Variceal transformation of the subendocardial microvasculature in regions of chronic myocardial ischemia.

The nature and cause of the striking regional dilatation of the microvasculature of the subendocardial myocardium seen in some patients with ischemic heart disease are unknown. To examine this question, we reviewed nine patients in whom regions of the left ventricular free wall had marked prominence of subendocardial vasculature on postmortem arteriography. All hearts had severe diffuse atherosclerosis of major epicardial coronary arteries. Histologic findings, including serial transmural sections, showed extreme dilatation of arterioles, capillaries, and venules of the subendocardial third of the myocardium. In this same region myocytes showed atrophy, vacuolization (a marker of chronic ischemia), and small foci of necrosis and fibrosis. The generalized small-vessel dilatation with adjacent ischemic myocytes makes it improbable that the vascular changes are caused by collateral flow. Previous anatomic studies have shown artery-vein arrangements in the myocardium providing for countercurrent regulation of regional blood flow. This mechanism, which produces vascular enlargement on the basis of metabolic need, may explain the regional variceal transformation of the subendocardial microvasculature seen with chronic ischemia.