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PubMed2000

Load dependent diastolic dysfunction in heart failure.

Congestive heart failure may result from cardiovascular overload, from systolic or from diastolic dysfunction. Diastolic left ventricular dysfunction may result from structural resistance to filling such as induced by pericardial constraint, right ventricular compression, increased chamber stiffness (hypertrophy) and increased myocardial stiffness (fibrosis). A distinct and functional etiology of diastolic dysfunction is slow and incomplete myocardial relaxation. Relaxation may be slowed by pathological processes such as hypertrophy, ischemia and by asynchronous left ventricular function. The present contribution analyses the occurrence of slow and incomplete myocardial relaxation in response to changes in systolic pressure and in response to changes in venous return. The regulation of myocardial relaxation by load is critically dependent on the transition from myocardial contraction to relaxation, which occurs in dogs when 82% of peak isovolumetric pressure has developed or at a relative load of 0.82. This corresponds to early ejection in normal hearts, but is situated even before aortic valve opening in severely diseased hearts. When load is developed beyond this transition, relaxation becomes slow and even incomplete. This is load dependent diastolic dysfunction. Load dependent diastolic dysfunction occurs in normal hearts facing heavy afterload and in severely diseased hearts even with normal hemodynamic parameters. This dysfunction should contribute to elevating filling pressures in most patients with severe congestive heart failure. This dysfunction can be reverted by decreasing systolic pressures or by decreasing venous return. Load dependent diastolic dysfunction gives us an additional reason to aggressively treat CHF patients with diuretics and vasodilators.

Animals↗
PubMed1996

[Sympathetic nervous system and endothelial function in heart failure].

Congestive heart failure is a frequent cardiovascular disease with a poor prognosis in advanced stages. Activation of neurohumoral systems such as the renin-angiotensin system and the sympathetic nervous system as well as impairment of local regulatory mechanisms (i.e. adrenoceptors, endothelial factors) play an important role in the pathogenesis and prognosis of the disease. The increase in peripheral resistance is due to imbalance of vasoconstrictors and vasodilators in favour of the vasoconstrictors and to changes in endothelial function, i.e. impaired production of nitric oxide, increased production of endothelin. Sodium and volume retention as well as the activation of the renin-angiotensin system increase preload. The sympathetic nervous system, which is known to be an independent negative prognostic factor, is activated and interacts with the renin-angiotensin system; however, up to now it is uncertain, whether these pathophysiological findings contribute to the development of congestive heart failure or if they are only secondary phenomena.

Amino Acid Sequence↗
PubMed2002

Cumulative effect of complete left bundle-branch block and chronic atrial fibrillation on 1-year mortality and hospitalization in patients with congestive heart failure. A report from the Italian network on congestive heart failure (in-CHF database).

BACKGROUND: Many clinical variables have been proposed as prognostic factors in patients with congestive heart failure. Among these, complete left bundle-branch block and atrial fibrillation are known to impair significantly left ventricular performance in patients with congestive heart failure. However, their combined effect on mortality has been poorly investigated. The aim of this study was to determine whether left bundle-branch block associated with atrial fibrillation had an independent, cumulative effect on mortality for congestive heart failure. METHODS AND RESULTS: We analysed the Italian Network on congestive heart failure (IN-CHF) Registry that was established by the Italian Association of Hospital Cardiologists in 1995. One-year follow-up data were available for 5517 patients. Complete left bundle-branch block and atrial fibrillation were associated in 185 (3.3%) patients. In this population the cause of congestive heart failure was dilated cardiomyopathy (38.4%), ischaemic heart disease (35.1%), hypertensive heart disease (17.3%), and other aetiologies (9.2%). This combination of electrical defects was associated with an increased 1-year mortality from any cause (hazard ratio, HR: 1.88; 95% CI 1.37-2.57) and sudden death (HR: 1.89; 95% CI 1.17-3.03) and 1-year hospitalization rate (HR: 1.83; 95% CI 1.26-2.67). CONCLUSIONS: In patients with congestive heart failure, the contemporary presence of left bundle-branch block and atrial fibrillation was associated with a significant increase in mortality. This synergistic effect remained significant after adjusting for clinical variables usually associated with advanced heart failure. We can conclude that this combination of electrical disturbances identifies a congestive heart failure specific population with a high risk of mortality.

