DIURETICS AND ELECTROLYTE ABNORMALITIES IN CONGESTIVE HEART FAILURE. 3. ELECTROLYTE DISTURBANCES IN CONGESTIVE HEART FAILURE.
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Electrocardiographic remodeling in patients paced for heart failure.
Congestive heart failure due to advanced coronary artery disease or dilated cardiomyopathy is often associated with intraventricular conduction delays. Electrical resynchronization is an evolving method to improve clinical and functional status. To evaluate whether pacing-induced changes in the electrocardiogram are related to hemodynamic changes, we analyzed electrocardiograms of patients enrolled in the Pacing Therapies in Congestive Heart Failure trial. The study population consisted of 42 patients, New York Heart Association functional class III-IV with a baseline QRS complex of 175 +/- 32 msec and a PR interval of 196 +/- 33 msec. The mean left ventricular ejection fraction was 0.23. Using high-resolution computer scans, we measured QRS duration of intrinsic and paced electrocardiographs at different times during the study. Results of the electrocardiographic measurements were correlated with functional results. During the crossover period, 34 episodes of biventricular pacing, 27 episodes of left ventricular pacing, and 5 episodes of right ventricular pacing occurred, each at an individual optimized atrioventricular (AV) delay. The only significant difference was that right ventricular pacing increased the QRS width by 40 msec as compared with baseline or biventricular pacing. Functional benefit, as indicated by relative increase of peak oxygen uptake (VO2) compared with baseline, was significantly correlated with shortening of paced QRS width (correlation coefficient, r = 0.55; p <0.05). After 12-month follow-up of 28 patients, we saw a slight, nonsignificant decrease of intrinsic QRS width. With regard to the underlying disease, intrinsic QRS width at baseline and at 12 months was also not significantly different between patients with coronary artery disease and dilated cardiomyopathy. This study found that right ventricular pacing causes an increase in QRS duration in patients with left bundle-branch block, whereas in left ventricular and biventricular pacing, QRS width remains unchanged. Shortening of QRS width is correlated with a pronounced relative increase of peak VO2, and thus may become a noninvasive marker of clinical efficacy. There is no evidence of remodeling of the intrinsic electrocardiogram after 12 months of pacing.
Arrhythmias, Cardiac↗
Current guidelines for the treatment of congestive heart failure.
Overt congestive heart failure (CHF) has a prevalence of 1% of the population. The predominant symptoms of patients with CHF are fatigue and dyspnoea. Fatigue is thought to result from changes in peripheral muscle metabolism secondary to decrease vasodilative capacity and physical inactivity. An increase of peripheral perfusion by vasodilator therapy and physical activity are therefore recommended. Beside overt decompensation, where dyspnoea results from acute pulmonary congestion due to backward failure, increased physiological dead space ventilation caused by pulmonary ventilation/perfusion mismatch accounts, to a large degree, for dyspnoea, and can be improved by vasodilator therapy. According to the pathophysiology of CHF, normalisation of loading conditions and myocardial inotropy are the parameters addressed by various pharmacological agents in order to alleviate symptoms and slow progression of the disease. Diuretics are rapidly acting and effective agents to improve congestion and decrease filling pressures. Digitalis improves haemodynamics and symptomatology by increasing inotropy and slowing resting heart rate in atrial fibrillation; however, prognostic effects have yet to be proved. The introduction of vasodilators has significantly improved the prognosis of the disease, and the administration of ACE inhibitors in particular has been shown to slow progression of CHF. This results in a substantial decrease in morbidity and mortality. The present article appraises the role of the currently used drugs in the treatment of CHF, considering effects on pathophysiology and clinical outcome and provides an approach to a differential drug regimen.
Adrenergic beta-Antagonists↗
The mechanism of adaptation of left atrial stretch receptors in dogs with chronic congestive heart failure.
Chronic congestive heart failure (CHF) was induced in dogs by the construction of an aorto-caval fistula below the level of the renal arteries. Aorto-caval fistula dogs showed signs of CHF which included ascites, hind limb edema, and pulmonary congestion. Ventricular catheterization indicated a significantly higher left ventricular end diastolic pressure and lower maximum velocity of left ventricular pressure development/left ventricular end diastolic pressure in CHF dogs when compared to sham-operated controls. Heart weight/body weight ratios were significantly higher in CHF dogs. Electrophysiological recordings from medullated left atrial type B receptors from the cervical vagus indicated a depressed sensitivity of these receptors in CHF dogs when compared to sham-operated control dogs. For any given change in left atrial pressure, the discharge of left atrial receptors was significantly reduced in CHF dogs compared with sham-operated controls. The mechanism for this depressed sensitivity was investigated. Sonomicrometry of the left atrial appendage indicated a decreased compliance of the left atrial appendage in the dogs with chronic CHF. In addition, microscope examination of the complex unencapsulated receptor endings taken from the left atrial endocardium indicated a marked alteration in receptor morphology. A loss of the end arborization was the most typical finding. It is concluded that chronic CHF brought about by an aorto-caval fistula results in a depressed left atrial stretch receptor response and that both decreased left atrial compliance and structural alterations in the receptor endings may account for this depressed sensitivity.
