AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Background

Acute myocardial infarction (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 due to concomitant arrhythmias, most often ventricular fibrillation (VF).

Almost all MIs are caused by rupture of the coronary atherosclerotic plaques with superimposed coronary thrombosis. Patients with MI usually present with signs and symptoms such as crushing chest pressure, diaphoresis, malignant ventricular arrhythmias, heart failure (HF), or shock. MI can also manifest as sudden cardiac death, which may not be apparent on autopsy (because necrosis takes time to develop). Presentations can be atypical and clinically subtle, especially in women. Findings may include new-onset or accelerated angina, atypical chest 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 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 can be induced only at 6 hours or later after the onset of symptoms, that is, when salvaging substantial amounts of jeopardized ischemic myocardium is no longer likely. An opened 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. Evidence also suggests a benefit from the use of beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, or angiotensin II receptor blockers (ARB), and possibly from insulin infusion (with potassium and glucose) to inhibitapoptosis(cell death).

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 called 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. Subsequent branches, called anterior branches, supply the free wall of the RV, followed by the origination of acute marginal branches that supply RV. When the RCA extends to the crux (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 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, it is most likely to produce extensive injury, impairing function with 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, changing 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 independent 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 when compressing the abdomen by hand) often accompany elevated CVP. In severe cases, the forward delivery of blood from the RV to the LV may be insufficient to fill the LV and cause 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 can further lower blood pressure. Adenosine may accumulate in the infarct zone secondary to a local inhibition of adenosine deaminase that aminophylline can pharmacologically antagonize. 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 coronary blood flow does not resume relatively promptly after medical therapy with fibrinolytic drugs, percutaneous intervention with angioplasty, surgery, or after spontaneous resolution, good myocardial perfusion may not be achieved despite restoration of luminal patency. This situation is known as the no-reflow phenomenon that 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) can lead to the formation of ventricular mural thrombi with 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 can appear like an acute MI.

Effect on systolic function

Lack of adequate oxygen and metabolite delivery to the myocardium diminishes the force of muscular contraction and decreases systolic wall motion in the affected territory.

Abnormal regional wall motion

Even brief deprivation of oxygen and requisite metabolites to the myocardium diminishes diastolic relaxation and causes abnormal regional systolic contractile function and wall thickening and abnormal wall motion. If the area affected is extensive, diminished stroke volume and cardiac output can result.

Myocardial hibernation and stunning

After one or more ischemic insults occur, 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.

Differential diagnosis is usually accomplished by performing tests for the muscle viability by using positron emission tomography (PET), MRI with delayed enhancement, 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 due to the induction of ischemia.

Hypokinesis and dyskinesis M

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. 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 is now encountered much less often than this. When rupture occurs, it may be associated with large infarctions, as indicated by cardiogenic shock, hemodynamically significant arrhythmia, or 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 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 due to coronary occlusion. Well-developed collaterals can greatly limit or even completely eliminate MI despite complete occlusion of a coronary artery. The number of patients who have collaterals at the time of a MI varies, and many patients develop collaterals in the hours and days after an occlusion occurs (De Wood, 1980, Fujita, 1999). Collaterals have normal blood flow at rest, accounting for absence of resting ischemia. However, they cannot increase blood flow with exercise; this inability accounts for ischemia during periods of stress (Vanoverschalde, 1993).

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 can increase the myocardial ischemic injury.

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 room, death is most often sudden. Acute MI accounts for 1 million hospital admissions each year.

Despite 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. Part of this effect may be due to 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 become closely aligned with that affecting developed countries. With a decline in infectious disease-related deaths accompanied by accelerated economic development and life-style changes that promoting atherosclerosis, rates of ischemic heart disease and MI are expected to sharply increase in developing countries, especially those 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 fatal event in most patients.

Race

• Acute MI more often occurs in white men.
• An increased incidence of MI is observed in Asian Indians.
• Lowest rates are seen in Japanese and French populations, a finding known as the French paradox.

Sex

Men are predominately affected; however, diabetes and a postmenopausal state equalize the risk in women.

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 using 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 and 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 precipitate an acute coronary event.

The spectrum of myocardial injury depends on not only the intensity of impaired myocardial perfusion but also the duration and the level of metabolic demand at the time of 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.

Typical MI initially manifests as coagulation necrosis ultimately followed by myocardial fibrosis. Contraction-band necrosis is also seen in many patients when ischemia. This is followed by reperfusion, or it is accompanied by massive adrenergic stimulation, often with concomitant myocytolysis.

Clinical Details

Signs and symptoms of typical Q-wave MI

Typical Q-wave MI may manifest with prodromal symptoms of fatigue, chest discomfort, or malaise in the days preceding the event, or it may occur suddenly, without warning.

MI most often in the early morning hours, perhaps partly because of the increased catecholamine-induced platelet aggregation and increased serum concentrations of plasminogen activator inhibitor-1 (PAI-1) 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 also may be described as an ache, a burning pain, a of feeling 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. On the contrary, 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 with reduced cardiac output.