Adolescent↗
PubMed1987

The role of hepatic venous congestion and endotoxaemia in the production of fulminant hepatic failure secondary to congestive heart failure.

The present study was undertaken to clarify the role of congestion of the liver and endotoxemia in the production of fulminant hepatic failure secondary to congestive heart failure. Induction of congestion of the liver, i.e. an elevation of hepatic venous pressure, in rats was accomplished by partial obstruction of the inferior vena cava. A close relationship was demonstrated between venous pressure and serum levels of transaminases as a measure of hepatic dysfunction. Hepatic dysfunction was mild in rats with venous hypertension alone, and only centrilobular congestion was seen on microscopy. In contrast, severe abnormalities of hepatic function were induced by venous hypertension and endotoxaemia. Histologically, the liver revealed bridging centrilobular necrosis as seen in patients with congestive heart failure who develop fulminant hepatic failure. These data suggest that coexistence of endotoxaemia and congestion of the liver may induce fulminant hepatic failure, and that the latter alone is associated only with slight hepatic dysfunction and liver damage.

Alanine Transaminase↗
PubMed1989

Short- and long-acting angiotensin-converting enzyme inhibitors: a randomized trial of lisinopril versus captopril in the treatment of congestive heart failure. The Multicenter Lisinopril-Captopril Congestive Heart Failure Study Group.

A randomized, parallel, double-blind study was performed with lisinopril, a long-acting angiotensin-converting enzyme inhibitor, versus captopril, a shorter-acting angiotensin-converting enzyme inhibitor, in the treatment of congestive heart failure. All patients were in New York Heart Association class II, III or IV and had remained symptomatic despite therapy with digoxin and diuretics. After a 4 to 14 day placebo baseline period, patients were randomized to receive either lisinopril, 5 mg orally once per day (n = 94), or captopril, 12.5 mg orally three times per day (n = 95), in addition to continuation of digoxin and diuretics. The dose of study drug could be doubled at 4 week intervals for a total of 12 weeks of double-blind therapy. The maximal dose was 20 mg once per day of lisinopril or 50 mg three times per day of captopril. The addition of either lisinopril or captopril to a regimen of diuretics or digoxin, or both, caused an increase in exercise duration as assessed on a motorized treadmill. When protocol violators were excluded, patients receiving lisinopril had a statistically greater increase in exercise duration than that of patients receiving captopril. In patients with renal impairment (serum creatinine greater than 1.6 mg/dl at baseline), lisinopril was superior to captopril in improving exercise duration. Lisinopril, but not captopril, increased left ventricular ejection fraction in patients with moderately to severely (less than 35%) decreased function (p less than 0.05). Improvement in functional capacity and quality of life, as assessed by the Yale Scale dyspnea/fatigue index, was significantly greater for the lisinopril group.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Predictors of sudden death and death from pump failure in congestive heart failure are different. Analysis of 24 h Holter monitoring, clinical variables, blood chemistry, exercise test and radionuclide angiography.

One hundred and ninety consecutive patients discharged with congestive heart failure were examined with clinical evaluation, blood chemistry, 24 h Holter monitoring, exercise test and radionuclide angiography. Median left ventricular ejection fraction was 0.30, 46% were in New York Heart Association class II and 44% in III. Total mortality after 1 year was 21%, after 2 years 32%. Of 60 deaths, 33% were sudden and 49% due to pump failure. Multivariate analyses identified totally different risk factors for sudden death: ventricular tachycardia, s-sodium < or = 137 mmol/l, s-magnesium < or = 0.80 mmol/l, s-creatinine > 121 mumol/l, and maximal change in heart rate during exercise < or = 35 min-1, and for death from progressive pump failure: New York Heart Association class III + IV, delta heart rate over 24 h < or = 50 min-1, low ejection fraction, high resting p-noradrenaline, s-urea > 7.6 mmol/l, s-potassium < 3.5 mmol/l, and maximal exercise duration < or = 4 min. In conclusion, this study demonstrated different risk factors for sudden death and for death from progressive pump failure.

