart block; it is characterized by regular coupling of 2 beats with the interval between a pair of beats greater than that between the coupled beats themselves.
Pulsus paradoxus is defined as a decline in systolic blood pressure of 10 mm Hg or more on inspiration; it is seen in cases involving cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, hypotensive shock, severe chronic lung disease, or pulmonary embolism.
In patients with associated aortic regurgitation, a pulse with sharp descent, or a water-hammer pulse, may be observed.
Jugular venous pulsations normally have several waves. The A wave results from venous distention (caused by RA systole), followed by the X descent (resulting from atrial relaxation and inferior movement of the floor of the RA during RV systole). The C wave follows, occurring at the same time as the carotid arterial pulse. The V wave is caused by the rise in RA pressure when blood flows in during RV systole while the tricuspid valve is closed; this is followed by the Y descent, which is related to the drop in RA pressure on reopening of the tricuspid valve. Between the Y descent and beginning of the A wave is a period of slow filling, or the diastasis period, which is sometimes called the H wave.
Jugular venous distention may accompany RV MI or RV failure secondary to profound LV dysfunction and pulmonary hypertension. It may also be elevated as a result of an increase in RA pressure in patients with HF, decreased RV compliance, pericardial disease, fluid overload, or tricuspid or superior vena cava obstruction. The Kussmaul sign, characterized by a paradoxical increase in jugular venous pressure during inspiration, may occur in patients with constrictive pericarditis, congestive HF (CHF), or tricuspid stenosis.
In atrial fibrillation, the A wave and X descent disappear, and the V wave and Y descent become prominent. The A wave becomes prominent in patients with RV hypertrophy, pulmonary hypertension, or LV hypertrophy when the thickened septum interferes with RV filling, tricuspid stenosis or atresia, and RA myxoma.
Cannon (amplified) A waves are seen in patients with AV dissociation, which results from RA contraction while the tricuspid valve is shut. In patients with RV failure and sinus rhythm, both A and V waves may be tall.
The X descent may be prominent in patients with RV volume overload, such as occurs in the presence of atrial septal defect. Constrictive pericarditis is characterized by a rapid and deep Y descent, followed by a rapid rise to a diastolic H wave without a prominent A wave. Sometimes, the X descent is also prominent, causing a W -shaped venous pulse. By contrast, in patients with cardiac tamponade, the X descent is prominent, and the Y descent is absent.
A prominent V wave or a cV wave (in which the "c" relates to the carotid pulse and the "V" relates to valve closure) occurs in patients with tricuspid regurgitation; it sometimes causes a systolic movement of the earlobe and a side-to-side head movement. A steep Y descent is seen in patients with myocardial dysfunction and ventricular dilatation.
Chest
Rales or wheezes may be auscultated; these occur secondary to pulmonary venous hypertension, which is associated with extensive acute LV MI. Unilateral or bilateral pleural effusions may produce egophony at the lung bases. On chest radiographs, they are evidenced by blunted costophrenic angles; on MRI, they are evidenced by dependent fluid signal intensity; on echocardiography, they are evidenced by echolucent zones adjacent to the heart.
Heart
On palpation, lateral displacement of the apical impulse, dyskinesis, a palpable S4 gallop, and a soft S1 sound may be found. These indicate diminished contractility of the compromised LV.
Paradoxical splitting of S2 may reflect the presence of left bundle-branch block or prolongation of the preejection period with delayed closure of the aortic valve, despite decreased stroke volume.
Increased S4 and S3 gallops may suggest increased LV stiffness; they represent the rapid filling phase (S3) or atrial contraction (S4).
A mitral regurgitation murmur (typically holosystolic near the apex) indicates papillary muscle dysfunction or rupture or mitral annular dilatation; it may be audible even when cardiac output is substantially decreased.
A holosystolic systolic murmur that radiates to the midsternal border and not to the back, possibly with a palpable thrill, suggests a ventricular septal rupture; such a rupture may occur as a complication in some patients with full-thickness (or Q-wave) MIs. With resistive flow and an enlarged pressure difference, the VSD murmur becomes harsher, louder, and higher in pitch than before.
A pericardial friction rub may be audible as a to-and-fro rasping sound with 1-3 components; it is produced through sliding contact of inflammation-roughened surfaces.
Neck vein and pulse patterns, splitting of S2, or ECG findings may suggest premature ventricular beats, brief runs of ventricular tachycardia, accelerated idioventricular rhythm, atrial flutter or atrial fibrillation, or conduction delays.
Abdomen
Patients frequently develop tricuspid incompetence; hepatojugular reflux may be elicited even when hepatomegaly is not marked.
