This review discusses some of the mechanisms inherent in diabetes that pred
ispose patients to increased cardiac morbidity and mortality.
Single photon emission computerized tomography or photon emission tomograph
y with radioactive labeled analogues of norepinephrine have shown that card
iac sympathetic dysfunction and incompetence are early and also late abnorm
alities in patients with Type I (insulin-dependent) and Type II (non-insuli
n-dependent) diabetes mellitus. Furthermore, myocardial blood flow assessme
nt with photon emission tomography has shown that in patients without myoca
rdial perfusion deficits, endothelial-dependent vasodilatation is severely
reduced in relation to cardiac sympathetic dysfunction. In addition, signs
of endothelial activation have also been found early in patients with Type
I and Type II diabetes in whom vascular disease has not been clinically det
ected. This activation in conjunction with glycaemic control is important i
n determining macrovascular mortality. Cardiac sympathetic dysfunction is p
artially restored to normal with near normalisation of glycaemia.
Interpretations. Recently unrecognized "subtle" changes predispose the hear
t to failure, after ischaemia-induced remodelling, and arteriosclerotic pla
ques to instability and rupture. These changes act in conjunction with effe
cts, driven by hyperglycaemia and diabetes, on the endothelium of large blo
od vessels, e.g. on nitric oxide release or on protein kinase-C beta activa
tion. Meticulous glucose control early on and rapid recompensation of hyper
glycaemia in patients with acute coronary syndrome are part of a successful
intensive multifactorial approach to prevent the heart in diabetes convert
ing from ailing to failing.