Adult↗
PubMed2006

Laparoscopic implantation of the Tenckhoff catheter for the treatment of end-stage renal failure and congestive heart failure: experience with the pelvic fixation technique.

BACKGROUND: Peritoneal dialysis is a widely accepted route for renal replacement. With the advent of endoscopy, many surgical techniques for the prevention of catheter failure have been proposed. OBJECTIVES: To evaluate the outcomes of patients undergoing laparoscopic Tenckhoff catheter implantation using the pelvic fixation technique. METHODS: Data analysis was retrospective. All procedures were performed under general anesthesia. A double-cuffed catheter was inserted using two 5 mm trocars and one 10 mm trocar, fixing its internal tip to the dome of the bladder and its inner cuff to the fascia. Catheter failure was defined as persistent peritonitis/exit-site/tunnel infection, severe dialysate leak, migration or outflow obstruction. RESULTS: LTCI was performed in 34 patients. Mean patient age was 65 +/- 17 years. In 12 of the 34 patients the indication for LTCI was end-stage renal failure combined with NYHA class IV congestive heart failure. Operative time was 35 +/- 15 minutes. A previous laparotomy was performed in 9 patients. Hospital stay was 1.5 +/- 0.6 days. The first continuous ambulatory peritoneal dialysis was performed after 20 +/- 12 days. Median follow-up time was 13 months. There were several complications, including 5 (14%) exit-site/tunnel infections, 27 episodes (0.05 per patient-month) of bacterial peritonitis, 3 (9%) incisional hernias, 1 case of fatal intraabdominal bleeding, 2 (5.8%) catheter migrations (functionally significant), and 10 (30%) cases of catheter plugging, 8 of which were treated successfully by instillation of urokinase and 2 surgically. A complication-mandated surgery was performed in 8 patients (23.5%). The 1 year failure-free rate of the catheter was 80.8%. One fatal intraabdominal bleeding was recorded. CONCLUSIONS: LTCI is safe, obviating the need for laparotomy in high risk patients. Catheter fixation to the bladder may prevent common mechanical failures.

Adult↗
PubMed1992

Increased plasma concentrations of endothelin in congestive heart failure in humans.

Congestive heart failure is characterized by decreased cardiac output and increased peripheral vascular resistance. Endothelin, a peptide found in plasma, is a potent vasoconstrictor. We hypothesized that plasma concentrations of endothelin are increased in humans with congestive heart failure. Plasma samples were obtained from 71 healthy control subjects and 56 patients with congestive heart failure. The mean plasma concentration of endothelin, measured by radioimmunoassay, was 7.1 +/- 0.1 pg/ml in the 71 normal control subjects but 12.6 +/- 0.6 pg/ml in the 56 patients with heart failure (P = 0.001). To evaluate the relationship between circulating endothelin and clinical stage of congestive heart failure, we categorized patients into two groups--those with mild heart failure (New York Heart Association class I or II) and those with severe heart failure (class III or IV). Circulating endothelin in the 24 patients with mild disease was 11.1 +/- 0.7 pg/ml, significantly higher than in normal subjects (P < 0.001). Endothelin in the 32 patients with severe heart failure was 13.8 +/- 0.9 pg/ml, a level significantly higher than that in the group with mild disease (P = 0.029). In the 56 patients with congestive heart failure, a negative correlation was found between plasma concentration of endothelin and left ventricular ejection fraction (r = -0.279; P = 0.037). These data demonstrate that the plasma concentration of endothelin is increased in humans with congestive heart failure and that the level correlates with the severity of disease. Endothelin may have a role in the increased vascular resistance in patients with chronic congestive heart failure.

