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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Type I and type II diabetes is associated with increased cardiovascular complications, the most common of which are ischaemic cardiomyopathy and left ventricular dysfunction. The existence of an independent disease, diabetic cardiomyopathy, was suggested by initial anatomic studies, experimental models, and, more recently, by epidemiological studies. The exact cause of this ventricular dysfunction is not known: several mechanisms have been proposed, such as metabolic abnormalities of glucose transport, cellular overload in fatty acid metabolites, alteration of calcium uptake by the sarcoplasmic reticulum leading to cellular calcium overload, coronary microangiopathy, structural collagen abnormalities, interstitial and perivascular fibrosis or the presence of an autonomic neuropathy. The condition is characterised by abnormal left ventricular filling suggesting poor compliance or prolongation of left ventricular relaxation. Left ventricular systolic function is usually normal at rest but abnormally decreased on effort. The value of strict metabolic control and the place of drug therapy, especially calcium antagonists which oppose cellular calcium overload, has yet to be established. The natural history of diabetic cardiomyopathy should be defined by clinical studies taking care to differentiate it from the cardiovascular consequences of hypertension or obesity which aggravate or stimulate this condition.
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PMID:[Diabetic cardiomyopathy]. 764 66

Heart failure, arrhythmia, or chest pain can be a consequence of diabetes independent of coronary disease or hypertension. Diastolic myocardial dysfunction is common, contributing to the high mortality during acute infarction. The authors discuss diabetic cardiomyopathy and its management.
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PMID:Diabetic cardiomyopathy: experimental and clinical observations. 780 91

Diabetic cardiomyopathy as a distinct entity was first recognized by Rubler et al. in diabetics with congestive heart failure (CHF), who had no evidence of coronary atherosclerosis. The Framingham study showed a 2.4-fold increased incidence of CHF in diabetic men and a 5.1-fold increase in diabetic women over 18 years. Pathological studies show left ventricular hypertrophy and fibrosis with varying degrees of small vessel disease, the functional significance of which is uncertain. Hypertension was recognized as an important cofactor in the development of fatal congestive heart failure in diabetics. On cardiac catheterization, in patients symptomatic of heart failure, either congestive or restrictive patterns have been observed. In contrast, asymptomatic diabetics had decreased left ventricular compliance but normal systolic function on hemodynamic study. Noninvasive studies show alterations in systolic and especially diastolic function, particularly in diabetics with microvascular complications and/or coexistent hypertension. Using load-independent measures of contractility, however, systolic function was generally found to be normal in asymptomatic normotensive diabetics. Experimental studies have focused on the mildly diabetic dog and the severely diabetic rat. Decreased left ventricular compliance and increased interstitial connective tissue were observed in chronically diabetic dogs. In contrast, ventricular myocardium from diabetic rats exhibits a reversible decrease in the speed of contraction, prolongation of contraction, and a delay in relaxation. These mechanical changes are associated with a decreased myosin ATPase, a shift in myosin isoenzyme distribution, alterations in a variety of Ca2+ fluxes, and changes in responses to alpha- and beta-adrenergic and cholinergic stimulation. These biochemical changes may be secondary to alterations in carbohydrate, lipid, and adenine nucleotide metabolism in the diabetic heart.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetic cardiomyopathy. 808 30

The functional and morphological changes in myocardium of diabetic patients is caused by diabetic macroangiopathy, diabetic microangiopathy, autonomic neuropathy and metabolic disorders. Mechanism of these changes in the course of diabetes is not fully known. To determine whether there are myocardial ultrastructure differences between patients with diabetic cardiomyopathy (normal coronary angiograms) and diabetic patients with coronary artery disease, electron microscopy examination were performed of 70 sections received from seven biopsied patients (1F, 6M), average age 53 years (range: 42-60) with diabetes type II WHO (group A) without clinical evidence of prior coronary artery disease and hypertension, and 100 sections from 10 patients (2F, 8M), average age 54 years (range: 42-65) with diabetes and coronary atherosclerosis. These patients had clinical evidence of heart failure and were submitted to bypass-graft operations (group B). Endomyocardial biopsy tissues were obtained from the right ventricle without complications either during or after the procedure. Obtained biopsy specimens were fixed in 3% glutaraldehyde stabilized with 1M cacodylate buffer at pH 7.4, postfixed in 1% OsO4 on cacodylate buffer. The materials were then dehydrated and embedded in epon. The Irvin-Fischer test for statistical analysis was used. A p value < 0.05 was considered significant. The presence of focal mild loss of myofibrils (+) was statistically more frequent in the patients in A group (p < 0.05). It was found in 86% (6/7) of cases in A group, while in the B group was observed in 20% of (2/10) cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiomyopathy in diabetes. Ultrastructural examinations]. 828 30

