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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both the QT interval and QT dispersion in diabetic patients have been reported to increase with the progression of cardiac autonomic neuropathy and to have a prognostic value. We assessed the cardiac autonomic influences on QT indices using the measurements of baroreflex sensitivity, heart rate variability, and cardiac (123)I-metaiodobenzylguanidine scintigraphic findings in patients with type 2 diabetes mellitus. Forty-two consecutive patients with type 2 diabetes (mean+/-SD: 54+/-10 years, 22 women and 20 men) were studied. Baroreflex sensitivity negatively correlated with the maximum and minimum QTc intervals as well as QT/QTc dispersion. However, the high-frequency power and the ratio of low-frequency power to high-frequency power of heart rate variability did not correlate with any QT indices. The percent washout rate of (123)I-metaiodobenzylguanidine positively correlated with QT/QTc dispersion, but not with maximum and minimum QTc intervals. Our findings suggest that cardiac vagal dysfunction is related to QT interval prolongation while both sympathetic and vagal dysfunctions are related to increased QT dispersion in type 2 diabetic patients. Baroreflex sensitivity and percent washout rate of (123)I-metaiodobenzylguanidine may be useful parameters indicating the abnormalities of the cardiac ventricular repolarization in this population.
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PMID:Regulation of QT indices mediated by autonomic nervous function in patients with type 2 diabetes. 1530 90

Diabetic cardiomyopathy is characterized by a prominent interstitial fibrosis. Postulated etiologies include microangiopathy, autonomic neuropathy, and metabolic factors. A common root of these pathologies is hyperglycemia or hyperinsulinemia, both of which are prominent in type 2 diabetes mellitus, which has the highest incidence of cardiovascular morbidity and mortality. The relative importance of each factor is a matter of debate; it is likely that both of these factors in addition to the concomitant risk factors seen in diabetics (dyslipidemias, hypertension, obesity, coagulation abnormalities) contribute to the spectrum of myocardial disease in diabetes. A discussion of these contributive pathologies and the hyperglycemia and hyperinsulinemia that underlie them is the subject of this review. Treatment methodologies to control the development of such pathology also are discussed.
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PMID:Preventing heart failure in patients with diabetes. 1533 15

The main purpose of this study was to determine whether cardiac autonomic neuropathy or coronary atherosclerosis is the more important factor affecting prolongation of the corrected QT interval (QTc) in patients with type 2 diabetes. We studied the association between QTc and the coefficient of variance of the heart rate variation (CV(RR)), which reflects cardiac autonomic neuropathy, and the combined intimal-medial thickness (IMT) of the common carotid artery, which reflects coronary atherosclerosis. In addition, we also investigated the relationship between the QTc and blood pressure, serum lipid concentrations, hemoglobin A(1C) (HbA(1C)) concentration, and duration of diabetes. We studied 75 patients with type 2 diabetes and 30 age-matched healthy individuals. The QT interval was measured in lead II of the electrocardiogram (ECG) and was corrected using Bazett's formula. Cardiac neuropathy was assessed by measuring CV(RR). Atherosclerosis was evaluated by measuring the combined IMT of the common carotid artery using B-mode ultrasonography. The QTc in patients with type 2 diabetes was significantly longer than in healthy individuals (P <.0001). The QTc more closely correlated with the IMT of the carotid artery (r = 0.7206, P <.0001), compared with CV(RR) (r = -0.3188, P =.0053), although both were statistically significant. The QTc also correlated positively with the systolic (SBP) and diastolic blood pressure (DBP) (r = 0.4371, P <.0001, r = 0.3632, P =.0014, respectively). Based on stepwise regression analysis with the QTc interval as the dependent variable, the IMT of the carotid artery had the most significant association with the QTc (beta = 0.6882, P =.0004). In conclusion, QTc prolongation in the setting of diabetes might be caused primarily by coronary atherosclerosis rather than by cardiac autonomic neuropathy.
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PMID:Association between the corrected QT intervals and combined intimal-medial thickness of the carotid artery in patients with type 2 diabetes. 1533 77

