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Patients with congestive heart failure had higher scores than control subjects using a case-finding instrument for depression; such patients also were more likely to exceed the diagnostic threshold for depression with this instrument. Identification and treatment of depressed CHF patients may significantly improve level of functioning in these patients.
Patients with congestive heart failure have been considered to have augmented sympathetic drive both at rest and during dynamic exercise. The augmentation observed during exercise may be related to the state of near exhaustion experienced by patients with heart failure at relatively low work loads. To compare the response of the sympathetic nervous system to exercise in normal subjects and patients with heart failure when they are working in a comparable physiologic frame of reference, the data for both groups can be expressed as percent peak oxygen consumption achieved (percent peak VO2) rather than as a function of absolute oxygen consumption (VO2). Ten healthy control subjects and 31 patients with chronic clinical class II and III heart failure were studied during upright maximal bicycle exercise. Eighteen of the 31 patients had primary cardiomyopathy and 13 had ischemic cardiomyopathy. The average ejection fraction at rest was 24 +/- 10% (+/- SD) in the group with heart failure. Heart rate, systolic blood pressure, VO2 and plasma norepinephrine levels were measured at rest and throughout exercise. When the data were expressed as a function of percent peak VO2 achieved, patients with heart failure demonstrated a flatter slope (p = 0.004) than normal in the response of plasma norepinephrine to exercise, indicating a relative blunting of sympathetic drive. This was accompanied by attenuated heart rate (p = 0.001) and blood pressure (p less than 0.001) responses. These differences were not apparent when the data are expressed as a function of absolute VO2.(ABSTRACT TRUNCATED AT 250 WORDS)
Patients with congestive heart failure (CHF) constitute a substantial portion of the caseloads of home care agencies. Home care is one strategy suggested for delaying or preventing hospital readmissions. This study examined the relationship between home care nursing services and hospital readmissions after 1176 discharges of patients with a primary diagnosis of CHF. It also described the home nursing care of such patients. Findings indicate that patients receiving home care nursing services were readmitted to the hospital significantly less often within a period of 90 days after hospital discharge.
Patients with congestive heart failure (CHF) are at increased risk of thromboembolic events. However, there is much debate and uncertainty over the use of antithrombotic therapy in these patients. The evidence for oral anticoagulation is limited, although large randomised trial data are forthcoming. Aspirin may be detrimental for heart failure due to a possible interaction with angiotensin-converting enzyme inhibitors, leading to increased hospitalisations from decompensated heart failure. The objective of this review article is to summarise the available evidence regarding the risk of stroke and thromboembolic events in CHF patients, as well as the effectiveness and risks of antithrombotic therapy in these patients.
Patients with congestive heart failure (CHF) are prone to increased skeletal muscle fatigue. Elevated circulatory concentrations of tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein-1, which may stimulate matrix metalloproteinase (MMP) activity and, thereby, contribute to skeletal muscle dysfunction, are frequently found in CHF. However, whether skeletal muscle MMP activity is altered in CHF is unknown. Hence, we have used a gelatinase assay to assess the activity of MMP and tissue inhibitors of MMP in single skeletal muscles of rats with CHF 6 wk after induction of myocardial infarction. Sham-operated (Sham) rats were used as controls. We also measured the gene expression and protein contents of MMP-2 and MMP-9 in skeletal muscles of these rats. Plasma MMP activity was nearly seven times higher (P < 0.05) in CHF than in Sham rats. Concomitantly, the MMP activity within single slow- and fast-twitch skeletal muscles of CHF rats increased two- to fourfold compared with Sham animals, whereas tissue inhibitor of MMP activity did not differ (P > 0.05). Preformed MMP-2 and MMP-9 were probably activated in CHF, because neither their gene expression nor protein levels were altered (P > 0.05). Serum concentrations of TNF-alpha and monocyte chemoattractant protein-1 remained unchanged (P > 0.05) between CHF and Sham rats during the 6-wk observation period. We conclude that development of CHF in rats enhances MMP activity, which in turn may distort the normal contractile function of skeletal muscle, thereby contributing to increased skeletal muscle fatigue.
