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PubMed2003

Thiamine deficiency in congestive heart failure patients receiving long term furosemide therapy.

OBJECTIVE: To assess the presence of thiamine deficiency in congestive heart failure patients receiving furosemide therapy. DESIGN: Prospective, biochemical analysis of thiamine status was performed in outpatients and inpatients of the University of Ottawa Heart Institute. SUBJECTS: Thirty-two patients with congestive heart failure who received at least 40 mg/day of furosemide were included. Patients were then separated into two groups depending on whether the dose of furosemide was greater than or equal to 80 mg/day. METHODS: The primary measure was actual thiamine status as assessed by the erythrocyte transketolase enzyme activity and the degree of thiamine pyrophosphate effect. RESULTS: Biochemical evidence of severe thiamine deficiency was found in 98% (24 of 25) patients receiving at least 80 mg/day of furosemide and in 57% (four of seven) of patients taking 40 mg furosemide daily, odds ratio (OR) 19.0 (1.13<OR<601.29). Thiamine status was not associated with any other clinical variables. CONCLUSIONS: These findings suggest that thiamine deficiency occurs in a substantial proportion of congestive heart failure patients being treated with furosemide.

Aged↗

PubMed2005

Prognostic value of elevated circulating heart-type fatty acid binding protein in patients with congestive heart failure.

BACKGROUND: Heart-type fatty acid binding protein (H-FABP) is released into the circulation when the myocardium is injured and is a novel marker for the diagnosis of acute myocardial infarction. The purpose of the present study was to examine the clinical significance of increased serum H-FABP levels in patients with congestive heart failure. METHODS AND RESULTS: Serum levels of H-FABP were measured in 179 patients admitted with congestive heart failure and 20 age-matched normal controls by using a sandwich enzyme-linked immunosorbent assay. Patients were prospectively followed during a mean follow-up period of 20 months with the end points of cardiac death and progressive heart failure requiring rehospitalization. Serum levels of H-FABP were higher in patients with congestive heart failure than in control subjects (5.7 +/- 4.8 ng/mL versus 2.7 +/- 0.8 ng/mL, P < .01) and increased with advancing NYHA class (P < .01). The cardiac event rate was markedly higher in patients with elevated H-FABP levels than in those with normal levels (43% versus 7%, P < .0001). Furthermore, the Cox multivariate proportional hazard analysis revealed that the elevated H-FABP level was the only independent predictor for cardiac events (chi2= 7.397, P < .01). CONCLUSIONS: Elevation of H-FABP indicates latent and ongoing cardiomyocyte damage and identifies patients at high risk for future cardiac events in congestive heart failure.

Aged↗

PubMed1990

Failure of captopril to prevent nitrate tolerance in congestive heart failure secondary to coronary artery disease.

The possible role of angiotensin-converting enzyme inhibition in preventing or minimizing tolerance to intravenous nitroglycerin in severe congestive heart failure (CHF) was studied by quantitating the degree of tolerance in 12 patients receiving nitroglycerin (group 1) and in 9 patients (group 2) receiving nitroglycerin and concurrent treatment with captopril (60 +/- 29 mg/day). At peak effect, nitroglycerin produced almost identical hemodynamic changes in both groups, with significant decreases in right atrial and pulmonary arterial wedge pressure, systolic blood pressure and systemic and pulmonary vascular resistances. Cardiac index increased. The extent of nitrate tolerance was calculated for each hemodynamic parameter as the percentage loss of the peak effect achieved by the drug. At 24 hours, 98 +/- 80% of the benefit achieved with respect to right atrial pressure was lost in group 1 and 61 +/- 74% in group 2 (group 1 vs 2, difference not significant). For pulmonary arterial wedge pressure, 51 +/- 31% (group 1) and 85 +/- 53% (group 2) (difference not significant) of the effect was lost, and for cardiac index, 53 +/- 58% (group 1) and 54 +/- 44% (group 2) (difference not significant). Tolerance was also almost identical regarding systolic blood pressure and systemic and pulmonary vascular resistance. Thus, the extent of tolerance to high-dose intravenous nitroglycerin in CHF was unaltered by administration of captopril, indicating that in clinical dosage, counter-regulatory neurohumoral mechanisms involving the renin-angiotensin system appear to be unimportant in its development.