Adult↗
PubMed1976

Fulminant hepatic failure secondary to congestive heart failure.

An elderly female with an acute episode of congestive heart failure, unaccompanied by any periods of hypotension, developed fulminant hepatic failure with an accompanying coagulopathy. Attempts to establish an etiology for her acute hepatic insufficiency, other than cardiac failure, proved negative. Fulminant hepatic failure as a consequence of congestive heart failure, without prolonged periods of hypotension preceding alteration in hepatic function, has not heretofore been described. Liver function is adversely effected in congestive heart failure. Hepatic ammonia clearance is impaired in cardiac failure and may be diminished to the point of resulting in hepatic encephalopathy. Coagulopathy is a frequent concomitant of fulminant hepatic failure. Establishing a clear etiology for a coagulopathy in the face of concomitant liver disease is difficult, thus making any therapeutic intervention fraught with peril.

Aged↗
PubMed1991

Atrial natriuretic peptide concentration in dogs with congestive heart failure, chronic renal failure, and hyperadrenocorticism.

The function of atrial natriuretic peptide (ANP) is claimed to be control of salt and water homeostasis, and thus, the hormone may be involved in the pathogenesis of certain diseases with impaired volume regulation. We, therefore, studied plasma ANP concentration in dogs with chronic renal failure, congestive heart failure, and hyperadrenocorticism. Dogs with chronic renal failure had twofold higher plasma ANP concentration (16.2 +/- 5.8 fmol/ml), compared with healthy dogs (8.3 +/- 3.5 fmol/ml). An even more distinct increase (sixfold) of plasma ANP concentration was found in dogs with congestive heart failure (52.9 +/- 29.7 fmol/ml). In contrast, dogs with hyperadrenocorticism did not have high ANP plasma concentration (5.5 +/- 2.0 fmol/ml). High-performance liquid chromatographic analysis of plasma from dogs with congestive heart failure indicated that, in addition to the normal circulating form of ANP (99-126), the unprocessed precursor ANP (1-126) is detectable in the circulation. These qualitative and quantitative alterations of plasma ANP concentration in dogs further suggest involvement of this peptide in the development and/or maintenance of diseases associated with impaired volume regulation.

Adrenocortical Hyperfunction↗
PubMed1997

Pulmonary effect of amiodarone in patients with heart failure. The Congestive Heart Failure-Survival Trial of Antiarrhythmic Therapy (CHF-STAT) Investigators (Veterans Affairs Cooperative Study No. 320).

OBJECTIVES: The purpose of this study was to evaluate the pulmonary effects of amiodarone in patients with heart failure, in those with chronic obstructive pulmonary disease (COPD) and in those undergoing a surgical procedure. BACKGROUND: Amiodarone has been known to cause pulmonary complications; especially in those with COPD and in those undergoing a surgical procedure. METHODS: Patients receiving vasodilator therapy for congestive heart failure were prospectively randomized to placebo or amiodarone at 800 mg/day for 14 days, 400 mg/day for 50 weeks and then 300 mg/day thereafter. Chest X-ray film and pulmonary function tests with diffuse capacity of carbon monoxide (DLCO) were obtained at baseline and annually. The power to detect a 20% difference in DLCO at 1 year exceeded 90% in all patients and in those with COPD (two-sided alpha = 0.05). The sample allowed a 75% power to detect pulmonary complications (1% vs. 5%) between the two treatment groups. RESULTS: There was no difference in baseline characteristics between patients randomized to amiodarone (n = 269) or placebo (n = 250). The DLCO measurements at randomization were 18.3 +/- 6.9 and 17.7 +/- 7.6 ml/min per mm Hg for the amiodarone and placebo groups, respectively (p = 0.3). At 1 and 2 years, DLCO measurements were 17.7 +/- 7.0 and 18.3 +/- 7.7 ml/min per mm Hg for the amiodarone group and 17.9 +/- 7.2 and 18.2 +/- 7.2 for the placebo group, respectively. There were no significant differences between the groups, with corresponding p values of 0.73 ad 0.96 at years 1 and 2, respectively. Among patients with COPD, DLCO measurements at randomization were 17.9 +/- 6.7 and 15.8 +/- 6.8 ml/min per mm Hg for the amiodarone and placebo groups, respectively. At years 1 and 2, DLCO measurements were 16.6 +/- 7.8 and 17.8 +/- 9.5 ml/min per mm Hg for the amiodarone group and 16.5 +/- 6.6 and 16.3 +/- 7.0 ml/min per mm Hg for the placebo group, with corresponding p values of 0.95 and 0.48, respectively. There was no difference in survival free of noncardiac or perioperative deaths between patients assigned to amiodarone or placebo. Pulmonary fibrosis was diagnosed in four patients (1.1%) treated with amiodarone and in three patients (0.8%) receiving placebo. CONCLUSIONS: Our study shows that amiodarone can be safely used, with an acceptable pulmonary toxicity, in patients with heart failure.

