Abstract

Patients with diabetes mellitus are excessively vulnerable to myocardial ischemia and often suffer from autonomic cardiac dysfunction. They are also known to have specific capillary pathology and abnormalities of substances essential for the neoangiogenic cascade. These background data led us to the hypothesis that the severity of ischemic heart disease in diabetes is attributable (at least in part) to microcirculatory and autonomic inadequacy caused by microangiopathy and failure of postischemic adaptive neoangiogenesis. To test this hypothesis we compared myocardial capillaries, autonomic nerve endings of 19 diabetics, 30 normoglycemics with ischemic heart disease, and 9 valve replacements serving as nonischemic controls. Right atrial appendages obtained during coronary bypass surgery were utilized for light, fluorescent, and electron microscopic morphometry. Although in this series there were no significant differences in the clinical and laboratory hemodynamic values between the ischemic normoglycemic and diabetic patients, the latter showed marked capillary and nerve terminal pathology, and their capillary density as well as capillary to myofiber ratios were significantly lower. In addition, the mean capillary area, volume fraction, and intercapillary distance were higher in diabetics. The mean area of the nerve varicosities was also smaller, and this was correlated with capillary density. We concluded that the findings support the hypothesis that cardiac vulnerability in diabetes is connected with inadequate adaptive neoangiogenesis and that this seems to be associated with atrophic changes in the nerve terminals.

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