Extremities
Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and RV dysfunction or failure. Pulse and neck-vein patterns may reveal other associated abnormalities, as described above under Venous Pulsations. Dependent edema may be graded 0-4 by assessing the depth of persistent pitting after thumb pressure is applied to the patient's inner shin for more than 10 seconds or by evaluating the lower back if the patient has had his or her legs elevated.
Nervous system
Patients with acute MI are prone to cerebrovascular injury as a result of emboli from ventricular mural thrombi; the rate is approximately 1%. MRI depicts mural thrombi with approximately twice the sensitivity of echocardiography.
The combination of acute MI and psychological depression appears to worsen the patient's prognosis. Acute MI may precipitate reactive depression whether or not beta-adrenergic blocking agents or other CNS-active agents are administered.
Laboratory determinations
The objectives of laboratory testing include the following:
- To determine the presence or absence of MI for diagnosis and differential diagnosis
- To characterize the locus, nature (Q-wave MI or non-Q-wave MI, also known as ST-segment elevation MI or non-ST-segment elevation MI), and extent of MI (ie, to estimate infarct size)
- To detect recurrent ischemia or MI (extension of MI)
- To detect early and late complications of MI
- To estimate the patient's prognosis
Serum levels of CK, CK-MB isoform, troponin I, and troponin T are routinely obtained to determine the presence, progression, or recurrence of acute MI in patients with prolonged chest pain or pain that occurs at rest. The troponin level is measured to determine whether myocardial damage of any cause has occurred during the 2 weeks (or longer) before testing; false-positive results may occur in patients with renal failure. Levels of CK and CK-MB typically increase and decrease within 1-3 days; these measurements clarify the acuteness of the event. The peak level and the area under the curve may indicate the size of the MI and may be of prognostic value. Although CK and myoglobin values may be elevated as a result of injury to skeletal muscle, an elevation of the percentage of CK-MB indicates the myocardial source.
Other markers that are less diagnostically accurate than these are also elevated in patients with MI. These markers include the WBC count; the erythrocyte sedimentation rate (ESRs); the lactate dehydrogenase (LDH) level; the aspartate aminotransferase (AST) level; and the alanine aminotransferase (ALT) level.
Laboratory evaluation is particularly helpful in the presence of comorbid conditions that may affect the patient's prognosis and influence his or her care. Such comorbidities include diabetes, renal or hepatic failure, anemia, bleeding disorders, and respiratory failure.
The platelet count may become dangerously low after the use of heparin because of heparin-induced thrombocytopenia (HIT). The leukocyte count may be normal initially, but it generally increases within 2 hours and peaks in 2-4 days, with predominance of polymorphonuclear leukocytes and a shift to the left. Elevations generally persist for 1-2 weeks.
Other components of the acute-phase reaction contribute to elevations of the ESR within 48 hours with subsequent changes that parallel those in the leukocyte count; this finding is of limited clinical value.
Blood oxygenation should be checked and repeatedly corrected if any clinical findings suggest hypoxemia; hypoxemia may result from pulmonary congestion, atelectasis, or ventilatory impairment secondary to complications of MI or excessive sedation or analgesia. Fingertip oximetry may be adequate in the absence of CO2 retention and may obviate puncture to assess arterial blood gases (ABGs). Such puncturing may lead to bleeding in patients being treated with thrombolytic drugs. However, normal oxygen saturation does not exclude impending respiratory failure.
Electrocardiography
Acute inferior myocardial infarction on an ECG.
After thrombolytic therapy, reperfusion arrhythmias, such as an accelerated idioventricular rhythm (AIVR), may occur.
Characteristic findings on sequential ECGs remain hallmarks of diagnosis despite the fact that occasionally, MIs occur without any acute changes and that some ECG changes are nonspecific (see Electrocardiographic Images above).
The diagnosis may be established with certainty when typical ST-segment elevation persists for hours and is followed by inversion of T waves during the first few days and by the development of Q waves. However, initial ST depression or T-wave inversion that is associated with MI is difficult to differentiate from that seen with ischemia without MI or in unrelated conditions. ST-segment depression followed by T-wave inversion without the evolution of Q waves may result from non–Q-wave MI or subendocardial ischemia without MI. True posterior-wall MIs may cause precordial ST depression, inverted and hyperacute T waves, or both. ST-segment elevation and upright hyperacute T waves may be evident with the use of right-sided chest leads.
RV MI commonly is manifested by ST-segment elevation or Q waves detectable in right-sided precordial leads. The appearance of abnormalities in a large number of ECG leads often indicates extensive injury or concomitant pericarditis.