Treatment of congestive heart failure has changed dramatically during the past 20 years, but diuretic drugs remain an essential component. Diuretics are essential despite the fact that these drugs stimulate the renin-angiotensin-aldosterone (RAA) axis and lead to adaptive responses that may be counterproductive. In this paper, new diuretic drugs and new uses of older drugs are discussed. These approaches emphasize low-dose combination therapy and may prove superior to traditional approaches that rely exclusively on loop diuretics. Such approaches aim to prevent adverse compensatory processes that appear to result from chronic diuretic treatment. These include acute and chronic increases in plasma renin activity and stimulation of the sympathetic nervous system, both of which increase afterload and may tend to increase mortality. They also include adaptive changes in nephron structure and function resulting from diuretic-induced increases in distal sodium load and diuretic-induced neurohormonal stimulation. These adaptations blunt the effectiveness of diuretic therapy. Diuretic strategies that rely on combinations of diuretics are emphasized as a method to prevent resistance. If diuretic resistance does develop, higher-dose combination regimens, continuous diuretic infusions and mechanical ultrafiltration can be used to overcome diuretic adaptations and restore diuretic efficacy. The goal of reducing the extracellular fluid volume with the least stimulation of the RAA axis and minimal changes in nephron architecture can be achieved in many patients.
Congestive heart failure (CHF) is a major and increasing chronic disease in Western society, with a high mortality, morbidity and cost for unplanned hospital admissions. Continuous cardiorespiratory monitoring is required to detect Cheyne-Stokes respiration (CSR). We have tested a new wireless monitoring system and compared it with polysomnography (PSG) and respiratory inductance plethysmography (RIP) in six CHF patients with CSR in a sleep laboratory. The wireless system compared well with RIP for the detection of CSR but less well with PSG, which had unexpected but significant respiratory sensing errors that led to misclassification of the respiratory disorder present. The wireless system could be used to select CHF patients for better-customized treatment at home as part of a specialist-supported community telemedicine programme.
With developing congestive heart failure (CHF), activation of the vasopressin V(1a) and angiotensin II type 1 (AT(1)) receptors can occur. In the present study, we examined the direct effects of V(1a) receptor blockade (V(1a) block), selective AT(1) receptor blockade (AT(1) block), and dual V(1a)/AT(1) receptor blockade (dual block) with respect to left ventricular (LV) function and contractility during the progression of CHF. LV and myocyte functions were examined in pigs with pacing CHF (rapid pacing, 240 beats/min, 3 weeks, n = 10), pacing CHF with concomitant V(1a) block (SR49059, 60 mg/kg, n = 8), pacing CHF with concomitant AT(1) block (irbesartan, 30 mg/kg, n = 7), or pacing CHF with dual block (n = 7). LV end-diastolic dimension and peak wall stress were reduced in all receptor blockade groups compared with CHF values. However, LV fractional shortening was increased only in the dual block group compared with CHF values (29 +/- 3 versus 21 +/- 2, P <.05). Basal LV myocyte percent shortening increased in the dual block group compared with CHF values (3.44 +/- 0.23 versus 2.88 +/- 0.11, P <. 05). Although V(1a) or AT(1) block reduced LV loading conditions, only dual block resulted in improved LV and myocyte shortening.
Pathophysiology of congestive heart failure (CHF) has undergone a remarkable evolution during the last two decades. CHF is now regarded especially as a neurohormonal disease and not only as a cardiocirculatory impairment. Many studies have emphasized that an abnormal neuroendocrine activation precedes the development of clinically recognized heart failure and plays an important pathogenetic role in progression of this disease. In patients with CHF, moreover, circulating levels of some neurohormonal factors have an independent negative prognostic value. More recently immunological and molecular biology studies have also demonstrated the negative effects exerted by some cytokines and by apoptosis. Correction of neurohormonal disorder is the rationale of therapeutical approach to patients with CHF and appears the only way to significantly decrease mortality. In this review the role of neuroendocrine activation in the pathophysiology of CHF is analyzed.
