True LV aneurysms develop in less than 5% of all patients with ST-elevation myocardial infarctions (STEMI) 1, 5 days to three months after the infarction.
They may present with symptoms of decompensated heart failure. Classic ECG findings are persistent ST elevation and deep Q waves in the same leads.
The wall of the true LV aneurysm is thinner than the wall of the rest of the left ventricle and is usually composed of fibrous tissue as well as necrotic muscle, sometimes mixed with viable myocardium.
A true aneurysmal sac contains an endocardium, epicardium and thinned fibrous tissue (scar) which is a remnant of the left ventricular muscle, while a pseudoaneurysm sac represents a pericardium that contains a ruptured left ventricle 5.
Aneurysm formation occurs when intraventricular tension stretches the non-contracting infarcted myocardium, causing bulging of the infarcted area with each contraction.
Usually, they involve the anterior or anterolateral wall.
Echocardiography, cardiac MRI and cardiac ventriculography can detect LV aneurysms.
The ratio of the maximum diameter of the orifice to the maximum internal diameter of the cavity may higher (0.9-1.0) than for a pseudoaneurysm 7.
Treatment and prognosis
The rate of mortality in patients with LV aneurysms is up to 6x higher than in patients without aneurysms. Death is often sudden and may be related to the high incidence of ventricular tachyarrhythmias associated with LV aneurysms 2.
Recognised complications include:
- intramural thrombus formation
- impairment in cardiac output
- rupture of the aneurysm: rare (the rupture rate is higher with pseudoaneurysms)
In certain situations consider:
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