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The hypothesis that diabetes mellitus provokes a specific cardiomyopathy is supported by numerous clinical, epidemiological and anatomopathological studies. However, the frequent association of diabetes mellitus with other conditions, such as hypertension and coronary atherosclerosis, both capable of causing the dysfunction of the cardiac muscle, makes it difficult to interpret many of the data reported in the literature and contributes to the continuing debate regarding the effective existence of diabetic cardiomyopathy and its possible pathogenetic mechanisms. In clinical terms, diabetic cardiomyopathy is manifested both as an altered diastolic and/or systolic phase, assessed using various non-invasive techniques, or as congested cardiac decompensation. The pathogenesis of diabetic cardiomyopathy is still not altogether clear. The alteration of the smallest coronary vessels might be responsible for the increased interstitial fibrosis found in the heart of diabetic patients. In this paper numerous data from the literature on this argument are reported and the authors advance the hypothesis that endothelial dysfunction may play a pathogenetic role in the development of cardiopathy.
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PMID:[Diabetic cardiomyopathy: possible pathogenetic role of coronary microcirculation]. 163 Jun 65

Patients with diabetes mellitus are particularly vulnerable to cardiovascular disease. Although both the macrovascular and microvascular complications are present in patients with diabetes alone, they are particularly severe in patients with both diabetes and hypertension. While there is no doubt that a primary diabetic cardiomyopathy occurs with functional consequences, considerable evidence--both in humans and in experimental animal models--points to hypertension as of critical importance in the pathogenesis of severe pathological and symptomatic diabetic heart disease. In hypertensive-diabetic cardiomyopathy, the histopathologic myocardial damage has been attributed to hypertension, while the myocellular dysfunction has been attributed to diabetes. Together, the consequences to the myocardium are devastating. Strict control of the hypertension and diabetes mellitus, along with prevention of the microvascular consequences of both conditions, may have an ameliorative effect on the subsequent development of diabetic heart disease.
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PMID:The diabetic heart: clinical, experimental and pathological features. 192 63

The hearts obtained at autopsy of 67 patients with hypertension, diabetes mellitus, or both were examined microscopically and histochemically, and the amount of fibrosis was determined. Significant differences in heart weight, interstitial fibrosis, replacement fibrosis, and perivascular fibrosis were found among the groups. The mean heart weight of the hypertensive-diabetic patients was significantly greater than that of the hypertensive patients and the diabetic patients. The amount of microscopic fibrosis increased between the groups, the lowest in hypertensive hearts, midrange in diabetic hearts, and highest in hypertensive-diabetic hearts. Total fibrosis correlated with heart weight among diabetic and hypertensive-diabetic patients and was significantly greater among patients with congestive heart failure, most of whom had histories of both hypertension and diabetes. The microscopic grade of fibrosis correlated significantly (p less than 0.01) with a quantitative, histochemical determination of the amount of collagen per milligram of total noncollagenous protein in the heart tissue. Myocardial fibrosis may contribute to the diastolic dysfunction typical of hypertensive-diabetic cardiomyopathy, in which congestive heart failure is a common sequela. The importance of hypertension in the pathogenesis of severe diabetic heart disease is discussed.
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PMID:A comparison of the pathological spectrum of hypertensive, diabetic, and hypertensive-diabetic heart disease. 202 37

Diabetes mellitus is a significant condition affecting major segments of all population groups studied. With the introduction of insulin and oral hypoglycemic therapy, and with better understanding of diet and weight control over the past half century, the primary causes of diabetic morbidity and mortality have shifted in varying proportions from metabolic derangements, infection, and renal insufficiency to different types of cardiovascular disease. Despite extensive clinical and laboratory research on the etiology, pathogenesis, and even the existence of cardiovascular disease associated with diabetes mellitus, however, considerable debate is still apparent in this field. Our purpose is to present an overview of the subject of diabetic heart disease, with a critical analysis of epidemiologic, clinical, and pathological data. Some of this material will be addressed from the perspective of research in this area over the past decade by one of us (SMF), particularly in experimental hypertensive and diabetic cardiomyopathy. However, overall, an attempt will be made to provide an objective and balanced analysis, in order to answer the question: does diabetic heart disease exist?
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PMID:Diabetic heart disease: the clinical and pathological spectrum--Part I. 268 Jan 99

