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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Scientific investigations indicate similarities in the pathophysiology of heart insufficiency and that of physical inactivity: similar changes in peripheral hemodynamics (increased peripheral vascular resistance, worsening of oxygen utilization during exercise), in autonomic control (activation of neurohumoral compensatory mechanisms, e.g. the renin-angiotensin system, overactivation of the sympathicus, reduction of vagal tonus, reduced pressosensitivity), in functional activity (reduced exercise tolerance and reduced maximum oxygen uptake), in skeletal muscle (decrease in mass, changes in structure), and in the psychological state (reduction in activity and feeling of well-being). In several, although small-scale studies it could be shown that patients with advanced left ventricular failure were able to take part in training programs without experiencing any ill effects, and that there was a positive shift in the usual typical effects of physical training, such as increase of heart rate, change in respiratory frequency, and maximum oxygen uptake. It could be shown that exercise therapy can result in a shift in the balance between the sympathetic and the parasympathetic tonus in the low- and high-frequency maxima of the R-R interval variability. The pre-training general predominance of the sympathetic tonus over the vagal tonus was changed dramatically by the training, leading to a predominance of the vagal tonus. Recent controlled studies with a randomized and controlled cross-over design and the application of a training program which was carried out regularly and independently have confirmed the positive effect of aerobic fitness training in cases of heart disease. At the end of the exercise phase, the patients experienced a significant improvement of the symptoms of left ventricular failure and of their capacity for exercise; furthermore, the training altered parts of the neurohumoral activation, which count as the main factors in the progression and death rate of patients with chronic cardiac disease.
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PMID:[Literature review of the latest research results concerning the positive effect of exercise therapy in chronic heart insufficiency]. 1262 77

In managing atrial fibrillation (AF), the main therapeutic strategies include rate control, termination of the arrhythmia, and the prevention of recurrences and thromboembolic events. Safety and efficacy considerations are important in optimizing the choice of an antiarrhythmic drug for the treatment of AF. Recently approved antiarrhythmics, such as dofetilide, and promising investigational drugs, such as azimilide and dronedarone, may change the treatment landscape for AF. For medical conversion of recent-onset AF, class IC antiarrhythmic drugs, administered as an oral bolus, have been demonstrated to be the most efficacious pharmacologic conversion agents. Intravenous ibutilide and oral dofetilide both have efficacies superior to placebo in controlled trials for converting persistent AF. Comparative trials in paroxysmal AF have demonstrated that flecainide, propafenone, quinidine, and sotalol are equally effective in preventing recurrences of AF. Amiodarone has been demonstrated to be more efficacious than propafenone or sotalol in the Canadian Trial of Atrial Fibrillation. In persistent AF, twice-daily dofetilide has been shown to be as or more effective than low-dose sotalol given twice daily for the maintenance of sinus rhythm in patients with AF. Trials have demonstrated that subjective adverse effects are less frequent with class IC drugs, sotalol, and dofetilide compared with such drugs as quinidine. In patients without structural heart disease, flecainide, propafenone, and D,L-sotalol are the initial drugs of choice, given their reasonable efficacy, low incidence of subjective side effects, and lack of significant end-organ toxicity. Treating AF in patients with left ventricular dysfunction can be difficult because of associated electrophysiologic derangements, potential proarrhythmic concerns, and negative inotropic effects of antiarrhythmics. Some data exist suggesting that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can prevent AF either by preventing atrial dilation and stretch-induced arrhythmias or by blocking the renin-angiotensin system. In post-myocardial infarction patients, D,L-sotalol, dofetilide, and amiodarone-and in congestive heart failure patients, amiodarone and dofetilide-have demonstrated neutral effects on survival in controlled trials. In the Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHF-STAT), amiodarone lowered the frequency of AF development and improved left ventricular ejection fraction over time. In CHF-STAT, there was lower mortality in patients who converted from AF to sinus rhythm. Dofetilide decreased rehospitalization for congestive heart failure in the Danish Investigations of Arrhythmia and Mortality on Dofetilide (DIAMOND) trials. Neutral effects on survival and favorable hemodynamics have positioned amiodarone and dofetilide as the antiarrhythmics of choice in patients with left ventricular dysfunction. In post-myocardial infarction patients, sotalol is an additional agent to consider for treatment of AF in this setting.
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PMID:Old and new antiarrhythmic drugs for converting and maintaining sinus rhythm in atrial fibrillation: comparative efficacy and results of trials. 1267 Jun 38

