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Part of the book series: Progress in Experimental Cardiology ((PREC,volume 2))

Summary

Cardiac hypertrophy is associated with the accumulation of extracellular matrix (ECM), cardiac fibrosis, and abnormal diastolic stiffness. Intra-coronary fibrosis in the hyper-trophied myocardium can lead to occlusion of a major coronary artery with resulting ischemia. Angiotensin (Ang) II is associated with cardiac hypertrophy and fibrosis as well as angiogenesis, but the mechanisms are unknown. Tissue levels of angiotensin are elevated in the ischemic and nonischemic regions of the failing heart, and there is evidence that Ang II contributes to myocardial cellular hypertrophy and cardiac fibrosis. Also, Ang II may contribute to angiogenesis in the infarcted heart, thereby increasing collateral circulation. Angiotensin-converting enzyme inhibitor (ACEI) treatment opposes hypertrophy and ischemic heart failure. The mechanisms responsible for this cardioreparative effect of ACEI are largely unknown, but may due to inhibition of Ang II formation as well as other mechanisms. In the infarcted and noninfarcted ischemic heart, interstitial matrix metalloproteinases (MMPs) are activated. Recent experiments suggest that ACEI improves cardiac function and reduces myocardial ischemic damage, in part, by inhibiting MMP activity.

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Tyagi, S.C., Hayden, M.R., Hall, J.E. (1998). Role of Angiotensin in Angiogenesis and Cardiac Fibrosis in Heart Failure. In: Dhalla, N.S., Zahradka, P., Dixon, I.M.C., Beamish, R.E. (eds) Angiotensin II Receptor Blockade Physiological and Clinical Implications. Progress in Experimental Cardiology, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5743-2_40

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