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)

When first introduced in 1981, angiotensin-converting enzyme (ACE) inhibitors were indicated only for treatment of refractory hypertension. Since then, they have been shown to reduce morbidity or mortality in congestive heart failure, myocardial infarction, diabetes mellitus, chronic renal insufficiency, and atherosclerotic cardiovascular disease. Pathologies underlying these conditions are, in part, attributable to the renin-angiotensin-aldosterone system. Angiotensin II contributes to endothelial dysfunction. altered renal hemodynamics, and vascular and cardiac hypertrophy. ACE inhibitors attenuate these effects. Clinical outcomes of ACE inhibition include decreases in myocardial infarction (fatal and nonfatal), reinfarction, angina, stroke, end-stage renal disease, and morbidity and mortality associated with heart failure. ACE inhibitors are generally well tolerated and have few contraindications. (Am Fam Physician 2002;66:473.)
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PMID:Using ACE inhibitors appropriately. 1248 85

Fatal and nonfatal complications (stroke, myocardial infarction, chronic heart failure, sudden coronary death, chronic renal insufficiency) were registered during long term follow-up of 529 patients with hypertensive disease and results were analyzed retrospectively. Duration of ambulatory treatment in two thirds of patients exceeded 15 years. There were 243 deaths in 1993-1999. Mean age of those who died was 75 years. Main fatal complications were strokes and myocardial infarctions. Their rates were similar. Strokes comprised one third of all deaths irrespective of age. There were no significant differences between rates of ischemic and hemorrhagic strokes. Among causes of death proportion of sudden death was the highest in patients younger than 60 years while that of chronic heart failure rose with age. There were no cases of chronic renal failure. Atherosclerotic lesions in coronary and cerebral vessels were found at autopsies irrespective of cause of death.
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PMID:[Fatal and nonfatal cardiovascular complications in patients with essential hypertension (hypertensive disease) during follow-up for many years]. 1249 62

Traditionally, the term complex hypertension has been applied to patients who have clinical evidence of target organ damage. However, this definition can be expanded to include many hypertensive patients who either present without manifest disease but harbor silent concomitant organ damage, or belong to a high-risk group and are likely to develop such damage. Thus, the number of patients who deserve special consideration as complex patients is considerable. Various factors may contribute toward classifying a patient as having complex hypertension. These include severe hypertension, concomitant conditions such as diabetes, chronic renal insufficiency, coronary artery disease, orcongestive heart failure; and high-risk populations such as the elderly and African Americans. Recent evidence demonstrates that aggressive goal blood pressure (BP)-lowering therapy is the key toward halting the progression of vascular disease. Although the choice of initial therapy seems less important than achieving goal BP, the drug selected must impart efficacy, organ protection, and tolerability. Combination therapy consisting of calcium-channel blockers and angiotensin-converting enzyme inhibitors seems to achieve these desirable effects. Several clinical trials have demonstrated these agents to have favorable effects on BP and organ protection even in complex hypertension, particularly when used in combination.
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PMID:Getting to goal in complex patients. 1262 19

Cardiovascular (CV) disease in uremic patients is a major concern to the nephrologist because it represents the main cause of morbidity and mortality in chronic renal failure patients, both predialysis and while on dialysis therapy. CV mortality is 3 to 20 times higher in dialysis patients than in the general population at similar age. Of note, a high prevalence of CV comorbidity is already present at start of maintenance dialysis, and is predictive of subsequent mortality on dialysis. CV disease progresses over years prior to the onset of ESRD, because risk factors develop from the early stage of chronic renal insufficiency. However, CV disease may be prevented or attenuated in patients who benefit from early, regular care of CV risk factors. Mechanisms of uremic cardiopathy, the major cause of mortality in uremic patients, are multifactorial and their effects are cumulative. Risk factors for left ventricular hypertrophy are hypertension, anemia, fluid overload and arteriosclosis, all of which are amendable by therapy. Risk factors for accelerated atherosclerosis, responsible for ischemic cardiopathy and myocardial infarction, are both common factors (e.g., hypertension, tobacco smoking and diabetes) and factors more specific for the uremic state (e.g., dyslipidemia, hyperhomocysteinemia and oxidative stress), all of which also are amendable by proper therapy. As a result, mixed hypertensive and ischemic cardiomyopathy develops, ultimately leading to cardiac failure, together with accidents resulting from valvular and arterial calcifications (favored by calcium-phosphate disorders), and from occlusion of coronary, cerebral and peripheral arteries. Cardioprotective therapy thus has become a cornerstone in the management of chronic renal failure patients, in conjunction with renoprotective therapy. Cardioprotective strategy involves optimal treatment of hypertension, anemia, fluid overload, dyslipidemia, hyperhomocysteinemia and calcium-phosphate disorders, and smoking cessation. To achieve a maximal efficacy, such treatment has to be initiated as early as possible in the course of renal failure. Because of its complexity, the integrated combined nephrotective and cardioprotective therapy requires early and sustained guidance by a nephrologist throughout the whole predialysis period.
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PMID:[Cardioprotection: an essential component for predialysis chronic renal failure treatment]. 1272 13

