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)

Cardiovascular effects of doping drugs are numerous, with different mechanisms: vasoconstriction of amphetamines, erythropoietin and cocaine; sodium water retention of anabolic steroids and corticosteroids; elevation in blood viscosity of erythropoietin, perflurocarbon emulsion, recombinant hemoglobin and anabolic steroids; sympathetic nervous system activation of amphetamines, beta 2 agonists and clenbuterol; lipids profile disorder of anabolic steroids. Physical activity consequences, particularly bradycardia and dehydration, are worsening. Thrombosis and arrythmogenic effects, with possibility of sudden death, are the severe immediate events. Hypertension and coronary diseases are medium-term effects; acute myocardial infarction is frequent. Heart failure can be secondary to cardiac muscle direct fibrosis, like with anabolic steroids. These cardiovascular effects are serious and it is necessary to early detect the doping drugs use in sporstmen; all prescribing physician should be aware of existing drugs and their clinical events.
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PMID:[Cardiovascular effects of doping]. 1255 90

Left ventricular (LV) volume and pressure overload occur frequently in chronic kidney disease (CKD). Anemia is a risk factor for left ventricular hypertrophy (LVH) and dilatation, heart failure, and death. Normalization of hemoglobin with erythropoietin may prevent LVH and dilatation in CKD, but in patients in later phases of their cardiac disease, this intervention is not of benefit. Increased vascular volume causes hypertension, which in turn causes LVH, cardiac failure, and ischemic heart disease (IHD). Manifestations of arteriosclerosis are associated with adverse cardiac outcomes, and angiotensin converting enzyme (ACE) inhibitors may improve LVH and markers of arteriosclerosis. Aortic stenosis in dialysis patients occurs infrequently, but may deteriorate rapidly. The hemodialysis milieu is the quintessential model of LV overload cardiomyopathy.
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PMID:Hemodynamic cardiovascular risk factors in chronic kidney disease: what are the effects of intervention? 1264 77

In recent years, rapid growth in the understanding of the pathophysiology of chronic heart failure has allowed for insights into many potential new therapeutic strategies. Yet until now, despite sound biological basis for efficacy and success in early-Phase studies, novel agents have not stood up to the scrutiny of late-Phase clinical trials. Indeed, remarkably negative results have been observed for vasopeptidase inhibitors, endothelin receptor antagonists and agents which block immune activation. However, efficacy data from other novel agents are still awaited, including the selective aldosterone receptor antagonist eplerenone, arginine vasopressin inhibitors, erythropoietin and hydroxy-methyl-glutaryl coenzyme A reductase inhibitors. Other classes of drugs which may enter clinical development include cardiac metabolic agents, matrix metalloproteinase inhibitors and advanced glycation end product antagonists. That the mortality and morbidity of patients with chronic heart failure remain unacceptably high makes the ongoing commitment to exploration of new drug therapies for the condition critical.
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PMID:New developments in the pharmacological treatment of chronic heart failure. 1272 Apr 87

Erythropoietin is a hypoxia-induced hormone that is essential for normal erythropoiesis. The production of recombinant human erythropoietin (rHuEpo) has revolutionized the treatment of anemia associated with chronic renal failure and chemotherapy, and has been used as prophylaxis to prevent anemia after surgery. The erythropoietin receptor is widely distributed in the cardiovascular system, including endothelial cells, smooth muscle cells and cardiomyocytes. Epo has potentially beneficial effects on the endothelium including anti-apoptotic, mitogenic and angiogenic activities. On the other hand, some reports suggest that rHuEpo may have pro-thrombotic or platelet-activating effects. Hypertension develops in 20-30% of renal patients treated with rHuEpo. Many patients with heart failure have anemia. Despite some potential adverse effects, early studies in heart failure patients with anemia suggest that rHuEpo therapy is safe and effective in reducing left ventricular hypertrophy, enhancing exercise performance and increasing ejection fraction. Further studies are warranted to define the role of rHuEpo in chronic heart failure and other cardiovascular settings.
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PMID:The cardiovascular effects of erythropoietin. 1449 55

Patients with end-stage renal disease (ESRD) have much higher rates of cardiovascular disease than the healthy population. Left ventricular hypertrophy (LVH), in particular, is common in this patient group. The impact of a decline in haemoglobin concentration on left ventricular mass index has been well documented. Partial correction of anaemia with recombinant human erythropoietin (epoetin) treatment has been recognized as a significant step forward in decreasing left ventricular mass and improving cardiovascular morbidity and mortality. However, LVH and cardiac failure in patients with ESRD comprise a complex condition, which is influenced by a number of factors in addition to anaemia. This article examines some of the pathophysiological aspects of LVH in patients with ESRD.
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PMID:Left ventricular hypertrophy: why does it happen? 1460 92