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

Diabetic cardiomyopathy, a condition characterized by the accumulation of carbohydrate-containing material surrounding the myocardial small blood vessels, has been studied in alloxan-diabetic normotensive and hypertensive rats. Immunochemical techniques were used to monitor several extracellular matrix constituents present in extracts of cardiac tissue, namely types I, IV and VI collagen, laminin and fibronectin, as well as myosin. These studies have indicated that after induction of diabetes, type VI collagen but none of the other matrix components studied, was significantly increased (from 2.29 +/- 0.04 mg/g in normal to 2.85 +/- 0.18 mg/g in diabetic ventricles, p < 0.01). Hypertension, whether induced by the clipping of one renal artery or genetically determined (spontaneously hypertensive rats), resulted in a similar elevation in type VI collagen (2.71 +/- 0.12 mg/g, p < 0.005 compared to normal rats). In the presence of diabetes plus hypertension the effect was not additive, the type VI collagen level being 2.93 +/- 0.15 (p < 0.001 compared to normal rats). Basement membrane collagen (type IV) in the myocardium appeared to be unaffected by diabetes or hypertension and the myosin contents of the hearts of the four experimental groups were similar. Quantitative determinations indicate that compared to type IV collagen, laminin or fibronectin, type VI collagen represents the major periodic acid-Schiff-reactive extracellular constituent of the rat ventricle. Its preferential increase in the heart in diabetes may provide insight into the molecular mechanisms of the diabetic microvascular disease.
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PMID:Increased rat myocardial type VI collagen in diabetes mellitus and hypertension. 845 34

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

Diabetes mellitus is a complex group of diseases that has hyperglycemia as a common metabolic abnormality. Although it is well-known that diabetic patients are susceptible to the effects of large vessel atherosclerosis with specific cardiac and cerebral complications, the association of diabetes mellitus with cardiac dysfunction caused by cardiomyopathy in the absence of significant coronary artery disease has been recognized for many years. However, the pathogenesis of diabetic cardiomyopathy remains unknown and has been somewhat controversial. Specifically, whether diabetes mellitus with its metabolic effects is sufficient to account for cardiomyopathy remains to be proven. This paper reviews the evidence for and against a metabolic etiology. In addition, we review the clinical and experimental evidence that supports the view that diabetes mellitus acts together with hypertension to produce structural damage in the heart that manifests as ventricular dysfunction and ultimately congestive heart failure. The concomitant effects of the metabolic derangements of diabetes and the vascular abnormalities associated with hypertension may lead to microvascular-induced tissue injury. Findings supporting this hypothesis are presented, along with observations suggesting that treatment with vasodilating calcium channel blockers or angiotensin converting enzyme inhibitors may be beneficial in regard to tissue pathology and mortality in experimental models. Recent clinical studies also support a role for the microcirculation in diabetics. Finally, it is suggested that if the microcirculation is pathogenetically involved in diabetic cardiomyopathy, then agents that improve microcirculatory flow along with tight control of hypertension may be as beneficial in the treatment or prevention of diabetic cardiomyopathy as strict metabolic control of hyperglycemia.
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PMID:Myocardial alterations in diabetes and hypertension. 886 52

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

The existence of a distinct diabetic cardiomyopathy, characterized by a raised left ventricular mass, has previously been suggested. However, as diabetes mellitus is associated with both left ventricular hypertrophy and hypertension a confounding effect of raised blood pressure in diabetic patients has to be considered. In the present cross-sectional study an echocardiographical examination was performed as part of a health screening survey in 582 males, aged 70 years. After the exclusion of subjects with coronary heart disease or those on regular antihypertensive treatment, 30 normotensive subjects with diabetes were compared with 10 subjects with non-insulin-dependent diabetes (NIDDM) and a diastolic blood pressure 90 mm Hg or more and 203 normotensive control subjects with normal glucose tolerance. Both groups with NIDDM showed a significantly increased left atrial diameter (4.4 +/- 0.7 vs 4.0 +/- 0.5 cm, p < 0.05) and an increased atrial component in diastole (A-wave, p < 0.01) compared to the control subjects. Left ventricular mass was, however, only marginally and not significantly elevated in the diabetic subjects when compared to the healthy control subjects (133 +/- 19 and 133 +/- 28 vs 128 +/- 25 g/m2). Only in the subjects with concomitant diabetes and a raised blood pressure was the intraventricular septum significantly enlarged (p < 0.05). Thus, in the present sample no distinct diabetic cardiomyopathy with an increased left ventricular mass, independent of the influence of hypertension could be detected. The myocardial alterations in these diabetic males were restricted to an increased left atrial size and an impaired diastolic function.
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PMID:Relationship between diastolic hypertension and myocardial morphology and function in elderly males with diabetes mellitus. 896 Aug 49


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