Diabetic heart disease (DHD) is one of the most important contemporary management problems confronting the entire diabetic management team. DHD is multifactorial and multifaceted. The three major problems are: coronary artery disease (CAD), autonomic cardiac denervation and a specific heart muscle disease in diabetes (diabetic cardiomyopathy). Various other ancillary problems include obesity, hypertension, lipid aberrations and rheological alterations etc. CAD and diabetes mellitus (DM) have a greater association; the disease is more severe, sets in early and has many atypical features including painless, silent onset, delayed arrival at intensive coronary care unit, increased incidence of pump failure and arrhythmias and high case fatality rate. Autonomic cardiac denervation is an important and a common companion of diabetic peripheral neuropathy and has serious repercussions in DHD. Simple, sensitive screening tests may identify such a group so as to exercise caution in management. Various clinical (non-invasive, invasive and autopsy) and experimental studies provide evidence for the existence of a specific diabetic heart muscle disease comprising of small vessel disease and metabolic aberrations. Recent advances in literature and our own experience are reviewed. The practical management aspects of each facet, such as maintenance of high index of suspicion, early diagnosis and referral, close monitoring, role of rigid blood glucose control and specific role of each member of the diabetic team is outlined. The possible preventative strategies are discussed.
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PMID:Diabetic heart disease--current problems and their management. 268 Nov 39

Diabetes mellitus is a significant condition, affecting major segments of all population groups studied. With the introduction of insulin and oral hypoglycemic therapy, together with better understanding of diet and weight control gained over the past half century, the primary causes of diabetic morbidity and mortality have shifted in varying proportions from metabolic derangements, infection, and renal insufficiency to different types of cardiovascular disease. Despite extensive clinical and laboratory research on the etiology, pathogenesis, and even the existence of cardiovascular disease associated with diabetes mellitus, however, considerable debate is still apparent in this field. Our purpose is to present an overview of the subject of diabetic heart disease, with a critical analysis of epidemiologic, clinical, and pathological data. Some of this material will be addressed from the perspective of research in this area over the past decade by one of us (SMF), particularly in experimental hypertensive and diabetic cardiomyopathy. However, overall, an attempt will be made to provide an objective and balanced analysis in order to answer the question: does diabetic heart disease exist?
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PMID:Diabetic heart disease--Part II: The clinical and pathological spectrum. 268 60

One of the leading causes of mortality in diabetics is myocardial disease. In the past few years this subject has generated a significant amount of interest with the result that myocardial problems associated with diabetes are far better understood. Though originally thought to occur as a result of atherosclerosis, various studies have shown that heart disease can occur in the absence of atherosclerosis, suggesting a diabetic cardiomyopathy. Using diabetic animals, it has been possible to characterize diabetes-induced myocardial abnormalities. Diabetic rat hearts do not respond to conditions of high stress as well as controls. The functional depression is accompanied by altered cardiac enzyme systems. A decrease in myosin ATPase activity which appears to be a result of diabetes-induced hypothyroidism is seen. Also, a depression of sarcoplasmic reticular calcium ATPase, along with a depression of calcium uptake by the SR, is seen in diabetic rat hearts. Na+, K+ ATPase activity has also been shown to be depressed and the depression appears to correlate with depressed atrial contractility. High levels of circulating fats in diabetics may alter the integrity of membranes leading to altered enzyme activities. Insulin treatment has been relatively successful at reversing or preventing myocardial changes in the diabetic rat. Other treatments that have been studied include thyroid hormone treatment, since the depression of myosin ATPase can be corrected by such treatment; and carnitine treatment, as the elevation of long chain acyl carnitines (LCAC) and the resulting depression of calcium uptake in the SR can be so normalized. These treatments have not been successful at normalizing cardiac function. A combination of the two treatments normalized function only partially, suggesting that factors besides myosin ATPase and SR calcium uptake are involved. Other treatments that have been tried include vanadate, methyl palmoxirate, and choline and methionine. Vanadate treatment has proved to be encouraging in that it normalizes both function and hyperglycemia. Methyl palmoxirate, a fatty acid analog, normalized only the elevation of LCAC but did not affect function. Methionine and choline were only partially successful in preventing the functional alterations of diabetic rat hearts. The purpose of the present article is to review our understanding of diabetes-induced myocardial problems and their possible causes. Findings from our laboratory and others are described in which attempts have been made to normalize cardiac function.
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PMID:Diabetes-induced abnormalities in the myocardium. 293 41

