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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The literature on the new nosologic unit diabetic cardiomyopathy is reviewed and the justification of the assigned term is discussed. Current knowledge on the epidemiology and pathological findings is presented. Particular attention is paid to noninvasive methods, especially echocardiography in patients with type I diabetes mellitus. Subclinical changes in diabetes suggesting deranged left ventricular function in systole and diastole are demonstrated.
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PMID:[Diabetic cardiomyopathy]. 268 32

The presence of diabetic cardiomyopathy and its relationship to concurrent hormonal and metabolic status have not been defined in patients with uncomplicated type I diabetes mellitus. Accordingly, radionuclide left ventricular angiograms and simultaneous metabolic profiles were obtained in 8 type I diabetic patients who had no major diabetic complications and in 11 normal subjects. Occult coronary artery disease was excluded by electrocardiogram exercise testing. Hemodynamics and systolic function did not differ between the groups. However, the peak filling rate (PFR; end-diastolic volumes per s) was less in the diabetic patients at rest [mean, 4.1 +/- 0.2 (+/- SE) vs. 4.8 +/- 0.2; P less than 0.05] and during aerobic (6.8 +/- 0.2 vs. 8.30 +/- 0.3; P less than 0.01) and anaerobic exercise (8.8 +/- 0.3 vs. 9.8 +/- 0.4; P less than 0.05). The time to PFR was prolonged in the diabetic patients at rest (174 +/- 10 vs. 133 +/- 7 ms; P less than 0.01) and during anaerobic exercise (126 +/- 5 vs. 103 +/- 6 ms; P less than 0.01). Plasma glucose and insulin levels were elevated in the diabetic patients at rest and during exercise. Otherwise, the metabolic and hormonal levels did not differ between the groups. In the diabetic patients, no single metabolic or hormonal parameter correlated with PFR or time to PFR. Impairment of diastolic filling also did not correlate with level of glycosylated hemoglobin or duration of diabetes. The alteration in diastolic filling present in type I diabetic patients who have no other diabetic complications may represent the earliest functional effect of diabetic cardiomyopathy.
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PMID:The relationship of cardiac diastolic dysfunction to concurrent hormonal and metabolic status in type I diabetes mellitus. 327 82

Diabetes mellitus is associated with severe and premature cardiovascular disease. The reasons for this have not been identified. It is now apparent that diabetics often have elevated circulating insulin levels compared to non-diabetics. In non-insulin dependent diabetes this is due to the associated obesity while in insulin treated diabetics exogenous insulin is responsible for hyperinsulinaemia between meals and at night. Two reports of high insulin levels in non-insulin dependent diabetics with cardiovascular disease are consistent with clinical and epidemiological studies linking hyperinsulinaemia with coronary, cerebral and peripheral arterial disease in non-diabetics. The arterial wall is an insulin sensitive tissue. Insulin promotes proliferation of arterial smooth muscle cells and enhances lipid synthesis and low density lipoprotein receptor activity. Insulin also promotes experimental atherosclerosis in a number of species. The evidence linking hyperinsulinaemia to the cardiovascular complications and diabetes is suggestive but incomplete and much more information on predictive factors for arterial disease in diabetes is urgently required. Diabetes mellitus is associated with severe and premature cardiovascular disease (reviewed by Stout 1982). Ischaemic heart disease, stroke and peripheral vascular disease are all more common in diabetics, particularly diabetic women. Although there is evidence for the existance of a specific diabetic cardiomyopathy, much of the cardiovascular disease in diabetics is due to atherosclerosis and its complications. Arterial disease in diabetics in distinct from microvascular disease affecting capillaries, and does not differ morphologically or biochemically from atherosclerosis in non-diabetics. The reason for the increased incidence of atherosclerosis in diabetes has not been established. Both non-insulin dependent and insulin dependent diabetes appear to be associated with cardiovascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperinsulinaemia--a possible risk factor for cardiovascular disease in diabetes mellitus. 390 79

To evaluate the presence of diabetic cardiomyopathy, we measured various parameters of left ventricular systolic and diastolic function by means of M-mode and Doppler echocardiography in 50 IDDM children (mean age 13 +/- 3 years; mean IDDM duration 5.9 +/- 4.1 years) free of cardiovascular symptoms. As compared to age-matched healthy control subjects, diabetic children evidenced a significant increase in mean values of pressure half time (PHT), an index of the early diastolic phase (53.7 +/- 10.2 msec vs 44.5 +/- 9, p < 0.002). When the patients were subdivided on the basis of IDDM duration, metabolic control and the presence of retinal microangiopathic abnormalities, those with longer IDDM duration and poor glycemic balance had higher PHT values. These data indicate that an early diastolic dysfunction, expressed by reduced left ventricular compliance, can be found in children with Type 1 diabetes mellitus of relatively short duration. Doppler echocardiography is a reliable non-invasive means to assess early impairment of cardiac function in IDDM patients.
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PMID:Evaluation of left ventricular diastolic function in insulin dependent diabetic children by M-mode and Doppler echocardiography. 787 23