Adult↗

PubMed1988

Changes of molecular forms of atrial natriuretic peptide after treatment for congestive heart failure.

In the present study, an attempt was made to clarify whether ANP molecular forms in the plasma of severe congestive heart failure patients differ from those in healthy persons and whether ANP molecular forms in the plasma of the patients were changed by successful treatment of cardiac disease. Twenty patients with congestive heart failure were treated at Kitasato University Hospital. They were classified as class III or IV by New York Heart Association criteria at the time of admission. Plasma ANP concentrations decreased after treatment from 356 +/- 58.2 to 72.3 +/- 14.8 pg/ml. The gel permeation chromatograms from the plasma of healthy persons showed low, or low and high molecular weight ANP peaks which correspond to the elution positions of authentic alpha-ANP or ribonuclease A (mol. wt., 13.7 kdalton). In patients with severe congestive heart failure at a severe stage, middle molecular weight ANP consisted with the elution position of authentic beta-ANP was particularly noted in addition of low and high molecular weight ANP peaks. This middle molecular weight peak disappears in most of cases by successful treatment. Molecular forms in the plasma obtained from the coronary sinus and the inferior or superior vena cava were essentially the same. These results indicate that the middle molecular weight ANP supposed as beta-ANP may particularly be secreted in severe congestive heart failure patients.

Adult↗

PubMed1982

Drug-induced conditioning in congestive heart failure.

Continuous 72-hour infusions of dobutamine reportedly effect sustained clinical improvement in patients with congestive heart failure. This study was designed to determine if shorter, more frequent infusions, delivered in an outpatient setting, elicit a similar response. Twenty-six patients with moderately severe congestive heart failure were randomized, 11 into a control group and 15 into a dobutamine treatment group. Baseline data were collected for 4 weeks in each group. Thereafter, the dobutamine treatment group received 4-hour infusions of dobutamine weekly for 24 weeks. Systolic time intervals, echocardiography, cardiac index and treadmill exercise tolerance were used to follow the progress of the control and dobutamine treatment groups. The ratio of preejection period to left ventricular ejection time and the cardiac index did not change significantly in either group. The velocity of circumferential fiber shortening and the percent change in the minor axis of the left ventricle during systole improved modestly (p less than 0.05) above baseline in the dobutamine group after 14 weeks of treatment and above the corresponding control values (p less than 0.05) after 22 weeks. Exercise tolerance (duration) improved 25--51% (all p less than 0.05) above baseline in the dobutamine group compared with 10--17% (all p greater than 0.05 vs baseline) in the control group. Heart rate at maximal exercise did not change significantly from baseline for either group and did not differ significantly between the two groups. Functional classification improved in 12 of 15 dobutamine treatment patients and in only two of 11 control patients (p less than 0.05). In our patients with congestive heart failure, weekly 4-hour dobutamine infusions did not elicit a major change in resting left ventricular function; however, exercise performance and clinical status improved considerably.

Adult↗

PubMed2001

Association between exogenous atrial natriuretic peptide and hemodynamics in dogs with congestive heart failure produced by experimental mitral regurgitation.