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BACKGROUND: In congestive heart failure (CHF), endothelial dysfunction may contribute to impairment of exercise induced vasodilatation and decreased exercise capacity. We hypothesised that administration of L-arginine, a precursor of nitric oxide (NO) and postulated antioxidant, may improve endothelium-dependent vasodilatation and exercise capacity and also exert antioxidant activity. AIMS: To investigate the effect of oral supplementation with L-arginine on exercise capacity and markers of oxidative stress in patients with mild to moderate CHF. METHODS: The study had a randomised double-blind cross-over design. Twenty one patients with stable NYHA II-III CHF underwent three exercise tests: initially, after oral administration of L-arginine (9 g/day for 7 days) or placebo. Blood was sampled prior to each test for plasma lipid peroxides, reduced sulphydryl groups and leukocyte oxygen free radical production. RESULTS: We found a higher prolongation of exercise duration time after L-arginine than after placebo (99+/-106 vs 70+/-99 s, p<0.05). There were no significant differences in markers of free radical activity. CONCLUSIONS: In patients with chronic stable CHF, oral supplementation with L-arginine prolongs exercise duration which may be due to NO-induced peripheral vasodilatation. The antioxidant properties of L-arginine have not been confirmed in this ex vivo study.
Patients with congestive heart failure are at risk for hiperkaliemia because of coexisting comorbidities and use of multiple medications that impair potassium excretion--such as angiotensin-converting enzyme inhibitors or spironolactone. This is the case report about the patient with late drug-induced hyperkalemia. Causes and prevention methods used against development of this adverse event were explained.
Causes of congestive heart failure include hypertension, coronary artery disease, alcohol abuse and valvular heart disease. Two-dimensional echocardiography with Doppler examination is excellent for identifying valvular heart disease. While noninvasive screening for coronary artery disease may seem cost-effective, the consequences of a missed diagnosis are such that coronary angiography should be strongly considered if there is any suggestion of ischemic heart disease. Medical management primarily consists of vasodilators, diuretics and inotropic agents. Vasodilator therapy may prolong the patient's life. Digoxin and diuretics improve symptoms and hemodynamic abnormalities. With advanced heart failure, adequate control of fluid retention and dyspnea may require diuretic doses associated with azotemia, and systolic blood pressure may have to be maintained at less than 100 mm Hg in spite of postural hypotension.
Congestive heart failure (CHF) represents the inability of the heart to pump enough blood to meet tissue requirements for oxygen, resulting in a discrepancy between myocardial oxygen supply and demand. It can result from any clinical situation that alters myocardial performance, including end stage renal disease (ESRD). The purpose of this article is to describe the pathophysiology of CHF, major signs and symptoms, medical management, and nursing interventions in patients with ESRD.
Angiotensin-converting enzyme (ACE) inhibitors are used in the management of a wide range of cardiovascular conditions, including congestive heart failure (CHF). Although the experimental evidence in support of their use in CHF is incontrovertible, their pattern of usage has failed to keep pace with the research findings. One factor that has fueled the hesitancy to use ACE inhibitors in CHF has been the concern that renal function might worsen upon their receipt. Although the glomerular filtration rate may decline when ACE inhibitor or angiotension receptor blocker therapy is started in CHF, in most cases it is not a reason to discontinue therapy other than temporarily. Although ACE inhibitors and angiotensin receptor blockers may differ theoretically in their renal effects, published information to date has not shown such a difference. (c)2001 by CHF, Inc.