Anterior and anterolateral MIs tend to involve more LV myocardium than do inferior or true posterior MIs. Hyperacute (symmetrical and often but not necessarily pointed) T waves are frequently an early sign of MI at any locus. The characteristic ECG changes may be seen in conditions other than acute MI. For example, patients with previous MI and LV aneurysm may have persistent ST elevation, resulting from dyskinetic wall motion, rather than acute ischemic injury. ST-segment changes may also be the result of misplaced precordial leads, hypothermia (elevated J point or Osborne waves), or hypothyroidism.
False q waves may be seen in septal leads in HOCM. They may also result from cardiac rotation.
Substantial T-wave inversion may be seen in some forms of LV hypertrophy with secondary changes. The Q-T segment may be prolonged because of ischemia or hypomagnesemia. Saddleback ST-segment elevation (Brugada epsilon waves) may be seen in leads V1-V3 in patients with a congenital predisposition to life-threatening arrhythmias. This elevation may be confused with that observed in acute anterior MI. Brugada ECG changes may be seen during the administration of procainamide or a beta blocker in patients whose ECG was previously normal. Brain injuries also may trigger changes in T waves.
Preferred Examination
Assessment of MI markers
The detection of elevated concentrations in plasma of macromolecules released from irreversibly injured myocardium has become the definitive diagnostic criterion for MI.10,11,12
CK-MB, cardiac troponin I, and troponin T egress from irreversibly injured ischemic myocardium within several hours after the onset of the insult; elevations in the plasma concentrations of these markers are sensitive diagnostic findings. These macromolecules are abundant in myocardium and are virtually absent from most other tissues.
Characteristic sequential changes of plasma CK-MB include elevations above normal within 4 hours, a peak increase of 2- to 10-fold in 16-24 hours, and a return to baseline within 3-4 days. The magnitude and persistence of elevations are useful in estimating the extent of MI. Analysis of subforms (isoforms) of individual CK isoenzymes may provide accurate estimates of the time of onset of MI and of when recanalization occurred; in addition, analysis of subforms may possibly permit detection of MI earlier than would be possible with isoenzyme or total-CK analysis. False-positive elevations in cardiac markers may be seen after surgical procedures, trauma, injury, vigorous exercise, rhabdomyolysis, cocaine use, or statin use.
Troponins
Levels of cardiac-specific troponins T and I increase within 4-6 hours after the onset of MI; levels peak within about 24 hours. However, levels continue to be elevated for 10-14 days. Therefore, concentrations of these troponins are useful for late diagnosis. Available data suggest that the troponin levels are only slightly more likely than CK-MB levels to be elevated when the patient first presents to the emergency department. False-positive troponin elevations may be encountered in patients with renal insufficiency, acute HF decompensation, or pulmonary embolism.
LDH1 and LDH2
The ratio of LDH1 to LDH2 isoenzymes remains elevated for several days after acute MI and is useful for late diagnosis. However, these isoenzymes are now rarely assayed, given the availability of troponin assays.
Other enzymes and proteins
Concentrations of other enzymes and proteins, such as total CK, serum AST, myoglobin, and myosin light chains, increase in patients with acute MI but are rarely assessed because of their low specificity for acute MI.
Limitations of Techniques: Elevations in the CK-MB level occur in association with skeletal muscle inflammation or necrosis; with renal failure; and (in rare cases) with other conditions. Elevations in the troponin T level, but not the troponin I level, occur in patients with renal insufficiency.
Imaging
Chest radiography
Chest radiography is useful in determining the presence of cardiomegaly, pulmonary edema, pleural effusions, Kerley B lines, and other criteria of HF. In some patients, cephalization (evidence of vascular congestion) may be associated with peripheral pulmonary arterial pruning (decreased prominence).
A small cardiac silhouette and clear lung fields in a patient with systemic hypotension may indicate relative or absolute hypovolemia. A large cardiac silhouette with similar hemodynamics may reflect hemopericardium and tamponade or RV MI that is compromising cardiac output.
Chest radiographic findings indicative of pulmonary venous hypertension may occur late and persist because of delay in fluid shifts among vascular, interstitial, and alveolar spaces.
Echocardiography
The preferred noninvasive modality for evaluating regional wall motion and overall ventricular performance is usually color-flow Doppler transthoracic echocardiography. If image quality is good and if the apex is visualized, the sensitivity and specificity of abnormal wall motion for diagnosing acute MI exceeds 90%, particularly in patients without previous MI.