Aged↗
PubMed1996

Case report: reversible mitral regurgitation and congestive heart failure complicating thyrotoxicosis.

Congestive heart failure is a relatively uncommon manifestation of thyrotoxic heart disease, and different mechanisms have been proposed. The authors present a possible explanation of congestive heart failure in some cases of thyrotoxicosis. A 39 year-old woman with Graves' disease was hypermetabolic, in atrial fibrillation, and had signs of congestive heart failure. She had a loud murmur of mitral regurgitation, clinical cardiomegaly, accentuated pulmonic sound, and peripheral edema. Propranolol reduced the heart rate to 60 beats per minute, but the loud mitral regurgitation murmur persisted. Echocardiographic and angiographic data were consistent with moderate to severe mitral regurgitation, serious enough to consider mitral valve replacement. As the patient's hyperthyroid state came under control, weight increased and the cardiac murmur resolved. After radioactive iodine treatment and the return to a eumetabolic state, an echocardiogram revealed only trace mitral regurgitation, with near normal left ventricular function and pulmonary arterial systolic pressures. These findings were confirmed by subsequent cardiac catheterization. The authors believe that mitral regurgitation, perhaps secondary to intrinsic papillary muscle dysfunction from hyperthyroidism, was the major cause of reversible congestive heart failure in this case. Valvular disease may play a more substantive role in thyrotoxic heart disease than previously recognized.

Adult↗
PubMed1995

ACE inhibitors and calcium antagonists in the treatment of congestive heart failure.

The increased mortality after myocardial infarction is related to the risk of reinfarction, sudden death, and the development and progression of heart failure; in congestive heart failure it is due to the progression of heart failure and sudden death. ACE inhibitors have been proven to prevent cardiovascular events, especially the progression of heart failure, in postinfarct patients with reduced ejection fraction and heart failure in the SAVE and AIRE trials. In patients with congestive heart failure, ACE inhibitor treatment has prevented cardiovascular death and reduced morbidity due to progressive heart failure in the SOLVD trials. In post-myocardial infarction patients, the calcium antagonist nifedipine did not affect mortality or morbidity; diltiazem improved prognosis in patients without congestive heart failure and in patients with non-Q-wave infarction; and verapamil improved prognosis by prevention of reinfarction and sudden death. Combination treatment with both verapamil, which has pronounced antiischemic properties and prevents sudden death and reinfarction, and an ACE inhibitor, which prevents the progression of heart failure, is a possibility for future cardiovascular therapy that should be evaluated.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

What is the role of the coronary circulation in congestive heart failure?

Manifestations of congestive heart failure are frequently observed in patients with coronary disease. However, they may be predominant in patients who have sustained prior myocardial infarction, in whom left ventricular aneurysm or papillary muscle dysfunction may induce left ventricular dysfunction. A small group of patients can develop severe cardiac insufficiency and pump failure on the basis of diffuse occlusive coronary artery disease. Heart failure can also be induced by congenital coronary abnormalities and in congestive cardiomyopathy some previous studies have suggested a decrease of coronary blood flow per unit of myocardial mass. Moreover, coronary artery disease can be associated and worsened congestive heart failure can result from other causes (e.g. valvular disease). However, congestive heart failure per se can also disturb coronary circulation as a result of changes in subendocardial myocardial perfusion or metabolism.