Animals↗
Changes in circulating norepinephrine with hemofiltration in advanced congestive heart failure.
In congestive heart failure (CHF), hemofiltration is associated with an obvious decrease in circulating norepinephrine. This method was used for investigating the mechanisms whereby plasma norepinephrine is increased in chronic CHF. In 23 cases of advanced CHF, hemofiltration (2,983 +/- 1,228 ml) lowered plasma norepinephrine by 515 +/- 444 pg/ml. This effect was prompt, persisted or became greater in the next 24 hours. It was not associated with significant changes in cardiac output, aortic pressure or systemic vascular resistance. It did not appear to depend on variations in parameters related to the sympathetic activity, such as plasma renin, right atrial, wedge pulmonary artery and renal perfusion pressures, and was independent of duration and amount of hemofiltration. These observations did not support the concept that the norepinephrine decrease was the main consequence of a neural sympathetic inhibition. Hemofiltration increased diuresis by 606 +/- 415 ml; changes were prompt and correlated inversely (r = -0.7; p less than 0.01) with those in plasma norepinephrine. The same unknown mechanism of the increased urinary output might potentiate the norepinephrine removal from the blood by the kidney, or hemofiltration and the augmented diuresis might result in a regression of congestion of lungs and kidneys, leading to an improved extraction of norepinephrine. In CHF, a relation may exist between fluid retention and norepinephrine and in advanced stages, circulating norepinephrine, although strikingly increased, is devoid of important cardiovascular effects. At these stages, plasma norepinephrine is probably unreliable as an index of the sympathetic neural activity.
Adult↗
Retinopathy and risk of congestive heart failure.
CONTEXT: Congestive heart failure (CHF) affects a substantial proportion of adults including those without preexisting coronary heart disease. The pathogenesis of CHF is uncertain, but microvascular disease has been hypothesized as a possible factor. OBJECTIVE: To determine the relationship of retinopathy, a marker of systemic microvascular disease, to risk of CHF. DESIGN, SETTING, AND PARTICIPANTS: Population-based, prospective 7-year cohort study in 4 US communities using the Atherosclerosis Risk in Communities Study database. Participants (n = 11,612, aged 49 to 73 years) had retinal photographs taken between 1993 and 1995. The photographs were graded according to a standardized protocol for the presence of retinopathy (eg, microaneurysms, retinal hemorrhages, soft exudates), arteriovenous nicking, focal arteriolar narrowing, and generalized arteriolar narrowing. MAIN OUTCOME MEASURES: Association between retinopathy and incident CHF, identified from hospitalization and death records. RESULTS: The 7-year cumulative incidence of CHF was 5.4% (492 events). Participants with retinopathy had a higher incidence of CHF compared with those without retinopathy (15.1% vs 4.8%, P<.001). After controlling for age, sex, race, preexisting coronary heart disease, mean arterial blood pressure, diabetes, glucose level, cholesterol level, smoking, body mass index, and study site, the presence of retinopathy was associated with a 2-fold higher risk of CHF (relative risk, 1.96; 95% confidence interval, 1.51-2.54). Among participants without preexisting coronary heart disease, diabetes, or hypertension, retinopathy was associated with a 3-fold higher risk of CHF (relative risk, 2.98; 95% confidence interval, 1.50-5.92). CONCLUSIONS: Retinopathy is an independent predictor of CHF, even in persons without preexisting coronary heart disease, diabetes, or hypertension. This suggests that microvascular disease may play an important role in the development of heart failure in the general population. Some asymptomatic persons with retinopathy on an ophthalmologic examination may benefit from further assessment of CHF risk.
Adult↗
Factors causing arrhythmias in chronic congestive heart failure.
