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.