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

Brain natriuretic peptide (BNP) has been established as a new and reliable laboratory marker for chronic heart failure (CHF). BNP is a neurohormone secreted by the cardiac ventricles in response to volume expansion and pressure overload. It is released as N-terminal pro-brain natriuretic peptide and then Korrelaenzymatically cleaved into the NT fragment and the immunoreactive BNP. BNP promotes vasodilatation, natriuresis, diuresis, and inhibits the renin-angiotensin- aldosterone system. BNP values depend on sex, age, renal function, and the assay used. BNP exhibits a high sensitivity and specificity for the diagnosis of CHF. BNP determination improves the differential diagnosis of acute dyspnea. Normal BNP levels are found, if dyspnea is caused by pulmonary disease, pathologic BNP values are typical of a cardiac disorder. In CHF, BNP levels can be used as a reliable independent predictor of cardiac death or deterioration of cardiac functional status at follow-up. As a general screening test for CHF, BNP is of limited value due to a substantial number of false positive test results, which lead to further cardiac diagnostic testing. BNP is helpful for the assessment of the success of CHF therapy in acute cardiac decompensation and outpatients. An individually tailored CHF therapy with serial determination of BNP opens up new perspectives for a more objective and effective treatment of CHF patients.
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PMID:[Brain natriuretic Peptide. Diagnostic and prognostic value in chronic heart failure]. 1458 10

Chronic obstructive pulmonary disease (COPD) often leads to massive oedema and the development of what is usually called cor pulmonale. The mechanisms by which patients with COPD retain salt and water are not completely understood. Several abnormalities have been found including reduced renal blood flow with relatively preserved glomerular filtration rate and elevated levels of renin, aldosterone, arginine vasopressin and atrial natriuretic peptide. Generally, these abnormalities worsen with the severity of COPD and are most marked during the oedematous phases. Cardiac output is remarkably normal, suggesting that "cor pulmonale" is not primarily a cardiac disorder but rather a condition of volume overload due to activation of sodium-retaining mechanisms. The stimulus for this activation could be underfilling of the arterial system (reduced effective circulating volume) secondary to a fall in total peripheral vascular resistance. The latter is caused by hypercapnia-induced dilation of the precapillary sphincters. Apparently, the massive sodium retention by the kidney is not able to restore the circulating volume and a vicious cycle ensues ultimately leading to a clinical picture which resembles right-sided heart failure. Predictably, only blockade of the effects of carbon dioxide at the level of the precapillary sphincters would be able to halt this process.
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PMID:Fluid homeostasis in chronic obstructive lung disease. 1462 Nov 5

Cardiovascular disease is a major cause of death in both sexes. Women suffer almost as many myocardial infarctions as men, although they tend to occur at a greater age. Prevention programs for heart disease have impacted more positively on men than women and relatively young women aged 35-54 years may have fared worse. Hypertension is more prevalent amongst younger men than women, but above 65 years of age it becomes more common in women. Adequate treatment of hypertension has many rewards, but is only received by a minority of hypertensives. Heart failure, too, is a major burden of cardiovascular disease, particularly in older women. Approximately 30% of all cardiac surgery is performed on women, who have a worse short-term postoperative prognosis than men, although the two sexes fare equally in long-term survival. Hypertension, heart failure and diabetes have been identified as key preoperative factors determining a poorer prognosis for cardiac surgery amongst women. The renin-angiotensin-aldosterone system is thought to be central to the development of cardiovascular disease, with elevated levels of angiotensin II hypothesized as the factor which stimulates the formation of large insulin-resistant adipocytes, en route to diabetes. At the cellular level, estrogens have many effects on cardiovascular cells capable of being interpreted as beneficial in terms of cardiovascular disease. New studies demonstrate that approximately 5% of proteins produced by human myocardial cells are modulated by estrogens, estrogens receptors are modulated by age and disease, and estrogens modulate expression of receptors for endothelin-1, a neurohormone implicated in cardiovascular disease.
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PMID:Cardiovascular disease in postmenopausal women. 1501 44

