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

Chronic heart failure is a well-recognized syndrome in which left ventricular impairment produces a constellation of secondary changes in other organ symptoms leading to symptoms such as muscular fatigue and dyspnoea and objective limitation to exercise tolerance. With modern drug therapy of diuretics and ACE inhibitors, the majority of patients have minimal if any signs of congestion, and yet severe symptomatic limitation remains. This limitation bears little relationship to conventional measures of either left ventricular function or the haemodynamic profile of the patient. The symptoms limiting exercise are predominantly fatigue or dyspnoea, and yet the classical pathophysiological explanations for their genesis now seem inadequate. Recent investigations, as demonstrated, in part, by the research presented in this symposium, attest to the importance of abnormalities in peripheral blood flow and in skeletal muscle in producing both objective limitation to exercise and in explaining the generation of the exercise-limiting symptoms of the syndrome of stable optimally treated chronic heart failure. In addition it is now evident that these muscle changes may in addition have pathophysiological significance for the maintenance of sympatho-excitation during exercise and potentially therefore in the progression of left ventricular remodelling and in the susceptibility to ventricular arrhythmias. This paper presents some of the background evidence which leads to the hypothesis that a feedback loop links changes in skeletal muscle to abnormal reflex cardiopulmonary control which may both limit exercise and be harmful in the progression of the syndrome.
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PMID:The "muscle hypothesis" of chronic heart failure. 893 79

Chronic heart failure (HF) is a leading cause of morbidity and mortality in the United States, affecting >4 million people. The increasing prevalence of HF has placed an enormous burden on the US healthcare system. For many patients with cardiovascular disease, HF is the final common pathway. Treatment strategies for HF are aimed at preventing and delaying progression of the disease and ultimately improving survival. This article reviews recent clinical drug trials for HF, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin II antagonists, vasodilators, beta-adrenergic blockers, positive inotropic agents, calcium antagonists, and antiarrhythmics. The benefits and shortcomings of these agents and the study designs are discussed. For patients with left ventricular (LV) systolic dysfunction, ACE inhibitors are the only agents that consistently improved survival and decreased the rate of HF progression. It is likely that beta-adrenergic blockers have the same effect. The syndrome of HF is complex with both peripheral and cardiac factors contributing to disease progression. The addition of a diuretic and/or digoxin is often needed to prevent worsening heart failure. Although an angiotensin II antagonist may also be beneficial in the treatment of HF, further studies are needed to clarify their precise role in the management of this condition. Calcium anatagonists, antiarrhythmics excluding amiodarone, and positive inotropes other than digoxin do not appear to prevent progression of HF nor improve survival. The most common cause of HF in the United States is related to coronary artery disease. Reduction of cardiac risk factors, such as smoking cessation, lowering serum cholesterol with diet and a lipid lowering agent, and blood pressure control, is likely to prevent the development or progression of HF.
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PMID:Pharmacotherapy for systolic dysfunction: a review of randomized clinical trials. 937 94

