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)

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

Anemia, defined as a hemoglobin level of less than 12 g/dL, often is seen in congestive heart failure (CHF). It is associated with an increased mortality and morbidity and increased hospitalizations. Compared with nonanemic patients the presence of anemia also is associated with worse cardiac clinical status, more severe systolic and diastolic dysfunction, a higher beta natriuretic peptide level, increased extracellular and plasma volume, a more rapid deterioration of renal function, a lower quality of life, and increased medical costs. The only way to determine if anemia is merely a marker for more severe CHF or actually is contributing to the worsening of the CHF is to correct the anemia and see if this favorably influences the CHF. In several controlled and uncontrolled studies, correction of the anemia with subcutaneous erythropoietin (EPO) or darbepoetin in conjunction with oral and intravenous iron has been associated with an improvement in clinical status, number of hospitalizations, cardiac and renal function, and quality of life. However, larger, randomized, double-blind, controlled studies still are needed to verify these initial observations. The effect of EPO may be related partly to its nonhematologic functions including neovascularization; prevention of apoptosis of endothelial, myocardial, cerebral, and renal cells; increase in endothelial progenitor cells; and anti-inflammatory and antioxidant effects. Anemia also may play a role in increasing cardiovascular morbidity in chronic kidney insufficiency, diabetes, renal transplantation, asymptomatic left ventricular dysfunction, left ventricular hypertrophy, acute coronary syndromes including myocardial infarction and chronic coronary heart disease, and in cardiac surgery. Again, controlled studies of correction of anemia are needed to assess its importance in these conditions. The anemia in CHF mainly is caused by a combination of renal failure and CHF-induced increased cytokine production, and these can both lead to reduced production of EPO, resistance of the bone marrow to EPO stimulation, and to cytokine-induced iron-deficiency anemia caused by reduced intestinal absorption of iron and reduced release of iron from iron stores. The use of angiotensin-converting enzyme inhibitor and angiotensin receptor blockers also may inhibit the bone marrow response to EPO. Hemodilution caused by CHF also may cause a low hemoglobin level. Renal failure, cardiac failure, and anemia therefore all interact to cause or worsen each other--the so-called cardio-renal-anemia syndrome. Adequate treatment of all 3 conditions will slow down the progression of both the CHF and the chronic kidney insufficiency.
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PMID:The interaction between heart failure and other heart diseases, renal failure, and anemia. 1694 68

The review depicts the findings of the foreign and Ukrainian researches focused on high blood level of natriuretic peptide (NP), which possesses, by itself, the risk of cardiovascular diseases in patients with diabetes mellitus regardless of its stage.
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PMID:[Natriuretic peptide--independent marker of cardiovascular diseases in patients with diabetes mellitus]. 1710 Jan 79

The streptozotocin (STZ)-treated rat is a widely studied experimental model of diabetes mellitus (DM). Its pathophysiology includes hypoinsulinemia, hyperglycemia, cardiac hypertrophy, and a cardiomyopathy that is characterized by the presence of diastolic and/or systolic contractile dysfunction. As part of their endocrine function cardiomyocytes in the heart produce and secrete a family of related peptide hormones called the natriuretic peptides that include A-type natriuretic peptide (ANP) and B-type natriuretic peptide (BNP). ANP and BNP levels are variously augmented in patients with hypertension, cardiac overload, in the ventricles of failing or hypertrophied heart, in cardiac heart failure, in acute myocardial infarction (MI), and in some circumstances in DM. In this article, the effects of BNP on ventricular myocyte contraction and Ca2+ transport in STZ-induced diabetic rats have been investigated. BNP concentration was significantly increased in blood plasma and in atrial muscle in STZ-induced diabetic rats compared to age-matched controls. BNP was 11.9 +/- 0.9 ng/mL in plasma from diabetic rats compared to 6.7 +/- 1.6 ng/mL in controls and 15.8 +/- 2.0 ng/mg protein in diabetic atrial muscle compared to 8.5 +/- 1.0 ng/mg protein in controls. The heart weight to body weight ratio, an indicator of hypertrophy, was significantly increased in diabetic rat heart (4.3 +/- 0.1 mg/g) compared to controls (3.7 +/- 0.04 mg/g). The amplitude of shortening was not significantly altered in diabetic myocytes (10.3 +/- 0.4%) compared to controls (10.9 +/- 0.4%). BNP reduced the amplitude of shortening to a greater extent in diabetic myocytes (8.1 +/- 0.6%) compared to controls (10.1 +/- 0.4%). The time to peak (TPK) shortening was significantly prolonged in diabetic myocytes (254 +/- 8 ms) compared to controls (212 +/- 5 ms) and was not additionally altered by BNP. The time to half relaxation of shortening was also significantly prolonged in diabetic myocytes (131 +/- 8 ms) compared to controls (111 +/- 5 ms). BNP (10(-8) to 10(-6) M) normalized the time to half relaxation of shortening in diabetic myocytes to that of controls. Time to peak (TPK) shortening of Ca2+ was not different between diabetic and control rats. However, BNP (10(-7) M) increases TPK of Ca2+ significantly. The amplitude of the Ca2+ transient was significantly increased in diabetic myocytes (0.42 +/- 0.02 Ratio units [RU]) compared to controls (0.36 +/- 0.02 RU) and was not additionally altered by BNP. BNP may have a protective role in STZ-induced diabetic rat heart.
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PMID:Effects of brain natriuretic peptide on contraction and intracellular Ca2+ in ventricular myocytes from the streptozotocin-induced diabetic rat. 1715 Dec 99

