Left ventricular hypertrophy of the myocardium is a mechanism of adaptation to chronic pressure and volume increase in the left ventricle. This is caused, for example, by hemodynamically relevant shunt volumes in extensive arteriovenous malformations (AVM). In addition, there is disruption of macrovascular and microvascular blood circulation.
The increased pressure load on the myocardium leads to concentric hypertrophy of the myocardium. As myocardial contractility decreases and ventricular end-diastolic filling increases, dilatation of the heart increases. The developing heart failure may lead to sudden cardiac death from ventricular fibrillation.
An additional potential complicating factor is the development of coronary artery disease at an older age in patients with arteriosclerosis and arteriovenous malformation. Arteriosclerosis may develop independently of the underlying disease due to common cardiovascular risk factors (diabetes mellitus, nicotine abuse, etc.) and complicate the high-output situation in AVM. The increasingly stenosed coronary arteries can no longer meet the high demands placed on the hypertrophied myocardium by the increased volume load in arteriovenous malformation, and myocardial infarction may result.
Concomitant diseases, especially pneumonias, can cause additional stress on the pulmonary circulation and the right heart, which can also be fatal for patients with large arteriovenous malformations.