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At least 199 records · Page 11Linked to original sources
PubMed1996

Congestive heart failure: increased cardiac and extracardiac atrial natriuretic peptide gene expression.

OBJECTIVES: The present investigation was designed to determine if atrial natriuretic peptide (ANP) gene expression increases in extracardiac as well as within the heart in congestive heart failure. METHODS: Congestive heart failure (CHF) was induced by producing cardiac hypertrophy secondary to an aortocaval fistula in Sprague-Dawley rats. To characterize this model, control and CHF rats had cardiac catheterizations and transthoracic echocardiography. ANP messenger RNA was measured by RNAase protection analysis in atria, ventricles, liver, colon, and stomach of CHF and sham rats and quantitated by 2-D scanning. The product of ANP gene expression was determined in each of these tissues with high performance-gel permeation chromatography. To help determine if increased degradation of atrial natriuretic peptides occur in congestive heart failure, the circulating concentrations and the excretion of the atrial natriuretic peptides into urine were measured by specific radioimmunoassays. RESULTS: ANP steady-state mRNA increased 4.2 +/- 0.05 and 4.3 +/- 0.06-fold, respectively, in the antrum of the stomach and within the heart ventricle of CHF rats compared with age-matched sham rats. ANP gene expression was present but not increased in atria, liver, and gastrointestinal tract of the CHF rats. High-performance gel permeation chromatography revealed that the product of this ANP gene expression within the stomach and heart ventricle in CHF animals was the ANP prohormone. There was not any decrease in the metabolism of these peptides by the kidney in CHF. CONCLUSIONS: ANP steady-state mRNA increases in extracardiac (i.e., stomach antrum) tissue as well as in the ventricle of the heart in CHF. The product of the ANP gene expression, i.e., the ANP prohormone is the same in the extracardiac tissues as within the heart. Whether the increased extracardiac ANP steady-state mRNA and its resultant increased atrial natriuretic peptides helps prevent bowel wall edema in CHF needs to be elucidated.

Animals↗
PubMed1999

Effect of isosorbide-5-mononitrate on exercise performance and clinical status in patients with congestive heart failure. Results of the Nitrates in Congestive Heart Failure (NICE) Study.

BACKGROUND AND AIMS: Nitrate therapy improves hemodynamics in patients with heart failure, but the chronic effects of oral nitrates on exercise performance and clinical status have not been well studied. METHODS: Oral isosorbide-5-mononitrate (ISMN) (50 mg once daily) or placebo was administered to 136 patients (NYHA Class 2-3) treated for heart failure, all receiving captopril and most also furosemide. Endpoints were treadmill exercise time at 12 weeks by modified Naughton protocol (primary), with an additional 12-week follow-up period. Secondary endpoints included left ventricular dimensions, ejection fraction, cardiothoracic ratio, functional class, quality of life, hospitalizations and plasma norepinephrine and atrial natriuretic peptide in a four-center substudy. RESULTS: Intention-to-treat analysis showed that mean change in treadmill exercise duration tended to be greater in patients receiving ISMN than placebo (treatment difference +42 s, 95% CI -5, +90 s at 12 weeks and +21 s, 95% CI -25, +74 s after 24 weeks) (NS). Treatment difference was greater in the prespecified subgroup with ejection fraction 31-40% (+55 s, 95% CI -11, +136 s at 12 weeks and +65 s, 95% CI +3, +147 s) (p = 0.035) at 24 weeks. No deleterious effects (i.e. hypotension) were observed with ISMN, although headache was reported in 19% of the active treatment group (p = 0.0001). CONCLUSIONS: ISMN added to captopril increased treadmill exercise time in patients with heart failure and a lesser reduction in baseline ejection fraction, although for the group as a whole, the increase in treadmill time was not significant.

Administration, Oral↗
PubMed2003

The rational use of diuretics in heart failure.

Congestive heart failure is a progressive hemodynamic disorder associated with significant morbidity and mortality. Concomitant renal dysfunction is frequently seen in patients with heart failure, and can compromise fluid regulation, leading to acute decompensation, and increased morbidity and mortality. Diuretic therapy has been the mainstay for treatment of congestive symptoms, despite documented mortality benefits. Misuse or overuse of diuretics can have negative consequences in heart failure, and optimizing diuretic efficiency may improve outcomes. In addition, new agents targeting elevated neuropeptides may prove to be beneficial in regulating fluid status and optimizing renal function.

