Microvascular involvement in cardiac pathology

Citation
Jb. Gavin et al., Microvascular involvement in cardiac pathology, J MOL CEL C, 30(12), 1998, pp. 2531-2540
Citations number
127
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
ISSN journal
00222828 → ACNP
Volume
30
Issue
12
Year of publication
1998
Pages
2531 - 2540
Database
ISI
SICI code
0022-2828(199812)30:12<2531:MIICP>2.0.ZU;2-S
Abstract
Abnormalities of the microvasculature are centrally involved in the pathoge nesis of some forms of heart disease, but in others are consequences of it. Microvascular abnormalities may contribute to the progression of viral myo carditis and Chagas' disease. Focal abnormalities may occur early in some c ardiomyopathies and do occur later in most types of myocarditis. The thicke ning of arteriolar walls in chronic hypertension is likely to contribute si gnificantly to the impairment of coronary haemodynamics associated with ada ptive ventricular hypertrophy and the consequent diminution of coronary res erve, increasing diffusion distances and failure of angiogenesis to compens ate. However, the resulting myocyte necrosis stimulates inflammatory angiog enesis. When ischemic myocyte injury becomes irreversible there is a concom itant loss of capacity for reperfusion, the no-renew phenomenon. Less sever e temporary ischemia reduces the proportion of functional capillaries. Mult iple mechanisms are involved in this microvascular stunning, including: rep erfusion injury; leukocyte activation, adhesion and accumulation; and impai red endothelium-dependent vasodilation. Many of the microvascular changes a re those of the inflammatory response to cell death and form part of a fina l common pathway in myocarditis, cardiomyopathy, cardiac hypertrophy and fa ilure, and ischemic heart disease. Stimulation of angiogenesis prior to myo cyte necrosis in hypertrophy and control of leukocyte activity in ischemic heart disease could minimize myocyte loss. (C) 1998 Academic Press.