The objective of this study was to determine the incidence of and risk factors for poststernotomy mediastinitis (PSM) due to methicillin-resistant Staphylococcus aureus (MRSA) infection in a hospital in which MRSA was endemic. A retrospective case-control study of patients with PSM after cardiac surgery during January 1997 through July 2002 was conducted. The incidence of PSM was 1.01% (48 of 4746 patients), and 31 episodes (64.6%) were due to MRSA infection. We analyzed the findings for 48 case and 65 control patients. Univariate analysis revealed that the risk factors for PSM were previous hospitalization, resternotomy, chronic renal insufficiency, longer operation time, postoperative heart failure, postoperative renal failure, and reoperation for bleeding. Multivariate analysis revealed that the independent risk factors for PSM were previous hospitalization and reoperation for bleeding. Previous hospitalization was the only significant risk factor for PSM due to MRSA infection. The hospital mortality rate associated with PSM was 41.7%, and there was a higher mortality rate associated with PSM due to MRSA infection.
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PMID:Poststernotomy mediastinitis due to methicillin-resistant Staphylococcus aureus endemic in a hospital. 1294

In two men, aged 19 and 64, with chronic renal insufficiency and subacute symptoms of malaise and weakness of the leg muscles, broad QRS complexes were seen in the ECG. The younger patient developed an asystole and resuscitation was unsuccessful. His blood potassium level was found to be 8.3 mmol/l. The older patient recovered after administration of calcium gluconate. His blood potassium level was found to be 8.5 mmol/l. An 80-year-old woman who was taking various drugs because of heart failure also complained of muscle weakness. Her blood potassium level was 7.2 mmol/l and her ECG showed narrow complexes. She recovered without calcium gluconate after a change in medication. Hyperkalemia is a potentially life-threatening electrolyte disorder that may require immediate treatment. The changes in the ECG, especially widening of the QRS complexes, are the most important clues to the severity of the hyperkalemia. A treatment protocol based on ECG changes may reduce the mortality in these patients.
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PMID:[Life threatening hyperkalemia: the value of the electrocardiogram]. 1518 20

Vascular access for hemodialysis is crucial for appropriate course of the treatment as well as for good prognosis for patients with chronic renal insufficiency. In this paper we present the case of chronically hemodialysed patient who developed high-output cardiac failure after several days before creation of the upper arm brachio-cephalic arteriovenous fistula. Ultrasonographic imaging of the fistula showed an over-functioning anastomosis with flow reaching 41/min. The surgical correction of the anastomosis length to 4 mm and reduction of the cephalic vein diameter to 5 mm, significantly improved general status of the patient, simultaneously maintaining an accurate function of the fistula, with the maximal flow up to 850 ml/min.
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PMID:[Acute cardiac failure secondary to brachiocephalic arteriovenous fistula in patient on chronic haemodialysis]. 1577 35

We examined the efficacy of candesartan in reducing cardiovascular events in hypertensive patients with coexisting chronic kidney disease and cardiovascular diseases. This open-label, prospective study was conducted from 1999 to 2002, and 141 hypertensive subjects 60 to 75 years old with non-diabetic chronic renal insufficiency were enrolled. Before randomization of the patients, we examined their past medical history and found that 69 patients had been hospitalized due to myocardial infarction (MI) or stroke. Therefore, the patients were divided into 2 groups, one with previous histories of MI or stroke and the other with no previous history of Ml or stroke. The patients were randomized to receive either the angiotensin receptor blocker candesartan or conventional treatment. The mean duration of follow-up was 3.1 +/- 0.4 years. The primary outcome was a primary cardiovascular event (MI, stroke, or heart failure) verified by hospitalization. At the end of the study, in the patients with past history of cardiovascular diseases, blood pressure was reduced from 146.4 +/- 7.2/79.2 +/- 5.1 to 34.4 +/- 6.1/72.3 +/- 4.0 mmHg in the candesartan group and from 145.3 +/- 5.1/80.1 +/- 3.8 to 133.4 +/- 5.8/73.8 +/- 4.2 mmHg in the conventional treatment group. In the patients without past history of cardiovascular diseases, blood pressure was reduced from 143.2 +/- 4.3/78.3 +/- 4.8 to 133.8 +/- 5.3/ 73.1 +/- 3.8 mmHg in the candesartan group and from 143.9 +/- 6.8/78.1 +/- 4.2 to 132.6 +/- 5.4/74.5 +/- 4.4 mmHg in the conventional treatment group at the end of the study. There were no significant differences between the candesartan group and the conventional treatment group in the reduction of blood pressures. Among patients with a past history of cardiovascular disease, the serum creatinine concentration increased from 1.49 +/- 0.38 to 1.58 +/- 0.42 by candesartan treatment and from 1.50 +/- 0.32 to 1.89 +/- 0.37 by conventional treatment. On the other hand, in patients with no past history of cardiovascular disease, the serum creatinine concentration increased from 1.44 +/- 0.42 to 1.46 +/- 0.40 by candesartan treatment and from 1.46 +/- 0.44 to 1.51 +/- 0.38 by conventional treatment. Although, there was no significant difference in the incidence of cardiovascular events between the 2 groups with the candesartan-based and conventional-based antihypertensive treatment, in patients without cardiovascular events (12/36 vs. 7/34: these figures indicate events per total participated persons per 3 years; following figures are the same as this), treatment with candesartan reduced the incidence of cardiovascular events in the patients with past history of cardiovascular diseases (20/33 vs. 32/ 38). In particular, candesartan-based treatment reduced the incidence of congestive heart failure by 66.4% in these patients. In conclusion, this prospective, open-labeled randomized study suggests that 1) previous history of cardiovascular diseases is a major risk factor for cardiovascular events; and 2) candesartan is effective for reduction of cardiovascular events in hypertensive patients with coexisting chronic kidney disease and cardiovascular diseases, especially for prevention of congestive heart failure.
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PMID:An angiotensin receptor blocker reduces the risk of congestive heart failure in elderly hypertensive patients with renal insufficiency. 1615 5