Association between exogenous atrial natriuretic peptide (ANP) and hemodynamic changes was ascertained in 3 dogs with overt congestive heart failure (CHF(+)) and 3 dogs without congestive heart failure (CHF(-)) caused by experimental mitral regurgitation (MR). The hemodynamic measurements were recorded in all dogs during and after 1 hr infusion of ANP at the rate of 0.1 (low dose), 0.5 (medium dose) and 1.0 (high dose) microg/kg/min, respectively. Heart rate, mean arterial pressure, pulmonary capillary wedge pressure (PCWP) and systemic vascular resistance decreased significantly during and after ANP infusion even with low dose in the CHF(+). Stroke volume, stroke volume index and cardiac output in the CHF(+) during and after ANP infusion showed an increasing trend as compared with the CHF(-). Double product, an indicator of myocardial oxygen consumption, significantly decreased during and after ANP administration at all doses in the CHF(+). These findings indicate that even at low dose, exogenous ANP improves cardiac performance and reduces myocardial oxygen consumption in the CHF(+), and suggest that ANP has beneficial effects in the treatment of dogs with overt congestive heart failure resulting from MR.

Animals↗

PubMed1998

Explaining price variations for the inpatient treatment of congestive heart failure.

OBJECTIVE: To identify key factors affecting hospital charge variations in the treatment of congestive heart failure. STUDY DESIGN: The determinants of total charges and average charges (the latter being a measure of treatment intensity) were evaluated using hospital discharge abstract data from 1994. Multivariate regression methods were used to help isolate the impact of key predictors of charges. In addition to relating a variety of factors (e.g., drug treatment regimens, patient comorbidities, demographic characteristics, insurance status, treatment course) to hospital charges, the analysis controlled for hospital-specific fixed effects. The study includes the effects of pharmacologic agents--information typically unavailable on inpatient claims-based data. RESULTS: Drug treatment regimens, particularly treatment with inotropic agents, were associated with substantially higher total charges. Comorbidities also increased the cost of treating congestive heart failure, particularly when septicemia, pneumonia, or acute myocardial infarction were involved. In contrast, gender, race, and insurance status bore little relationship to total charges or average charges. CONCLUSION: The fixed-effects estimates revealed that substantial interhospital variations in charges persisted, suggesting that there may be significant opportunities to control the inpatient costs of treating congestive heart failure.

Demography↗

PubMed1997

A randomized controlled trial of epoprostenol therapy for severe congestive heart failure: The Flolan International Randomized Survival Trial (FIRST).

This trial evaluated the effects of epoprostenol on patients with severe left ventricular failure. Patients with class IIIB/IV congestive heart failure and decreased left ventricular ejection fraction were eligible for enrollment if angiography documented severely compromised hemodynamics while the patient was receiving a regimen of digoxin, diuretics, and an angiotensin-converting enzyme inhibitor. We randomly assigned 471 patients to epoprostenol infusion or standard care. The primary end point was survival; secondary end points were clinical events, congestive heart failure symptoms, distance walked in 6 minutes, and quality-of-life measures. The median dose of epoprostenol was 4.0 ng/kg/min, resulting in a significant increase in cardiac index (1.81 to 2.61 L/min/m2), a decrease in pulmonary capillary wedge pressure (24.5 to 20.0 mm Hg), and a decrease in systemic vascular resistance (20.76 to 12.33 units). The trial was terminated early because of a strong trend toward decreased survival in the patients treated with epoprostenol. Chronic intravenous epoprostenol therapy is not associated with improvement in distance walked, quality of life, or morbid events and is associated with an increased risk of death.

Aged↗

PubMed1993

Congestive heart failure in neonates due to intracranial arteriovenous malformation: endovascular treatment.

Newborns with intracranial arteriovenous malformations and congestive heart failure have an extremely poor prognosis. This report describes two infants with intracranial arteriovenous malformations and severe congestive heart failure successfully treated in the newborn period with endovascular embolization. Both infants had immediate improvement in symptoms and both had second embolization procedures performed. Ventriculoperitoneal shunting was necessary in both children because of progressive hydrocephalus. At follow-up of more than 4 years, neither patient has any sign of congestive heart failure, and one is developmentally normal.

Cardiac Catheterization↗

PubMed1990

Development of dopaminergic drugs for the chronic treatment of congestive heart failure.