Chronic heart failure (CHF) is accompanied by a reduced exercise capacity, and the symptoms can be at least in part explained by qualitative and quantitative changes in the skeletal muscle composition and metabolism. We have correlated the myosin heavy chain (MHC) composition of the gastrocnemius in 20 patients with different degrees of CHF to expiratory gases measured during maximal cardiopulmonary exercise testing, NYHA functional class and echocardiographic parameters. MHC composition was determined electrophoretically in skeletal muscle needle microbiopsies and the percent distribution calculated by laser densitometry. There was no correlation between ejection fraction, left ventricular end-diastolic and end-systolic diameters and MHC composition. The percentage of MHC 1 (slow aerobic isoform) was positively correlated with peak VO2 (r2 = 0.5, p = 0.0004), ventilatory threshold (VT, r2 = 0.33, p = 0.008), and O2 pulse (peak VO2/HR, r2 = 0.40, p = 0.003). There was a negative correlation between MHC 2a and 2b (fast isoforms) and peak VO2 (r2 = 0.38 and 0.37, p = 0.004, respectively), VT (r2 = 0.2, p = 0.05; r2 = 0.34, p = 0.007, respectively) and O2 pulse (r2 = 0.39, p = 0.003; r2 = 0.23, p = 0.03, respectively). NYHA functional class was also negatively correlated with the same parameters (r2 = 0.2, p = 0.01; r2 = 0.4, p = 0.001; r2 = 0.34, p = 0.006, respectively) as well as with MHC 1 (r2 = 0.62, p = 0.0001). A positive correlation was found between NYHA functional class and MHC 2a and 2b (r2 = 0.46, p = 0.001; r2 = 0.41, p = 0.002, respectively). The severity of heart failure is paralleled by a shift of the MHC pattern toward the fast MHC 2b. The correlation between the magnitude of the MHCs shift, from the slow aerobic to the fast type, with both clinical parameters (NYHA functional class) and functional measurements (peak VO2, VT, O2 pulse) of exercise capacity seem to suggest that changes in skeletal muscle composition may play a key role in exercise tolerance in patients with CHF.
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PMID:[Myosin isoforms in skeletal muscle in patients with chronic heart decompensation: distribution and correlation with with exercise tolerance]. 941 May 67

Clearly at present, the one perfect surrogate marker for mortality remains elusive. Chronic heart failure is a complex syndrome: as such it may perhaps be too simplistic to expect any single parameter to be universally predictive of drug effects on mortality, especially when each drug works by different mechanisms. Nevertheless, neurohormonal antagonists, such as ACE inhibitors and beta-blockers, seem to benefit both mortality and all surrogate markers of mortality. Equally, inotropic drugs and Class I antiarrhythmics appear to worsen both mortality and many surrogates. This is encouraging. However, significant discrepancies exist, particularly for digoxin, ibopamine and hydralazine-nitrates, although it is only with the latter two that diametrically opposite effects occurred, whereby favourable surrogate effects turned into unfavourable mortality effects (or vice versa). It appears appropriate to have guarded optimism about the potential use of these surrogates to predict drug effects in chronic heart failure. Given our current understanding, none of the parameters discussed above is perfect when used alone. Perhaps a battery of surrogates would be more appropriate rather than there being any single surrogate. The most promising surrogates are heart rate variability, QT dispersion and plasma neurohormones, the first two for sudden death and the last one for death from progressive disease.
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PMID:Can drug effects on mortality in heart failure be predicted by any surrogate measure? 944 12

Conductance of alveolar capillary membrane (DM) and capillary blood volume (VC) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLCO). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced DM and subsequent impairment of DLCO. Angiotensin-converting enzyme inhibition improves DLCO in patients with chronic heart failure. This study was aimed at investigating which of the two subcomponents of DLCO is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (group 1) and 13 age- and sex-matched normal subjects underwent pulmonary function testing with determination of DM and VC, while receiving placebo and 48 h and 1 and 2 months after starting enalapril treatment (10 mg twice daily). Nine similar patients (group 2) received isosorbide dinitrate (40 mg thrice daily) for a month then enalapril for another month, and underwent pulmonary function testing at 48 h and 1 month after starting treatments. Effects of angiotensin-converting enzyme inhibition in normal controls were not significant in the short- or mid-term. In group 1 patients, the only change observed at 48 h was a reduction in VC (probably due to a decrease in capillary pulmonary pressure). There was a marked increase in DM to a similar extent at 1 and 2 months, resulting in a significant improvement in DLCO despite a decrease in VC. In group 2 patients, nitrates failed to improve DLCO and DM, whereas enalapril was as effective as in group 1. These observations suggest a modulatory effect of angiotensin-converting enzyme inhibition on the membrane function which emerges gradually and persists over time and is probably dissociated from changes in pulmonary capillary pressure and VC. Chronic heart failure disturbs the alveolar capillary interface and increases gas diffusion resistance; angiotensin-converting enzyme inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.
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PMID:Angiotensin-converting enzyme inhibition restores the diffusing capacity for carbon monoxide in patients with chronic heart failure by improving the molecular diffusion across the alveolar capillary membrane. 985 2

