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)

Recent studies with eluting stents showed encouraging results in preventing in-stent restenosis. We report a case of a patient in whom the implantation of carbon-coated and eluting stents in two different vessels was associated with different angiographic results. A diabetic hypertensive 67-year-old woman with an acute inferior myocardial infarction underwent direct coronary angioplasty on the right coronary artery with the implantation of two carbon-coated stents. In view of the severity of an additional lesion of the left anterior descending coronary artery and diabetes, coronary angioplasty and stenting with an eluting stent was performed in this vessel. Five months later the patient presented with acute pulmonary edema and an increase in troponin I levels. A new coronary angiography showed a long subtotal in-stent restenosis of the right coronary artery, whereas the left anterior descending coronary artery was normal. Our case report suggests that eluting stents should be considered a precious and effective tool in preventing in-stent restenosis.
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PMID:Eluting stents: an effective, promising solution? 1532 May 74

Chronic diabetes is often associated with cardiomyopathy, which may result, in part, from defects in cardiac muscle proteins. We investigated whether a 20-wk porcine model of diabetic dyslipidemia (DD) would impair in vivo myocardial function and yield alterations in cardiac myofibrillar proteins and whether endurance exercise training would improve these changes. Myocardial function was depressed in anesthetized DD pigs (n = 12) compared with sedentary controls (C; n = 13) as evidenced by an approximately 30% decrease in left ventricular fractional shortening and an approximately 35% decrease in +dP/dt measured by noninvasive echocardiography and direct cardiac catheterization, respectively. This depression in myocardial function was improved with chronic exercise as treadmill-trained DD pigs (DDX) (n = 13) had significantly greater fractional shortening and +dP/dt than DD animals. Interestingly, the isoform expression pattern of the myofibrillar regulatory protein, cardiac troponin T (cTnT), was significantly shifted from cTnT1 toward cTnT2 and cTnT3 in DD pigs. Furthermore, this change in cTnT isoform expression pattern was prevented in DDX pigs. Finally, there was a decrease in baseline levels of cAMP-dependent protein kinase-induced phosphorylation of the myofibrillar proteins troponin I and myosin-binding protein-C in DD animals. Overall, these results indicate that 20 wk of DD lead to myocardial dysfunction coincident with significant alterations in myofibrillar proteins, both of which are prevented with endurance exercise training, implying that changes in myofibrillar proteins may contribute, at least in part, to cardiac dysfunction associated with diabetic cardiomyopathy.
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PMID:Exercise improves impaired ventricular function and alterations of cardiac myofibrillar proteins in diabetic dyslipidemic pigs. 1546 90

Risk stratification of patients presenting to the hospital with acute coronary syndrome (ACS) is usually based on ECG assessment, and several clinical and biochemical criteria, which are all intended to identify subjects with more severe disease, who might benefit from aggressive medical or interventional treatment. However, no one widely accepted jeopardy score is available. Our aim was to determine whether the initial ECG, biochemical data and past medical history correlate with the extent of coronary artery disease in patients with ACS thus identifying subjects with severe coronary artery disease (CAD) who may benefit from the early invasive strategy. Patients' data was prospectively collected and retrospectively analysed according to the result of angiography examination. Our cohort consisted of 220 consecutive patients hospitalised due to typical chest pain (> 5 min.) occurring at rest within the last 24 hours. Study group comprised of 115 patients, who were subsequently subjected to coronary angiography Blood for qualitative troponin I test (Cardiac STATus, Spectral Inc., NJ, USA), and other routine biochemistry tests was drawn and ECG was done on admission. Chi-square and Pearson correlation tests were used for statistical analysis, p < 0.05 being considered statistically significant. Stepwise forward regression analysis was used to identify variables predictive of significant coronary artery stenosis. We have identified 65 patients with significant and 5 patients with insignificant multivessel stenosis, 33 patients with significant and 7 patients with insignificant single vessel disease. Five patients had normal coronary arteries. Male sex was significantly more prevalent among patients with coronary artery disease than with normal arteries (71% vs. 40%, p = 0.02). No differences in biochemistry values were seen among the groups. There was a significant difference in the prevalence in ST segment depression (p = 0.03) among these patients and in the incidence of plasma fibrinogen levels of >380 mg% (p = 0.02), those findings being most frequently encountered in significant multi- and single-vessel disease subjects. Hypertension, myocardial infarction more than 10 days ago, history of smoking, hypercholesterolemia and diabetes were independent predictors of the presence of significant stenosis. Assessment of admitting ECG and troponin I together with patients medical history may allow for identification of ACS patients with significant CAD that may benefit from early invasive treatment.
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PMID:[Severity of coronary artery disease in patients with acute coronary syndrome without ST segment elevation]. 1616 13

