Abstract

Ventricular aneurysms are circumscribed, thin-walled fibrous, noncontractile outpouchings of the ventricle. The majority are apically located, true aneurysms of the left ventricle (LV) that occur as a consequence of transmural myocardial infarction (MI). The precursor of aneurysm formation appears to be infarct expansion early after acute MI and occurrence generally relates to infarct size. The presence of underlying hypertension and the use of steroids and nonsteroidal antiinflammatory agents may promote aneurysm formation. The clinical sequelae include congestive heart failure (CHF), thromboembolism, angina pectoris, and ventricular tachyarrhythmias. Late rupture is a particular complication of false aneurysms in which the pericardium is the aneurysm wall. The diagnosis may be suspected by the clinical finding of a diffuse, pansystolic apical thrust, persistent ST-segment elevation on the electrocardiogram, and distortion of the cardiac silhouette on chest x-ray. This can be confirmed using echocardiography, radionuclide ventriculography, and cardiac catheterization. The latter has the additional advantage of being able to delineate the coronary anatomy. Management involves prevention, specific therapy for the various clinical manifestations, and surgery. Therapeutic interventions with thrombolytic agents, aspirin, heparin, and beta blockers that are applied early in the evolution of an MI may limit infarction size, thereby reducing the tendency toward infarct expansion and aneurysm formation. Patients with mild CHF can usually be controlled with the standard combination of angiotensin-converting enzyme inhibitors, diuretics, and digoxin. Thromboembolism is best prevented by anticoagulation with warfarin for at least 3 months after the acute MI. The choice of pharmacotherapy for ventricular tachyarrhythmias should be guided by electrophysiologic studies. The treatment of patients with angina pectoris utilizes conventional therapeutic modalities.(ABSTRACT TRUNCATED AT 250 WORDS)

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