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

Dyslipidemia is a causative, yet modifiable risk factors for the development of adverse outcomes secondary to coronary artery disease. Recent trials have focused on the level of low-density lipoprotein cholesterol (LDL-C) necessary to achieve maximum reduction in clinical events. Data also exist demonstrating that intensive lowering of LDL-C in patients with unstable angina reduces the incidence of adverse clinical events. The statins appear to be fundamental therapy in patients with established coronary disease as well as a mainstay for those with early evidence of atherosclerosis. The angiotensin-converting enzyme (ACE) inhibitors have demonstrated a reduction in ischemic events in patients with heart failure. Recent trials of ACE inhibitors in patients with vascular disease who do not have the traditional indications for ACE inhibition have shown a reversal of endothelial dysfunction and a reduction in adverse clinical endpoints. A role for the use of calcium antagonists in patients with atherosclerosis is less well established, despite the evidence of excellent results in patients with symptomatic coronary disease. A recent clinical trial, using a third-generation dihydropyridine calcium antagonist with novel mechanisms, found promising results with regard to its effects on atherosclerosis
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PMID:Effect of lipid-lowering agents, angiotensin-converting enzyme inhibitors, and calcium antagonists on coronary disease risk. 1170 18

Previous investigations of adults with the Prader-Willi syndrome (PWS) are few and have demonstrated severe obesity with increased morbidity and mortality in cardiovascular disease. It is, thus, important to identify risk factors and, if possible, start prevention. We studied the clinical, genetic, endocrinological, and metabolic findings in 19 adult PWS patients (10 men; mean age, 25 yr). The PWS karyotype was demonstrated in 13 patients. The mean body mass index was 35.6 kg/m(2), and total body fat was increased. Two thirds were biochemically hypogonadal. Fifty percent had severe GH deficiency (GHD). Four were hypertensive. One patient had heart failure and diabetes. Impaired glucose tolerance was seen in 4 patients, elevated homeostasis model assessment index in 9 patients, and modest dyslipidemia in 7. IGF-binding protein-1 correlated negatively with insulin levels. Four patients had osteoporosis, and 11 had osteopenia. There was no significant difference between the group with the PWS karyotype and the group without the karyotype in age, body mass index, waist/hip ratio, percent body fat, insulin values, homeostasis model assessment index, or lipid profile, except for lipoprotein(a), which was significantly higher in the group with the negative karyotype. IGF-I and lumbar spine bone mineral density were significantly lower in patients with genetic alteration, indicating a more severe GHD. The risk factors found in this study predicting cardiovascular disease are interpreted as secondary to GHD. These findings point to the importance of evaluating treatment of GHD in adults with PWS.
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PMID:Metabolic profile and body composition in adults with Prader-Willi syndrome and severe obesity. 1216 80

Age is the main clinical determinant of large artery stiffness. Central arteries stiffen progressively with age, whereas peripheral muscular arteries change little with age. A number of clinical studies have analyzed the effects of age on aortic stiffness. Increase of central artery stiffness with age is responsible for earlier wave reflections and changes in pressure wave contours. The stiffening of aorta and other central arteries is a potential risk factor for increased cardiovascular morbidity and mortality. Arterial stiffening with aging is accompanied by an elevation in systolic blood pressure (BP) and pulse pressure (PP). Although arterial stiffening with age is a common situation, it has now been confirmed that older subjects with increased arterial stiffness and elevated PP have higher cardiovascular morbidity and mortality. Increase in aortic stiffness with age occurs gradually and continuously, similarly for men and women. Cross-sectional studies have shown that aortic and carotid stiffness (evaluated by the pulse wave velocity) increase with age by approximately 10% to 15% during a period of 10 years. Women always have 5% to 10% lower stiffness than men of the same age. Although large artery stiffness increases with age independently of the presence of cardiovascular risk factors or other associated conditions, the extent of this increase may depend on several environmental or genetic factors. Hypertension may increase arterial stiffness, especially in older subjects. Among other cardiovascular risk factors, diabetes type 1 and 2 accelerates arterial stiffness, whereas the role of dyslipidemia and tobacco smoking is unclear. Arterial stiffness is also present in several cardiovascular and renal diseases. Patients with heart failure, end stage renal disease, and those with atherosclerotic lesions often develop central artery stiffness. Decreased carotid distensibility, increased arterial thickness, and presence of calcifications and plaques often coexist in the same subject. However, relationships between these three alterations of the arterial wall remain to be explored.
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PMID:Influence of age, risk factors, and cardiovascular and renal disease on arterial stiffness: clinical applications. 1246 Jul 8