MI may be clinically silent in as many as 25% of elderly patients, a population in whom 50% of MIs occur, and the diagnosis 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 sometimes do not recognize chest pain because of stoicism, an unusually high pain threshold, disorders that impair function of the nervous system and that result in a defective anginal warning system (eg, diabetes mellitus), or obtundation caused by medication or impaired cerebral perfusion.

Physical examination

General appearance

Patients may appear acutely ill. They often clutching their chest and cannot lay 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 and 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 due to 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 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 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 (variation in systolic pressure >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 and can be palpated in associated hypertrophic obstructive cardiomyopathy (HOCM) or mixed aortic stenosis and regurgitation. A dicrotic pulse is encountered in 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, where 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, which is defined as a greater than or equal to 10-mm Hg decline in systolic blood pressure with inspiration, is seen in cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, hypotensive shock, severe chronic lung disease, and pulmonary embolism.

In patients with associated aortic regurgitation, a pulse with sharp descent, or a water-hammer pulse, may be observed.

Venous pulsations

Jugular venous pulsations normally have several waves. The A wave results from venous distention due to RA systole, followed by the x descent (due to 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 followed by the Y descent 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 due to increased RA pressure in HF, decreased RV compliance, pericardial disease, fluid overload, and tricuspid or superior vena cava obstruction. The Kussmaul sign, characterized by a paradoxical rise during inspiration in the jugular venous pressure, 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 due to 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 can be prominent in patients with RV volume overload, such as in 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. On the contrary, in patients with cardiac tamponade, the X descent is prominent, and the Y descent is absent.

A prominent V wave or a cV wave (c from the carotid pulse and V from valve closure) occurs in patients with tricuspid regurgitation and 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 can be auscultated, and these occur secondary to pulmonary venous hypertension associated with extensive acute LV MI. Unilateral or bilateral pleural effusions may produce egophony at the lung bases and may be observed in the form of blunted costophrenic angles on chest radiographs, dependent fluid signal intensity on MRI, or echolucent zones adjacent to the heart on echocardiography.

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 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, and 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 and may be audible even when cardiac output is substantially decreased.

A holosystolic systolic murmur radiating to the midsternal border and not to the back, possibly with a palpable thrill, suggests a ventricular septal rupture, which 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 due to 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, and 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 can 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 or non-Q-wave, also known as ST-elevation vs non-ST-elevation MIs), and extent of MI (ie, 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. Troponin indicates if myocardial damage of any cause occurred in the 2 weeks (or longer) before testing, though false-positive results may occur in patients with renal failure. Levels of CK and CK-MB typically increase and decrease within 1-3 days, clarifying the acuteness of the event. The peak level and the area under the curve may indicate the size of the MI and may have prognostic value. CK and myoglobin values may also rise with injury to skeletal muscle, but elevation of the percentage of CK-MB indicates the myocardial source.

Other markers that are less diagnostically accurate than these are also elevated. These markers include WBC counts; erythrocyte sedimentation rates (ESRs); and levels of lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and alanine aminotransferase (ALT).

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 persist generally 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, eg, that resulting 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 can obviate puncture to assess arterial blood gases (ABGs). Such puncturing might lead to bleeding in patients treated with thrombolytic drugs. However, normal oxygen saturation does not exclude impending respiratory failure.

Electrocardiography

Characteristic findings on sequential ECGs remain hallmarks of diagnosis despite the occasional occurrence of MI without any acute changes and the nonspecific nature of some of ECG changes.

The diagnosis can be established with certainty when typical ST elevation persists for hours and when it is followed by inversion of T waves in the first few days and the development of Q waves. However, initial ST depression or T-wave inversion 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 can 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 elevation and upright hyperacute T waves may be evident with right-sided chest leads.

RV MI commonly is manifested by ST 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 due to dyskinetic wall motion rather than acute ischemic injury. ST-segment changes may also be due to misplaced precordial leads, hypothermia (elevated J point or Osborne waves), or hypothyroidism.

False q waves may be seen in septal leads in HOCM. They can 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 ischemia, or hypomagnesemia. Saddleback ST-segment elevation (Brugada epsilon waves) can be seen in leads V1-V3 in patients with a congenital predisposition to life-threatening arrhythmias. This elevation can 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 with a previously normal ECG. Brain injuries also can 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.

CK-MB, cardiac troponin I, and troponin T egress from irreversibly injured ischemic myocardium within several hours after the onset of the insult, and their elevated concentrations in plasma 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 increased 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 can provide accurate estimates of the time of onset of MI and of when recanalization occurred, and it may possibly permit detection of MI earlier than that possibly 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 also increase within 4-6 hours after the onset of MI, and they 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 troponins are only slightly more likely than CK-MB to be elevated when the patient first presents to the emergency department. False-positive troponin elevations can 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 to perform 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: False-positive CK-MB elevations are found with skeletal muscle inflammation or necrosis, with renal failure, and (in rare cases) with other conditions. False-positive troponin T, but not troponin I, elevations 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 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 to evaluate 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, sensitivity and specificity of abnormal wall motion for 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 using enzymatic criteria, or when it is complicated by shock or profound HF. In part, this assessment is done to identify potentially surgically correctable complications and to detect ventricular true or false aneurysms or thrombi.

