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Acute Myocardial Infarction Imaging

Practice Essentials

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. (See the images below.) 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). 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 electrocardiographic criteria
or by performing imaging with 2-dimensional (2-D) echocardiography or magnetic resonance imaging (MRI).

Acute inferior myocardial infarction on an ECG.

Acute inferior myocardial infarction on an ECG.

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Apical left ventricular (LV) dyskinesis (ventricul

Apical left ventricular (LV) dyskinesis (ventricular aneurysm) after an anterior myocardial infarction.

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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. (See the image below.)
 Evidence suggests a benefit from the use of beta blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARB), and possibly insulin infusion (with potassium and glucose) to inhibit apoptosis (cell death).

After thrombolytic therapy, reperfusion arrhythmia

After thrombolytic therapy, reperfusion arrhythmias, such as an accelerated idioventricular rhythm (AIVR), may occur.

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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). Chest roentgenographic findings are usually nonspecific.

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 right ventricular (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.

Multidetector-row computed tomography (CT) scanning (ie, CT scanning 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 (more so than with cardiac catheterization).


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.

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.

Positron-emission tomography

Positron-emission tomography (PET) scanning 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.
 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.

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