A 46-year-old Japanese man with type 2 diabetes mellitus, whose only diabetic complication was simple retinopathy, developed acute painful neuropathy. This presented as paresthesia and hyperesthesia restricted to the abdomen. The patient's haemoglobin A(1c) had dropped from 12% to 7.5% within 5 months, following a rapid improvement in glycaemic control. On investigation, there were no indications of disease in the intraabdominal area. Nerve conduction studies were consistent with mild sensorimotor peripheral and autonomic neuropathy. The patient required medication (mexiletine, sulpiride and imipramine hydrochloride) to control the pain. Four months after presentation, the symptoms showed a dramatic improvement and the treatment for pain relief was discontinued without any recurrence of paresthesia or hyperesthesia in the patient's abdomen. This was a very unusual case of diabetic post-treatment painful neuropathy in which the prominent features were severe pain, paresthesia and hyperesthesia restricted to the abdomen.
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PMID:Acute painful neuropathy restricted to the abdomen following rapid glycaemic control in type 2 diabetes. 1545 90

The macro- and microvascular burden of type 2 diabetes is well established. A number of recent single risk factor intervention trials targeting hyperglycemia, dyslipidemia, hypertension, procoagulation, microalbumuria, and existing cardiovascular disorders have, however, shown major beneficial effects on long-term outcome. The results from these studies are anticipated to change the future management of type 2 diabetes, and most of the updated national guidelines for the treatment of type 2 diabetes recommend a multipronged approach driven by ambitious treatment targets. The outcome of this intensive integrated therapy has, however, only been investigated in a few studies of patients with type 2 diabetes. One of these trials, the Steno-2 Study, showed that intensive intervention for an average of 7.8 years cuts cardiovascular events as well as nephropathy, retinopathy, and autonomic neuropathy by about half when compared with a conventional multifactorial treatment. The challenge for now is to ensure that the trial experiences are widely adopted in daily clinical practice.
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PMID:Intensive integrated therapy of type 2 diabetes: implications for long-term prognosis. 1556 20

The metabolic abnormalities associated with diabetes mellitus result in macrovascular and microvascular complications in multiple organ systems; it is the cardiovascular impact that accounts for the greatest morbidity and mortality associated with this disease. Heart failure, both with reduced and preserved systolic function, is a major complication, arising from the frequent associations with coronary atherosclerosis, hypertension, and a specific heart muscle dysfunction (cardiomyopathy) that occurs independently of coronary artery disease. Hyperglycemia, insulin resistance, and hypertension, together with activation of both circulating and tissue renin-angiotensin-aldosterone systems, contribute to structural fibrosis and autonomic neuropathy. Thus it becomes imperative to identify cardiac abnormalities early in the course of both type 1 and type 2 diabetes in order to allow early and aggressive intervention to control glucose and blood pressure and to normalize blood lipid profiles. Patients with diabetes should be treated to secondary prevention targets, including blood pressure less than 130/80 mm Hg and LDL less than 100 mg/dL. Angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, certain calcium channel blockers, statins, and aspirin have all been demonstrated to significantly reduce cardiovascular morbidity and mortality in patients with diabetes.
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PMID:Heart failure in diabetes mellitus: causal and treatment considerations. 1572 10

Cardiovascular disease (CVD) is the major cause of death in patients with type 2 diabetes mellitus. However, the diagnosis of CVD is delayed due to concealment of antecedent symptoms by factors such as autonomic neuropathy. In this study, we aimed to investigate the frequency of silent ischemia by using exercise electrocardiogram (ECG). The present study included 500 Turkish patients with type 2 diabetes (male/female: 222/278), who showed no evidence of CAD and angina pectoris or no sign(s) of ischemic changes in resting ECGs. All patients underwent treadmill exercise test according to Bruce protocol, and 62 cases (12.4%) exhibited abnormal changes. These patients identified by exercise ECG consisted of 28 males (28/222, [12.6%]) and 34 females (34/278, [12.2%]) and were then examined by coronary angiography. CAD was diagnosed in 53 individuals by coronary angiography. The abnormalities of exercise test are associated with the age of the patients or the duration of diabetes (p < 0.05). There is no significant difference in the severity of coronary disease or in the prevalence of silent ischemia between male and female patients. However, among the patients identified by exercise ECG females have higher body mass index than males, suggesting that obesity may represent the risk factor of CAD in women with type 2 diabetes.
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PMID:The prevalence of silent ischemia in Turkish patients with type 2 diabetes mellitus. 1575 Mar 31