Severe congestive heart failure (CHF) is a common syndrome with a high mortality rate (about 50% in 1 year among patients with symptoms at rest). Severity of left ventricular dysfunction is the most important adverse prognostic factor. Serious arrhythmias are common in CHF and also increase the mortality rate. Sudden death is the mode of death in about 40% of patients with severe heart failure. Multiple factors contribute to arrhythmias in CHF, including left ventricular dysfunction, myocardial ischemia, catecholamines, electrolyte disturbances, and drugs used to treat the heart failure. Minimizing or correcting these influences may be important in reducing serious arrhythmias. Antiarrhythmic drugs may be important in reducing the incidence of sudden death among patients with severe heart failure, although this has not yet been proved.
Arrhythmias, Cardiac↗
Characterization of systemic oxygen transport in end-stage chronic congestive heart failure.
Chronic congestive heart failure (CHF) is characterized by low cardiac index (CI) and low systemic oxygen delivery (DO2), which frequently are associated with lethal cardiogenic shock after acute myocardial infarction. Nevertheless, patients with severe CHF are able to survive with these low levels of systemic DO2 and CI. It was hypothesized that patients with CHF survive low CI and DO2 by downregulation of global metabolism and resting oxygen consumption (VO2) and a concomitant increase in systemic oxygen extraction ratio (O2ER). Therefore the objective of this study was to characterize the resting pattern of systemic oxygen transport (O2T) and utilization in patients with stable CHF. Seventeen patients with CHF (New York Heart Association functional class III or IV) for > or = 3 months and with left ventricular ejection fraction (EF) < 25% and whose condition was stable with conventional oral therapy were studied. The control group comprised 10 subjects (NYHA class I) who had coronary angiography and who were found to have normal left ventricular function and EF > 60%. Subjects underwent right-heart catheterization for measurement and calculation of hemodynamic and O2T variables (VO2, DO2, and O2ER). There were no significant differences in mean age (67 +/- 6 vs 64 +/- 17 years) or gender ratio (male:female 14:3 vs 7:3) between CHF and control groups, respectively. The cause of CHF was ischemic in 13 and idiopathic in 4 patients. There were 9 patients in NYHA class III and 8 in class IV.(ABSTRACT TRUNCATED AT 250 WORDS)
Adaptation, Physiological↗
Intact systolic left ventricular function in clinical congestive heart failure.
Clinical congestive heart failure (CHF) is traditionally associated wtih significant left ventricular (LV) systolic dysfunction. Over a 1-year period, 58 patients with CHF and intact systolic function (LV ejection fraction [EF] 62 +/- 11%) were identified. An objective clinical-radiographic CHF score was used to document the clinical impression. Based on radionuclide evaluation of peak filling rate, 38% of these patients were found to have a significant abnormality in diastolic function as measured by peak filling rate (less than 2.50 end-diastolic volume/s). An additional 24% of the patients had probable diastolic dysfunction with borderline abnormal peak filling rate measurements (2.5 to 3.0 end-diastolic volume/s). The disease states most frequently associated with CHF and intact systolic function were coronary artery disease and systemic hypertension. During a 3-month sampling period 42% of patients with clinical diagnosis of CHF referred to the nuclear cardiology laboratory were found to have intact systolic function; thus, intact systolic function is not uncommon in patients with clinical CHF. Abnormal diastolic function is the most frequently encountered mechanism for the occurrence of CHF. Definition of systolic and diastolic function appears relevant for development of optimal therapeutic strategies for the treatment of patients with CHF.
Adult↗
Abnormalities in the regional circulations accompanying congestive heart failure.
In congestive heart failure, patients appear to have alimited ability to dilate their resistance vessels in skeletal muscle in response to a metabolic stimulus. This is true whether the metabolic stimulus is ischemia, dynamic, or static exercise. The mechanism for this limited arteriolar capacity is at least twofold; an increased sodium content of the vessels as well as an increased tissue pressure which is seen in edematous states. This can be considered a positive compensatory mechanism in that it helps to maintain systemic arterial pressure during exercise when the cardiac output fails to increase normally. If the resistance vessels were to dilate normally, then in the face of a limited cardiac output, exercise syncope would be expected to occur...
Basement Membrane↗
Differences in atrial versus ventricular remodeling in dogs with ventricular tachypacing-induced congestive heart failure.
