UMLS:C0018801 - FACTA Search

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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic elevation of plasma aldosterone contributes to heart failure. Mineralocorticoid receptor (MR) antagonism is cardioprotective in such a setting, but whether such protection occurs in the presence of low-aldosterone concentrations remains unclear. We investigated whether MR blockade attenuates cardiac hypertrophy and failure in rats with salt-sensitive hypertension. Dahl salt-sensitive (DS) rats fed a high-salt diet from 7 weeks develop concentric left ventricular (LV) hypertrophy secondary to hypertension at 12 weeks followed by heart failure at 19 weeks (DS-CHF). DS rats on such a diet were treated with a non-antihypertensive dose of the selective MR antagonist eplerenone from 12 to 19 weeks. Renin activity and aldosterone concentration in plasma were decreased in DS-CHF rats compared with controls. LV hypertrophy and fibrosis, as well as macrophage infiltration around coronary vessels, were apparent in DS-CHF rats. The amounts of mRNAs for 11beta-hydroxysteroid dehydrogenase type 1, MR, monocyte chemoattractant protein 1, and osteopontin were increased in these hearts. Treatment of DS-CHF rats with eplerenone inhibited these changes in gene expression, as well as coronary vascular inflammation and heart failure. Eplerenone attenuated both the decrease in the ratio of reduced to oxidized glutathione and the increase in NADPH oxidase activity apparent in DS-CHF rat hearts. MR blockade with eplerenone thus resulted in attenuation of LV hypertrophy and failure, without an antihypertensive effect, in rats with low-aldosterone hypertension. The beneficial cardiac effects of eplerenone are likely attributable, at least in part, to attenuation of myocardial oxidative stress and coronary vascular inflammation induced by glucocorticoid-activated MRs.
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PMID:Mineralocorticoid receptor antagonism attenuates cardiac hypertrophy and failure in low-aldosterone hypertensive rats. 1650 9

It is well known that insulin resistance (IR) and inflammation (IF) are associated with macroangiopathy. However, whether IR and IF are related to cardiac disease (myocardial infarction, angina pectoris, and heart failure), stroke or both remains elusive. The present hospital-based prospective study was designed to investigate this issue. The study subjects were 300 Japanese patients with type 2 diabetes mellitus and negative history of cardiac disease and stroke. IR (K index of insulin tolerance test; K(ITT)) and IF (high-sensitivity C-reactive protein [hs-CRP]) were measured in each patient at baseline. Patients were followed-up for a mean period of 5.5 years. The time of first evidenced cardiac disease or stroke was monitored. During the follow-up, 35 patients developed cardiac disease and 26 patients developed stroke. Age, smoking, K(ITT), and hs-CRP were independently related to cardiac disease, while age, systolic blood pressure, low HDL, and anti-platelet drug use were independently related to stroke. When patients were subdivided into IR(-) and IR(+), and IF(-) and IF(+), Kaplan-Meier survival analysis showed that the rate of cardiac disease, but not of stroke, was significantly higher in IR(+)IF(+) than IR(-)IF(-) patients (p < 0.01). In conclusion, coexistence of IR and IF effectively predicted cardiac disease but not stroke in Japanese patients with type 2 diabetes mellitus.
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PMID:Coexistence of insulin resistance and inflammation effectively predicts cardiac disease but not stroke in Japanese patients with type 2 diabetes mellitus. 1673 Aug 41

Diabetic nephropathy (DN) is one of the main causes of end stage renal disease (ESRD) and a leading cause of diabetes mellitus related morbidity and mortality. Recently, sirtuin are reported to have emerging pathogenetic roles in cancer, muscle differentiation, heart failure, neurodegeneration, diabetes and aging. The aim of the present study was to study the role of intermittent fasting (IF) on DN and studying the expression of Sir2 and p53. At biochemical level, we found that IF causes significant improvement in blood urea nitrogen (BUN), creatinine, albumin and HDL cholesterol, parameters that are associated with the development of DN. Diabetic rats on IF also show significant improvement in onset of hypertension. Interestingly, the expression of Sir2, a NAD dependent histone deacetylase, decreases in diabetic rat kidney and this decrease is overcome by IF. Moreover, we provide evidence for involvement of mitogen activated protein kinases (MAPK) cascade in mediating the effects of IF as there is reduction in the expression of p38 which gets induced under diabetic condition. This was further accompanied by the concomitant decrease in cleavage of caspase3 and p53 expression. These findings suggest that IF significantly improves biochemical parameters associated with development of DN and changes the expression of Sir2 and p53.
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PMID:Intermittent fasting prevents the progression of type I diabetic nephropathy in rats and changes the expression of Sir2 and p53. 1731 25

