Gasser R N
Dept. of Internal Medicine, University of Graz, Austria.
Angiology. 1988 Aug;39(8):761-72. doi: 10.1177/000331978803900809.
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.
众所周知，系统性高血压是心肌梗死（MI）的主要危险因素之一。对高血压大鼠的广泛研究表明，这些动物的心肌细胞以及冠状动脉壁中的钙含量过度升高，这导致这些肌肉条带的静息张力更高，收缩反应更强。多年来，许多作者认为冠状动脉痉挛在急性心肌梗死（AMI）早期的病理生理学中起很大作用。可以证明，聚集在动脉粥样硬化斑块旁受损血管壁处的血小板会释放血管收缩因子，这些因子会在内皮有缺陷的部位引发一系列严重痉挛，最终导致心肌梗死；这种病理生理途径称为血栓 - 缺血再入机制。由于冠状动脉平滑肌中的细胞内钙升高，在系统性高血压存在的情况下，这种局部收缩反应可能会增强。另一方面，已经表明，一旦游离钙离子过度穿过肌膜进入肌浆，心肌纤维就会发生严重改变，最终导致坏死，从而使钙结合或排出过程的能力不堪重负；在缺血期间尤其如此。由于在系统性高血压中，心肌细胞内的游离钙已经升高了十倍，因此心肌可能更容易因缺血而进一步钙超载，坏死也会加剧。系统性高血压时心血管系统心肌细胞内钙的升高会增强冠状动脉和心肌的病理反应。这项工作全面概述了系统性高血压伴发的AMI所涉及的病理生理原理。