Disease Progression↗
PubMed1998

Nocturnal oxygen and hypercapnic ventilatory response in patients with congestive heart failure.

Patients with congestive heart failure and Cheyne-Stokes respiration have a low arterial oxygen saturation, especially during sleep, which can be increased by breathing oxygen. Chronic alterations in blood gases are known to modulate the hypercapnic ventilatory response (HCVR). We therefore evaluated whether the HCVR is influenced by nocturnal nasal oxygen in patients with heart failure and Cheyne-Stokes respiration. Twenty patients with chronic congestive heart failure and a left ventricular ejection fraction < or = 35% (mean 18.3% +/- SD 6.0%) as well as 25 healthy control subjects were studied. The patients were assigned to 1 week each of nocturnal nasal oxygen and room air with a flow of 41 min-1 in a randomized cross-over fashion. After each week resting ventilation and HCVR were evaluated by the rebreathing technique. Breathing oxygen during the night for 1 week increased the basal nocturnal oxygen saturation from 92.5% +/- 1.6% to 96.5% +/- 0.9% (P < 0.000,01) and reduced Cheyne-Stokes respiration. HCVR was 1.22 +/- 0.90 l min-1 mmHg-1 after nocturnal room air and did not differ from that in the control subjects (1.31 +/- 0.62 l min-1 mmHg-1). In the patients HCVR decreased to 0.91 +/- 0.52 l min-1 mmHg-1 after nocturnal oxygen (P = 0.019). There were no significant changes with nocturnal oxygen in resting minute ventilation, respiratory rate or end-tidal PCO2. We conclude that nocturnal nasal oxygen reduces HCVR in patients with congestive heart failure and Cheyne-Stokes respiration.

Carbon Dioxide↗
PubMedDate not supplied

Successful weaning from milrinone of a patient with severe congestive heart failure using carvedilol.

Congestive heart failure is a major and growing health care concern worldwide, and mortality in patients with severe heart failure is high. Few options are available to patients with New York Heart Association class IV heart failure refractory to oral medical therapy. Over the last 15-20 years milrinone, a phosphodiesterase-III inhibitor, has been used occasionally to treat patients with acute heart failure and as a bridge to heart transplantation and, more recently, has been used intermittently or continuously on an outpatient basis. We report a patient with severe, chronic congestive heart failure, whom we treated successfully with continuous milrinone infusions as an outpatient. We were able to wean him of the milrinone after successful up-titration of carvedilol. Nine months after discontinuation of milrinone the patient remains stable in New York Heart Association class I on high dose carvedilol. Research is required to validate the possibility that patients with severe heart failure may be successfully weaned from milrinone using carvedilol and achieve significant improvement of their functional status and quality of life. This may prove to be an effective strategy for the treatment of selected patients with severe, chronic congestive heart failure. (c)2001 by CHF, Inc.

Journal Article↗
PubMed2004

Interleukin-6 and B-type natriuretic peptide are independent predictors for worsening of heart failure in patients with progressive congestive heart failure.

BACKGROUND: Neurohormones and cytokines have been associated with poor prognosis in patients with congestive heart failure. However, direct comparisons between them are rare and the best predictor for worsening of heart failure remains to be elucidated. The aim of the study was to identify independent predictors for worsening of heart failure. METHODS: We studied 100 patients with congestive heart failure (LVEF <or=25%). Serum levels of interleukin-6 (IL-6), tumor necrosis factor (TNF)-alpha, aminoterminal atrial natriuretic peptide (N-ANP), B-type natriuretic peptide (BNP), aminoterminal B-type natriuretic peptide (N-BNP), norepinephrine (NE) and big endothelin (big ET) were measured at entry into the study. Univariate and stepwise multivariate regression analyses were performed to compare variables and clinical parameters. The end-point was defined as worsening of heart failure. RESULTS: During follow-up (mean 378 days), 30 patients reached the defined end-point. Univariate risk factors of worsening of heart failure were IL-6 (p = 0.0001), log BNP (p = 0.0001), log N-ANP (p = 0.0259), big ET (p = 0.0032), log N-BNP (p = 0.0495), NE (p = 0.0013) and LVEF (p = 0.0498). Multivariate regression analysis identified IL-6 as the strongest independent predictive value for worsening of heart failure (p = 0.0001), followed by log BNP (p = 0.0002). Mean IL-6 levels were 1.76 +/- 1.73 in stable patients and 4.62 +/- 7.98 pg/ml in patients who developed worsening of heart failure. Using a cut-off value of 1.66 pg/ml for IL-6 Kaplan-Meier freedom from worsening, heart failure was significantly higher in patients below this cut-off point compared with those above (p = 0.0002). CONCLUSIONS: IL-6 and BNP independently predict worsening of heart failure. A single measurement could help to identify patients at high risk for worsening of heart failure and these individuals should be monitored more closely.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Cardiac troponin levels in heart failure.