Dilated cardiomyopathy, owing to any cause, usually culminates in the clinical syndrome of congestive heart failure. Heart failure is characterized by exertional dyspnea and fatigue, but the precise mechanisms that produce these symptoms are still not clear. Sodium retention occurs early in heart failure, but this disturbance is dynamic in nature and is not always present in the patient. The mechanism of early salt and water retention in heart failure is not defined. Gross edema and ascites occur much later, undoubtedly owing to the convergence of a number of factors. The peripheral adaptations to heart failure include activation of the renin-angiotensin system and the sympathetic nervous system, and the release of AVP. The result is an increase in preload with a resultant increase in stroke volume for some patients, but the price is paid in the form of heightened impedance to ejection and circulatory congestion. The sympathetic nervous system disturbances in heart failure are striking, as disturbances in both circulating and myocardial NE levels are consistently found. Vasorelaxant and natriuretic hormones, as well as certain prostaglandins, may be released in an attempt to offset excessive "compensatory" pressor-sodium retentive mechanisms, but the net result seems to be excessive peripheral vasoconstriction and a downward spiral of deterioration in many patients. One would hope that an unraveling of the complex pathophysiology of heart failure would lead to therapy that would change the natural history of the disease. The results of the first V-HeFT trial give room for cautious optimism in this regard.
The present study was undertaken to verify the hypothesis that infusion of atrial natriuretic peptide (ANP) might lower preload and be beneficial in the treatment of pulmonary congestion even without a diuresis in patients with acute renal failure (ARF) secondary to severe congestive heart failure (CHF). We studied 22 patients with ARF secondary to CHF. The mean age of the patients (14 men and 8 women) was 72 years (range 36 to 85 years). Seven of the patients had dilated cardiomyopathy, ten had ischemic heart disease, and five had valvular heart disease. ANP was infused intravenously and the following data before and 1 hour after the start of ANP infusion were recorded; urinary output, systemic blood pressure (SBP), pulmonary blood pressure (PBP), right atrial pressure (RAP), cardiac index (CI), heart rate (HR), and arterial blood oxygen partial pressure. Diastolic PBP were employed as pulmonary capillary wedge pressure. Urinary output did not change. Mean SBP decreased from 92 to 85 mmHg (p < 0.05), and mean PBP decreased from 34 to 28 mmHg (p < 0.01). Mean RAP decreased from 11 to 9 mmHg (p < 0.01) and diastolic PBP decreased from 25 to 19 mmHg (p < 0.01). HR did not change significantly and CI increased 2.4 to 2.5 mi/min/m2 (p < 0.05). Arterial blood oxygen partial pressure increased significantly from 71 to 82 mmHg (p < 0.05). In conclusion, ANP decreased preload and improved arterial blood oxygen partial pressure, though diuretic response to ANP is attenuated in ARF secondary to CHE. Infusion of ANP will be very beneficial in cases in which dyspnea and pulmonary edema due to elevation of preload are the principal clinical problems.
BACKGROUND: Patients with congestive heart failure have a high mortality rate and are also hospitalized frequently. We studied the effect of an angiotensin-converting-enzyme inhibitor, enalapril, on mortality and hospitalization in patients with chronic heart failure and ejection fractions less than or equal to 0.35. METHODS: Patients receiving conventional treatment for heart failure were randomly assigned to receive either placebo (n = 1284) or enalapril (n = 1285) at doses of 2.5 to 20 mg per day in a double-bind trial. Approximately 90 percent of the patients were in New York Heart Association functional classes II and III. The follow-up averaged 41.4 months. RESULTS: There were 510 deaths in the placebo group (39.7 percent), as compared with 452 in the enalapril group (35.2 percent) (reduction in risk, 16 percent; 95 percent confidence interval, 5 to 26 percent; P = 0.0036). Although reductions in mortality were observed in several categories of cardiac deaths, the largest reduction occurred among the deaths attributed to progressive heart failure (251 in the placebo group vs. 209 in the enalapril group; reduction in risk, 22 percent; 95 percent confidence interval, 6 to 35 percent). There was little apparent effect of treatment on deaths classified as due to arrhythmia without pump failure. Fewer patients died or were hospitalized for worsening heart failure (736 in the placebo group and 613 in the enalapril group; risk reduction, 26 percent; 95 percent confidence interval, 18 to 34 percent; P less than 0.0001). CONCLUSIONS: The addition of enalapril to conventional therapy significantly reduced mortality and hospitalizations for heart failure in patients with chronic congestive heart failure and reduced ejection fractions.