BACKGROUND: Congestive heart failure (CHF) causes arrhythmogenic remodeling in both atria and ventricles, but differences between atrial and ventricular remodeling in CHF have not been well characterized. METHODS AND RESULTS: We examined atrial and ventricular tissues from dogs with CHF induced by ventricular tachypacing (220-240/min) for 0 (control) or 24 h, or 1, 2 or 5 weeks. Histopathology was used to assess apoptosis, fibrosis, white blood cell infiltration and cell death, ELISA to measure angiotensin-II concentration and Western blot to evaluate protein expression. Ventricular tachypacing-induced CHF was associated with substantially more fibrosis in left atrium (maximum 10 +/- 1% at 5 weeks) than in left ventricle (0.4 +/- 0.1% at 5 weeks, P < 0.01 versus left atrium). Tissue angiotensin-II concentration increased to steady state in atrial tissue at 24 h but increased more slowly in left ventricle, with a maximum that was significantly higher in atrium than ventricle. Ventricular tachypacing caused tissue apoptosis, inflammatory cell infiltration and cell death, with maximum changes in left atrium being faster, transient and larger than in left ventricle. Mitogen activated protein kinase activation was rapid (within 24 h) in left atrium, but smaller and slower (p38, c-Jun N-terminal kinase) or non-significant (extracellular signal-related kinase) in left ventricle. The 25-kDa activated form of transforming growth factor-beta1, a particularly important profibrotic mediator in atrium, increased significantly in left atrium, from 2.6 +/- 0.6 (control) to 9.2 +/- 1.7 (24 h) and 8.1 +/- 1.8 optical density units (1 week), but was not significantly changed in ventricle. CONCLUSIONS: There are qualitative and quantitative differences in atrial versus ventricular remodeling in experimental ventricular tachypacing-induced CHF, with potentially important consequences for understanding underlying mechanisms and developing new therapeutic approaches.
Angiotensin II↗
Depression increasingly predicts mortality in the course of congestive heart failure.
BACKGROUND: Congestive heart failure (CHF) is frequently associated with depression. However, the impact of depression on prognosis has not yet been sufficiently established. AIMS: To prospectively investigate the influence of depression on mortality in patients with CHF. METHODS: In 209 CHF patients depression was assessed by the Hospital Anxiety and Depression Scale (HADS-D). RESULTS: Compared to survivors (n=164), non-survivors (n=45) were characterized by a higher New York Heart Association (NYHA) functional class (2.8+/-0.7 vs. 2.5+/-0.6), and a lower left ventricular ejection fraction (LVEF) (18+/-8 vs. 23+/-10%) and peakVO(2) (13.1+/-4.5 vs. 15.4+/-5.2 ml/kg/min) at baseline. Furthermore, non-survivors had a higher depression score (7.5+/-4.0 vs. 6.1+/-4.3) (all P<0.05). After a mean follow-up of 24.8 months the depression score was identified as a significant indicator of mortality (P<0.01). In multivariate analysis the depression score predicted mortality independent from NYHA functional class, LVEF and peakVO(2). Combination of depression score, LVEF and peakVO(2) allowed for a better risk stratification than combination of LVEF and peakVO(2) alone. The risk ratio for mortality in patients with an elevated depression score (i.e. above the median) rose over time to 8.2 after 30 months (CI 2.62-25.84). CONCLUSIONS: The depression score predicts mortality independent of somatic parameters in CHF patients not treated for depression. Its prognostic power increases over time and should, thus, be accounted for in risk stratification and therapy.
Adult↗
Effects of omapatrilat on cardiac nerve sprouting and structural remodeling in experimental congestive heart failure.
BACKGROUND: Congestive heart failure (CHF) results in decreased cardiac sympathetic innervation. OBJECTIVES: The purpose of this study was to test the hypothesis that therapy with the vasopeptidase inhibitor omapatrilat (OMA) attenuates cardiac neuronal remodeling in CHF. METHODS: We induced CHF in dogs with rapid ventricular pacing for 5 weeks with (CHF+OMA group, n = 8) or without (CHF group, n = 10) concomitant OMA treatment (10 mg/kg twice daily). Cardiac catheterization and echocardiography were performed to determine cardiac structure and hemodynamic parameters. Myocardial nerve density was determined by immunocytochemical staining with anti-growth associated protein 43 (GAP43) and anti-tyrosine hydroxylase (TH) antibodies. Seven normal dogs were used as histologic controls. RESULTS: In the CHF group, ascites developed in 3 dogs and 4 dogs died, compared with no ascites or death in the CHF+OMA group (P = .07). In the 6 CHF dogs that survived, all had atrial fibrosis, severely depressed left ventricular systolic function, and increased atrial and ventricular chamber size. OMA treatment decreased the atrial and ventricular chamber sizes and the degree of atrial fibrosis. Most CHF dogs showed severe myocardial denervation, although some showed normal or abnormally high nerve counts. OMA treatment prevented heterogeneous reduction of nerve density. The left ventricular TH-positive nerve densities were 128 +/- 170 microm(2)/mm(2), 261 +/- 185 microm(2)/mm(2), and 503 +/- 328 microm(2)/mm(2) (P < .05), and the atrial GAP43-positive nerve densities were 1,683 +/- 1,365 microm(2)/mm(2), 305 +/- 368 microm(2)/mm(2), and 1,278 +/- 1,479 microm(2)/mm(2) (P < .05) for the control, CHF, and CHF+OMA groups, respectively. CONCLUSION: CHF results in heterogeneous cardiac denervation. Long-term OMA treatment prevented the reduction of nerve density and promoted beneficial cardiac structural remodeling.