Imaging is useful also to detect 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 to estimate the severity of mitral or tricuspid regurgitation, detect ventricular septal defects secondary to rupture, assess diastolic function, monitor cardiac output calculated from flow velocity and aortic outflow tract area estimates, and estimate 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 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 due to 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 can also define the effectiveness of therapeutic interventions designed 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 in 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, as not all parts of the heart are seen. One in 10 patients have inadequate views, most often because of lung disease.

Multidetector-row CT (ie, CT with 16-64 detectors) is emerging as a useful means to identify blockages of the coronary arteries. However, it involves substantial exposure to ionizing radiation and iodinated contrast agent (exposures more that those of cardiac catheterization).

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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

RADIOGRAPH

Section 4 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

In patients with MI, portable radiography is almost always performed in the emergency department or CCU.

When present, prominent pulmonary vascular markings on the radiograph reflect elevated LVEDP, but clinically significant temporal discrepancies may occur because of diagnostic and posttherapeutic lags. Up to 12 hours may elapse before pulmonary edema accumulates after ventricular filling pressure becomes elevated. The posttherapeutic phase lag is even longer; up to 2 days are required for pulmonary edema to resorb and for the radiographic signs of pulmonary congestion to clear after ventricular filling pressure returns toward normal.

The degree of congestion and the size of the left side of the heart on the chest radiograph are useful for defining groups of patients with MI who are at increased risk for dying after the acute event.

Complications of MI

When CHF persists despite treatment, certain complications of MI must be excluded. These include aneurysm, pseudoaneurysm, rupture of the ventricular wall or papillary muscle, and interventricular septal defect. In converse, MI may occur as a complication of aortic dissection.

Ventricular septal defect

An interventricular septal defect occurs in 0.5-1.0% of patients with recent septal infarction and is characterized by cardiomegaly, pulmonary edema, and poor myocardial contractility. On the plain radiograph, the typical shunt pattern may not be appreciated because of pulmonary edema, but it can emerge months later if the patient survives. Such defects usually involve the muscular septum and occur within 7-12 days after MI.

Post-MI syndrome

The radiographic picture of post-MI syndrome (ie, Dressler syndrome) is that of a heart enlarged because of pericardial effusion. Unilateral pleural effusions are common, though bilateral effusions can also occur, and lower-lobe consolidation, particularly on the left side, occurs in less than 20% of patients. These findings generally appear 2-6 weeks after MI and are analogous to postpericardiotomy syndrome.

LV aneurysm

Aneurysm of the LV is an abnormal bulge or outpouching of the myocardial wall that develops in 12-15% of patients after MI. It most commonly occurs at the cardiac apex or along the anterior free wall of the LV. It is true aneurysm if it is lined with myocardium. A false aneurysm is a contained rupture in which at least part of the wall is typically pericardium and possibly lined with thrombus. False aneurysm or pseudoaneurysm often has a narrow entrance to a large cavity.

The chest radiograph may show a localized bulge along the ventricular wall, with or without a thin rim of calcification. CT, MRI, and echocardiography may all demonstrate differences in dyskinesis of the damaged wall. High resolution may be needed to distinguish some cases of pseudoaneurysm from true aneurysm; for this purpose, MRI is preferred.

The differential diagnosis of LV aneurysm includes other deformities of the left heart border caused by pericardial cysts, mediastinal or pleural tumor, thymoma, and other mediastinal masses.

Cardiac rupture and pseudoaneurysm

Cardiac rupture usually occurs in patients who have had an acute transmural infarction. Most die immediately, but in a few, surrounding extracardiac soft tissue contain or enclose the rupture, and a pseudoaneurysm forms.

Radiographs show a paracardiac mass with sharply marginated edges free of calcification. On the lateral projection, the mass is usually posterior, unlike the relative anterior position of a true aneurysm.

Rupture of the papillary muscle

Papillary muscle rupture follows MI in approximately 1% of patients. Plain radiographic findings vary from a normal chest to gross cardiomegaly with left atrial and ventricular enlargement and pulmonary edema. Left ventriculography, MRI, and Doppler echocardiography demonstrate the flail leaflets of the mitral valve and help in estimating the degree of mitral regurgitation.

Degree of Confidence

Radiography is a nonspecific test. The degree of confidence is low. If findings from transthoracic echocardiography are not diagnostic, transesophageal echocardiography may be necessary.

False Positives/Negatives

False findings are frequent.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

CT can provide useful cross-sectional information in patients with MI. In addition to helping in the assessment of cavity dimensions and wall thickness, CT depicts LV aneurysms and intracardiac thrombi, which are particularly important in MI. New multidetector-row CT provides 3-dimensional (3D) visualization of the coronary artery anatomy and ramifications, its calcifications, stenoses, and even the presence of soft plaque in the wall of the coronary artery.

Complications of MI, such as pseudoaneurysm, are confirmed by means of echocardiography, MRI, or contrast-enhanced CT. Imaging of a pseudoaneurysm typically shows a relatively narrow neck and a complete absence of muscle in the wall of the pseudoaneurysm, unlike a true aneurysm, which has a rim of myocardial wall that may be identified on angiograms by the presence of mural vessels.