Coronary Circulation↗
PubMed2000

Plasma bradykinin levels in human chronic congestive heart failure.

Induction of congestive heart failure by high-frequency pacing has been reported to increase plasma levels of immunoreactive kinins in dogs. In the present study, we evaluated plasma bradykinin levels in human heart failure. Utilizing a recently developed method, we specifically measured plasma levels of bradykinin-(1-9) nonapeptide in 21 patients with chronic congestive heart failure [New York Heart Association (NYHA) stages III and IV). At the same time, we measured plasma atrial natriuretic peptide levels and plasma renin activity, and, as a marker of inflammation, plasma levels of tumour necrosis factor. In addition, 18 healthy subjects matched for gender and age served as normal controls. Plasma bradykinin concentrations were not higher in patients with chronic congestive heart failure (median 2.1 fmol/ml) than in healthy subjects (2.6 fmol/ml). In contrast, plasma atrial natriuretic peptide levels were clearly higher (patients, 63 fmol/ml; controls, 24 fmol/ml; P<0.0001), despite diuretic treatment and in the presence of high plasma renin activity (patients, 13.0 ng x h(-1) x ml(-1); controls, 0.3 ng x h(-1) x ml(-1); P<0.0001). Tumour necrosis factor was elevated in heart failure patients in NYHA class IV only (27 pg/ml, compared with 21 pg/ml in controls; P=0.013). Bradykinin, atrial natriuretic peptide and plasma renin activity levels were not correlated with the severity of the disease, as assessed by NYHA classification. These results indicate that a rather selective cytokine activation, without concomitant stimulation of the kallikrein-kinin system, occurs in human chronic congestive heart failure.

Aged↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: Vasopeptidase inhibition and its role in congestive heart failure.

Vasopeptidase inhibition--that is, the dual inhibition of ACE and neutral endopeptidase-reduces blood pressure in a potent manner. Preliminary studies suggest that vasopeptidase inhibition can also effectively treat congestive heart failure. Additional corroborating studies to support the use of vasopeptidase inhibition in heart failure are now underway. (c)2000 by CHF, Inc.

Journal Article↗
PubMed1991

Decreased coronary sinus oxygen content: a predictor of adverse prognosis in patients with severe congestive heart failure.

Patients with congestive heart failure have abnormal coronary hemodynamics, characterized by decreased coronary sinus oxygen content, increased coronary sinus blood flow and increased myocardial oxygen consumption. To evaluate their prognostic importance, the clinical characteristics and systemic and coronary hemodynamics were related to survival in 91 patients with severe congestive heart failure and decreased ejection fraction (25.5 +/- 10% [mean +/- SD]). In 69 patients congestive heart failure was due to or secondary to coronary artery disease (group 1) and in 22 it was due to idiopathic dilated cardiomyopathy (group 2). Five patients were in functional class II, 48 in class III and 38 in class IV. The median survival time was 20.7 months. As assessed with the Cox proportional hazards model, coronary sinus oxygen content was most strongly associated with a poor prognosis. On the basis of a comparison between the lowest (coronary sinus oxygen content less than or equal to 4.44 vol%) and highest quintile (coronary sinus oxygen content greater than 4.44 vol%), a low coronary sinus oxygen content was associated with a 2.34-fold increased risk of dying (95% confidence interval, 1.31 to 4.08). A low systolic blood pressure and a high diastolic pulmonary artery pressure were also significantly associated with increased mortality. Patients in the subgroup with a low coronary sinus oxygen content had values for functional class, ejection fraction and systemic hemodynamics similar to those of patients in the subgroup with high coronary sinus oxygen content. It is concluded that a low coronary sinus oxygen content indicative of noncompensated metabolic demand suggests a poor prognosis in patients with severe congestive heart failure.

Aged↗