Chronic heart failure (CHF) is a complex syndrome affecting many body systems. Body wasting (ie, cardiac cachexia) is a serious complication of CHF long known but little investigated. Although no specific diagnostic criteria have been established, we have suggested that cardiac cachexia be defined on the basis of the presence of documented nonintentional and nonedematous weight loss > 7.5% of the premorbid normal weight, occurring over a time period of > 6 months. Using this definition, 16% of an unselected CHF outpatient population was found to be cachectic. The cachectic state is predictive of impaired prognosis independently of age, functional disease classification, left ventricular ejection fraction, and peak oxygen consumption. The mortality in the cachectic cohort is 50% at 18 months. Analyzing body composition in detail, it has been found that patients with cardiac cachexia suffer from a general loss of fat tissue (ie, energy reserves), lean tissue (ie, skeletal muscle), and bone tissue (ie, osteoporosis). Cachectic CHF patients are weaker and fatigue earlier, which is due to both reduced skeletal muscle mass and impaired muscle quality. The pathophysiologic alterations leading to cardiac cachexia remain unclear, but initial cross-sectional studies have suggested that humoral neuroendocrine and immunologic abnormalities are linked, independently of established heart failure severity markers, to the presence of body wasting. Comparing the features of cachectic and noncachectic CHF patients with those of healthy control subjects, it is mainly the cachectic CHF patients who show raised plasma levels of epinephrine, norepinephrine, and cortisol; the highest plasma renin activity and aldosterone plasma concentrations; and the lowest plasma sodium level. Several studies have shown that cardiac cachexia is linked to raised plasma levels of tumor necrosis factor-ac. The degree of body wasting is strongly correlated with neurohormonal and immune abnormalities. The available evidence suggests that cardiac cachexia is a multifactorial neuroendocrine and metabolic disorder with a poor prognosis. A complex imbalance of different body systems may cause the development of body wasting.
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PMID:Cardiac cachexia: a syndrome with impaired survival and immune and neuroendocrine activation. 1008

The use of cardiac peptide measurements as possible diagnostic tools in congestive heart failure has been extensively discussed in the recent literature. Therefore, the aim of this study was to establish a model of experimental chronic heart failure, and thereby perform a comparative study of secretion and circulating levels of the cardiac peptides atrial natriuretic peptide (ANP), N-terminal proatrial natriuretic peptide (N-terminal proANP) and brain natriuretic peptide (BNP) during evolving heart failure. Chronic heart failure was induced in seven pigs by rapid left atrial pacing for three weeks. The effects of failure induction were documented 24 h after pacemaker deactivation. Hemodynamic indices of cardiac preload, like pulmonary capillary wedge pressure (PCWP) and right atrial pressure (RAP), were all considerably increased compared to sham operated controls. Likewise, plasma endothelin-L, noradrenaline, renin activity, aldosterone and angiotensin II were all markedly increased. Heart failure was accompanied by significant increases in both estimated cardiac secretory rate and plasma concentrations of all three cardiac peptides, significantly correlated to the PCWP. The directional changes during evolving heart failure were similar, although the percentage increase in plasma BNP was much larger than for ANP and N-terminal proANP. In absolute molar terms, however, the BNP concentration changes were minor compared to those of the other two peptides. The larger percentage increase of BNP might indicate its superiority as a marker of heart failure development, provided a functional assay suitable for clinical use can be designed for a peptide circulating in this low concentration range.
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PMID:An experimental study of cardiac natriuretic peptides as markers of development of congestive heart failure. 1008 6

Chronic heart failure is the most common reason for hospitalization among the elderly in western societies. To elucidate the meaning of the experience of care received in the hospital, as narrated by 12 elderly patients with severe chronic heart failure, interviews were analyzed by an approach inspired by Ricoeur's phenomenologic hermeneutics. The analysis revealed that the study respondents experienced the care as "unpredictable." This essential theme captured the divergent descriptions of 2 subthemes: care was either "confident but incomprehensible" or "nonconfident and incomprehensible." When the patients sought care, it was as though they were launching themselves into the unknown because they knew that many experiences would be unpredictable. Despite experiences of indifferent and unpredictable care, the narratives revealed a need to rely on the caregivers' expertise.
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PMID:The meaning of hospital care, as narrated by elderly patients with chronic heart failure. 1033 Feb 16

