Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic Syndrome X is a clinical entity which comprises the following factors: diabetes mellitus, arterial hypertension, high levels of triglyceride and/or low levels of HDL cholesterol, central obesity and microalbuminuria (by WHO criteria). The first goal of this study was to determine the frequency of the Metabolic Syndrome X (MSX) in patients with acute myocardial infarction compared with the general population. The second goal of the study was to examine the frequency of heart failure and reinfarction rate in the patients with myocardial infarction, with and without MSX. Furthermore, the relationship between gender and MSX was analyzed. A total of 101 patients with acute myocardial infarction took part in randomized trial (32 women and 69 men). MSX and all of its components were diagnosed according to WHO criteria. To determine statistical significance of our results, we used chi2 test and t-test for independent samples. From 101 patient 48 had MSX (47.52%), while in the general population incidence of MSX is 3-4%. The reinfarction and the heart failure rate were significantly higher in the group of patients with MSX (p = 0.0067 and p = 0.0217, respectively). To conclude, the results of the present study confirm that MSX is a high risk factor for myocardial infarction and its complications.
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PMID:Metabolic syndrome X--high risk factor for acute myocardial infarction and its complications. 1213 4

Ramipril is safe and effective in the treatment of hypertension and heart failure, but this is not reviewed here. Ramipril is a lipophilic angiotensin-converting enzyme inhibitor suitable for once-daily administration. In addition to decreasing angiotensin II and increasing bradykinin levels, ramipril increases the levels of vasodilatory renal medullary neutral lipids and inhibits platelet-derived growth factor-induced proliferation of glomerulus cells. Ramipril also decreases transforming growth factor-beta in the kidney. Changes in kidney structure and proteinuria are characteristics of the streptozotocin (STZ) rat model of diabetes, and these are prevented by ramipril. In STZ diabetes, doses of ramipril that have no effect on blood pressure reverse vascular hypertrophy. In animal models of kidney failure (subtotal nephrectomy, stroke-prone spontaneously hypertensive rats), ramipril is renoprotective and some of this renoprotective effect is independent of blood pressure lowering. In humans, clinical doses of ramipril probably do not modify glucose metabolism but do reduce the levels of LDL- and HDL-cholesterol. In clinical trials of renal effects, ramipril has been shown to increase cortical nephron flow in hypertension and to reduce proteinuria in patients with and without diabetes and/or hypertension. Some of the smaller clinical trials showed beneficial effects on kidney function with low doses of ramipril that do not lower blood pressure. A large clinical trial in nondiabetic proteinuria, the Ramipril Efficacy in Nephropathy (REIN) trial, has shown that ramipril 1.25 mg/day, which does not lower blood pressure, arrested the decline in glomerular filtration rate and prolonged the time to end-stage renal failure. In diabetic patients who have had a previous cardiovascular event or having one other cardiovascular risk factor, the MICRO-HOPE clinical trial showed that ramipril lowers the combined risk of myocardial infarction, stroke and cardiovascular death by 25%. In conclusion, ramipril has proven beneficial effects in kidney disease alone or in association with diabetes and in diabetes without kidney disease, and is the pril for diabetes and kidney disease. (c) 2001 Prous Science. All rights reserved.
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PMID:Is Ramipril the pril for diabetes and kidney disease? 1276 20

The scavenger receptor class B type I (SR-BI) was the first molecularly well-defined cell-surface HDL receptor to be described. SR-BI mediates selective HDL cholesterol uptake by formation of a productive lipoprotein/receptor complex, which requires specific structural domains and conformation states of apolipoprotein A-I present in HDL particles. SR-BI is abundantly expressed in several tissues, including the liver, where its expression is regulated by various mechanisms, including the transcriptional activity of nuclear receptors. The importance of SR-BI in overall HDL cholesterol metabolism and its antiatherogenic activity in vivo has been definitively established by SR-BI gene manipulation in mice. Remarkably, SR-BI/apolipoprotein E double-knockout mice develop complex coronary artery disease, myocardial infarction, and heart failure. Additional studies should help to define the importance of SR-BI in human health and disease.
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PMID:Influence of the HDL receptor SR-BI on lipoprotein metabolism and atherosclerosis. 1292 50

