The interdependence of hypertension, calcium overload, and coronary spasm in the development of myocardial infarction.

It is a well-known fact that systemic hypertension is one of the major risk factors for myocardial infarction (MI). Extensive studies on hypertensive rats revealed that calcium is excessively elevated in the myocytes, as well as in the coronary artery wall of these animals, which results in a higher resting tension and a stronger contractile response of those muscle strips. Over many years coronary spasm has been claimed by various authors to be greatly involved in the pathophysiology of early phase of acute MI (AMI). It can be shown that thrombocytes that aggregate at the injured vessel wall next to atherosclerotic plaques release vasoconstrictive factors that induce series of severe spasms at the sites with defective endothelium that end up in myocardial infarction; the pathophysiologic pathway is called the thrombo-ischemic reentry mechanism. This local contractile response may be enhanced in the presence of systemic hypertension since intracellular calcium is elevated in the coronary smooth muscle. On the other hand, it has been shown that heart muscle fibers undergo severe alterations finally resulting in necrotization, as soon as free calcium ions penetrate excessively through the sarcolemma membrane into the myoplasm so that the capacities of the calcium binding or extrusion processes become overpowered; this is especially the case during ischemia. Since free intracellular calcium is already ten times elevated in the myocytes in systemic hypertension, the myocardium may be more vulnerable to further calcium overload owing to the ischemia and necrotization is augmented. The elevation of intracellular Ca of the myocytes of the cardiovascular system in systemic hypertension enhances the pathologic response of the coronary arteries and the myocardium. This work gives a complete overview of the pathophysiologic principles involved in AMI occurring with systemic hypertension.