Among the general heart failure (HF) population, over half have diastolic HF (DHF). The proportion of DHF increases with age, from 46% in patients younger than 45 years to 59% in patients older than 85 years. The diagnosis of DHF is made by the combination of signs and symptoms of HF with preserved systolic function (left ventricular ejection fraction >50%), and evidence of diastolic dysfunction obtained by echocardiographic Doppler examination, invasive hemodynamic evaluation, or an elevation of serum B-type natriuretic peptide. The most common risk factors for the development of diastolic dysfunction and DHF include long-standing hypertension, older age, female sex, obesity, diabetes, chronic kidney disease, and coronary artery disease. Acute decompensation occurs in the setting of pressure overload, volume overload, or superimposed cardiac ischemia. The cornerstones of in-hospital management include blood pressure and volume control, heart rate control, and correction of precipitating factors. Priorities in the outpatient clinic include optimal blood pressure control, maintenance of euvolemia with minimal or no diuretics, and, potentially, use of disease-modifying drugs including angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, aldosterone receptor blockers, beta-blockers, and digoxin. Long-term regression of left ventricular hypertrophy, improvement in diastolic filling parameters, and sustained reductions in B-type natriuretic peptide may be future treatment targets for this condition.
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PMID:Curriculum in cardiology: integrated diagnosis and management of diastolic heart failure. 1758 43

Since 1) dilated cardiomyopathy (DCM) causes chronic heart failure (CHF), and 2) augmentation of neurohumoral factors such as angiotensin II impairs glucose metabolism, we examined the rate of abnormal glucose metabolism in patients having both DCM and CHF and whether correction of the impairment of glucose metabolism would improve the pathophysiology of CHF in DCM patients. A 75-g oral glucose tolerance test (OGTT) was performed in 56 patients with DCM-induced CHF and 168 age- and sex-matched control subjects. Among the CHF patients, 26.8% and 50.0% suffered from diabetes mellitus (DM) and impaired glucose tolerance (IGT), respectively, showing that abnormal glucose tolerance was more prevalent in DCM patients than in the control subjects (7.7% and 14.3%, respectively). In the patients with DCM-induced CHF, a correlation was observed between the brain natriuretic peptide (BNP) levels and the difference between the plasma glucose levels at the time of fasting and at 2 h of OGTT. Since neither DM nor IGT are thought to cause DCM, the abnormalities of glucose metabolism may be attributed to the progression of CHF. Furthermore, we tested whether correction of the abnormal glucose tolerance using voglibose (an alpha-glucosidase inhibitor) would improve the severity of CHF in another group of 30 patients with DCM-induced CHF and IGT. The patients treated with voglibose for 24 weeks showed decreases in left ventricular dimension, NYHA functional classification values, and plasma BNP levels, and an improvement in cardiac function. In conclusion, abnormal glucose tolerance was more prevalent among patients with DCM-induced CHF than controls, and the correction of IGT improved the pathophysiology of CHF.
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PMID:Abnormal glucose tolerance contributes to the progression of chronic heart failure in patients with dilated cardiomyopathy. 1728 58

Cardiovascular disease is a major cause of death in patients with systemic lupus erythematosus (SLE) especially during the late phase of the disease. This study was conducted to evaluate B-type natriuretic peptide (BNP) levels in female SLE patients without cardiac symptoms and to investigate whether BNP levels correlated with echocardiographic findings. We studied 59 women with SLE and 33 healthy women. SLE patients with history of cardiac disease, diabetes mellitus, hypertension, and other inflammatory diseases were excluded from the study. All subjects had a complete history and physical examination. Overall disease activity assessment in SLE patients at the time of the study were derived by calculation of SLE disease activity index (SLEDAI). BNP levels were determined, and transthoracic echocardiography were performed in all subjects. There was no difference between SLE patients and controls in terms of age, blood pressure, smoking status, plasma glucose, creatinine levels, and lipid profiles. Nine patients had SLEDAI score greater than 5. All subjects had an EF greater than 55%. Diastolic dysfunction was more frequent in lupus patients than in controls (15 [25.4%] vs. 2 [6%]; p = 0.022). BNP levels of SLE patients were significantly higher than controls (median 17.9 range [5-211] pg/ml vs. median 14.7 range [5-39.7] pg/ml; p = 0.033). Twenty-seven of the SLE patients (46%) and seven of the controls (21%) had BNP levels greater than or equal to 20 pg/ml (p = 0.019). There were no differences in BNP levels of SLE patients with and without diastolic dysfunction (median 17.8 range [5-117] pg/ml vs. median 18.5 range [5-211] pg/mL; p = NS). BNP levels were positively correlated with left atrium diameter (r (2) = 0.39, p = 0.001). BNP levels did not correlate with erythrocyte sedimentation rate/C-reactive protein levels, SLEDAI scores, total steroid dosage used, or other echocardigraphic parameters. BNP levels were increased in female SLE patients without cardiac symptoms as compared to healthy controls. Although none of the SLE patients in our study had clinical signs of ischemic heart disease, increased levels of BNP in SLE patients might be a reflection of a ischemic myocardial tissue.
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PMID:B-type natriuretic peptide (BNP) levels in female systemic lupus erythematosus patients: what is the clinical significance? 1731 74