Congestive heart failure (CHF) is a major cardiovascular disorder that is increasing in incidence, prevalence, and lethality. The prognostic significance of cardiac troponin levels among symptomatic and asymptomatic CHF has attracted recent interest. We sought to assess the significance of cardiac troponins in heart failure. These cardiac markers are associated with decreased left ventricular ejection fraction and poor prognosis in patients with CHF and are related to the severity of heart failure. The mechanism for the release of these markers seems to be from ventricular remodeling, ongoing myocyte degeneration, the presence of coronary artery disease, and reduced coronary reserve. In addition to B-type (brain) natriuretic peptide (BNP), cardiac troponin levels measured in patients admitted to the hospital could help risk-stratify patients and manage them effectively. BNP and cardiac troponins are easy to measure and can be repeated many times to follow patients, without interobserver variability. Theoretically, BNP is a marker of heart failure status and cardiac troponin is a marker of myocyte injury. The first therapeutic goal could be relief of circulatory congestion and lowering of BNP. The second goal could be attenuation of myocyte injury and lowering of cardiac troponins. Measuring and monitoring the levels of both could be highly effective means to reliably stratify the patients into low-, intermediate-, and high-risk groups for cardiac events and progression of heart failure. Furthermore, large-scale trials are necessary to establish them as noninvasive monitoring markers of heart failure and effectiveness of treatment.

Biomarkers↗
PubMed1997

Bone mass, vitamin D deficiency, and hyperparathyroidism in congestive heart failure.

PURPOSE: In contrast to renal and hepatic failure, congestive heart failure (CHF) has not been associated with a defined metabolic bone disorder. However, low bone mass has been reported in patients with CHF who receive a cardiac transplant. Both the pathophysiology and therapy of CHF may influence bone and mineral homeostasis and evidence that calciotropic hormones may affect cardiovascular function is accumulating. Therefore, we evaluated patients with severe CHF to determine the prevalence of osteoporosis and to characterize relationships between mineral homeostasis, bone turnover, bone mass, and severity of CHF. PATIENTS AND METHODS: One hundred one patients (79 men and 22 women, aged 25 to 70 years) with severe CHF (New York Heart Association functional class III or IV) referred for consideration for cardiac transplantation were evaluated with measurements of serum 25-hydroxyvitamin D (25-OHD), 1,25 dihydroxyvitamin D [1,25(OH)2D], intact parathyroid hormone (PTH), markers of bone turnover (serum osteocalcin, urinary hydroxyproline, and pyridinium crosslinks); bone mineral density (BMD) by dual energy x-ray absorptiometry was measured in 91 patients. Left ventricular ejection fraction (LVEF) and resting cardiac output (CO) were determined in 88 and maximal treadmill exercise testing and peak oxygen consumption were performed in 45 patients. RESULTS: Osteoporosis (T score < or = -2.5) was present in 7% at the lumbar spine, 6% at the total hip, and 19% at the femoral neck. Osteopenia (T scores between -1.0 and -2.5) was present in 43% at the lumbar spine, 47% at the total hip, and 42% at the femoral neck. Women were more severely affected (P = 0.007). Frankly low serum 25-OHD (< or = 9 pg/mL) and 1,25(OH)2D (< or = 15 pg/mL) levels were found in 17% and 26% of the patients, respectively, and elevated serum PTH (> or = 65 pg/mL) in 30%. Both low serum 1,25(OH)2D and increased serum PTH were associated with prerenal azotemia. Low serum vitamin D metabolites were associated with biochemical evidence of increased bone turnover, but BMD did not differ by vitamin D or PTH status. Patients with more severe CHF had significantly lower vitamin D metabolites and higher bone turnover, whereas elevated PTH was associated with better LVEF (21 +/- 1 versus 18 +/- 1%; P = 0.05) and correlated positively with resting CO (R = 0.220; P = 0.04). CONCLUSIONS: Osteopenia or osteoporosis were observed in approximately half of these patients with severe CHF. Abnormal calciotropic hormone concentrations, also common, were associated with evidence of increased bone resorption but were not related to BMD in this cross-sectional study. Abnormal concentrations of calciotropic hormones were related to the severity of cardiovascular compromise. Because both low BMD and low serum concentrations of 25-OHD in patients with CHF are associated with higher rates of bone loss and fracture after cardiac transplantation, patients should be evaluated for and receive appropriate therapy for these disorders.