HMG-CoA reductase inhibitors (statins) have recently been reported to improve cardiac function, and decrease the incidence of heart failure (HF) in hyperlipidemic patients. However, evidence for statin treatment in patients with HF remains a subject of debate. Thus, a study was initiated to examine the effects of pitavastatin on cardiac function evaluated by echocardiographic findings and plasma brain natriuretic peptide (BNP) levels in patients with HF. Twenty-three patients with HF were treated with pitavastatin 1-2 mg/day in addition to standard therapy for 7.5 +/- 3.8 months. Left ventricular end-diastolic dimension (LVDd) and left ventricular end-systolic dimension (LVDs) were determined by echocardiography. Left ventricular ejection fraction (LVEF) was calculated using Teichholz's formula. Serum lipid and plasma BNP levels were also measured. During the follow-up period, LVEF was increased from 42 +/- 11 to 48 +/- 13% (P = 0.002). LVDs was reduced from 43 +/- 10 to 40 +/- 10 mm (P < 0.001), while there was no change in LVDd. E/A (n = 10) and deceleration time (n = 7), obtained in some patients, did not change significantly (0.89 +/- 0.33 to 0.77 +/- 0.17%, and 215 +/- 46 to 227 +/- 72 msec, respectively). In addition, the plasma BNP level was moderately, but significantly decreased from 94 +/- 78 to 70 +/- 56 pg/mL (P = 0.005). In subgroup analysis, LVEF was improved in both patients with ischemic and nonischemic HF. There was no significant correlation between the percent change in serum total cholesterol and the percent change in LVEF by pitavastatin treatment. Serum total cholesterol, LDL-cholesterol, and triglycerides decreased by 21%, 30%, and 15%, respectively, and HDL-cholesterol increased by 12%. Pitavastatin improved cardiac function in patients with HF, which generally worsens with time. The results suggest that pitavastatin may be beneficial for treatment of HF.
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PMID:Beneficial effects of pitavastatin, a 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitor, on cardiac function in ischemic and nonischemic heart failure. 1836 64

The epidemiological literature supports an inverse association and a dose-response gradient between exercise training and both cardiovascular disease in general and coronary artery disease in particular. An overwhelming number of studies has supported similar findings for hypertension, dyslipidaemia, obesity, diabetes, inflammatory and coagulation markers related to cardiovascular disease and cardiac heart failure. Findings are highly suggestive that endurance type exercise training, of moderate intensity most days of the week can lower blood pressure in patients with hypertension, can decrease triglyceride levels and increase HDL cholesterol levels in patients with dyslipidaemia, reduces body weight when combined with diet, improves insulin sensitivity, modifies the inflammatory process and finally can improve stroke volume and reduce cardiomegaly in patients with cardiac heart failure.
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PMID:The role of exercise in cardiovascular rehabilitation: a review. 1837 84