Despite of dramatic improvement in diagnostic procedures and treatment of diabetic patients, cardio-vascular complications are still the most frequent causes of death in these patients. Diabetes influences myocardial and coronary vessels function by coexisting macroangiopathy, microangiopathy, metabolic disturbances and autonomic nervous system neuropathy. All these factors result in diastolic and systolic dysfunction of the heart. Cardiomyopathy, congestive heart failure and serious arrhythmias are the end stage of diabetic complications. Macroangiopathy demonstrates accelerated atherosclerosis (involving coronary arteries), which consequences can be observed in 1 type diabetes patients at around the age of 30. Causes of increased risk of macroangiopathy in type 1 diabetic patients are not clear. There are not many clinical, prospective trials which can allow for etiology determination of the increased incidence of atherosclerosis and mortality due to coronary artery disease in this population. Adding to traditional risk factors of atherosclerosis like genetic factors, hypertension, dyslipidemia, obesity, smoking and improper diet, other important risk factors are observed in diabetic patients. Only few clinical trials suggest that hyperglycemia, glycation, glycoxidation of proteins, lipoproteins, changes in their composition, microalbuminuria, coagulation, fibrinolytic disturbances are additional risk factors of endothelium dysfunction and atherosclerosis. Prevention and treatment of accelerated coronary artery disease and it's consequences are more complicated in the diabetic population than in others. Some of the clinical trials suggest that even improved glycemic control does not eliminate the elevated risk of coronary artery disease in type 1 diabetic patients.
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PMID:[Myocardial and coronary vessel dysfunction in diabetes I patients]. 1251 40

Patients with end-stage renal disease (ESRD) are at extreme cardiovascular risk. At least half of all patients starting dialysis therapy have overt cardiovascular disease (CVD). In addition, recent studies suggest annual incidence rates for new-onset cardiac failure, peripheral vascular disease, ischemic heart disease (IHD), and stroke of approximately 7%, 7%, 5%, and 1%, respectively. High-level exposure to traditional risk factors, such as smoking and dyslipidemia, hemodynamic overload factors, such as anemia and hypertension, and a myriad of metabolic factors related to uremia are all likely to play a role. There has been explosive growth in observational studies and a heartening, if less dramatic, increase in risk factor intervention trials, suggesting that risk factor modification can lead to meaningful benefit.
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PMID:Clinical epidemiology of cardiac disease in dialysis patients: left ventricular hypertrophy, ischemic heart disease, and cardiac failure. 1264 74

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

Type 2 diabetes mellitus substantially increases the lifetime risk of both developing and dying from heart failure. While this appears to be explained in part by the well-known association of diabetes with hypertension, dyslipidemia, and coronary atherosclerosis, additional pathophysiologic mechanisms linking type 2 diabetes and heart failure have recently been suggested. These include the potentially adverse effects of hyperglycemia on endothelial function and redox state, effects of excess circulating glucose and fatty acids on cardiomyocyte ultrastructure, intracellular signaling and gene expression, and the possibility that diabetes may impair recruitment of the myocardial insulin-responsive glucose transport system in response to ischemia. Because many of these putative pathophysiologic mechanisms should be amenable to normalization of the diabetic metabolic milieu, strategies designed to more carefully control circulating levels of glucose and fatty acids might conceivably delay or prevent the development of heart failure.
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PMID:Diabetes mellitus and heart failure. 1282 71