Hyperglycemia in the context of acute coronary syndrome (ACS) is a common observation, and existing data suggest that high glucose levels are associated with increased in-hospital mortality. We assessed the relation between random glucose and long-term mortality in 9,020 patients with ACS who were enrolled in the OPUS-TIMI 16 trial. A significant relation between glucose level and 10-month mortality was observed (2.7% in quartile 1 vs 7.0% in quartile 4, p <0.0001). After multivariable adjustment for co-morbidity, which included history of diabetes, this relation remained significant (quartile 4 vs 1, hazard ratio 1.70, 95% confidence interval 1.16 to 2.50, p = 0.006). These observations were similar in the TACTICS-TIMI 18 trial. In addition, we observed that B-type natriuretic peptide and troponin I levels increased across glucose quartiles in the OPUS-TIMI 16 trial (p values for trend = 0.002 and 0.0001, respectively) and the TACTICS-TIMI 18 trial (p values for trend = 0.006 and 0.0001, respectively). High blood glucose during ACS is an independent predictor of long-term mortality and is significantly correlated with prognostic biomarkers. Glucose levels during ACS may be an important addition to the risk stratification of patients with ACS and a potentially important target for therapy.
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PMID:Association between blood glucose and long-term mortality in patients with acute coronary syndromes in the OPUS-TIMI 16 trial. 1672 16

Diabetes is associated with increased cardiovascular morbidity and mortality. We studied the relationship between hyperglycaemia, troponin I concentrations and one-year mortality in 498 subjects admitted to hospital with an acute coronary syndrome. The proportion of deaths was higher in those with hyperglycaemia (random glucose > 11.1 mmol/L) compared to those without (27% and 12%, respectively, Chi-squared test = 9.84, p=0.002). There was a difference in troponin I concentration on admission between those patients who were alive and dead (median and interquartile range 0.14 [0 to 3.90] and 2.98 [0.23 to 18.53] respectively, p<0.001) and the risk of death was elevated in those with a myocardial infarction compared to those without (relative risk = 1.85, 95% confidence intervals 1.55 to 2.21). Despite adherence to guidelines for the management of acute coronary syndromes, the presence of hyperglycaemia confers a significant long-term mortality disadvantage.
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PMID:The association between hyperglycaemia and elevated troponin levels on mortality in acute coronary syndromes. 1705 27

Myocyte necrosis has been considered to play a fundamental role in the pathophysiology of congestive heart failure (CHF), which has usually evolved as a consequence of depletion of compensatory mechanisms and contractile reserve of myocardium. Elevated levels of creatine kinase MB (CK-MB) and troponin I (Tn-I) have been regarded as biochemical markers of myocyte necrosis. This study was planned to investigate the specificity and sensitivity of Tn-I and CK-MB in CHF and to examine the correlation of these markers with disease severity. A total of 104 patients (38 female, 66 male; mean age, 66 y [range, 36-89]) with symptoms and signs of heart failure on admission and with a reduced left ventricular ejection fraction (EF; by transthoracic echocardiography) were labeled "the patient group," and 58 patients (40 female,18 male; mean age, 61 y [range, 34-77]) with no signs or symptoms of CHF and with a normal EF detected by transthoracic echocardiography were included in the study as "the control group." Left ventricular EFs, end-diastolic diameters, and end-systolic diameters of patients in both groups were measured. Blood samples were drawn from all patients in both groups on admission, so that levels of CK-MB and Tn-I could be measured. All patients in both groups also underwent coronary angiography. Conditions leading to elevation of CK-MB or Tn-I were considered exclusion criteria. The 2 groups failed to show any significant differences in terms of mean age and the presence of coronary artery disease, hypertension, or diabetes mellitus (P>.05). Mean EF in the patient group was lower than that in the control group (P<.05). Mean CK-MB and Tn-I in the patient group were significantly higher than in the control group (P<.05). In the patient group, hypertensive patients were found to have significantly higher mean values of CK-MB than were seen in normotensive patients in the same group (P<.05). In the patient group, 52 cases were considered to be class I-II (New York Heart Association [NYHA]) (group 1), and 52 were considered to be class III-IV (group 2). Group 1, group 2, and the control group did not differ significantly from one another with regard to the presence of coronary artery disease, hypertension, and diabetes mellitus (P>.05). The mean EF in group 2 was significantly lower than that in group 1 and in the control group (P<.05); the mean EF in group 1 was significantly lower than that in the control group (P<.05). Group 1 values did not differ significantly from those of group 2 or the control group in terms of enzymatic markers (P>.05), but group 2 had significantly higher mean values of CK-MB and Tn-I than were noted in the control group (P<.05). The uphill course of CK-MB and Tn-I values from the control group to group 2 (NYHA class III-IV) was statistically significant (P<.05). Serum concentrations of CK-MB and Tn-I may become elevated in severely symptomatic patients with CHF (particularly NYHA class III-IV), demonstrating a relationship between clinical severity of the disease and elevation of myocardial enzymes (CK-MB and Tn-I).
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PMID:Clinical importance of elevated CK-MB and troponin I levels in congestive heart failure. 1727 73