Recent studies at our institution using positron emission tomography (PET) provide evidence that both myocardial blood flow (MBF) and glucose metabolism may be affected in patients with diabetes mellitus. A retrospective study revealed inadequate myocardial glucose uptake as assessed by 2-[18F]fluoro-2-deoxyglucose (18FDG) in 64% of type I (insulin-dependent diabetes mellitus, IDDM) and 36% of type II (non-insulin-dependent diabetes mellitus, NIDDM) patients. However, a study in 7 patients with IDDM and 9 controls showed that metabolic standardization using hyperinsulinemic-euglycemic clamp is associated with similar myocardial glucose uptake in both groups (0.43 +/- 0.16 vs 0.44 +/- 0.12 micromol/g per min; p = nonsignificant). Furthermore, we studied MBF as assessed by [13N]ammonia in 15 IDDM patients without coronary artery disease. We found an impairment in flow reserve in diabetic patients as compared with a control group of 13 healthy volunteers (2.6 +/- 1.3 vs 4.0 +/- 0.6; p <0.01), which was primarily due to a significantly higher resting MBF (95.3 +/- 27.7 vs 69.1 +/- 8.1 mL/100 g per min; p <0.01). Hyperemic flow during adenosine infusion tended to be lower in diabetics, but was not significantly different (236.3 +/- 105.7 vs 273.0 +/- 26.0 mL/100 g per min; p = nonsignificant). Morphologic and functional abnormalities of the coronary microcirculation have been reported in diabetic animals and humans. Furthermore, there is an ongoing controversy regarding the existence of a specific diabetic cardiomyopathy that is not related to epicardial coronary disease. However, few studies have explored the effect of diabetes, hyperinsulinemia, or hyperglycemia on MBF and glucose metabolism in humans. With PET it is possible to perform comprehensive noninvasive studies of various aspects of cardiac function in patients with diabetes mellitus.
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PMID:Myocardial blood flow and glucose metabolism in diabetes mellitus. 929 61

Disturbances of coronary circulation have been reported in diabetic patients with microvascular complications but without obstructive coronary atherosclerosis. The aim of the present study was to investigate coronary flow reserve in young adult patients with IDDM but without microalbuminuria and diabetic autonomic neuropathy. Coronary flow reserve was determined in 12 nonsmoking male patients with IDDM (age 30.0 +/- 6.6 years) and 12 healthy matched volunteers. Groups were similar with respect to blood pressure and serum lipid concentrations, and no subject had a positive family history of coronary heart disease. The patients with IDDM had normal exercise echocardiography and autonomic nervous function tests. Five patients had minimal background retinopathy, and none had microalbuminuria. Positron emission tomography and [15O]H2O were used to measure myocardial blood flow at rest and after dipyridamole administration. The studies were performed during euglycemic hyperinsulinemia (serum insulin approximately 70 mU/l). The baseline myocardial blood flow was similar in patients with IDDM and in control subjects (0.84 +/- 0.18 vs. 0.88 +/- 0.25 ml x g(-1) x min(-1), NS). The myocardial blood flow during hyperemia was 29% lower in patients with IDDM (3.17 +/- 1.57) compared with the control subjects (4.45 +/- 1.37 ml x g(-1) x min(-1), P < 0.05). Consequently, coronary flow reserve (the ratio of flow during hyperemia and at rest) was lower in diabetic patients than in control subjects (3.76 +/- 1.69 vs. 5.31 +/- 1.86, P < 0.05) and the total coronary resistance during hyperemia was higher in diabetic patients (53.7 +/- 31.5) compared with the control subjects (31.4 +/- 11.6 mmHg x min x g x ml(-1), P < 0.05). The coronary flow reserve was similar in diabetic patients with and without mild background retinopathy. No association was found between the coronary flow reserve and serum lipid or HbA1c values in either group. Coronary flow reserve is impaired in young adult males with IDDM and no or minimal microvascular complications and without any evidence of coronary heart disease. This abnormality cannot be explained by standard coronary heart disease risk factors. The results imply early impairment of coronary vascular reactivity in IDDM patients, which may represent an early precursor of future coronary heart disease or may contribute to the pathogenesis of diabetic cardiomyopathy.
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PMID:Coronary flow reserve is reduced in young men with IDDM. 951 21

Diabetic cardiomyopathy (DC) has been reported in type 2 diabetics with short duration of clinically overt diabetes. Impaired left ventricular function has been reported in young patients with diabetes mellitus type 1 (IDDM), but severe cardiomyopathy as the first early major complication of IDDM is very rare. We report a 14 year-old girl with a 5-year history of IDDM and very poor compliance with treatment and follow-up. She was referred to our clinic upon the development of congestive heart failure and dilated cardiomyopathy was diagnosed based on clinical findings, electrocardiogram, chest X-ray and echocardiography. She had no evidence of other major complications of IDDM such as retinopathy, nephropathy or neuropathy.
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PMID:Dilated cardiomyopathy as the first early complication in a 14 year-old girl with diabetes mellitus type 1. 1108 94