Erythropoietin is a hypoxia-induced hormone that is a major regulator of normal erythropoiesis. Over the last decade, the production of recombinant human erythropoietin has revolutionized the treatment of anemia associated with chronic renal failure, and has led to a greater understanding of anemia pathophysiology and to the elucidation of the interactions of erythropoietin, iron, and erythropoiesis. Anemia has been shown to be independently associated with increased mortality and disease progression. Potential survival benefits associated with correction of anemia have expanded considerably the indications of erythropoietin use in various patient populations and are leading to consideration of earlier, more aggressive treatment of mild to moderate anemia. The results of such treatment are promising in a variety of new clinical settings, including anemia associated with congestive heart failure. Furthermore, the erythropoietin receptor is widely distributed in the cardiovascular system, including endothelial cells, smooth muscle cells and cardiomyocytes and preclinical studies have established erythropoietin to be a pleiotropic cytokine with anti-apoptotic activity and tissue-protective actions in the cardiovascular system, beyond correction of hemoglobin levels. Despite some potential adverse effects, such as hypertension, and the occurrence of erythropoietin resistance, early studies in heart failure patients with anemia suggest that erythropoietin therapy is safe and effective in reducing left ventricular hypertrophy, enhancing exercise performance and increasing ejection fraction. Anemia is found in about one-third of all cases of congestive heart failure (CHF). The most likely common cause is chronic renal insufficiency, which is present in about half of all CHF cases. However, anemia can occur in CHF without renal insufficiency and is likely to be due to excessive cytokine production. The anemia itself can worsen cardiac function, both because it causes cardiac stress through tachycardia and increased stroke volume, and because it can cause a reduced renal blood flow and fluid retention, adding further stress to the heart. Long-standing anemia of any cause can cause left ventricular hypertrophy, which can lead to cardiac cell death through apoptosis and worsen CHF. Therefore, a vicious circle, cardio-renal anemia syndrome, is set up wherein CHF causes anemia, and the anemia causes more CHF and both damage the kidneys worsening the anemia and the CHF further and increasing mortality. There is now evidence that early correction of the CHF anemia with subcutaneous erythropoietin and intravenous iron improves shortness of breath and fatigue, cardiac function, renal function and exercise capacity, reducing the need for hospitalization and improving quality of life. In the present review we discuss the data on current clinical use of erythropoietin in cardiovascular disease, with the main focus on the treatment of congestive heart failure, and summarize the advances and progress made in the understanding of the hematopoietic and pleiotropic effects of erythropoietin in the cardiovascular system.
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PMID:Erythropoietin in heart failure and other cardiovascular diseases: hematopoietic and pleiotropic effects. 1624 29

Like the introduction of digitalis more than 200 years ago, novel medical therapies today have the potential to significantly alter the course of heart failure (HF) and save thousands of lives. This review outlines new directions in HF medical management beyond the foundation of neurohormonal blockade. Furthermore, the role of novel risk factors in HF such as chronic renal insufficiency, anemia, and sleep apnea present tantalizing therapeutic targets to extend the morbidity and mortality benefits of current therapies. The course of time will tell which of these risk factors and therapies can hold promise, given the recent litany of negative trials in the HF arena. Advancements in molecular and genetic techniques have allowed us to begin to consider patient specific therapies and lay the groundwork for even further improvements in treatment of symptomatic HF. Finally, advances in telemedicine and device technology will allow the clinician to remotely monitor useful clinical parameters such as heart rate variability and pulmonary filling pressures to make more informed clinical decision-making and improve outcomes.
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PMID:New directions in the medical management of heart failure. 1642 41


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