Familial HDL deficiency (FHD) is a rare autosomal dominant lipoprotein disorder. We describe a novel genetic variant of the apolipoprotein A-I (apoA-I) gene resulting in FHD. The proband is a 51-year-old woman who was hospitalized due to severe heart failure. Her plasma HDL-cholesterol (C) and apoA-I concentrations were 0.08mmol/l and 1mg/dl, respectively. She exhibited corneal opacities and planar xanthomas on eyelids and elbows. Coronary angiography demonstrated extensive obstructions in two major vessels. Genomic DNA sequencing of the patient's apoA-I gene revealed a homozygosity for a GC deletion between 5 GC repeats in exon 4, creating a frameshift and a stop codon at residue 178. We designated this mutation as apoA-I Shinbashi. The proband's father, son, and daughter were found to be heterozygous for this mutation and their HDL-C and apoA-I levels were about half of normal levels, demonstrating a gene dosage effect. The father underwent coronary bypass surgery at age of 70 years. Lecithin-cholesterol acyltransferase (LCAT) activity was decreased by 63% in the homozygote and 31% in heterozygotes, respectively. This new case of apoA-I deficiency, apoA-I Shinbashi, is the first case involving a single gene defect of the apoA-I gene to develop all the characteristics for apoA-I deficiency, including premature coronary heart disease.
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PMID:A novel two nucleotide deletion in the apolipoprotein A-I gene, apoA-I Shinbashi, associated with high density lipoprotein deficiency, corneal opacities, planar xanthomas, and premature coronary artery disease. 1470 55

Rosuvastatin is a new statin with a great number of pharmacological benefits related to the capacity of modifying favorably the lipid profile but also for the selective binding with 3-hydroxy-3-methylglutaryl coenzyme A reductase, relative hydrophilic properties and selectivity for hepatic cells. Rosuvastatin demonstrated to be more efficacious in reducing LDL cholesterol levels than other statins and to be capable of increasing HDL cholesterol levels. It is well tolerated in a wide range of dosages maintaining its effectiveness. Many trials are ongoing with the aim to evaluate not only the efficacy of rosuvastatin in terms of surrogate endpoints but also in terms of cardiovascular morbidity and mortality. The usefulness of rosuvastatin will be evaluated also in selective patient populations affected by advanced renal disease or chronic heart failure. Two relevant research projects have been started recently, the GALAXY Programme, designed for evaluating the efficacy of rosuvastatin in atherosclerosis and ischemic heart disease and the GISSI-HF trial planned with the aim of testing the efficacy of this statin on morbidity and mortality in chronic heart failure and investigating the pharmacological effects on the pathophysiological mechanisms of heart failure.
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PMID:[Ongoing trials and future prospects]. 1498 47

Beyond regulation of sexual function, male steroids play an important role in many physiological homeostasis systems, including the cardiovascular system. Via a specific androgen receptor, testosterone mediates cardiomyocyte trophicity both in physiological situations and in hypertrophy-related cardiac diseases. Androgens also regulate pathological levels of inflammatory cytokines such as Il-6 or TNF in advanced heart failure. They also mediate vascular resistance since coronary vasodilatation has been proven both in vitro and in vivo. Reduced free testosterone serum levels (age-mediated or premature coronary artery disease) promote a pro-atherogenic lipid profile expressed as lower serum HDL-cholesterol and up-regulation of triglyceride levels. This observation has relevant clinical implications for the evaluation and treatment of coronary artery disease. As most of normal and diseased cardiovascular system functions are influenced by androgens, further evaluation of their physiological implications should be undertaken as well as large-scale rigorous studies of the therapeutic implications in two disabling diseases, coronary heart disease and heart failure.
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PMID:[The heart and androgens]. 1524 76

Dietary n-3 polyunsaturated fatty acids (PUFA) derived from fatty fish or fish oil may reduce the incidence of lethal myocardial infarction and sudden cardiac death. This might be due to a prevention of fatal cardiac arrhythmias. So far, however, only few clinical data are available being adequate to define indications for an antiarrhythmic treatment with n-3 PUFA. In a randomized, double-blind, placebo-controlled study 65 patients with cardiac arrhythmias without coronary heart disease or heart failure were subdivided into 2 groups. One group (n = 33) was supplemented with encapsulated fish oil (3g/day, equivalent to 1g/day of n-3 PUFA) over 6 months. The other group (n = 32) was given 3g/day of olive oil as placebo. In the fish oil group a decrease of serum triglycerides, total cholesterol, LDL cholesterol, plasma free fatty acids and thromboxane B2 as well as an increase of HDL cholesterol were observed. Moreover, a reduced incidence of atrial and ventricular premature complexes, couplets and triplets were documented. Accordingly, higher grades of Lown's classification switched to lower grades at the end of the dietary period. No changes were seen in the placebo group. The data indicate an antiarrhythmic action of n-3 PUFA under conditions of clinical practice which might help to explain the reduced incidence of fatal myocardial infarction and sudden cardiac death in cohorts on a fish-rich diet or supplemented with n-3 PUFA. Further studies elucidating the possible link between the reduced incidence of cardiac arrhythmias and sudden cardiac death by dietary intake of n-3 PUFA are warranted.
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PMID:Can n-3 PUFA reduce cardiac arrhythmias? Results of a clinical trial. 1525 84