Degree of Confidence

CT angiography (CTA) may cause overestimation of obstructions, and its degree of confidence is lower than that of MRI for assessing mural thrombi and the locations of infarcts. Although cardiac CT is less convenient than echocardiography, it is probably more sensitive than echocardiography for detecting thrombi.

False Positives/Negatives

False findings are frequent.

MRI

Section 6 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

MRI enables direct visualization of the myocardium with excellent delineation of the epicardial and endocardial interfaces. As a consequence, it can accurately define segmental wall thinning that indicates previous MI. In some patients with a clinical history of transmural infarction, residual myocardium can be demonstrated at the site of the infarction. In others, MRI shows virtually complete replacement of muscle by scar. Direct visualization of the myocardium can be used to determine whether sufficient residual myocardium remains in the region jeopardized by a coronary arterial lesion to warrant bypass grafting. Delayed enhancement is the retention of contrast agent 10-20 min after bolus injection of gadolinium-based contrast agent (diethylenetriamine penta-acetic acid [DPTA] 0.1 mM/kg and indicates early myocardial injury if the imaging parameters are properly adjusted, MRI is the best method to define scarring and inflammation.

The recognition of decreased signal intensity of the myocardial wall at the site of old MI suggests that MRI can demonstrate replacement of myocardium by fibrous scar. MRI scar maps can be generated by using delayed enhancement, which consists of T1-sensitive imaging performed 10-20 minutes after the administration of a gadolinium-based contrast agent (0.1 mM/kg, 20 mL in typical adults). Damaged cells and collagen in scar tissue retain the contrast material, making the scar white with the normal wall dark. Scars less than one third the thickness of the wall indicate a good potential for improvement with revascularization, whereas scars greater than third thirds the thickness of the wall suggest limited recovery with therapy (except by research cell therapies or surgical scar revision) (see Image 5).

ECG- and respiratory-gated MRI can demonstrated complications of MIs, such as LV thrombus and aneurysms. Transverse or short-axis tomography facilitates the recognition of the small ostium connecting the LV chamber and the false aneurysm; this is a distinguishing feature of the false LV aneurysm compared with the true LV aneurysm.

MIs have been demonstrated on gated MRI. The region of ischemically damaged myocardium had increased signal intensity compared with normal myocardium. Contrast between infarcted and normal myocardium increases on images with increased T2 contribution to signal intensity. The administration of contrast medium (gadolinium chelates) with T1-weighted spin-echo imaging increases enhancement of infarcted myocardium, with increased signal intensity compared with normal myocardium.

Regional wall thickening can also be assessed during MRI with dynamic movies or grid-tag strain maps. A wall thinner than 6 mm at end diastole and wall thickening of less than 1 mm correspond to a myocardial scar, as defined by lack of uptake of technetium Tc 99m sestamibi single photon emission CT (SPECT), or FDG glucose on PET. Furthermore, MRI is a good predictor of recovery of regional function after myocardial revascularization.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.

As of late December 2006, the FDA had received reports of 90 such cases of NSF/NFD . Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

The degree of confidence is typically high unless arrhythmia impairs image quality. MRI is the most accurate test for identifying MIs and for delineating the size and depth of wall-thickness involvement. MRI is attractive because of its ability to show (1) perfusion of infarcted and noninfarcted tissue; (2) areas of jeopardized but not infarcted myocardium; (3) myocardial edema, fibrosis, wall thinning, and hypertrophy; (4) ventricular chamber size and segmental wall motion; (5) the temporal transition between ischemia and infarction, and (6) complications of MI.

MRI can also be used to image wall motion after dobutamine or adenosine infusion to assess ischemia. Dobutamine stress MRI, performed by using a low dose (5-15 mcg/kg/min) can be performed after a recent MI. The rationale for this study is that contractile function of viable tissue improves after inotropic stimulation, whereas scarred tissue does not. Criteria for viability include end-diastolic wall thickness (EDWT) of 5.5 mm or less and dobutamine-induced systolic wall thickness (SWT) 2 mm or more. In patients with an acute or recent MI, dobutamine stress MRI has a sensitivity of approximately 91% and a specificity of approximately 70%. For cardiac ischemia, uses dobutamine 10 to 40 mg/kg/min is used.

However, dobutamine stress MRI has several limitations. First, ECG changes due to ischemia cannot be detected reliably with standard ECG monitoring in the high-field MRI environment. Instead, wall-motion abnormalities are visually and subjectively detected to ensure the patient's safety during stress testing. Also, wall thickening in response to dobutamine is not entirely specific for ischemia.

False Positives/Negatives

The rate of false findings is low.

ULTRASOUND

Section 7 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Two-dimensional echocardiography

The portability of echocardiographic equipment makes this technique preferred for the assessment of patients with MI hospitalized in the CCU or in the emergency department before admission. In patients with chest pain compatible with MI but with a nondiagnostic ECG, a distinct segment of abnormal contraction on echocardiography indicates ischemic impairment.

