Coronary collateral circulation

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Overview
During contraction of the ventricular myocardium (systole), the subendocardial coronary vessels (the vessels that enter the myocardium) are compressed due to the high intraventricular pressures. However the epicardial coronary vessels (the vessels that run along the outer surface of the heart) remain patent. Because of this, blood flow in the subendocardium is greatly reduced. As a result most myocardial perfusion to the left anterior descending and the left circumflex occurs during heart relaxation (diastole) when the subendocardial coronary vessels are patent and under low pressure. The right coronary artery, which terminates in the thin walled right ventricle, has greater filling during systole. Failure of oxygen delivery to rise as a result of increases in blood flow to meet the increased oxygen demand of the heart results in tissue ischemia, a condition of oxygen debt.

Brief ischemia is associated with chest pain, a condition known as angina. Severe ischemia can cause the heart muscle to die of oxygen starvation, a condition termed myocardial infarction. Chronic moderate ischemia can result in weakening of myocardial contractility, a condition known as myocardial hibernation.

The coronary circulation possesses unique pharmacologic characteristics. Prominent among these is its reactivity to adrenergic stimulation. The majority of vasculature in the body constricts to norepinephrine, a sympathetic neurotransmitter the body uses to increase blood pressure. In the coronary circulation, norepinephrine elicits vasodilation, due to the predominance of beta-adrenergic receptors in the coronary circulation.

Agonists of alpha-receptors, such as phenylephrine, elicit very little constriction in the coronary circulation.

Additional Resources

 * Coronary Collateral Circulation by Levin, Kauff and Baltaxe