Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An echocardiographic study was carried out on 23 young diabetics, 19 of whom had retinopathy. Their diastolic function was analysed by comparing the timing and pattern of mitral valve opening with the pattern of left ventricular wall movement. Only six patients had all their values within the normal range. Fourteen patients had abnormalities similar to those seen in patients with cardiomyopathy; the close time relation between mitral valve movement and wall movement was lost and mitral valve opening delayed in eight patients. Three other patients had considerable outward wall movement before mitral valve opening, which is characteristic of ischaemic heart disease. Although these studies provide no definite evidence of a cause, the abnormalities found may reflect a subclinical diabetic cardiomyopathy due to small-vessel disease.
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PMID:Diabetic cardiomyopathy? An echocardiographic study of young diabetics. 62 29

The objective of this study was to test the hypothesis that excessive severity of ischaemic heart disease in diabetics is due, in part, to capillary inadequacy. Sections from autopsied hearts of diabetic patients with and without myocardial infarction as well as from those of patients with infarcts and no diabetes were used for morphometric studies of intramural microvessels in areas without infarction. Normoglycaemic patients with normal hearts were also examined. Two to five transverse sections from each of 44 hearts (stained with methenamine silver) were examined for capillary numerical density, capillary to myofibre ratios, and myofibre diameters. Averages for each case and totals for each group were calculated and compared. Normoglycaemic patients with infarcts had increased morphometric values. Diabetics with infarcts had significantly lower capillary densities than the other groups. In conclusion, it is suggested that in diabetes there is an inadequate ischaemia-induced, reactive angiogenesis. This may contribute towards increased myocardial vulnerability in further ischaemic injury and perhaps to diabetic cardiomyopathy.
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PMID:Human coronary microvessels in diabetes and ischaemia. Morphometric study of autopsy material. 151 82

Findings of research into the specific course of ischaemic heart disease (IHD) concurrent with diabetes mellitus are analysed. Diabetic patients were found to have a more severe course of IHD after myocardial infarction, which was more often complicated with arrhythmias, cardiac failure, and unstable angina. The incidence of painless IHD after myocardial infarction was found to be twice higher in diabetics. A consistent relationship between the severity of diabetes and an increase in painless IHD incidence was noted. Diabetes was found to aggravate the IHD course irrespective of the patient's age. A correlation was observed between the severity of IHD and insulinaemia. Certain functional-diagnosis methodologies are shown to be most informative in the differential diagnosis of IHD and diabetic cardiomyopathy. The high efficacy of a complex therapy including beta-blockers and angioprotectors in concurrent IHD and diabetes is demonstrated.
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PMID:[Characteristics of the course of ischemic heart disease and diabetes mellitus occurring jointly]. 275 81

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

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

Left ventricular function and morphology were assessed using M-mode echocardiography in 3 patients with diabetes mellitus associated with mitochondrial tRNA(Leu)(UUR) gene mutation, who were free of clinical, electrocardiographic, or thallium scan evidence of ischemic heart disease. Echocardiograms revealed hypertrophic cardiomyopathy in all 3 patients. Hypertrophy of the interventricular septum was mild in Cases 1 and 3 (12 and 13 mm, respectively) and severe in Case 2 (22 mm) (normal 7-10 mm). When they had neither signs nor symptoms suggestive of congestive heart failure, percentage fractional shortening (%FS), an index of wall motion of the left ventricle (normal > 28%), was normal in Cases 2 and 3 (28 and 32%, respectively) whereas it was slightly decreased in Case 1 (22%). In Case 1 with mild hypertrophy, the development of congestive heart failure was associated with a marked decrease in %FS to 13%; this patient responded well to diuretics and captopril and %FS rose to 22%. However, a mild decrease in %FS to 21% caused congestive heart failure in Case 2 with severe hypertrophy. His response to treatment was marginal. The present study indicates that mitochondrial DNA analysis should be done in patients with diabetic cardiomyopathy, and that sequential echocardiography is invaluable for the detection of hypertrophic cardiomyopathy and the management of subsequent myocardial dysfunction in patients with mitochondrial diabetes mellitus and cardiomyopathy.
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PMID:Hypertrophic cardiomyopathy in patients with diabetes mellitus associated with mitochondrial tRNA(Leu)(UUR) gene mutation. 856 88

The increased incidence of congestive heart failure and the increased mortality and morbidity in the diabetic patient following myocardial infarction or coronary artery bypass graft can be explained by the presence of diabetic cardiomyopathy. Noninvasive studies in young diabetic patients show no cardiac abnormality, but in older diabetic patients mild cardiac diastolic dysfunction is detectable. This mild cardiomyopathy can become clinically detectable in the presence of hypertension and can be severe in the presence of myocardial ischemia. Microvascular disease is unlikely to cause diabetic cardiomyopathy. Cellular changes, including defects in calcium transport and fatty acid metabolism, may lead to myocellular hypertrophy and myocardial fibrosis, initially causing diastolic dysfunction that may advance to systolic dysfunction. Glycemic control, energetic detection and treatment of hypertension with appropriate antihypertensive agents, and early detection and treatment of ischemic heart disease are essential in preventing and treating diabetic cardiomyopathy.
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PMID:Diabetic cardiomyopathy. A unique entity or a complication of coronary artery disease? 858 13