Complete 2D echocardiographic examination typically includes color-coded assessment of blood movement (red is toward the transducer; blue, away), which reveals valvular leaks and septal defects. Continuous and pulsed Doppler likewise help in evaluating blood movement by using shifts in sound frequency to measure velocity anywhere along a column or at a specific location, respectively. Because a pressure drop across a passage, such as a valve or VSD, is predominantly due to the change in kinetic energy (½MV² Doppler imaging can be used to estimate pressure gradients. Furthermore, equations based on conservation (ie, the observed fluid is not created or destroyed) results in a number of useful ways to estimate the severity of pressures, stenoses, and leakages.

Echocardiography is also useful in evaluating patients with chest pain with a suspected aortic dissection. Identification of an intimal flap consistent with aortic dissection is a crucial observation because it represents a major contraindication to thrombolytic therapy. Transthoracic echocardiography offers a limited view of the aorta, which improves by including views from the suprasternal notch. Transesophageal echocardiography improves the views, but portions of the aorta, particularly in the arch, can still be missed. CT and MRI are equally good and enable complete examination of the aorta.

Areas of abnormal regional wall motion are almost universally observed in patients with MI, and the degree of wall-motion abnormality can be categorized with a semiquantitative wall-motion score. Of note, infarcts can be missed during echocardiography when the infarction is small or when it involves just the apex. MRI is best for examining the apex and small or partial-thickness infarctions.

LV function estimated from 2D echocardiography is well correlated with angiographic measurements and is useful in establishing the patient's prognosis after MI. Furthermore, early use of echocardiography can aid in the detection of potentially viable but stunned myocardium (contractile reserve). Stress echocardiography is as good as nuclear imaging for detecting inducible ischemia.

Although transthoracic imaging is adequate in many patients, 10-20% have poor echocardiographic windows, especially if they have lung disease or if require a ventilator. In such patients, transesophageal echocardiography or MRI may be used.

Three-dimensional echocardiography

Computer-controlled rotation of the transducer used for 2D echocardiograph can be used to generate 3D movies. This technique has advantages for the evaluation of a diseased mitral valve and potentially other situations in which 3D tissue relationships may clarify the character and severity of an abnormality.

Stress echocardiography

Echocardiography is frequently used to assess myocardial ischemia by providing images at rest and stress. A typical treadmill or bicycle ergometer can be used as means of exercise. In patients who cannot exercise, chemical stress may be induced with dobutamine. During dobutamine-stress echocardiography, images are acquired during an infusion of dobutamine, which is given in increments of 10 mcg/kg/min to a rate of 40 mcg/kg/min. Normal walls show progressively increasing contractility (motion and thickening). Necrotic segments have reduced or reversed motion and no thickening, and their contractility fails to increase with increased stimulation. Viable but jeopardized myocardium (ie, ischemic myocardium) shows a biphasic response. Its contractility increases at low doses of dobutamine and declines, with perceptible wall wall-motion abnormalities, at high doses.

Degree of Confidence

The degree of confidence is moderately high, ie, 85% if adequate stress is achieved.

False Positives/Negatives

The rate of false-positive findings is low. False-negative results occur when the peak stress level is marginal, when rest and stress views do not match, or when views do not cover the entire heart. Poor views are acquired in about 10% of patients. Echocardiography requires a lung-free window that commonly excludes the true apex of the LV and that offers limited views of the RV.

NUCLEAR MEDICINE

Section 8 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Radionuclide angiography, perfusion imaging, infarct-avid scintigraphy, and PET have been used to evaluate patients with MI.

Nuclear cardiac-imaging techniques can be useful for detecting MI; assessing infarct size, collateral flow, and jeopardized myocardium; determining the effects of the infarct on ventricular function; and establishing the prognosis of patients with MI. However, the necessity of moving a critically ill patient from the CCU to the nuclear medicine department limits practical application of this study unless a portable gamma camera is available.

For the diagnosis of MI, cardiac radionuclide imaging should be restricted to special, limited situations in which the triad of the patient's clinical history, ECG findings, and serum marker measurements is unavailable or unreliable.

Radionuclides, such as thallium, sestamibi, and tetrofosmin are used along with mechanical (treadmill or bicycle) or pharmacologic (dobutamine or adenosine) stress testing. Images are obtained at rest and stress and compared to look for inducible ischemia (decreased counts with stress). When thallium is used, images must be obtained within a few minutes of infusion. Images obtained at rest sometimes do not show adequate redistribution, and reinjection and imaging performed at 24 hours reveals viability that was missed during immediate imaging. Background correction is performed by acquiring images before perfusion or by estimation by using low-resolution CT or other imaging means.

Degree of Confidence

The degree of confidence is fairly high.

False Positives/Negatives

False findings are often encountered.

ANGIOGRAPHY

Section 9 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Techniques

Selective coronary angiography requires the injection of an x-ray opaque material, typically iodine, through a catheter threaded through an artery to the aorta and to the origin of each coronary artery. It is the criterion standard for identifying coronary blockages.

Viability studies, such as MRI with delayed enhancement, PET, nuclear medicine studies, or dobutamine echocardiography, may be needed to determine if damaged tissue beyond a blockage can recover. However, the open-artery hypothesis is that opening all blocked arteries, even if the muscle they supply cannot recover function, may be best. Extensions of the catheterization technique needed for coronary angiography enable treatment accomplished by inserting balloons or stents and/or by locally delivering medications. These therapies are collectively known as percutaneous coronary interventions (PCIs).