Absorptiometry, Photon↗
PubMed1991

[A case of fulminant hepatic failure secondary to congestive heart failure].

It has been generally accepted that congestive heart failure does not lead to fulminant hepatic failure, unless it is associated with cardiac shock or low cardiac output. Only three cases have been reported, in which liver congestion is followed by fulminant hepatic failure without a history of shock or low cardiac output. Here we present a case of a 48-year-old man with dilated cardiomyopathy and pulmonary infarction, who developed fulminant hepatic failure from congestion. When he was admitted for the control of diabetes mellitus, hepatomegaly of 3-finger breadth and marked cardiomegaly without pulmonary congestion was noted. Diabetes was controlled using insulin. But 3 weeks after admission, he sometimes complained of back dullness because of pulmonary infarction. His heart gradually increased in size, and Jugular venous dilatation and pretibial pitting edema also worsened. Jaundice was noted and serum GOT and GPT increased. A large liver of 6-finger breath below the right costal margin was able to be felt. But within one week, the size of the liver markedly decreased and the signs of hepatic failure such as jaundice, hepatic encephalopathy and numerous petechiae appeared. Blood pressure was maintained and no hypotension or cardiac shock was noted. The patient died of fulminant hepatic failure on the 20th days after onset of the hepatic failure. The autopsy revealed liver atrophy with severe central lobular necrosis, and thrombus in the right main pulmonary artery which caused severe pulmonary infarction. The mechanism of fulminant hepatic failure not accompanied with low cardiac output is discussed.

Cardiomyopathy, Dilated↗
PubMed2000

Effect of mibefradil, a T-type calcium channel blocker, on morbidity and mortality in moderate to severe congestive heart failure: the MACH-1 study. Mortality Assessment in Congestive Heart Failure Trial.

BACKGROUND: Calcium antagonists have proved disappointing in long-term congestive heart failure (CHF) studies. Mibefradil, a new calcium antagonist that selectively blocks T-type calcium channels, has been shown to be an effective antihypertensive, antianginal, and anti-ischemic agent, and because of its different mechanism of action, it may be beneficial as adjunct therapy in CHF patients. METHODS AND RESULTS: This multicenter, randomized, double-blind study compared mibefradil with placebo as adjunct to usual therapy in 2590 CHF patients (NYHA class II to IV; left ventricular fraction <35%). The initial 50-mg daily dose of mibefradil was uptitrated to 100 mg after 1 month and continued up to 3 years. Patients were monitored at 1 week; 1, 2, and 3 months; and every 3 months thereafter. All-cause mortality, cardiovascular mortality, and cardiovascular morbidity/mortality were analyzed by use of the log-rank test (alpha=0.05). Substudies included exercise tolerance, plasma hormone and cytokines, echocardiography, and quality of life. Total mortality was similar between mibefradil- and placebo-treated patients (P=0.151). The 14% increased risk of mortality with mibefradil in the first 3 months was not statistically significant (P=0.093). Treatment groups had similar cardiovascular mortality (P=0.246), cardiovascular morbidity/mortality (P=0.783), and reasons for death or hospitalization. Patients comedicated with mibefradil and antiarrhythmics (class I or III), including amiodarone, had a significantly increased risk of death. Substudies demonstrated no significant differences between treatments. CONCLUSIONS: When used as adjunct therapy, mibefradil did not affect the usual outcome of CHF. The potential interaction with antiarrhythmic drugs, especially amiodarone, and drugs associated with torsade de pointes may have contributed to poor outcomes early in the study.

