Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) is characterized by transient left ventricular apical ballooning associated with symptoms, electrocardiographic changes and minimal cardiac enzyme release in the absence of coronary artery disease. Initially described in Japan, TTP occurs worldwide, predominantly in women and frequently after emotional or physical stress. Symptoms include anginal chest pain, dyspnea and syncope. Electrocardiographic ST elevations may be present only for several hours, and are followed by negative T waves that persist for months. Arterial hypertension is found in up to 76% of TTP patients, hyperlipidemia in up to 57% and diabetes mellitus in up to 12%. Potential pathophysiological mechanisms for TTP include catecholamine-induced myocardial stunning or hyperkinesis of the basal left ventricular segments, coronary vasospasm, plaque rupture, myocarditis and genetic factors. TTP patients should be monitored similarly to myocardial infarction patients because organ failure, cardiogenic shock, ventricular fibrillation or rupture may occur. Beta-blockers are indicated, whereas catecholamines and nitrates should be avoided. The long-term prognosis is unknown.
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PMID:Transient left ventricular dysfunction (tako-tsubo phenomenon): Findings and potential pathophysiological mechanisms. 1703 1

Atrial fibrillation (AF) is the most common arrhythmia after coronary artery bypass grafting (CABG). AF is a vexing problem that causes morbidity, prolongs hospital stay, and increases costs. Numerous factors have been suggested to play a role in the development of AF. The aim of this study was to evaluate the effect of intermittent aortic cross clamping (IACC) compared with hypothermic cardioplegic solution (HCS) in the development of postoperative AF. We evaluated data obtained from 345 patients undergoing CABG with HCS (HCS group, n = 212) and IACC (IACC group, n = 173) between April 2004 and August 2005. Diabetes mellitus was observed more often in the HCS group (P < .05), otherwise both groups had similar preoperative characteristics including sex, age, the number of distal anastomoses, left ventricle ejection fraction, history of myocardial infarction, and use of beta-blocker medication. The only statistically significant difference between the groups was higher postoperative Ca-antagonist use in the HCS group. Rates of postoperative AF, however, were significantly lower in the IACC group (21.52%) than that in the HCS group (11.05%; P < .01). Postoperative Ca-antagonist use in the HCS group and smoking in the IACC group were independent predictors of AF after CABG. The incidence of postoperative AF after CABG with IACC was reduced compared with HCS. IACC with ventricular fibrillation may exert a counteractive effect against AF.
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PMID:Does intermittent aortic cross clamping decrease the incidence of atrial fibrillation after coronary bypass surgery? 1759 84

Diabetes mellitus (DM) is an independent risk for cardiovascular disease. Furthermore, patients with DM have increased risk for ventricular arrhythmia that is thought to be secondary to coronary artery disease (CAD) or congestive heart failure (CHF). We hypothesized that DM may cause ventricular arrhythmias independent of CAD or CHF. Using a large database, we evaluated the occurrence of ventricular fibrillation in patients with DM adjusting for CAD and CHF. We used patient treatment files (PTF), documents of inpatients' admissions containing discharge diagnoses (ICD-9 codes) from all Veterans Health Administration Hospitals. The patients were stratified in two groups: ICD-9 code for DM (293 124) and a control group with ICD-code for hypertension (HTN) but no DM (552 623). ICD-9 codes for ventricular fibrillation were used for this study. We performed uni- and multivariant analysis adjusting for comorbid conditions. Ventricular fibrillation was present in 563 (0.2%) vs 781 (0.1%) in the control group. Using multivariate analysis, DM remained independently associated with ventricular fibrillation (odds ratio: 1.7; confidence interval: 1.5-1.9; P < 0.000). Patients with DM have significantly higher prevalence of ventricular fibrillation independent of CAD or CHF, which in part may explain the higher risk of sudden death in patients with DM.
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PMID:Increased prevalence of ventricular fibrillation in patients with type 2 diabetes mellitus. 1765 19

A 62-year-old man with multiple cardiac risk factors, including diabetes mellitus type II, treated hypertension, and hyperlipidemia, had a dobutamine stress echocardiogram performed as part of a preoperative evaluation. At peak stress the patient developed an apical regional wall motion abnormality. Approximately 12 minutes into the recovery period, the patient developed ventricular tachycardia that degenerated into ventricular fibrillation. He was successfully resuscitated and underwent emergency coronary angiography that showed a 95% distal left anterior descending coronary artery stenosis.
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PMID:Ventricular fibrillation in late recovery after dobutamine stress echocardiography. 1768 30

