The pathogenesis of diabetic cardiomyopathy is unknown. The synergistic, or enhanced, effect of hypertension on pathological changes in the heart of diabetic patients has been highly suspected. The purpose of this study was to evaluate the myocardial changes related to diabetes mellitus with and without hypertension, using biopsy specimens. We examined the ultrastructural changes in biopsy specimens of the endomyocardium obtained from 25 patients. They were divided into four groups: controls without hypertension or diabetes mellitus (n = 6), and patient with hypertension (n = 3), diabetes mellitus (n = 8), and diabetes with hypertension (n = 8). The diabetic patients showed nearly normal or mildly depressed systolic left ventricular function. Ultrastructural pictures were analyzed for thickening of the capillary basement membrane, presence of toluidine blue-positive materials (i.e., materials showing metachromasia) in the myocytes, size of myocytes, and interstitial fibrosis. The thickening of the capillary basement membrane, the accumulation of toluidine blue-positive materials, and interstitial fibrosis were all significantly greater in the patients with diabetes mellitus compared to the control subjects. The myocytes tended to be small (cell atrophy) in the diabetes group. Although these pathological changes in the heart were characteristic of diabetic patients, irrespective of the presence or absence of hypertension, the presence of hypertension increased the pathological changes of myocardial cells as well as abnormality in the capillary vessels in patients with diabetes mellitus. Alterations in the myocardial cells and capillaries, caused by diabetes mellitus, may lead to myocardial cell injury and interstitial fibrosis and, ultimately, to ventricular systolic and diastolic dysfunction, especially when the diabetes is accompanied by hypertension.
We report herein an adult case of anomalous origin of the left coronary artery from the pulmonary artery (Bland-White-Garland syndrome; BWG syndrome). The patient had chest discomfort during exercise and signs of mitral regurgitation. We diagnosed him as having BWG syndrome by angiography, and performed surgical treatment. At the operation, retrograde coronary blood flow was found through the left coronary artery during aortic cross-clamping. This suggested extracardiac anastomosis from peripheral arteries to the left coronary artery. Since the collateral blood flow was considerable during aortic cross-clamping, only the left coronary artery was closed. A collateral from the left bronchial artery to the left circumflex artery was demonstrated by postoperative angiography. Cases of adults with BWG syndrome are rare, and this may be the first report of a collateral from the bronchial artery.
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