We have developed an animal model of diabetic sympathetic autonomic neuropathy which is characterized by neuroaxonal dystrophy (NAD), an ultrastructurally distinctive axonopathy, in chronic streptozotocin (STZ)-diabetic rats. Diabetes-induced alterations in the sorbitol pathway occur in sympathetic ganglia and therapeutic agents which inhibit aldose reductase or sorbitol dehydrogenase improve or exacerbate, respectively, diabetes-induced NAD. The sorbitol dehydrogenase inhibitor SDI-711 (CP-470711, Pfizer) is approximately 50-fold more potent than the structurally related compound SDI-158 (CP 166,572) used in our earlier studies. Treatment with SDI-711 (5 mg/kg/day) for 3 months increased ganglionic sorbitol (26-40 fold) and decreased fructose content (20-75%) in control and diabetic rats compared to untreated animals. SDI-711 treatment of diabetic rats produced a 2.5- and 4-5-fold increase in NAD in the SMG and ileal mesenteric nerves, respectively, in comparison to untreated diabetics. Although SDI-711 treatment of non-diabetic control rat ganglia increased ganglionic sorbitol 40-fold (a value 8-fold higher than untreated diabetics), the frequency of NAD remained at control levels. Levels of ganglionic sorbitol pathway intermediates in STZ-treated rats (a model of type 1 diabetes) and Zucker Diabetic Fatty rats (ZDF, a genetic model of type 2 diabetes) were comparable, although STZ-diabetic rats develop NAD and ZDF-diabetic rats do not. SDI failed to increase diabetes-related ganglionic NGF above levels seen in untreated diabetics. Initiation of Sorbinil treatment for the last 4 months of a 9 month course of diabetes, substantially reversed the frequency of established NAD in the diabetic rat SMG without affecting the metabolic severity of diabetes. These findings indicate that sorbitol pathway-linked metabolic alterations play an important role in the development of NAD, but sorbitol pathway activity, not absolute levels of sorbitol or fructose per se, may be most critical to its pathogenesis.
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PMID:A potent sorbitol dehydrogenase inhibitor exacerbates sympathetic autonomic neuropathy in rats with streptozotocin-induced diabetes. 1575 58

The metabolic abnormalities associated with diabetes mellitus result in macrovascular and microvascular complications in multiple organ systems; it is the cardiovascular impact that accounts for the greatest morbidity and mortality associated with this disease. Heart failure, both with reduced and preserved systolic function, is a major complication, arising from the frequent associations with coronary atherosclerosis, hypertension, and a specific heart muscle dysfunction (cardiomyopathy) that occurs independently of coronary artery disease. Hyperglycemia, insulin resistance, and hypertension, together with activation of both the circulating and the tissue renin-angiotensin-aldosterone systems, contribute to structural fibrosis and autonomic neuropathy. Thus, it becomes imperative to identify cardiac abnormalities early in the course of both type 1 and type 2 diabetes to allow early and aggressive intervention to control glucose and blood pressure and to normalize blood lipid profiles. Patients with diabetes should be treated to secondary prevention targets, including blood pressure less than 130/80 mm Hg and low-density lipoprotein cholesterol level less than 100 mg/dL. Angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers,beta blockers, calcium channel-blockers, statins, and aspirin have all been demonstrated to significantly reduce cardiovascular morbidity and mortality in patients with diabetes.
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PMID:Diabetes mellitus and heart failure. 1581 21

Diabetic neuropathy is a debilitating disorder that occurs in nearly 50 percent of patients with diabetes. It is a late finding in type 1 diabetes but can be an early finding in type 2 diabetes. The primary types of diabetic neuropathy are sensorimotor and autonomic. Patients may present with only one type of diabetic neuropathy or may develop combinations of neuropathies (e.g., distal symmetric polyneuropathy and autonomic neuropathy). Distal symmetric polyneuropathy is the most common form of diabetic neuropathy. Diabetic neuropathy also can cause motor deficits, silent cardiac ischemia, orthostatic hypotension, vasomotor instability, hyperhidrosis, gastroparesis, bladder dysfunction, and sexual dysfunction. Strict glycemic control and good daily foot care are key to preventing complications of diabetic neuropathy.
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PMID:Evaluation and prevention of diabetic neuropathy. 1595 41


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