Antihypertensive therapy has been associated with 35 to 40% reduction in stroke incidence and 20 to 25% reduction in myocardial infarction. Antihypertensive drugs have various metabolic and endocrine activities. Their effect on electrolytes and hormones which modify the serum levels of electrolytes (such as aldosterone, angiotensine II and brain natriuretic peptide) is reviewed. Antihypertensive drugs may also modify risk factors for cardiovascular disease such as cholesterol, CRP hs, as well as urate acid and insulin resistance. Diuretics and betablockers increase this resistance whereas, it is decreased by certain enzyme conversion inhibitors and certain angiotensine II receptor blockers, partially through adiponectin release. Endocrine side effects of antihypertensive drugs such as weight gain, diabetes, gout, osteoporosis, impotence are discussed. They may decrease adherence to medication. Therefore we recommend if possible a low dose combination of antihypertensive drugs.
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PMID:[Metabolic and endocrine effects of antihypertensive drugs]. 1744 3

Management of heart failure (HF) remains complex with low 5-year survival. The Seattle Heart Failure Model (SHFM) is a recently described risk score derived predominantly from clinical trial populations that may enable the prediction of survival in patients with HF. This study sought to validate the SHFM in an independent, nonclinical trial-based HF population. Patients (n = 4,077) from the hospital-based Intermountain Heart Collaborative Study registry with a diagnosis of HF were evaluated using prospectively collected data (mean +/- SD follow-up 4.4 +/- 3.1 years). The SHFM was used to calculate a risk score for each patient. Receiver-operating characteristic area under the curve provided SHFM predictive ability for a composite end point of survival free from death, transplantation, or left ventricular assist device implantation. Addition of creatinine, serum urea nitrogen, diabetes status, and B-type natriuretic peptide (BNP) to the SHFM was also evaluated. Patient age averaged 67 +/- 13 years and 61% were men. Area under the curves were 0.70 (95% confidence interval 0.66 to 0.70), 0.67 (95% confidence interval 0.66 to 0.69), 0.67 (95% confidence interval 0.065 to 0.68), and 0.66 (95% confidence interval 0.63 to 0.67) for 1-, 2-, 3-, and 5-year survivals, respectively. Area under the curves were slightly attenuated in patients >75 years of age (n = 1,339), implantable cardioverter-defibrillator recipients (n = 693), and patients with an ejection fraction >40% (n = 1,634). BNP added significantly to the model (area under the curve +0.06). BNP was found to add additional predictive ability at 1 year (area under the curve change +0.05) and nominally at 5 years (area under the curve change +0.02). In conclusion, the SHFM predicts survival in patients with HF in a hospital-based population, with areas under the curve similar to those from data on which models were initially fit.
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PMID:Validation of the Seattle Heart Failure Model in a community-based heart failure population and enhancement by adding B-type natriuretic peptide. 1769 31

Despite good outcomes in pediatric renal transplantation, life expectancy is reduced, mostly as a result of accelerated atherosclerosis. A comprehensive evaluation of cardiac status and risk factors for cardiovascular disease was performed in 60 patients after renal transplantation (age 3 to 29 yr; mean 15.8). Posttransplantation diabetes was diagnosed in 7%. Half of the patients did not engage in any physical activity, and this was associated with increased body mass index. Uncontrolled hypertension was found in 13% of patient, and 53% were on antihypertensive medications. BP index was associated with left ventricular mass index (LVMI). Dyslipidemia was relatively uncommon, with hypercholesterolemia found in 15% and elevated LDL cholesterol found in 10% of patients. Hyperhomocysteinemia was frequent (58%); in most patients, it was not due to folate or B(12) deficiency. Lipid and homocysteine abnormalities were associated with cyclosporine therapy. Echocardiography demonstrated normal LVMI in 93% of patients, although LVMI was higher than in healthy control subjects. Cardiac troponin I was normal in all patients, but N-terminal pro-brain natriuretic peptide was elevated in 35% and was associated with LVMI and renal function. Although present cardiac status is relatively normal in pediatric renal transplantation patients, cardiac risk factors are common, and strategies to prevent cardiovascular disease need to be developed.
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PMID:Risk factors for cardiovascular disease in children and young adults after renal transplantation. 1769 60


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