Angiotensin-Converting Enzyme Inhibitors↗
Enhanced acetylcholine and P2Y-receptor stimulated vascular EDHF-dilatation in congestive heart failure.
OBJECTIVE: Congestive heart failure (CHF) is accompanied by impaired peripheral blood flow and endothelial dysfunction with decreased release of nitric oxide (NO). Strong evidence supports the existence of another vasodilatory substance, endothelium derived hyperpolarising factor (EDHF), which has not previously been studied in CHF. METHOD: CHF was induced by left coronary artery ligation resulting in a reproducible myocardial infarction in Sprague Dawley rats. Vasodilatory responses to acetylcholine and extracellular nucleotides (ATP, ADP beta S, ADP and UTP) were examined in cylindrical segments of the mesenteric artery, precontracted with noradrenaline. The combined NO- and EDHF-dilatation (after inhibition of cyclo-oxygenase pathways) was called "total dilatation", as indomethacin had only minor effects in this system. NO-dilatation was studied in segments pretreated with indomethacin and the potassium channel inhibitors charybdotoxin (10(-7.5) M) and apamin (10(-6) M), while EDHF-dilatations were studied in the presence of indomethacin (10(-5) M) and L-NOARG (10(-3.5) M). RESULTS: EDHF-dilatations in CHF were strongly up-regulated for ACh (36% vs. 73%; sham vs. CHF operated rats), ADP beta S (10% vs. 42%), ADP (0% vs. 21%) and UTP (3% vs. 35%). These dilatations were abolished by a combination of charybdotoxin and apamin, confirming that they were mediated by EDHF. The NO-dilatations on the other hand were down-regulated in CHF as compared to sham operated rats for ACh (93% vs. 76%; sham vs. CHF operated rats), ADP beta S (61% vs. 37%). ADP (60% vs. 30%), ATP (49% vs. 34%) and UTP (65% vs. 47%), while a minor decrease was seen in the total dilatation for ACh (87% vs. 75%; sham vs. CHF operated rats), ADP beta S (47% vs. 42%), ADP (59% vs. 39%), ATP (52% vs. 39%) and UTP (59% vs. 44%). CONCLUSION: In this model of non-atherosclerotic CHF there was a minor decrease in the total dilatation and a marked down-regulation of the NO-mediated dilatation, while the EDHF-dilatation was up-regulated. Increased EDHF-activity in CHF may represent a compensatory response to decreased NO-activity to preserve endothelial function and tissue perfusion.
Acetylcholine↗
Nursing management of congestive heart failure. Part I.
Congestive heart failure (CHF) is a common clinical problem and in its advanced stage has a poor prognosis. Approximately 400,000 individuals develop heart failure each year (Parmley 1989). CHF can be caused by coronary artery disease such as myocardial infarction, ischemia and hypertension. Should heart failure occur as a result of acute myocardial infarction, a classification tool developed by Killip can be used to assess the degree of CHF. Killip's classification is organised into the following four categories: Class I: no heart failure Class II: mild to moderate failure Class III: acute pulmonary oedema Class IV: cardiogenic shock (Killip, as cited by Benz 1989). This system helps in organising clinical signs and symptoms of heart failure. Due to the fact that CHF is now the most common hospital discharge diagnosis for those over the age of 65, critical care nurses need to be able to recognise complications and intervene rapidly (Parmley 1989) in collaboration with medical staff. The purpose of this paper is first to discuss cardinal signs and symptoms and clinical data associated with CHF. Second, critical care nurses' management of CHF is organised around common nursing diagnoses.
Cardiovascular Agents↗
Longstanding atrial fibrillation causes depletion of atrial natriuretic peptide in patients with advanced congestive heart failure.