Cardiovascular disease is the leading cause of perioperative morbidity and mortality after vascular surgery. The purpose of this study was to identify risk factors for myocardial ischemia after vascular surgery and to investigate a potential association of ischemia with mortality in a community hospital setting. A retrospective review was conducted after 190 major vascular procedures. Electrocardiogram (ECG) results and troponin I levels were obtained serially during the first 24 postoperative hours. Outcomes analyzed were ischemic ECG changes, troponin I level more than 2 ng/mL, 6-month mortality, and overall survival. The authors investigated any association of these outcomes with each other and the type of operation, history of coronary artery disease, diabetes, recent coronary intervention, age older than 70 years, or postoperative symptoms. Twenty-seven (14%) patients experienced ischemic ECG changes. Twenty-one (11%) patients experienced troponin I elevation. Univariate analysis revealed a history of coronary artery disease, diabetes, concerning symptoms, and troponin elevation to be predictive of ECG change (P < 0.05). ECG change and symptoms were predictive of troponin elevation (P < 0.01). Cox multivariate analysis revealed only infrainguinal bypass to predict 6-month mortality (odds ratio = 2.92, P = 0.02). Diabetes was the sole predictor of overall mortality (odds ratio = 1.94, P = 0.001). Nonsustained ischemic postoperative ECG changes during the first 24 postoperative hours do not independently influence 6-month or overall mortality after major vascular surgery. Postoperative troponin elevation likely conveys a mortality risk in the subsequent 6 months. In the community hospital setting, midterm survival rates after vascular surgery equivalent to those in higher volume centers can be achieved. Patients undergoing infrainguinal bypass and diabetics continue to be the most moribund vasculopaths.
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PMID:Predictors of electrocardiographic change, cardiac troponin elevation, and survival after major vascular surgery: a community hospital experience. 1767 44

Patients with diabetes mellitus (DM) have poor long-term outcome after percutaneous coronary intervention (PCI) partly because of microvascular disease and distal embolization. Microvascular obstruction can be assessed by measuring coronary flow reserve (CFR). The Prediction of CK-MB RElease During Successful Stenting Correlating with Indicators of Microvascular ObstruCTion (PREDICT) trial compared the CFR in patients with versus without DM during PCI. Patients undergoing elective PCI were prospectively enrolled according to diabetic (n = 36) and nondiabetic (n = 36) status. All patients received drug-eluting stent with abciximab and were followed for 30-day major adverse cardiac events. CFR and FFR (fractional flow reserve) before and after stenting were measured before and after intracoronary adenosine bolus. Procedural success, MB enzyme of creatine-kinase (CK-MB), troponin I, and high-sensitive C-reactive protein elevation, vascular complications, and major adverse cardiac events were not different. FFR before stenting was 0.77 +/- 0.03 in patients with DM versus 0.76 +/- 0.02 in patients without DM (p = 0.69). FFR after stenting was 0.97 +/- 0.03 and 0.99 +/- 0.01 (p = 0.26), respectively. CFR before stenting was 1.36 +/- 0.31 in patients with DM versus 1.49 +/- 0.25 in patients without DM (p = 0.064). However, CFR after stenting was significantly lower in patients with versus without DM (1.89 +/- 0.30 versus 2.44 +/- 0.67, p <0.001, respectively). CFR after stenting only moderately correlated with CK-MB and high-sensitive C-reactive protein after PCI but did not correlate with 30-day major adverse cardiac events. In conclusion, patients with DM have significantly lower CFR after stenting despite equivalent FFR and myonecrosis compared with patients without DM, indicating greater microvascular obstruction after PCI despite abciximab.
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PMID:Comparison of coronary flow reserve and fractional flow reserve in patients with versus without diabetes mellitus and having elective percutaneous coronary intervention and abciximab therapy (from the PREDICT Trial). 1832 43