The number of patients with chronic kidney disease-CKD is still growing. Overweight and obesity present also an important problem of world public health. However, there are not many data showing possible association between obesity and incresing risk of development of renal failure recently it has been demonstrated that in obese patients secondary focal segmental glomerulosclerosis and glomerular hypertrophy appear more frequently. The aim of this study was to estimate glomerular filtration rate-GFR in patients with normal serum creatinine concentration undergoing primary angioplasty according to body mass index. The study included 1413 patients udergoing primary angioplasty for acute myocardial infarction. The following parameters were assessed: age, gender, family history of cardiovascular disease, risk factors of cardiovascular disease (hypertension, diabetes mellitus, obesity etc.), previous myocardial infarction, pre-existing heart failure, treatment given, localization of infarct, coronary stenting, serum creatinine before angioplasty, cholesterol, LDL, HDL, triglycerides, glucose, blood pressure. Of a total of 1413 patients, 1337 (94.62%, 943 M, 394 F) had correct serum creatinine concentration (below 1.5 mg/dl for men, below 1.2 mg/dl for women). Glomerular filtration rate was calculated from serum creatinine levels by using the simplified Modification of Diet in Renal Disease Study formula--MDRD, Cockcroft-Gault equation and Jeliffe formula. An average value of GFR in study group was 79.94 +/- 24.51 ml/min (Cockcroft-Gault equation), 73.02 +/- 21.96 ml/min (Cockcroft-Gault adjusted to weight), 90.37 +/- 25.1 ml/min (MDRD equation) and 77.67 +/- 21.65 ml/min (Jeliffe formula). A significant lower serum creatinine levels and GFR (assessed by 3 formulas and Cockcroft-Gault using adjusted weight) were observed in women group. In the whole study group (with normal serum creatinine levels) substantial correlation was found between age and serum creatinine concentration (r = 0.13, p > 0.001), GFR (MDRD, r = -0.37, p < 0.001, Cockcroft-Gault, r = -0.62, p < 0.001, adjusted to weight r = -0.64, p < 0.001, Jeliffe r = -0.61, p < 0.001) and also between BMI and GFR (MDRD r = 0.28, p < 0.001, Cockcroft-Gault, r = 0.31, p < 0.001, adjusted to weight r = 0.08, p < 0.001, Jeliffe r = 0.341, p < 0.001), but not with serum creatinine concentration (r = 0.03, p = 0.3). In patients with normal serum creatinine levels percentage of patients with GFR below 60 ml/min ranges from 4.79% up to 30.74%. In patients with higher BMI, higher GFR may be partially caused by glomerular hyperfiltration. Overweight or obesity are significant, but potentially changeable risk factors for development of chronic renal failure. However, chronic kidney disease is one of the complications of obesity.
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PMID:[Obesity as a risk factor of chronic kidney disease in patients undergoing primary angioplasty]. 1841 92

The efficacy and safety of muraglitazar versus glimepiride were evaluated in patients with type 2 diabetes. After open-label metformin monotherapy, 1,805 patients received randomised therapy with muraglitazar 2.5 mg or 5 mg or with glimepiride 1 mg in a double-blind 52-week study. The primary end point was change in glycosylated haemoglobin (HbA1C); secondary end points were changes in fasting lipid levels and glycaemic indices. At week 52, the reduction in HbA1C with muraglitazar 5 mg plus metformin was superior (p<0.0001) and with muraglitazar 2.5 mg it was non-inferior in comparison with glimepiride. At week 12, muraglitazar significantly decreased triglyceride levels (p<0.0001) and increased levels of high-density lipoprotein cholesterol (HDL-C) (p<0.0001). Oedema, weight gain and heart failure were more evident with muraglitazar. Muraglitazar 5 mg plus metformin significantly improved HbA1C, triglyceride and HDL-C levels in patients with type 2 diabetes. Cardiovascular events were similar among groups (~2%), but there was an imbalance of total mortality in favour of glimepiride.
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PMID:Improvement of glycaemic and lipid profiles with muraglitazar plus metformin in patients with type 2 diabetes: an active-control trial with glimepiride. 1877 89