PCI is used instead of thrombolytic therapy to clear a blockage early in an acute MI (primary angioplasty), as adjunctive therapy with thrombolysis, as a management strategy in the subacute phase of acute MI (days 2-7), or late after MI. In the early stages of MI, intervention is typically limited to the infarct-related lesion.

Percutaneous coronary intervention

Indications for PCI according to guidelines from the American College of Cardiology and the American Heart Association

Coronary arteriography should be performed in patients with Q-wave or non-Q-wave MI who develop spontaneous ischemia; in those who have ischemia with a minimal workload; and in those who have MI complicated by CHF, hemodynamic instability, cardiac arrest, mitral regurgitation, or ventricular septal rupture. Patients with angina or provocable ischemia after MI should also undergo coronary arteriography because revascularization may reduce the high risk of repeat infarction in these patients. Guidelines from the American College of Cardiology/American Heart Association (ACC/AHA) list the following classes of indications for coronary angiography:

• Class I
• • Spontaneous myocardial ischemia or ischemia provoked with minimal exertion
  • Presurgical therapy for acute MI, ventricular septal defect, true aneurysm, or pseudoaneurysm
  • Persistent hemodynamic instability
• Class II A:
• • Suspected MI due to coronary embolism, arteritis, trauma, certain metabolic diseases, or coronary spasm
  • Survivors of acute MI with LV ejection fraction (LVEF) of less than 0.40, CHF, previous PCI or coronary artery bypass grafting (CABG), or malignant ventricular arrhythmias
• Class II B:
• • For a suspected persistent occlusion of the IRA to perform delayed PCI
  • Coronary arteriography performed without risk stratification to identify the presence of left main or 3-vessel coronary artery disease
  • All patients after non–Q-wave MI
  • Recurrent ventricular tachycardia despite antiarrhythmic therapy without ongoing ischemia

Contraindications

No absolute contraindications are described for coronary arteriography.

Relative contraindications include the following:

• Unexplained fever
• Untreated infection
• Severe anemia with hemoglobin level less than 8 g/dL
• Severe electrolyte imbalance
• Severe active bleeding
• Uncontrolled systemic hypertension
• Digitalis toxicity
• Previous allergy to contrast material but no pretreatment with corticosteroids
• Ongoing stroke
• Acute renal failure
• Decompensated CHF
• Severe coagulopathy
• Diabetic patients with Cr greater than 2
• Patients on metformin (Glucophage) or other oral hypoglycemic agents
• Active endocarditis

Risk factors for clinically significant complications after catheterization include advanced age, hemodynamic instability, multisystemic disease, large infarctions, bleeding disorders, and extensive atherosclerosis in the aorta or access arteries.

Magnetic resonance angiography and CTA

Contrast-enhanced magnetic resonance angiography (MRA) is a fast-growing, noninvasive modality for vascular imaging. Current clinical applications of MRI of the coronary arteries include evaluations of anomalous coronary arteries, Kawasaki disease, and bypass-graft patency. MRI of native coronary arteries remains the most challenging area of cardiac MRI. Several factors that contribute to this difficulty. The coronary arteries are small (2-4 mm in diameter) and frequently tortuous. They have continuous inherent cardiac and respiratory motions that cause motion artifact. Both black-blood and bright-blood techniques with 2D or 3D linear and nonlinear acquisitions during breath holding or free breathing with navigators have been used with limited success. ECG- and respiratory-gated MRI has decreased the overall severity of these artifacts.

CTA is widely used to examine the peripheral arteries and grafts. However, until recently, motion artifact hindered coronary angiography, as with MRI of the coronary arteries. Newer, faster 64-section CT angiography has substantively resolved this problem and is proving to be a convenient and useful test for confirming the absence of coronary artery disease and for constructing 3D models of coronary obstructions and calcifications. Also, soft plaque may be seen within arterial walls as areas of distinctly decreased Hounsfield attenuation.

Degree of Confidence

The degree of confidence is high.

False Positives/Negatives

False findings are extremely rare. Additional procedures may be required to identify the hemodynamic significance of observed lesions. Microvascular disease may cause ischemia with no evident obstructions by angiography. Catheterization may cause dissection of an artery (bleeding into the vessel lining) resulting in obstruction and an MI in a patient who may have had normal coronary arteries. Catheterization may also cause a perforation with bleeding into the pericardial space. Either of these may cause death.

INTERVENTION

Section 10 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Treatment in the prehospital phase

Most deaths caused by MI occurs early and are attributable to primary VF. Therefore, initial objectives are immediate ECG monitoring, electric cardioversion of VF should it occur, and rapid transfer of the patient to facilitate prompt coronary recanalization. Community-based systems in Belfast, Ireland; Columbus, Ohio; Los Angeles, California; and Seattle, Washington have conclusively documented the effectiveness of rapid response by rescuers (eg, police and firefighters) trained in defibrillation.