Despite the commonplace nature of hypertension in chronic dialysis patients, many issues remain unresolved. According to current JNC/V (see text) recommendation, a systolic blood pressure of < 120 mm Hg is optimal, 120-129 mm Hg is normal, and one of 130-139 mm Hg is high-normal. The majority of dialysis patients receiving treatment in the United States is probably not maintained in the optimal blood pressure range. However, if the J curve hypothesis has credence, many of our dialysis patients may be susceptible to overtreatment, especially of their diastolic blood pressure. In patients with ischemic cardiovascular disease, several studies show a decrease in survival with diastolic blood pressures < 85 mm Hg. This J curve phenomenon is seen predominantly in patients with ischemic heart disease. Since many, and possibly most, of the currently treated end-stage renal disease patients in the United States have existing atherosclerotic cardiovascular disease when they start chronic dialysis therapy, lowering of the diastolic blood pressure below a J threshold may be dangerous. This problem may be especially prevalent in diabetics with diabetic cardiomyopathy. Diabetics and other end-stage renal disease patients may be started on hemodialysis with glomerular filtration rates in the 10- to 15-cm2/min range. Patients with high residual renal function may have small intradialytic weight gains and frequent intradialytic hypotension. This 'overtreatment' may lead to postdialysis arrhythmias and sudden death in chronic dialysis patients. As in the nonrenal failure population, end-stage renal disease patients with left ventricular hypertrophy have a 2- to 3-fold increased risk of death from cardiovascular diseases, and all cause mortality. In contrast to nonrenal failure patients, normotensive ESRD patients may show an increase of left ventricular mass over time. Although left ventricular hypertrophy can be reversed with good blood pressure control, patients are often undertreated based on analysis of dialysis clinic blood pressures. Even if clinic systolic blood pressure levels are optimal, chronic dialysis patients may still have unacceptably high ambulatory blood pressure levels due to a rise in nocturnal blood pressure with sleep.
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PMID:Treatment of hypertension in renal failure patients: when do we overtreat? When do we undertreat? 887 57

Although lysophosphatidylcholine (lyso-PtdCho) accumulates in the sarcolemmal (SL) membrane and alters its function during myocardial ischemia and diabetic cardiomyopathy, the effects of lyso-PtdCho on SL signalling processes have not yet been investigated. The present study was carried out to examine the actions of lyso-PtdCho on the rat heart SL membrane enzymes involved in the phosphoinositide pathway. Different lyso-PtdCho species (10 to 200 microM) inhibited the activities of both phosphatidylinositol kinase and phosphatidylinositol-4-phosphate kinase in the SL membrane in a concentration-dependent manner. The inhibitory potency of lyso-PtdCho compounds for phosphatidylinositol kinase was lyso-PtdCho plasmalogen > 1-oleoyl-lyso-PtdCho > 1-stearoyl-lyso-PtdCho > 1-palmitoyl-lyso-PtdCho, and that for phosphatidylinositol-4-phosphate kinase was lyso-PtdCho plasmalogen > 1-oleoyl-lyso-PtdCho > 1-palmitoyl-lyso-PtdCho > 1-stearoyl-lyso-PtdCho. The inhibitory effect of lyso-PtdCho on phosphatidylinositol-4-phosphate kinase was greater than that on phosphatidylinositol kinase. Lyso-PtdCho structural analogues, such as phosphatidylcholine, lysophosphatidic acid, lysophosphatidylethanolamine, L-alpha-glycerophosphate, oleate and phosphorylcholine, did not affect the phosphoinositide kinases, suggesting that the intact structure of lyso-PtdCho was required for the inhibition of the kinases. The detrimental action of lyso-PtdCho on PtdIns kinase was potentiated by acidosis. Unlike Ca2+, ATP (0.1 and 4 mM) increased lyso-PtdCho-induced deactivation of the kinases. Both enzyme activities were found to be depressed in the ischemic-reperfused or diabetic hearts. None of the tested lyso-PtdCho species altered phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) hydrolysis by SL phospholipase C. These results indicate that accumulation of lyso-PtdCho in the SL membrane under pathological conditions may diminish the availability of the PtdIns(4,5)P2 substrate for the production of second messengers by receptor-linked phospholipase C.
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PMID:Modification of heart sarcolemmal phosphoinositide pathway by lysophosphatidylcholine. 943 41

Heart dysfunction in chronic diabetes has been observed to be associated with depressed myofibrillar adenosine triphosphatase activities as well as abnormalities in the sarcoplasmic reticular and sarcolemmal calcium transport processes. The evidence has been presented to show that alterations in the expression of myosin isozymes and regulatory proteins as well as myosin phosphorylation contribute to the development of myofibrillar remodeling in the diabetic heart. Defects in sarcoplasmic reticular and sarcolemmal calcium transport appear to be due to the accumulation of lipid metabolites in the membrane. Different agents, such as calcium-antagonists, beta-adrenoceptor blockers, angiotensin converting enzyme inhibitors, metabolic interventions and antioxidants, have been reported to exert beneficial effects in preventing subcellular remodeling and cardiac dysfunction in chronic diabetes. Clinical and experimental investigations have suggested that increased sympathetic activity, activated cardiac renin-angiotensin system, myocardial ischemia/functional hypoxia and elevated levels of glucose for a prolonged period, due to insulin deficiency, result in oxidative stress. It is proposed that oxidative stress associated with a deficit in the status of the antioxidant defense system may play a critical role in subcellular remodeling, calcium-handling abnormalities and subsequent diabetic cardiomyopathy.
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PMID:Subcellular remodeling and heart dysfunction in chronic diabetes. 989 15


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