Assessment of segmental function and overall LV performance provides prognostic information and is essential when MI is extensive, as judged by use of enzymatic criteria, or when MI is complicated by shock or profound HF. In part, this assessment is done to identify potentially surgically correctable complications and to detect true ventricular aneurysms, false ventricular aneurysms, or thrombi.
Imaging is also useful in detecting pericardial effusion, concomitant valvular or congenital heart disease, and marked depression of ventricular function that may interdict treatment in the acute phase with beta-adrenergic blockers. Echocardiography is also helpful in delineating recovery of stunned or hibernating myocardium.
Doppler echocardiography is particularly useful in estimating the severity of mitral or tricuspid regurgitation; in detecting ventricular septal defects secondary to rupture; in assessing diastolic function; in monitoring cardiac output, as calculated from flow velocity and aortic outflow tract area estimates; and in estimating pulmonary artery systolic pressure. For dobutamine echocardiography, images are acquired during an infusion of dobutamine, which is increased from 0 to 40 mcg/kg/min in 10-mcg/kg/min increments. If target stress is not achieved (>85% of the age-predicted maximum heart rate) and if the patient does not have glaucoma, atropine may be added to augment the peak heart rate.
Normal walls show a progressive increase in contractility (motion and thickening). Dead segments have poor motion and no thickening, and contractility fails to increase with high stimulation. Viable but jeopardized myocardium (ischemic myocardium) shows a biphasic response, wherein the contractility increases at lower doses of dobutamine and declines with perceptible wall-motion abnormalities at high doses of dobutamine. This kind of response is characteristic of ischemic myocardium and is most often the result of coronary stenosis.
Positron-emission tomography
PET performed with the use of tracers of intermediary metabolism, perfusion, or oxidative metabolism permits quantitative assessment of the distribution and extent of impairment of myocardial oxidative metabolism and regional myocardial perfusion. It may also be used to assess the effectiveness of therapeutic interventions intended to salvage myocardium, and it has been used to diagnostically differentiate reversible injury from irreversible injury in hypoperfused zones.
Limitations of Techniques
Chest roentgenographic findings are usually nonspecific.
For PET scanning, resolution is a frequent problem. Also, a glucose load is required, and patients with diabetes need an insulin-glucose lock to ensure adequate myocardial uptake.
MRI is generally excluded for patients with pacemakers, defibrillators, and other select metallic implants. Echocardiography is inferior to MRI in image quality, especially for the apex and for the RV, but it is portable. Although MRI can precisely depict the location of infarct and the percentage of wall thickness involved, echocardiography is generally used to estimate the location on the basis of wall motion and/or wall thickening. MRI is generally superior for evaluating complications of MI, such as VSD and pseudoaneurysm.
With echocardiography, endocardial dropout is common, because not all parts of the heart are seen. In 1 in 10 patients, the views are inadequate, most often because of lung disease.
Multidetector-row CT (ie, CT with 16-64 detectors) is emerging as a useful means of identifying blockages of the coronary arteries. However, it involves substantial exposure to ionizing radiation and iodinated contrast agent (moreso than with cardiac catheterization).
Differential Diagnoses
| Aorta, Dissection | Pneumothorax |
| Aortic Regurgitation | Ventricular Septal Defect |
| Brain, Stroke | |
| Congestive Heart Failure | |
| Mitral Regurgitation |
Other Problems to Be Considered
Acute pericarditis
Angina pectoris
Cardiac tamponade
Contusion
Depression
Dyspepsia
Esophageal spasm
Esophageal reflux
Heart arrhythmias
Heart rupture
Herpes zoster
Hypotension
Mitral valve prolapse
Myocarditis
Myopericarditis
Pulmonary embolism (as observed on helical CT)
Pulmonary hypertension
Pleurodynia
Radicular pain
Tachycardia myopathy
More on Myocardial Infarct, Acute |
 Overview: Myocardial Infarct, Acute |
| Imaging: Myocardial Infarct, Acute |
| Follow-up: Myocardial Infarct, Acute |
| Multimedia: Myocardial Infarct, Acute |
| References |
| Further Reading |
| Next Page » |
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Further Reading
Related eMedicine topics:
Myocardial Infarction (from Cardiology)
Myocardial Infarction (from Emergency Medicine)
Complications of Myocardial Infarction
Related Medscape topics:
Specialty Site Radiology
Specialty Site Cardiology
Resource Center Heart Failure
Resource Center COPD
Keywords
acute myocardial infarct, acute myocardial infarction, AMI, MI, heart attack, acute coronary syndrome, ACS, myocardial injury, ST-elevation myocardial infarction, STEMI, non–ST-elevation myocardial infarction, NSTEMI, coronary artery disease, CAD