TREATMENT OF ARTERIAL HYPERTENSION - Blood pressure (BP) should be regularly measured in all patients with CKD (Strength of Recommendation C). - BP control and proteinuria reduction delay progression of CKD (Strength of Recommendation A) and reduce cardiovascular risk (Strength of Recommendation C). Thus, control of both factors should be the treatment objective. - The BP target in patients with CKD should be < 130/80 mmHg, and 125/75 mmHg if proteinuria is > 1 g/24 hours (Strength of Recommendation A). - Lifestyle changes should be made: low-sodium diet (less than 100 mEq/day of sodium or 2.4 g/day of salt); weight reduction if patient is overweight (body mass index 20-25 kg/m2); regular aerobic physical exercise and moderate alcohol intake for BP control and prevention of cardiovascular risk (Strength of Recommendation A). - The choice of the antihypertensive drug in patients with CKD depends on the etiology of CKD, cardiovascular risk, or presence of clinical or subclinical cardiovascular disease (Strength of Recommendation A). - Two or more antihypertensive drugs are usually required to control blood pressure in patients with CKD (Strength of Recommendation B), and will frequently include a diuretic, which in stages 4-5 should be a loop diuretic (Strength of Recommendation B). - Renin-angiotensin-aldosterone system (RAAS) inhibitors are first choice drugs in patients with diabetic nephropathy, patients with non-diabetic nephropathy with a protein/creatinine ratio higher than 200 mg/g, and patients with heart failure (Strength of Recommendation A). The combination of ACEIs and ARBs is indicated for reducing proteinuria that remains high despite treatment with a RAAS inhibitor, provided potassium levels do not exceed 5.5 mEq/L (Strength of Recommendation B). - When RAAS blockers are started or their dose is changed in patients with advanced CKD, kidney function and serum potassium levels should be monitored at least after 1-2 weeks. DIAGNOSIS AND TREATMENT OF DYSLIPIDEMIA - A complete evaluation of the lipid profile including total cholesterol, LDL-C, HDL-C, and triglycerides should be performed in any patient with CKD at baseline and at least annually (Strength of Recommendation B). - In patients with stage 4-5 CKD and LDL-C >or= 100 mg/dL, treatment to decrease levels to < 100 mg/dL should be considered because of their high CV risk. This reduction is recommended in secondary prevention and in primary prevention in diabetic patients. Lipid-lowering treatment is recommended in all other patients, although no evidence showing its benefits is available yet (Strength of Recommendation C). - In patients with stage 4-5 CKD and triglyceride levels >or= 500 mg/dL which are not corrected by treating the underlying cases, treatment with triglyceride-lowering drugs may be considered to reduce the risk of pancreatitis. However, treatment with fibrates should be used with caution, and these drugs should not be associated to statins due to the risk of rhabdomyolysis (Strength of Recommendation C). There is little experience on the efficacy and safety of omega-3 fatty acids for the treatment of hypertriglyceridemia in patients with grade 4-5 CRF, but they may be considered a possibly safer alternative to fibrates (Strength of Recommendation C). SMOKING - Smoking is a cardiovascular risk factor and a risk factor for progression of kidney disease in patients with CRF (Strength of Recommendation B). - Use of active measures to achieve smoking cessation is recommended in patients with CRF (Strength of Recommendation C). HOMOCYSTEINE - Hyperhomocysteinemia has been postulated as a cardiovascular risk factor in the general population and in kidney patients, but the available evidence is not consistent. - There is no evidence that vitamin therapy decreases cardiovascular risk in patients with CRF, and recommendation of routine vitamin measurement and start of vitamin therapy to reduce cardiovascular risk in these patients is therefore questionable (Strength of Recommendation B). LEFT VENTRICULAR HYPERTROPHY - Left ventricular hypertrophy (LVH) is a cardiovascular risk factor in patients with CRF (Strength of Recommendation B). - It is advisable to perform an echocardiogram at baseline and every 12-24 months and to consider treatments allowing for LVH regression (Strength of Recommendation C). The approach to LVH should be early and multifactorial because its reversibility is limited once established (Strength of Recommendation C). - RAAS blockade with ACEIs or ARBs partially reverts LVH in patients with CRF (Strength of Recommendation B). ANTI-PLATELET AGGREGATION - Because of the high cardiovascular risk in patients with CKD, anti-platelet aggregant therapy, especially low-dose aspirin, would be indicated in patients with type 2 diabetes as primary prevention, and in all patients with CKD as secondary prevention. There is however no evidence of the benefits of anti-platelet aggregant therapy in primary prevention in patients with CKD, particularly in stages 4-5; indication for treatment in this situation should therefore be individualised because of its greater risk of bleeding. - Adequate good blood pressure control should previously be achieved to minimise the risk of haemorrhagic stroke (Strength of Recommendation C).
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PMID:[Arterial hypertension and dyslipidemia in patients with chronic kidney disease (CKD). Anti-platelet aggregation. Goal oriented treatment]. 1901 37