Type 2 diabetes is characterized by fasting hyperglycemia, secondary to hepatic insulin resistance and increased glucose production. Peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) is a transcriptional coactivator that is thought to control adaptive responses to physiological stimuli. In liver, PGC-1alpha expression is induced by fasting, and this effect promotes gluconeogenesis. To examine whether PGC-1alpha is involved in the pathogenesis of hepatic insulin resistance, we generated transgenic (TG) mice with whole body overexpression of human PGC-1alpha and evaluated glucose homeostasis with a euglycemic-hyperinsulinemic clamp. PGC-1alpha was moderately (approximately 2-fold) overexpressed in liver, skeletal muscle, brain, and heart of TG mice. In liver, PGC-1alpha overexpression resulted in increased expression of hepatocyte nuclear factor-4alpha and the gluconeogenic enzymes phosphoenolpyruvate carboxykinase and glucose-6-phosphatase. PGC-1alpha overexpression caused hepatic insulin resistance, manifested by higher glucose production and diminished insulin suppression of gluconeogenesis. Paradoxically, PGC-1alpha overexpression improved muscle insulin sensitivity, as evidenced by elevated insulin-stimulated Akt phosphorylation and peripheral glucose disposal. Content of myoglobin and troponin I slow protein was increased in muscle of TG mice, indicating fiber-type switching. PGC-1alpha overexpression also led to lower reactive oxygen species production by mitochondria and reduced IKK/IkappaB signaling in muscle. Feeding a high-fat diet to TG mice eliminated the increased muscle insulin sensitivity. The dichotomous effect of PGC-1alpha overexpression in liver and muscle suggests that PGC-1alpha is a fuel gauge that couples energy demands (muscle) with the corresponding fuel supply (liver). Thus, under conditions of physiological stress (i.e., prolonged fast and exercise training), increased hepatic glucose production may help sustain glucose utilization in peripheral tissues.
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PMID:Whole body overexpression of PGC-1alpha has opposite effects on hepatic and muscle insulin sensitivity. 1920 57

A 75-year-old woman with diabetes mellitus, hypertension, and hyperlipidemia came to the emergency department with generalized and upper-extremity weakness; she had experienced a fall 2 months earlier. On admission, her drug therapy included lovastatin 40 mg/day, controlled-release diltiazem 240 mg/day, and glimepiride 1 mg/day. Nineteen days earlier, sitagliptin 100 mg/day had been started; it was discontinued 2 weeks later, and glimepiride was begun. A cardiology consultation performed on the day of admission determined that a markedly elevated creatine kinase-myocardial band isoenzyme level and borderline-high troponin I level were diagnostic of rhabdomyolysis secondary to statin use. Because the patient had been taking lovastatin for the past 12 years, the possibility that the rhabdomyolysis may have been caused by a drug interaction between lovastatin and a concomitant drug was evaluated. As it had been 10 months since her last dosage adjustment of diltiazem, it was unlikely that the statin-induced rhabdomyolysis was precipitated by diltiazem. Use of the Drug Interaction Probability Scale to determine the strength of a lovastatin-sitagliptin interaction indicated a possible association (score of 4). Multiple drug interactions have been reported with lovastatin. To our knowledge, however, this is the first case report of a possible sitagliptin-lovastatin interaction that may have caused rhabdomyolysis. Studies must be performed to further evaluate the in vivo effect of sitagliptin on the cytochrome P450 3A4 enzyme system and to elucidate other mechanisms that may potentiate such a drug-drug interaction. In the meantime, however, clinicians should be aware of this possible drug interaction.
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PMID:Rhabdomyolysis caused by a potential sitagliptin-lovastatin interaction. 1924 53


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