This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Gasser, R. N. A. Search for Related Content PubMed PubMed Citation Articles by Gasser, R. N. A. Social Bookmarking                         What's this?

The Interdependence of Hypertension, Calcium Overload, and Coronary Spasm in the Development of Myocardial Infarction

Dept. of Internal Medicine, University of Graz, Austria Graz, Austria

It is a well-known fact that sys temic hypertension is one of the ma jor risk factors for myocardial in farction (MI). Extensive studies on hypertensive rats revealed that cal cium 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 patho physiology of the early phase of acute MI (AMI). It can be shown that thrombocytes that aggregate at the injured vessel wall next to athero slcerotic plaques release vasocon strictive factors that induce series of severe spasms at the sites with defec tive endothelium that end up in myocardial infarction; the patho physiologic pathway is called the thromboischemic reentry mechan ism. This local contractile response may be enhanced in the presence of systemic hypertension since intracel lular calcium is elevated in the coro nary smooth muscle.

On the other hand, it has been shown that heart muscle fibers un dergo severe alterations finally re sulting in necrotization, as soon as free calcium ions penetrate exces sively through the sarcolemma mem brane into the myoplasm so that the capacities of the calcium binding or extrusion processes become overpow ered ; this is especially the case during ischemia. Since free intracellular cal cium is already ten times elevated in the myocytes in systemic hyperten sion, the myocardium may be more vulnerable to further calcium over load owing to the ischemia and ne crotization is augmented.

The elevation of intracellular Ca of the myocytes of the cardiovascular system in systemic hypertension en hances the pathologic response of the coronary arteries and the myocar dium. This work gives a complete overview of the pathophysiologic principles involved in AMI occurring with systemic hypertension.

Angiology, Vol. 39, No. 8, 761-772 (1988)
DOI: 10.1177/000331978803900809


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				R. Gasser, W. Klein, and E. Kickenweiz Vasodilative Response to Hypoxia and Simulated Ischemia Is Mediated by ATP-Sensitive K + Channels in Guinea Pig Thoracic Aorta Angiology, March 1, 1993; 44(3): 228 - 243. [Abstract] [PDF]