Microvasculature in acute myocardial ischemia: part I: evolving concepts in pathophysiology, diagnosis, and treatment.

The microcirculation is generally defined as vessels 200 m in diameter, which are not visualized on coronary angiography. Flow through the microvasculature is therefore generally measured using noninvasive techniques. One of these techniques is myocardial contrast echocardiography (MCE), which has provided important new pathophysiological insights into acute myocardial ischemia. In this article, we shall discuss these insights in both stress-induced ischemia and spontaneously occurring ischemia. We shall also discuss other important issues such as collateral blood flow, myocardial viability, ischemia-reperfusion–induced myocardial injury, and evolving treatment strategies aimed at preserving microvascular flow and function in acute myocardial ischemia. There is 45 mL of blood in the adult human coronary circulation (termed coronary blood volume), of which about one-third resides in the arterial, venous, and capillary networks each.1 At baseline, 8% of the left ventricular (LV) mass is constituted by blood present in the microcirculation, 90% of which is in the capillaries—termed myocardial blood volume (MBV) (Figure 1).2 The velocity of blood in the coronary vessels is related to the size of the vessels, and at the level of the capillary (mean length 0.5 mm and mean diameter 7 m), the mean red cell velocity at rest is 1 mm · s .2 There are 8 million capillaries in the human heart, and it takes 1 mL of blood 1 year to travel through a single capillary.2 The microcirculation not only consists of a channel of passive networks through which blood is transported through the myocardium, but is an active site of blood flow control as well as metabolic activity. Indeed, the regulation of flow through these networks is complicated and depends on a number of metabolic, myogenic, and other control mechanisms. The capillary hydrostatic pressure is held constant within the myocardium at all times at 30 mm Hg, with the preand postcapillary pressures at 45 and 15 mm Hg, respectively.3 The coronary arterioles (ranging in size from 150 to 300 m) act as resistance vessels so that the aortic pressure (mean 90 mm Hg) is brought down to a precapillary pressure of 45 mm Hg. The arterioles have smooth muscles with a strong and immediate myogenic response such that the arteriolar resistance can change second to second to keep the precapillary pressure constant (autoregulation). Coronary venules also have weak myogenic responses, and they also control local resistance by changing the rheological properties of blood. In addition, the venules are the site of leukocyte adhesion during inflammation. Their endothelial surfaces express a number of adhesion molecules, whose production is upregulated at different times after the onset of tissue injury.