The renin-angiotensin system (RAS) and transforming growth factor-beta1 (TGF-beta1) play a pivotal role in the development of cardiac hypertrophy and heart failure. Recent studies indicate that angiotensin II (Ang II) and TGF-beta1 do not act independently from one another but rather act as part of a signalling network in order to promote cardiac remodeling, which is a key determinant of clinical outcome in heart disease. This review focuses on recent advances in the understanding, how Ang II and TGF-beta1 are connected in the pathogenesis of cardiac hypertrophy and dysfunction. Increasing evidence suggests that at least some of the Ang II-induced effects on cardiac structure are mediated via indirect actions. Ang II upregulates TGF-beta1 expression via activation of the angiotensin type 1 (AT1) receptor in cardiac myocytes and fibroblasts, and induction of this cytokine is absolutely required for Ang II-induced cardiac hypertrophy in vivo. TGF-beta induces the proliferation of cardiac fibroblasts and their phenotypic conversion to myofibroblasts, the deposition of extracellular matrix (ECM) proteins such as collagen, fibronectin, and proteoglycans, and hypertrophic growth of cardiomyocytes, and thereby mediates Ang II-induced structural remodeling of the ventricular wall in an auto-/paracrine manner. Downstream mediators of cardiac Ang II/TGF-beta1 networking include Smad proteins, TGFbeta-activated kinase-1 (TAK1), and induction of hypertrophic responsiveness to beta-adrenergic stimulation in cardiac myocytes.
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PMID:TGF-beta1 and angiotensin networking in cardiac remodeling. 1527 67

Despite recent advances, cardiovascular disease continues to be the leading cause of death among patients with diabetes. Diabetes-related heart disease makes up the majority of the cardiovascular morbidity and mortality and this clinical entity results from synergistic interaction amongst various overlapping mechanisms. Diabetes-related heart disease is characterised by a propensity to develop premature, diffuse atherosclerotic disease, structural and functional abnormalities of the microvasculature, autonomic dysfunction and intrinsic myocardial dysfunction (the so-called diabetic 'cardiomyopathy'), all of which are exacerbated by hypertension and diabetic nephropathy. The renin-angiotensin-aldosterone system possesses various autocrine and paracrine effects which drive most of the pathophysiological mechanisms in diabetes-related heart disease. This review aims to describe the expanding role of the renin-angiotensin-aldosterone system, the complex entity of diabetes-related heart disease and the (emerging) evidence for specific inhibition of the renin-angiotensin-aldosterone system in diabetes.
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PMID:Diabetes, the renin-angiotensin system and heart disease. 1532 Aug 46

Current evidence favors the view that regardless of etiology, there is a predictable sequence of neuroendocrine activation that operates in most dogs and cats with progressive heart disease and that it is largely, but not entirely, independent of etiology. The natriuretic peptides and sympathetic nervous system seem to be early responders to developing cardiac and hemodynamic perturbations in both species. BNP plays a particularly prominent role in cats, possibly as a reflection of disease etiology. Shortly thereafter, plasma endothelin concentrations rise, reflecting the impact of the hemodynamic alterations on the vasculature. Endothelin and the natriuretic peptides directly suppress plasma renin release but have divergent effects on aldosterone. Activation of the tissue RAAS may operate early on to further the progression of heart failure, but evidence of plasma RAAS activation occurs comparatively late and near the time of development of overt CHF. Finally, in animals with severe CHF that are prone to hypotension,vasopressin levels may also rise, contributing to the retention of free water and congestion that is refractory to diuretics. Although oversimplified, this scenario seems to be consistent with data obtained in human, canine, and feline patients. These observations provide some impetus for evaluating ACE inhibitors in cats and beta-receptor-blocking drugs in dogs and cats. Perhaps we are also a little closer to identifying useful biochemical markers that can aid in the diagnosis of heart disease, guide therapy, and improve our understanding of the biologic processes occurring in our patients.
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PMID:Neuroendocrine evaluation of cardiac disease. 1532 72

With diabetes mellitus reaching epidemic proportions, mainly secondary to obesity, the impact of cardiovascular disease due to this combination makes it a dominant public health problem during the first quarter of the 21st century. The complex interaction that results in diabetic heart disease is created by overlapping mechanisms. There is a propensity to develop premature, diffuse atherosclerotic coronary disease, which is associated with adverse short- and long-term morbidity and mortality. There are structural and functional abnormalities of the microvasculature, autonomic dysfunction, and intrinsic failure of myocardial contraction (so-called diabetic cardiomyopathy). These changes are amplified by arterial hypertension and kidney disease. In this review, we consider the role of the renin-angiotensin-aldosterone system and how it is a crucial driver of most of the pathophysiologic mechanisms behind diabetic heart disease and why in the past 5 years blocking this system in diabetic patients has emerged as a critical therapeutic intervention.
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PMID:Diabetes mellitus, the renin-angiotensin-aldosterone system, and the heart. 1536 66


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