Approximately 65% of deaths caused by MI occur in the first hour. More than 60% of these deaths (ie, 39% of patients who would otherwise die) can be prevented with defibrillation by a bystander or a first-responding rescuer.

Additional objectives of prehospital care by paramedical and emergency personnel include adequate analgesia (generally achieved with morphine); pharmacologic reduction of excessive sympathoadrenal and vagal stimulation; treatment of hemodynamically significant or symptomatic ventricular arrhythmias (generally with lidocaine); and support of cardiac output, systemic blood pressure, and respiration.

Prehospital administration of tissue-type plasminogen activator (tPA), aspirin, and heparin may be given to patients with bona fide MI by paramedics, as guided by ECG findings within 90 minutes of the onset of symptoms. This treatment improves outcome compared with thrombolysis begun after the patient arrives at the hospital.

Atropine 0.5 mg given intravenously (IV) at 5-minute intervals to a maximum of 2-4 mg is useful to counteract excessive vagal tone that often underlies bradyarrhythmias and hypotension. If bradycardia persists, transthoracic pacing may be life saving.

Treatment in the emergency department

Treatment in the emergency department begins with focused cardiovascular history taking and physical examination, the establishment of IV access, 12-lead ECG, and continuous rhythm monitoring. All patients with suspected MI should be given chewable aspirin 160-325 mg unless they have a documented allergy to aspirin.

Cardiac enzyme levels should be measured, as should hematocrit, electrolyte, creatinine, and oxygen levels. (For the last measurement, fingertip oximetry is usually sufficient.)

Initial stabilization of patients with suspected MI and ongoing acute chest pain should include sublingual nitroglycerin, which may be repeated for 2 additional doses at 5-minute intervals if pain persists. Patients should not have contraindications, such as hypotension (systolic blood pressure < 90 mm Hg), bradycardia, tachycardia, or findings suggestive of RV infarction.

Refractory or severe pain should be treated symptomatically with IV morphine, meperidine, or pentazocine. Doses of morphine 4-8 mg IV can be repeated every 5-15 minutes with relative impunity until the pain is relieved or toxicity is manifested by hypotension, vomiting, or depressed respiration. Should toxicity occur, a morphine antagonist, such as naloxone, can reverse it. The patient's blood pressure and pulse must be monitored to keep the systolic blood pressure above 100 mm Hg and, optimally, below 140 mm Hg.

Relative hypotension may be treated by elevating the lower extremities or by given fluids, except in patients with concomitant pulmonary congestion, in whom treatment for cardiogenic shock may be required. Atropine, in doses similar to those given in the prehospital phase, may increase blood pressure if hypotension reflects bradycardia or excess vagal tone.

Oxygen should be given to prevent hypoxemia. High concentrations may be counterproductive because of vasoconstriction and the lack of augmented myocardial oxygen delivery in normoxemic patients.

The assignment of patients to subsets guide triage decisions.

For patients with probable MI who are appropriate candidates for reperfusion because of a new ST elevation of 1 mm or more in 2 or more leads or presumably because of a new bundle-branch block in the setting of a typical clinical syndrome, plans should be made for prompt treatment to induce recanalization even while the patient is in the emergency department. Options include IV thrombolysis (started immediately in the emergency department) or immediate transfer to the cardiac catheterization laboratory for primary percutaneous transluminal coronary angioplasty (PTCA).

For patients whose clinical presentations and ECGs strongly suggest ischemia, especially those with ST-segment depression or T-wave inversion on ECG, thrombolysis is not recommended. However, anti-ischemic therapy for suspected non-Q-wave infarction or unstable angina should be started, and the patient should then be transferred to a CCU or an intermediate care or step-down unit.

Low-risk patients without obvious ischemia should be observed and monitored in either a step-down or intermediate care unit or a unit to evaluate or observe for chest pain.

Treatment in the hospital phase

CCUs have reduced early mortality rates from acute MI by approximately 50%, initially by providing immediate defibrillation and most recently by facilitating the implementation of beneficial interventions. These interventions include the administration of IV medications and therapy designed to limit the extent of MI, to salvage jeopardized ischemic myocardium, and to recanalize infarct-related arteries, as well as to diagnose and treat other conditions.

Coronary revascularization

Alternatives for coronary recanalization include the IV administration of thrombolytic agents or catheter-based approaches.

Thrombolysis can be accomplished with a variety of IV medications and regimens, with or without the use of adjunctive therapies.

Catheter-based recanalization with PTCA, with or without stenting, can induce patency in more infarct-related arteries (about 90% compared with about 50-80% for pharmacologic thrombolysis). This intervention decreases residual stenosis, recurrent ischemia, the risks of reocclusion, and the need for later mechanical revascularization. Catheter-based approaches also avoid the risk of bleeding, including intracerebral bleeding, observed with thrombolysis. Patients who are treated with primary PTCA generally have shorter lengths of stay and consume fewer medical resources than patients treated with IV thrombolysis. Several randomized trials have demonstrated that rapidly available primary PTCA performed by skilled operators for acute MI is associated with long-term outcomes similar to those achieved with IV thrombolysis, though this comparison remains a topic of active investigation.

Disadvantages of primary PTCA include the fact that the procedure is highly dependent on the operator's skill and that immediate access to highly skilled operators is necessary.