BACKGROUND: Congestive heart failure (CHF) is characterized by neurohormonal activation, including increased plasma concentrations of atrial natriuretic peptide (ANP) and N-terminal ANP (N-ANP). Onset of atrial fibrillation (AF) further increases these peptides, but it may be hypothesized that concentrations decrease during longstanding AF due to inherent atrial degeneration. AIM: We sought to investigate the relation between neurohormonal activation in patients with CHF and the duration of concomitant AF. METHODS: The study group comprised 60 patients (age 70 +/- 8 years) with advanced CHF due to left ventricular systolic dysfunction (left ventricular ejection fraction (LVEF) < 0.35) and chronic AF (duration 21 (1-340) months). Plasma neurohormone concentrations were measured, and multiple regression analysis was performed to identify their clinical predictors. RESULTS: Median plasma neurohormone concentrations were: ANP 113 pmol/l, N-ANP 1187 pmol/l, norepinephrine 496 pg/ml, renin 127 micro units/l, aldosterone 128 pg/ml and endothelin 8.1 pg/ml. Norepinephrine, renin, aldosterone and endothelin were not significantly related to the duration of AF. In contrast, ANP decreased along with the duration of AF (P = 0.03), while the same trend was observed for N-ANP (P = 0.10). However, for these peptides a first order interaction with LVEF was present, which was not observed in the other neurohormones. In patients with LVEF > 0.25 ANP and N-ANP increased along with the duration of AF, whereas in patients with LVEF < or = 0.25 an inverse relation between ANP (P = 0.02) and N-ANP (P = 0.04) and the duration of AF was present, longer-standing AF being associated with lower concentrations. CONCLUSION: In patients with advanced CHF with low LVEF plasma ANP and N-ANP concentrations decrease during longstanding AF. This finding agrees with the concept that longstanding AF leads to impaired ability of the atria to produce these neurohormones due to inherent degenerative changes.
Aged↗
Carvedilol does not alter the insulin sensitivity in patients with congestive heart failure.
BACKGROUND: Congestive heart failure (CHF) has previously been shown to be associated with insulin resistance and hyperinsulinemia. A beneficial effect of the non-selective beta-blocker carvedilol has been demonstrated in patients with CHF. However, whether the drug affects the insulin sensitivity (S(i)) is unknown. AIMS: To investigate whether treatment with carvedilol alters the S(i) in patients with CHF during a prospective, double-blinded, placebo-controlled study. METHODS AND RESULTS: The patients were randomized to receive either carvedilol (n=29) or matched placebo (n=17). Insulin and glucose responses were measured during a 0.3 g/kg intravenous glucose tolerance test, and S(i) was calculated according to Bergman's Minimal Model. Baseline S(i) values correlated significantly with body mass index (r=-0.42, P=0.002), plasma urate (r=-0.42, P=0.002), plasma HDL-cholesterol (r=0.39, P=0.003), maximal oxygen uptake (r=0.35, P=0.009), plasma triglycerides (r=-0.34, P=0.01) and weight (r=-0.29, P=0.03). During the study the insulin sensitivity was unchanged in the carvedilol group compared with placebo (2.63+/-1.45 to 2.38+/-1.64 vs. 2.81+/-2.36 to 2.48+/-1.84x10(-4) min(-1)/mUl(-1), P=0.83). CONCLUSION: Additional treatment with carvedilol is neutral with regard to influence the insulin sensitivity in patients with mild to moderate CHF.
Adrenergic beta-Antagonists↗
The association between disease severity, functional status, depression and daily quality of life in congestive heart failure patients.
Congestive heart failure significantly compromises quality of life by contributing to severe physical, role, and social functioning impairment as well as increased psychological distress. Previous research examining quality of life in CHF patients has typically been conducted using global self-report instruments that may exceed a patient's ability to accurately recall their experiences. This investigation examines the impact of disease severity, functional status, and level of depression on daily quality of life (i.e., mean level and variability) in CHF patients during a 2-week monitoring period. Indices of quality of life included emotional and physical quality of life, social support and conflict, positive and negative mood, and coping responses. Fifty-eight patients with CHF participated in the investigation. Depressive symptoms were positively associated with a number of quality of life indices (i.e., physical and emotional quality of life, social support and conflict, mood, and coping behaviours). Left ventricular ejection fraction and functional impairment had a much weaker association with quality of life. These findings suggest that depressive symptoms may have a greater impact on quality of life in CHF patients than severity of cardiac dysfunction or functional impairment.
Activities of Daily Living↗