Several studies showed that anaemia is commonly observed in patients with Chronic Heart Failure (CHF) and is associated with worsened symptoms and survival. When anaemia in these patients is treated with erythropoietin (EPO), a significant improvement in cardiac function and symptoms was observed. Although it was originally believed that EPO specifically acted on haematopoietical cells, recent evidence demonstrated several non-haematopoietical effects. Ischaemia/reperfusion experiments in rat heart and brain showed large infarct reduction when treated with EPO. Other effects of EPO are related to its pro-angiogenic effects on endothelial cells, which could be of potential value in patients with ischaemic heart disease. These preclinical findings suggest that EPO may have potential effects in cardiovascular disease beyond correction of haemoglobin levels.
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PMID:Erythropoietin in cardiovascular diseases. 1498 16

Anemia can be the cause of heart failure, but also its consequence. The pathogenesis of anemia in chronic heart failure (CHF) has yet to be fully elucidated, but is likely to be complex. Epidemiologic studies suggest that kidney dysfunction (by reducing the erythropoietic response to anemia), inflammation (by inducing erythropoietin resistance), decreased body mass index, old age, female gender, and poor clinical status may be important factors in the development of anemia in CHF. Intestinal malabsorption, chronic aspirin use, and proteinuria predisposes to iron deficiency. Proinflammatory cytokines are likely to play a significant role in anemia in CHF by generating the "anemia of chronic illness" that is a hallmark of inflammatory conditions. Few studies have investigated the mechanisms of anemia in CHF. There is a need for such studies.
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PMID:Anemia in chronic heart failure: pathogenetic mechanisms. 1500 93

Anemia occurs frequently in chronic heart failure (CHF) patients and is associated with increased morbidity and mortality risk. Clinical trials with recombinant human erythropoietin in patients with chronic kidney disease and concomitant structural heart disease have demonstrated beneficial effects on ventricular remodeling but variable effects on clinical outcome. Preliminary clinical trials in patients with CHF demonstrate that erythropoietin therapy is well-tolerated and associated with short-term clinical benefits. The optimum target hemoglobin, erythropoietin dosing regimen, and role of iron supplementation in patients with CHF are not known. Darbepoetin alfa is a glycosylated derivative of erythropoietin with a prolonged half-life that may allow less frequent dosing in CHF populations. Additional studies are needed to determine the safety and efficacy of long-term erythropoietic therapy in CHF patients.
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PMID:Treatment of anemia in patients with chronic heart failure. 1500 95

In the last three decades, numerous reports have shown that patients with chronic pulmonary disease and with heart failure with hypoxemia cleared drugs at a lower rate than healthy volunteers. As a consequence decreased clearance, drug toxicity is frequent in these patients. The reduction in drug clearance is due to a decrease in activity of cytochrome P450 isoforms, partly associated to the hypoxemia. With in vivo animal models, acute moderate hypoxia (PaO2 of around 35-50 mm Hg) reduces the clearance of drugs biotransformed by CYP1A1, CYP1A2, CYP2B6, CYP2C9, CYP2C19 and CYP2E1, although hypoxia does not affect the clearance of drugs biotransformed by CYP3A6. Ex vivo and in vitro experiments demonstrate that hypoxia down-regulates CYP1A1, CYP1A2, CYP2B6, CYP2C9 and CYP2C19, decrease preceded by a reduction in activity. On the other hand, acute moderate hypoxia up-regulates CYP3A6. The changes in protein expression are preceded by modifications in the mRNA coding for the proteins. The effect of hypoxia on hepatic cytochrome P450 is carried out by serum mediators, e.g. interferon-gamma, interleukin-1beta, and interleukin-2 are responsible for the decrease in activity and in expression of cytochrome P450 isoforms, and erythropoietin accounts for the increase in CYP3A6. Probably several mechanisms underlie and contribute to the decrease in activity and down-regulation of cytochrome P450 isoforms by hypoxia, e.g. reducing potentiation factors, inducing repressor elements and activating negative regulatory elements. The up-regulation of CYP3A6 implies a PTK- and p42/44MAPK-dependent stabilization/activation, nuclear translocation of HIF-1 and AP-1, binding to CYP3A6 promoter, and transactivation of the gene to induce CYP3A6 expression.
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PMID:Effect of hypoxia on cytochrome P450 activity and expression. 1518 Apr 95

Heart failure is defined as the inability of the heart to pump blood at an amount sufficient to meet the metabolic needs of the body. In heart failure, the inability to meet the body's metabolic needs is based on hemodynamic derangement and suboptimal oxygen-carrying capacity of the blood itself. Current pharmacologic therapy attempts to improve survival and reduce symptomatology by optimizing hemodynamics to increase oxygen delivery, but does not address oxygen-carrying capacity. Unfortunately, there is a high prevalence of anemia in patients with heart failure, which compromises oxygen-carrying capacity, is an independent predictor of mortality, and may be caused in part by pharmacologic agents that confer morbidity and mortality benefits in this population. Recombinant human erythropoietin supplementation improves the functional capacity of the failing myocardium, reverses and antagonizes the detrimental remodeling induced by autoimmune activity, and may reduce mortality and morbidity among patients receiving maximal pharmacologic therapy for heart failure. However, limited clinical data prohibit widespread recommendations for its use in patients with heart failure.
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PMID:Anemia management in heart failure: a thick review of thin data. 1522 66


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