There are two major components to this chapter: (1) regulation of coronary blood flow, mainly under physiologic conditions, and (2) mechanisms of myocardial ischemia, both reversible and irreversible, where coronary blood flow is compromised.
The defining characteristic of the coronary circulation is the direct relationship existing between coronary blood flow and myocardial oxygen consumption. The physiologic rationale is based on the requirement for coronary blood flow to meet the energy requirements of the heart. The main parameters dictating cardiac oxygen consumption are heart rate (chronotropy), cardiac contractility (inotropy), and left ventricular (LV) wall stress. Whereas coronary perfusion at rest in humans is approximately 200 mL/min, it can increase up to 1000 mL/min on maximal exercise. The difference between values at rest and maximal levels of coronary blood flow represents the coronary blood flow reserve. The mechanisms by which the coronary bed adapts blood flow to the cardiac workload represent one component of coronary autoregulation, that is, the recruitment of the coronary blood flow reserve to match coronary blood flow (O2 supply) to energy needs (O2 demand). This is accomplished via metabolic byproducts and adenosine, but it can also be modulated through an integrated regulation of substance release from the endothelium or from the myocardium itself, neural control, myocardial compressive forces, and aortic perfusion pressure. First, the myogenic tone of the small-caliber coronary resistance vessels is controlled by endothelial factors (such as nitric oxide), metabolic products (such as adenosine), and the autonomic nervous system (both cholinergic and α- and β-adrenergic receptors). Second, this chemical control of coronary blood flow is additional to the control exerted by physical forces (aortic perfusion pressure and intramyocardial compression forces). All of these components will be discussed in the first part of this chapter.
Unique Characteristics of Coronary Blood Flow
In contrast to most other vascular beds, the myocardium is perfused mainly during diastole and shows a sharp decrease in perfusion during systole, which can be attributed to myocardial compression (Fig. 54–1). The myocardial compressive forces are largely responsible for this phasic nature of coronary perfusion throughout the cardiac cycle. Because of this, a measurement of mean coronary vascular resistance is less meaningful than a calculation of vascular resistance at end-diastole prior to atrial contraction when compressive forces are minimal. A fall of coronary perfusion at the onset of ventricular systole is due to the squeezing forces of the contracting myocardium, when the intraventricular pressure that opposes coronary blood flow is roughly equal to the aortic perfusion pressure. Blood flow through large coronary arteries can even be transiently reversed during early systole. Reciprocally, ventricular relaxation during diastole is accompanied by a decrease in intraventricular pressure that is far greater than the decrease in aortic pressure, which allows optimal coronary perfusion early in diastole. In addition, the position of the coronary ostia just above the aortic valve leaflets favors the perfusion of the coronary ...