Beyond sexual function regulation, male steroids are operative in several physiologic homeostastic systems including the cardiovascular system. By ways of specific androgen receptors,testosterone can mediate cardiomyocyte trophycity, in physiologic states as in diseases involving cardiac hypertrophy. Androgenic hormones also regulate pathologic levels of inflammatory cytokines as 11-6 or TNF, in advanced heart failure. They also mediate vascular resistance with, in vitro and in vivo, proved coronary vasodilatation. Reduced free testosterone serum levels (age-mediated or in premature coronary artery disease patients (CAD) promote a pro-atherogenic lipid profile expressed as HDL-cholesterol decrease and up-regulation of triglycerids levels). The latter observation has relevant clinical significance for evaluation and treatment of CAD disease. As most of normal and diseased cardiovascular system functions are influenced by androgens, we can foresee an increasing interest for further evaluation of their physiologic implications as well as for large and rigourous studies of their therapeutic potential in two leading disabling pathologies, CAD and heart failure.
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PMID:[Heart and androgens]. 1549 57

Hypercholesterolemia is a risk factor for development of coronary artery disease (CAD), however, several reports have suggested that low serum cholesterol is associated with a worse prognosis in patients with congestive heart failure (CHF). The objective of this study was to determine the prognostic value of cholesterol for CHF. The study subjects consisted of 133 consecutive patients hospitalized in our institution for progressive heart failure from April 2000 to March 2003. Thirty-two percent of the patients had CAD. After improvement of congestive heart failure and discharge from the hospital, lipid profiles, including serum total cholesterol (TC), triglycerides, and high and low density lipoprotein cholesterol (HDL, LDL, respectively), were obtained. During the follow-up period (2.3 +/- 0.9 years), 21 patients died. There was a significant difference between survivors and nonsurvivors in HDL (53 +/- 15, 43 +/- 15 mg/dL, P = 0.01), but no differences were observed in other variables. In patients with CAD, survivors had significantly lower TC concentrations (179 +/- 30 versus 246 +/- 55 mg/dL, P = 0.004), although in patients without CAD, survivors had significantly higher TC concentrations (203 +/- 37 versus 170 +/- 40 mg/dL, P = 0.02). Multivariate analysis showed high TC predicted a worse outcome in patients with CAD (odds ratio (OR) = 1.052, 95% confidence interval (CI) 1.002-1.104, P = 0.04), but a better outcome in patients without CAD (OR = 0.972, 95% CI 0.948-0.997, P = 0.03), independent of age, gender, medication, and complications. Thus, low serum cholesterol is associated with an improved outcome in patients with CAD, while it predicts a worse outcome in patients without CAD.
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PMID:The association between cholesterol and mortality in heart failure. Comparison between patients with and without coronary artery disease. 1615 53

Epidemiologic data from the Framingham Study provide insights into the population burden of heart failure (CHF), its prognosis and modifiable risk factors that promote it. In the general population CHF is chiefly the end stage of hypertensive, coronary and valvular cardiovascular disease. It is a major and growing problem in most affluent countries because of aging populations of increased size, and the prolongation of the lives of cardiac patients by modern therapy. Once clinically manifest, CHF, despite recent innovations in therapy, carries an unacceptably high mortality rate. In the Framingham Study, median survival is only 1.7 y for men and 3.2 y for women, with only 25% of men and 38% of women surviving 5 y. This is a mortality rate 4-8 times that of the general population of the same age. This poor outlook is observed for all etiologies of CHF and sudden death is a prominent feature of the mortality. Based on population attributable risks, hypertension has the greatest impact, accounting for 39% of CHF events in men and 59% in women. Despite its much lower prevalence in the population (3-10%) myocardial infarction also has a high attributable risk in men (34%) and women (13%). Valvular heart disease only accounted for 7-8% of CHF. Hypertension increased the age and risk factor adjusted hazard of CHF 2-fold in men and 3-fold in women, with a greater impact of the systolic than diastolic blood pressure. Diabetes increased CHF risk 2-8 fold with risk ratios twice as large in women as men. About 19% of CHF cases have diabetes. It accounted for 6-12% of the CHF in the Framingham Study cohort. Dyslipidemia characterized by a high total/HDL cholesterol ratio, but not the total cholesterol alone was a risk factor for CHF. An enlarged heart on X-Ray, ECG-LVH, a reduced vital capacity and rapid heart rate usually signified deteriorating cardiac function. CHF risk associated with ECG-LVH was independent of X-Ray cardiomegaly but risk was further augmented when both coexist. Echocardiographic left ventricular hypertrophy signifies a high risk of CHF proportional to the degree of increase in left ventricular mass without a critical value that delineates compensatory from pathological hypertrophy. Risk of CHF in persons predisposed by hypertension, diabetes or cardiac conditions varies over a 10-fold range depending on the aforementioned modifiable risk factors and indicators of deteriorating left ventricular function. Using multivariate risk formulations it is possible to identify 20% of the population from which 70% of the CHF will evolve. Those in the upper quintile of multivariate risk are good candidates for echocardiographic testing to delineate those needing aggressive preventive measures to delay the onset of CHF. Therapy of CHF must begin with treatment of presymptomatic left ventricular dysfunction to reverse the dysfunctional maladaptive changes.
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PMID:Incidence and epidemiology of heart failure. 1622 42


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