We review the macroscopic and microscopic anatomy of myocardial disease associated with heart failure (HF) and sudden cardiac death (SCD) and focus on the prevention of SCD in light of its structural pathways. Compared to patients without SCD, patients with SCD exhibit 5- to 6-fold increases in the risks of ventricular arrhythmias and SCD. Epidemiologically, left ventricular hypertrophy by ECG or echocardiography acts as a potent dose-dependent SCD predictor. Dyslipidemia, a coronary disease risk factor, independently predicts echocardiographic hypertrophy. In adult SCD autopsy studies, increases in heart weight and severe coronary disease are constant findings, whereas rates of acute coronary thrombi vary remarkably. The microscopic myocardial anatomy of SCD is incompletely defined but may include prevalent changes of advanced myocardial disease, including cardiomyocyte hypertrophy, cardiomyocyte apoptosis, fibroblast hyperplasia, diffuse and focal matrix protein accumulation, and recruitment of inflammatory cells. Hypertrophied cardiomyocytes express "fetospecific" genetic programs that can account for acquired long QT physiology with risk for polymorphic ventricular arrhythmias. Structural heart disease associated with HF and high SCD risk is causally related to an up-regulation of the adrenergic renin-angiotensin-aldosterone pathway. In outcome trials, suppression of this pathway with combinations of beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin-II receptor blockers, and mineralocorticoid receptor blockers have achieved substantial total mortality and SCD reductions. Contrarily, trials with ion channel-active agents that are not known to reduce structural heart disease have failed to reduce these risks. Device therapy effectively prevents SCD, but whether biventricular pacing-induced remodeling decreases left ventricular mass remains uncertain.
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PMID:Structural pathways and prevention of heart failure and sudden death. 1293 Feb 59

The aging of the population of the United States (US) will bring with it higher numbers of patients with coronary heart disease and heart failure (HF). Because HF already imposes severe economic and medical burdens on our health care system, it is imperative to optimize primary and secondary prevention of cardiovascular (CV) disease. In most cases, HF develops as a result of either long-standing hypertension or a myocardial infarction (MI). Other than cardiac death, HF represents the last stage in the progression of CV disease, which begins with CV risk factors such as hypertension, dyslipidemia, obesity, and smoking. These risk factors lead to the development of left ventricular (LV) hypertrophy or an MI (or both), which lead to LV dysfunction and, finally, to HF. The prognosis of HF is poor, the 5-year survival rate being approximately 25%. Heart failure may be due to either LV systolic or diastolic dysfunction, the latter having a normal ejection fraction. Because CV disease is progressive, interventions are possible at all stages along the CV continuum. Beta-blockers (betaB) are recommended agents at several stages of CV disease. Large-scale trials have shown that betaB significantly reduce risks for morbidity and mortality in patients with HF. Ongoing studies should help to clarify further the optimal cardioprotective therapies in patients with HF.
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PMID:From hypertension to heart failure: update on the management of systolic and diastolic dysfunction. 1451 98

Patients with diabetes are at high risk for cardiovascular (CV) events and heart failure. Approximately 2-3 million diabetics in the U.S. have had a history of prior CV events. The prevalence of diabetes in patients with heart failure ranges from 24% reported in clinical trials to 47% among hospitalized patients, and an estimated 1-2 million persons in the U.S. have diabetes and heart failure. Diabetes substantially increases the risk of mortality after acute coronary syndromes and also increases the risk of hospitalizations and mortality in patients with heart failure. It is now recognized that activation of multiple neurohormonal systems is central in the pathophysiology of diabetes, CV events, and heart failure. Pharmacologic intervention in these systems (eg, angiotensin-converting enzyme (ACE) inhibition, aldosterone-receptor antagonism, and beta-blockade) has been shown to decrease morbidity and mortality in diabetics with prior CV events and/or heart failure. Despite this awareness, ACE inhibitors, aldosterone antagonists, and beta-blockers are underutilized, and deaths and hospitalizations caused by CV events and heart failure in diabetic patients have steadily increased. Concerns about an increased incidence of hypoglycemia, worsening dyslipidemia, and decreased insulin sensitivity resulting from the use of beta-blockers may be preventing physicians from prescribing these agents for diabetic patients. Beta-blockade in conjunction with ACE inhibition should be standard therapy for all diabetic patients. Optimal glycemic control therapy for patients with heart failure has not been well-defined, and there is an urgent need for randomized clinical trials to determine optimal treatment.
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PMID:The management of the diabetic patient with prior cardiovascular events. 1466 2


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