Blood pressure (BP) control remains unsatisfactory worldwide. Better knowledge of BP management in clinical practice is needed to develop more effective improving strategies. Using a large Italian primary care database, we selected the subjects diagnosed with hypertension, and extracted the diagnosis of myocardial infarction, angina pectoris/coronary disease, stroke/transitory ischemic attack (TIA), heart failure, atrial fibrillation, peripheral arterial disease, diabetes mellitus, the serum total cholesterol, HDL cholesterol, triglycerides, creatinine, BP, electrocardiogram, weight, height and the prescription of cardiovascular (CV) drugs. Hypertension was recorded in 119.065 individuals (prevalence 19.3%), 19.134 (16%) had no ambulatory visit and 33.183 (27.8%) had no BP value recorded. Overall, 14.594 (21.9%) had at least one recorded diagnosis showing high CV risk. BP was controlled (mean of BP values <140/90 mm Hg) in 28.918 patients (16.690 women, 12 189 men and 40 gender not recorded), that is, 43.23% of the subjects with recorded BP. Among the non-controlled patients, 21.866 (57.8%) were non-high risk grade 1 (mean BP 142.5/84.5 mm Hg; s.d. 13.1/8.2) and 7.123 (18.8%) high-risk grade 1 hypertensives (mean BP 150/83 mm Hg; s.d. 6.2/7.2). Less than three drugs were prescribed in 29.919 (79.1%) of non-controlled patients. Low attendance rate, BP under-recording and suboptimal use of politherapy are major obstacles to hypertension control. Most uncontrolled individuals are low-CV risk, grade 1 hypertensive patients, for whom the personal benefit of adding another drug is modest. Aiming at the recommended BP target in uncontrolled grade 2-3 hypertensive/high-CV risk patients would probably require two additional drugs.
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PMID:Blood pressure control and drug therapy in patients with diagnosed hypertension: a survey in Italian general practice. 1924 92

It has been demonstrated that there is an association between serum lipoproteins and survival rate in patients with ischemic cardiomyopathy, as well as in patients with non-ischemic causes of heart failure. We tested the hypothesis of an association between serum lipoprotein levels and prognosis in a cohort of outpatients with heart failure, including Chagas' heart disease. The lipid profile of 833 outpatients with heart failure in functional classes III and IV of the New York Heart Association, with a mean age of 46.9 +/- 10.6 years, 655 (78.6%) men and 178 (21.4%) women, was studied from April 1991 to June 2003. The survival rate was estimated by the Kaplan-Meyer's method and the Cox proportional hazards models. Etiology of heart failure was ischemic cardiomyopathy in 171 (21%) patients, Chagas' heart disease in 144 (17%), hypertensive cardiomyopathy in 136 (16%), and other etiologies in 83 (10%). In 299 (36%) patients, heart failure was ascribed to idiopathic dilated cardiomyopathy. Variables significantly associated with mortality were age (hazard ratio, HR = 1.02; 95%CI = 1.01-1.03; P = 0.0074), male gender (HR = 1.77; 95%CI = 1.2-2.62; P = 0.004), idiopathic dilated cardiomyopathy (HR = 1.81; 95%CI = 1.16-2.82; P = 0.0085), serum triglycerides (HR = 0.97; 95%CI = 0.96-0.98; P < 0.0001), and HDL cholesterol (HR = 0.99; 95%CI = 0.99-1.0; P = 0.0280). Therefore, higher serum HDL cholesterol and higher serum triglycerides were associated with lower mortality in this cohort of outpatients with heart failure.
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PMID:Association of HDL cholesterol and triglycerides with mortality in patients with heart failure. 1937 90

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