The study was designed to characterise the influence of a novel acyl-CoA:cholesterol acyltransferase inhibitor, VULM 1457, on the severity of myocardial ischaemia-reperfusion injury in a model of diabetes mellitus and hypercholesterolaemia induced by co-administration of streptozotocin and a high fat-cholesterol diet. We used Langendorff-perfused rat hearts to measure the size of myocardial infarction after 30 min of regional ischaemia, followed by a 2-h reperfusion period, and open-chest rats were exposed to 6 min of ischaemia and 10 min of reperfusion to analyse ventricular arrhythmias. In addition to the high fat-cholesterol diet, VULM 1457 was administered to the diabetic-hypercholesterolaemic rats for 5 days. Decreased plasma and liver cholesterol levels and a significantly reduced occurrence of ventricular fibrillation (29% vs. 100%, P<0.01), determined via the mean number and duration of episodes (0.6+/-0.4 and 2.1+/-1.4 s vs. 2.8+/-0.8 and 53.5+/-14.4 s in diabetic-hypercholesterolaemic rats, both P<0.01), were observed in these animals. Lethal ventricular fibrillation was suppressed, and arrhythmia severity was also significantly decreased in these animals as compared to the non-treated animals (2.9+/-0.6 vs. 4.9+/-0.2; P<0.05). A smaller infarct size, normalised to the size of area at risk, was observed in the treated diabetic-hypercholesterolaemic group as compared to the non-treated group (16.3+/-1.9% vs. 37.3+/-3.1%; P<0.01). Aside from remarkable hypolipidaemic activity, VULM 1457 improved the overall myocardial ischaemia-reperfusion injury outcomes in the diabetic-hypercholesterolaemic rats by suppressing arrhythmogenesis as well as by reducing myocardial necrosis.
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PMID:The myocardial infarct size-limiting and antiarrhythmic effects of acyl-CoA:cholesterol acyltransferase inhibitor VULM 1457 protect the hearts of diabetic-hypercholesterolaemic rats against ischaemia/reperfusion injury both in vitro and in vivo. 1776 71

This study examined the prevalence of major and minor depression in patients with acute coronary syndrome and their relation with heart rate and heart-rate variability, and clinical characteristics. The study group included 297 patients, 200 men and 97 women, between ages of 21 and 70 years (M age = 57.5 +/- 9.6), who were admitted to a coronary care unit with acute coronary syndrome and survived to discharge from the hospital. Major and minor depression were diagnosed using DSM-IV. There were 44.1% patients with acute coronary syndrome without depression, 29.3% with minor depression, and 26.6% with major depression. The prevalence of minor and major depression was more elevated in patients with non-ST-segment elevation myocardial infarction and unstable angina than in patients with ST-segment elevation myocardial infarction. Ventricular fibrillation and atrial fibrillation were more common in patients with major and minor depression than in patients without depression. The 24-hr. duration of heart-beat intervals and heart-rate variability were significantly lower in patients with major and minor depression than in patients without depression. This study implies that clinical depression was significantly comorbid with the acute coronary syndrome and was related to hypertension, diabetes mellitus, age, sex, type of acute coronary syndrome, left ventricular failure, higher heart rate, and lower heart-rate variability.
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PMID:Relation between major and minor depression and heart rate, heart-rate variability, and clinical characteristics of patients with acute coronary syndrome. 1788 12

We examined whether thyroid hormones affect myocardial epsilon-PKC signalling, downstream target substrate, connexin-43 (Cx43) and arrhythmogenesis in non-diabetic and diabetic rats. Diabetes was induced by a single streptozotocin injection (50mg/kg, i.v.). Triiodothyronine (T(3)) was applied by gavage (1microg/kg of body weight for 10 days) to 4 weeks and 9 weeks diabetic and age-matched non-diabetic rats. Western blot analysis of Cx43 and epsilon-PKC, immunofluorescence of Cx43, ultrastructure of cardiomyocytes and myocardial conduction velocity were performed. Isolated perfused heart preparation was used to test ventricular fibrillation susceptibility. T(3) significantly decreased epsilon-PKC expression in non-diabetic and suppressed in diabetic rat heart ventricles. Decline of epsilon-PKC signalling was associated with decrease of Cx43 phosphorylation in diabetic and to a greater extent in non-diabetic rat hearts. However, conduction velocity was significantly decreased in diabetic while enhanced due to T(3) and increased in non-diabetic T(3)-treated rat heart ventricles compared to non-treated. T(3)-induced down-regulation of Cx43 was associated with increased cardiac propensity to ventricular fibrillation. Findings indicate that activation of epsilon-PKC signalling linked with phosphorylation of Cx43 is one of the mechanisms involved in the adaptation of the heart to hyperglycemia. Suppression of epsilon-PKC and Cx43 phosphorylation by T(3) abolish benefit of adaptation rendering the heart prone to lethal arrhythmias.
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PMID:Thyroid hormones suppress epsilon-PKC signalling, down-regulate connexin-43 and increase lethal arrhythmia susceptibility in non-diabetic and diabetic rat hearts. 1862 45