In this study we assess the mechanisms of exercise-induced left ventricular (LV) dysfunction in asymptomatic patients with Type 1 diabetes mellitus (T1DM) without coronary artery disease. Fourteen patients and 10 volunteers were enrolled. LV volume, LV ejection fraction (LVEF) and end-systolic wall stress were calculated by two-dimensional echocardiography at rest and during isometric exercise. Myocardial iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy was performed to assess adrenergic cardiac innervation. Diabetic subjects were classified into group A (n=7), with an abnormal LVEF response to handgrip (42 +/- 7%), and group B (n=7), with a normal response (72 +/- 8%). Baseline LVEF was normal in both group A and B patients. In group A patients, the LV circumferential wall stress-LVEF relation showed an impairment in LVEF disproportionate to the level of LV after load. No significant changes in LVEF occurred during dobutamine, whereas post-extrasystolic potentiation (PESP) significantly increased LVEF (60 +/- 6% vs 74 +/- 6%,p < 0.001); PESP at peak handgrip normalized the abnormal LVEF (42 +/- 7% vs 72 +/- 5%, p < 0.001); and MIBG uptake normalized for body weight or for LV mass was lower than in normal subjects (1.69 +/- 0.30 vs 2.98 +/- 0.82 cpm/MBq per g,p = 0.01) and group B diabetic patients (vs 2.79 +/- 0.94 cpm/MBq per g,p = 0.01). A linear correlation between LVEF at peak handgrip and myocardial MIBG uptake normalized for LV mass was demonstrated in the study patients. A defective blunted recruitment of myocardial contractility plays an important role in determining exercise LV dysfunction in the early phase of diabetic cardiomyopathy. This abnormal response to exercise is strongly related to an impairment of cardiac sympathetic innervation.
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PMID:Myocardial dysfunction and adrenergic innervation in patients with Type 1 diabetes mellitus. 1123 60

Heart failure is known to be a complication of insulin-dependent (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) even in the absence of coronary heart disease or hypertension. The mechanisms leading to diabetic cardiomyopathy are unknown. The aim of the study was to characterize structural and functional alterations in hyperinsulinemic Zucker diabetic fatty (ZDF) rats treated with or without insulin. Diabetic animals showed a twofold increase in cardiomyocyte volume with increased left ventricular ANP but not BNP mRNA levels in spite of a reduced plasma renin activity (PRA) 2 months after onset of diabetes compared to nondiabetic littermates. These changes were associated with an increase in left ventricular performance as assessed by echocardiography. Insulin treatment led to a significant increase in body weight (BW), total heart weight, myocardial protein content, and left ventricular mass (LVM). Perivascular fibrosis and laminin thickness were significantly augmented in diabetic rat myocardium irrespective of insulin treatment, whereas interstitial collagen I and fibronectin were similarly found in diabetic and control myocardium. Initial stages of diabetic cardiomyopathy in hyperinsulinemic rats are characterized by cardiomyocyte hypertrophy and enhanced cardiac contractility. It is suggested that hyperinsulinemia may be involved in cardiac hypertrophy.
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PMID:Myocardial hypertrophy and enhanced left ventricular contractility in Zucker diabetic fatty rats. 1476 80

Diabetic cardiomyopathy is a common complication leading to heightened risk of heart failure and death. In the present report, we performed proteomic analysis on total cardiac proteins from the OVE26 mouse model of type 1 diabetes to identify protein changes that may contribute to diabetic cardiomyopathy. This analysis revealed that a surprising high proportion (12 of 20) of the altered proteins that could be identified by mass spectrometry were of mitochondrial origin. All but one of these proteins were upregulated by diabetes. Quantitative RT-PCR, performed for two of these proteins, indicated that part of the upregulation was attributed to increased messenger RNA levels. Morphological study of diabetic hearts showed significantly increased mitochondrial area and number as well as focal regions with severe damage to mitochondria. Diabetic mitochondria also showed reduced respiratory control ratio (9.63 +/- 0.20 vs. 6.13 +/- 0.41, P < 0.0001), apparently due to reduced state 3 rate, and diminished GSH level (5.5 +/- 0.9 vs. 8.2 +/- 2.5 micromol/mg protein, P < 0.05), indicating impaired mitochondrial function and increased oxidative stress. Further examination revealed increased mitochondrial DNA (1.03 +/- 0.18 vs. 0.69 +/- 0.13 relative copy number, P < 0.001) and a tendency to higher protein yield in OVE26 cardiac mitochondria, as well as increased mRNA level for mitochondrial transcription factor A and two mitochondrial encoded proteins. Taken together, these results show that mitochondria are a primary target in the diabetic heart, probably due to oxidative stress, and that this damage coincides with and may stimulate mitochondrial biogenesis.
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PMID:Cardiac mitochondrial damage and biogenesis in a chronic model of type 1 diabetes. 1528 Jan 50


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