Data from nonrandomized studies suggest an advantage with primary PTCA in patients with acute MI complicated by cardiogenic shock. It is clearly the treatment of choice in patients with contraindications to thrombolytic agents. Whether certain subsets of patients respond better to PTCA or thrombolysis is unclear. For example, in patients with type 2 diabetes, elective PTCA is inferior to CABG, and it may be the case that similar or other characteristics will ultimately guide the choice among reperfusion therapies in acute MI.

The first generation of fibrinolytic drugs (eg, streptokinase, urokinase, acetylated plasminogen streptokinase activator complexes [APSACs], reteplase, and novel plasminogen activator [nPA]), indiscriminately induce activation of circulating plasminogen and clot-associated plasminogen. First-generation drugs invariably elicit a systemic lytic state characterized by depletion of circulating fibrinogen, plasminogen, and hemostatic proteins and by marked elevation of concentrations of fibrinogen degradation products in plasma.

Second-generation drugs (eg, tPA, single-chain urokinase plasminogen activator) includes recently developed agents, such as tenecteplase (TNK), preferentially activate plasminogen in the fibrin domain compared with free plasminogen in the circulation. Therefore, they have clot selectivity. In optimal regimens, these agents induce clot lysis without inducing a systemic lytic state, they are less prone than nonselective agents to predispose the patient to transfusion-requiring hemorrhage, and they are effective in inducing recanalization in 80-90% of infarct-related arteries within 90 minutes. Therefore, tPA recanalizes 75-80% of infarct-related arteries in contrast to approximately 50% with IV streptokinase.

Coronary thrombolysis with IV activators of plasminogen improves ventricular function and decreases mortality, especially early after MI and when initiated given a few hours after the onset of ischemia. Even when started late (>6 h after the onset of MI), restored patency of the infarct-related artery may confer an early mortality benefit, perhaps because of improved collateral blood flow and ventricular remodeling and function or decreased infarct expansion, arrhythmogenicity, ventricular aneurysm formation, and late arrhythmia associated with aneurysms that do develop.

In the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) trial, second-generation agents significantly improved 24-hour, 30-day, and 1-year mortality, as well as survival without disabling stroke.

The risks of coronary thrombolysis include bleeding, much of which is confined to sites of vascular access. Marked depletion of fibrinogen or prolongation of the bleeding time may be markers of pharmacologic effects that lead to bleeding. With thrombolysis, the incidence of hemorrhagic stroke is increased, but the risk of thrombotic or embolic stroke is somewhat reduced, and overall any small increase in fatal cerebrovascular accidents is more than offset by the favorable effect on survival. Plasminogen activators should not be given to patients with active internal bleeding or a bleeding diathesis, suspected aortic dissection, recent trauma, intracranial neoplasm, or hypertensive crisis. Relative contraindications include prolonged or traumatic cardiopulmonary resuscitation, peptic ulcer disease, remote cerebrovascular accident, and hepatic failure. Safety has not been established for pregnant women, although it has been for menstruating women.

In general, use of thrombolytic agents has been well demonstrated to be effective in patients aged 75 years or younger who present with suspected Q-wave MI within 6 hours after the onset of symptoms, and in whom contraindications are not present. Although the absolute risk of complications is greatest in the elderly, overall mortality reduction is at least as great in this group than in others because the prognosis with MI managed conservatively is also worse for elderly patients than that for younger patients.

Treatment may be helpful in some patients first seen 6-12 hours after the onset of symptoms, particularly those with stuttering infarcts. It has not been demonstrated to be effective in patients with non-Q-wave MI or unstable angina. The clinical effectiveness of coronary thrombolysis depends on the frequency, rapidity, and persistence of recanalization. All of these factors depend not only on the intensity of fibrinolysis but also on the inhibition of coagulation and platelet-induced thrombosis, which undoubtedly occur concomitantly.

At present, IV heparin is routinely administered in addition to orally administered aspirin. Alternatives include low-molecular-weight heparin, other inhibitors of coagulation (eg, hirudin), and antagonists of binding of fibrinogen to the platelet surface glycoprotein IIb/IIIa (GPIIb/IIIa) receptor (eg, abciximab, eptifibatide, tirofiban, and orbofiban).

Even optimally effective coronary thrombolysis is compromised by early thrombotic reocclusion in 6-20% of patients with initial recanalization unless vigorous conjunctive anticoagulation is started immediately.

Use of thrombolytic medications and mechanical revascularization may be required. For example, low-dose IV t-PA combined with early PTCA appears to be superior to PTCA alone. CABG may be needed in patients whose condition fails to respond to PTCA with stenting, and it is feasible even after the administration of IV thrombolytic agents if necessary. Despite a high perioperative mortality rate for CABG within 24 hours of failed pharmacologic thrombolysis or PTCA, subsequent 1-year mortality among survivors may be as low as 2% and not different from the rate in those who survived CABG performed late after MI. CABG is an option for patients in whom other efforts to establish reperfusion fail and who have ongoing major complications. Contrary to initial expectations, not all patients treated with thrombolytic drugs need obligatory early cardiac ca