Diabetic patients have a higher incidence of cardiac arrhythmias, including ventricular fibrillation and sudden death, and show important alterations in the electrocardiogram, most of these related to the repolarization. In myocytes isolated from diabetic hearts, the transient outward K+ current (Ito) is the repolarizing current that is mainly affected. Type 1 diabetes alters Ito at 3 levels: the recovery of inactivation, the responsiveness to physiologic regulators, and the functional expression of the channel. Diabetes slows down Ito recovery of inactivation because it triggers the switching from fast-recovering Kv4.x channels to the slow-recovering Kv1.4. Diabetic animals also have decreased responsiveness of Ito towards the sympathetic nervous system; thus, the diabetic heart develops a resistance to its physiologic regulator. Finally, diabetes impairs support of various trophic factors required for the functional expression of the channel and reduces Ito amplitude by decreasing the amount of Kv4.2 and Kv4.3 proteins.
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PMID:Transient outward potassium channel regulation in healthy and diabetic hearts. 1923 70

1. Rosiglitazone is widely used in the treatment of Type 2 diabetes. However, in recent years it has become evident that the therapeutic effects of peroxisome proliferator-activated receptor gamma ligands reach far beyond their use as insulin sensitizers. Recently, the ability of rosiglitazone pretreatment to induce cardioprotection following ischaemia-reperfusion (I/R) has been well documented; however, the protective mechanisms have not been elucidated. In the present study, examined the role of the phosphatidylinositol 3-kinase (PI3-K)/Akt signalling pathway in rosiglitazone cardioprotection following I/R injury. 2. Mice were pretreated with 3 mg/kg per day rosiglitazone for 14 days before hearts were subjected to ischaemia (30 min) and reperfusion (2 h). Wortmannin (1.4 mg/kg, i.p.), an inhibitor of PI3-K, was administered 10 min prior to myocardial I/R. Then, activation of the PI3-K/Akt/glycogen synthase kinase (GSK)-3alpha signalling pathway was examined. The effects of PI3-K inhibition on rosiglitazone-induced cardioprotection were also evaluated. 3. Compared with control rats, the ratio of infarct size to ischaemic area (area at risk) and the occurrence of sustained ventricular fibrillation in rosiglitazone-pretreated rats was significantly reduced (P < 0.05). Rosiglitazone pretreatment attenuated cardiac apoptosis, as assessed by ELISA to determine cardiomyocyte DNA fragmentation. Rosiglitazone pretreatment significantly increased levels of phosphorylated (p-) Akt and p-GSK-3alpha in the rat myocardium. Pharmacological inhibition of PI3-K by wortmannin markedly abolished the cardioprotection induced by rosiglitazone. 4. These results indicate that rosiglitazone-induced cardioprotection in I/R injury is mediated via a PI3-K/Akt/GSK-3alpha-dependent pathway. The data also suggest that modulation of PI3-K/Akt/GSK-3alpha-dependent signalling pathways may be a viable strategy to reduce myocardial I/R injury.
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PMID:Rosiglitazone-induced myocardial protection against ischaemia-reperfusion injury is mediated via a phosphatidylinositol 3-kinase/Akt-dependent pathway. 1956 39

50 years old female patient, with history of diabetes mellitus and hypertension, receiving metformin (500 mg BID) and atenolol (50 mg BID), presented to the Emergency Room with asthenia and dizziness. The patient was also receiving alternative medication (Dragon Blanco) which contains no licorice. During the emergency workup she developed syncope and three episodes of ventricular fibrillation. She was electrically defibrillated and treated with amiodarone and potassium replacement. The patient was admitted to the Intensive Care Unit. Physical exam: BP: 160/90 mm Hg, RR: 15, Pulse: 83: Cardiovascular: grade II systolic murmur which irradiated to the neck. The rest of the examination was unremarkable. Labs: Na: 138 meg/dl, K: 1.6 meg/dl, Cl: 84 meg/dl, BUN: 17 mg/dl, Creat.: 1.1 mg/dl, Gluc.: 148 mg/dl, Renin: < 0.15 mcgr/ml, Aldosterone: 20.1 mcg%. Aldosterone-Renin ratio: 133. Chest X-Ray: cardiomegaly. EKG: RBBB, long QT segment and prominent broad "u" waves compatible with severe hypokalemia. A CT SCAN of the Abdomen/Pelvis showed a 3.2 cm right adrenal mass, most likely adenomatous. The patient was discharged with the diagnosis of primary aldosteronism. Due to the diagnosis of diabetes mellitus, hypertension and the three episodes of ventricular fibrillation, surgical treatment was postponed until stress tests and eventual coronary angiographic studies were performed. We found in our review of the medical literature 9 reports of fibrillation associated with hyperaldosteronism. Of those, only two were associated with primary aldosteronism, one of them with a fatal outcome. This case is highly unusual and emphasizes the importance of an adequate diagnosis of secondary hypertension.
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PMID:Ventricular fibrillation as the first manifestation of primary hyperaldosteronism. 1961 May 66


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