Aged↗
PubMed1991

Congestive heart failure. New frontiers.

Congestive heart failure is a common syndrome with high mortality in its advanced stages. Current therapy includes the use of vasodilator drugs, which have been shown to prolong life. Despite current therapy, mortality remains high in patients with severe heart failure. Potent new inotropic vasodilators have improved ventricular performance but have not prolonged life in patients with end-stage heart failure. Serious arrhythmias are implicated in the sudden deaths of 30% to 40% of patients with severe heart failure, but the benefits of antiarrhythmic therapy have not been established. Upcoming trials will address this question. Ventricular remodeling and progressive dilatation after myocardial infarction commonly lead to congestive heart failure; early unloading of the ventricle with an angiotensin-converting enzyme inhibitor may attenuate these events. These findings support the concept that angiotensin-converting enzyme inhibitors may be useful in managing heart failure of all degrees of severity, including left ventricular dysfunction and end-stage heart failure. Part of the damage that may occur with acute myocardial infarction, particularly in this era of thrombolysis therapy, is reperfusion injury, which may be mediated by oxygen-derived free radicals. Better knowledge of the mechanisms and treatment of myocardial infarction, the leading cause of congestive heart failure, may help prevent or attenuate the development of this syndrome.

Anti-Arrhythmia Agents↗
PubMed2002

Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure: a report from the Italian network on congestive heart failure.

BACKGROUND: A deleterious effect of complete left bundle-branch block (LBBB) on left ventricular function has been established. Nevertheless, the independent effect of a widened QRS on mortality rate in congestive heart failure (CHF) is still controversial. Therefore, we carried out this analysis to determine whether LBBB is an independent predictor of mortality in CHF. METHODS AND RESULTS: We analyzed the large Italian Network on CHF Registry of unselected outpatients with CHF of different causes. The registry was established by the Italian Association of Hospital Cardiologists in 1995. Complete 1-year follow-up data were available for 5517 patients. The main underlying cardiac diagnosis was ischemic heart disease in 2512 patients (45.6%), dilated cardiomyopathy in 1988 patients (36.0%), and hypertensive heart disease in 714 patients (12.9%). Other causes were recorded in the remaining 303 cases (5.5%). LBBB was present in 1391 patients (25.2%) and was associated with an increased 1-year mortality rate from any cause (hazard ratio, 1.70; 95% confidence interval, 1.41 to 2.05) and sudden death (hazard ratio, 1.58; 95% confidence interval, 1.21 to 2.06). Multivariate analysis showed that such an increased risk was still significant after adjusting for age, underlying cardiac disease, indicators of CHF severity, and prescription of angiotensin-converting enzyme inhibitors and beta-blockers. CONCLUSION: LBBB is an unfavorable prognostic marker in patients with CHF. The negative effect is independent of age, CHF severity, and drug prescriptions. These data may support the rationale of randomized trials to verify the effects on mortality rate of ventricular resynchronization with multisite cardiac pacing in patients with CHF and LBBB.

Adolescent↗
PubMed1985

Surgical treatment of an aneurysm of the vein of Galen in a newborn with heart failure.

Congestive heart failure is the usual complaint and cause of death in neonates with aneurysms of the great vein of Galen. Direct surgical obliteration of the feeding arteries cures the heart failure, but few such newborns survive the operation. The authors report a case of primary aneurysm of the great vein of Galen treated successfully by clipping the afferent arteries and reduction of the bulk of the aneurysm by bipolar coagulation. Five months after the operation the child's development is normal.

Cerebral Angiography↗
PubMed2005

Mechanisms of ventricular arrhythmias in heart failure.

Congestive heart failure continues to be a leading cause of mortality and morbidity worldwide. In approximately 50% of these patients, the mode of death is sudden. Ventricular tachycardia and fibrillation represent the majority of arrhythmias; the mechanisms responsible are heterogeneous and complex. Myocardial scar, a potent environment for reentry, is likely to contribute to many of the ventricular arrhythmias in ischemic heart failure. Altered calcium handling and changes in potassium currents may contribute to the increase in early and delayed afterdepolarizations seen in the failing heart. In addition, compensatory mechanisms may become deleterious and potentially arrhythmogenic via a variety of mechanisms. This article provides a general overview of the mechanisms thought to be responsible for ventricular arrhythmias in chronic heart failure.

Action Potentials↗