To determine if cardiac autonomic neuropathy (CAN) contributes to diabetic cardiomyopathy, left ventricular function was assessed by resting and exercise radionuclide ventriculography (RVG) in 30 patients with long-standing insulin-dependent diabetes mellitus who had no clinical, electrocardiographic, or tomographic thallium scan evidence of heart disease. In 11 of 30 patients (37%), RVG revealed abnormal left ventricular performance. CAN was found in 91% of these patients. RVG was abnormal in 59% of patients with CAN and in only 8% of patients without CAN (P less than 0.005). There were significant reductions in mean (+/- SE) ejection fractions (EF) in patients with CAN at rest (62.8 +/- 2.2% vs. 75.2 +/- 2.5%; P less than 0.001) and with maximal exercise (65.8 +/- 2.6% vs. 80.9 +/- 2.3%; P less than 0.001) compared to patients without CAN. There was an inverse correlation between the autonomic function score and both resting EF (r = -0.53; P less than 0.002) and exercise EF (r = -0.55; P less than 0.002). Systolic function did not correlate with age, sex, duration or control of diabetes, microvascular complications, or plasma norepinephrine levels. Thus, approximately one third of our study population had evidence for depressed left ventricular function in the absence of ischemic heart disease, and the cardiac dysfunction was related to the severity of CAN. CAN may be a contributor to cardiac dysfunction in diabetes mellitus.
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PMID:Abnormal cardiac function in diabetic patients with autonomic neuropathy in the absence of ischemic heart disease. 371 Dec 60

Diabetic cardiomyopathy apparently has an important role in the increased cardiovascular morbi-mortality of diabetic patients and its cause is likely to be secondary to small vessel disease. We undertook the present study to compare small and large vessel disease in hearts of patients who died with coronary disease, and determine how diabetes and/or hypertension correlates with these findings. The paraffin blocks of 52 hearts were used in this study. Cases were selected if they died from coronary artery disease and excluded if they had a previous angioplasty, revascularization surgery, congenital, rheumatic or other causes of heart disease. They were divided in two groups; diabetics and non-diabetics and each group was subdivided in hypertensives an non hypertensives. They were matched by age and sex. DM duration was 11 +/- 6 years and known hypertension of 10 +/- 4 years with no significant differences between both groups. The results were recorded without knowledge of patients clinical findings. Atherosclerotic heart disease was more advanced in DM patients, with an increased prevalence of three vessels disease, and more extensive myocardial infarctions. Diabetic subjects had increased (non significant) basal membrane thickening of the capillaries. We could not find differences in parenchymal hypertrophy, interstitial edema, proliferative endothelial lesions and luminal width in middle and large size vessels. Hypertensive patients had increased perivascular fibrosis (NS). Our results suggest that advanced atherosclerotic heart disease is more common in diabetic patients and diabetic cardiomyopathy, if present, seems not to related to a particular structural microvascular disease.
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PMID:[The absence of characteristics lesions in the microcirculation of non-insulin-dependent diabetic patients]. 834 50

Prior to 1972, the increased cardiovascular morbidity and mortality that diabetics endure had been attributed to vascular disease. In 1972, Rubler et al. proposed the existence of a diabetic cardiomyopathy based on their expereince with four adult diabetic patients who suffered from congestive heart failure (CHF) in the absence of discernable coronary artery disease, valvular or congenital heart disease, hypertension, or alcoholism. Alternative explanations for CHF, such as anemia and vascular and renal disease in these four patients, gave rise to criticisms, but a wave of subsequent studies in the 1970s and 1980s provided credence to this new disease entity. This review of the studies done since 1972 appears to support the concept of a diabetic cardiomyopathy independent of atherosclerotic cardiovascular disease. The exact mechanism is still questionable, and several mechanisms have been proposed including small and microvascular disease, autonomic dysfunction, metabolic derangements, and interstitial fibrosis. However, the weight of evidence leans toward the development of fibrosis, possibly caused by the accumulation of a peroxidase acid schiff (PAS)-positive glycoprotein, leading to myocardial hypertrophy and diastolic dysfunction.
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PMID:Diabetic cardiomyopathy. 985 79


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