Chronic heart failure (CHF) patients frequently show sleep-disordered breathing consisting of periodic breathing (PB) and Cheyne-Stokes respiration (CSR) with central sleep apnoea (CSA). Since the diagnosis of sleep-disordered breathing, in CHF patients, can be made only by means of full polysomnography, the aim of the present study was to evaluate whether or not daytime respiratory function can identify patients at risk of nocturnal PB and/or CSR/CSA. Twenty-seven patients (mean age 54 +/- 8.5 yrs), eight New York Heart Association Functional Class (NYHAFC) II, 17 NYHAFC III and two NYHAFC IV, with severe cardiac failure (cardiac output 2.0 +/- 0.66 L.min-1, ejection fraction 22.5 +/- 5.77%, pulmonary capillary wedge/pressure 23 +/- 9.05 mmHg). Mouth occlusion pressure (P0.1)/maximal inspiratory pressure (MIP) was significantly higher in patients with nocturnal CSR/CSA (5.04 +/- 1.49 versus 3.24 +/- 2.13%, analysis of variance (ANOVA) 0.03), whereas their arterial carbon dioxide tension (Pa,CO2) was significantly lower (4.15 +/- 0.56 (31.2 +/- 4.23 mmHg) versus 4.67 +/- 0.53 kPa (35.1 +/- 4 mmHg), ANOVA 0.02). Logistic regression analysis demonstrated that CSR/CSA occurrence may be predicted by daytime measurement of P0.1/MIP and Pa,CO2 (p = 0.04 and 0.01 respectively; odds ratio 1.93 and 0.76 respectively). The sensitivity was 70%, specificity 76.5%, false positive rate 36.4%, false negative rate 18.8%, positive predictive value 71.4% and negative predictive value 85%. This model seems useful for predicting respiratory pattern changes in chronic heart failure patients and the authors suggest that polysomnography be performed only in high-risk patients, saving costs and the resources of sleep laboratories.
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PMID:Identification of chronic heart failure patients at risk of Cheyne-Stokes respiration. 1054 73

Cardiac preload reduction through venodilatation is beneficial in chronic heart failure. The recent development of endothelin receptor antagonists for possible therapeutic use in heart failure has hastened the need for a clearer understanding of the venoconstrictor actions of endothelin-1 in this disease. Two main subtypes of endothelin receptor, ET(A) and ET(B), exist in human blood vessels. We studied the venoconstrictor effects of endothelin-1 (a non-selective ET(A) and ET(B) agonist) and sarafotoxin S6c (a selective ET(B) agonist) in vivo in patients with chronic heart failure and in age-matched healthy controls. On separate days at least 1 week apart, locally active doses of endothelin-1 or sarafotoxin S6c were infused into a suitable dorsal hand vein for 1 h, and the venous internal diameter was measured using a displacement technique. Venoconstriction in response to endothelin-1 was significantly blunted in heart failure patients compared with controls (26+/-7% and 51+/-6% peak reduction in vein calibre respectively; P=0.013). Venoconstriction to sarafotoxin S6c was similar in heart failure patients and controls (17+/-5% and 17+/-4% peak reduction in vein calibre respectively). Both ET(A) and ET(B) receptors mediate venoconstriction in healthy subjects and in patients with chronic heart failure. Optimal inhibition of the venoconstrictor effects of endothelin-1 in chronic heart failure may therefore require administration of an antagonist with ET(A)- and ET(B)-receptor-blocking properties. Chronic heart failure may be associated with a selective decrease in venous ET(A) receptor sensitivity, but further studies are required to clarify the functional significance of this observation.
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PMID:Venous endothelin receptor function in patients with chronic heart failure. 1060 Jun 60


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