1. The search of orally active dopaminergic drugs for the chronic treatment of congestive heart failure has followed two different approaches. 2. On the one hand, a selective DA-1 receptor agonist, such as fenoldopam, has been investigated as an agent developed for the stimulation of vascular and tubular DA-1 receptors in the kidney. On the other hand, orally active prodrugs were synthetized with the aim of mimicking the full pattern of dopaminergic and adrenergic actions of intravenous dopamine. 3. Ibopamine, the diisobutyric ester of N-methyldopamine, has shown effects comparable to those of dopamine in various animal models and in clinical investigations. Furthermore, patients suffering from mild or severe congestive heart failure were shown to benefit from ibopamine treatment in a number of therapeutic trials. 4. Limited experience is currently available on other prodrugs, such as docarpamine and Sim 2055, i.e. the 4-0-phosphate ester of N-methyldopamine. The latter is an analogue of ibopamine designed for a preferential delivery of N-methyldopamine in the kidney. 5. Based upon some additional studies with levodopa, the results suggest that a combination of DA-1 and DA-2 agonistic activity is a desirable feature of a new drug, since it appears suitable to provide vasodilation while counteracting the neurohumoral abnormality of congestive heart failure.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMedDate not supplied

Physiologic sequelae of prematurity: the nurse practitioner's role. Part III. Congestive heart failure.

The premature infant with resultant respiratory disease may also have signs and symptoms of impending congestive heart failure that have a variety of causes. The nurse practitioner can be instrumental in the early identification and treatment of congestive heart failure. This article, the third in a series, provides a discussion of the pathophysiology, signs and symptoms, data collection, treatment modalities, and parental education that can assist parents when coping and dealing with congestive heart failure in their premature infant.

Heart Failure↗

PubMed1978

Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure.

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).

Aorta↗

PubMed1977

Chronic congestive heart failure after repair of tetralogy of Fallot.

The etiology of chronic congestive heart failure (CHF) after repair of tetralogy of Fallot was determined in 102 patients consecutively catheterized 1 to 12 years postoperatively. Chronic CHF was observed in 36/102 patients. The most prevalent abnormality leading to congestive failure (31/36) was a large residual ventricular septal defect alone or in combination with other lesions. All postoperative patients with pulmonary to systemic flow ratios greater than 2:1 (25/102) had congestive failure and evidence of biventricular dysfunction. Significant tricuspid regurgitation (N = 11) and persistent systemic to pulmonary artery shunts (N = 6) contributed to volume overload and congestive failure in the patients with large residual ventricular septal defect. Isolated severe residual right ventricular outflow tract obstruction was a common cause of chronic CHF. Pulmonary artery hypertension was present in 20/36 patients with CHF. The increased pulmonary pressure was not wholly due to an increased pulmonary flow since 7/20 patients had pulmonary vascular resistance greater than 3 mm Hg/L/min/m2. Our findings indicate that persistent or chronic congestive heart failure in postoperative tetralogy of Fallot patients requires bilateral cardiac catherterization since an identifiable and surgically correctable lesion is nearly always present.

Adolescent↗

PubMed2006

Statins associated with reduced mortality in patients admitted for congestive heart failure.

BACKGROUND: Statins may be of potential benefit in patients with congestive heart failure (CHF) due to modulation of neurohormones and their antioxidant, antiinflammatory, and antifibrotic properties. To test this hypothesis, we performed a case-control study by using a prospective registry of patients admitted to our hospital for CHF. METHODS AND RESULTS: The Maastricht Registry of Congestive Heart Failure consists of a cohort of all patients who were admitted to the University Hospital Maastricht because of CHF for the first time between 1998 and 2000. Elective admissions were not included in the database. Drug treatment was left at the discretion of the attending physician. From a total of 840 patients admitted, we selected patients with an uncomplicated survival for at least 1 month after hospital discharge. For each survivor a nonsurvivor was matched for age, sex, left ventricular ejection fraction, and renal function. Drugs were considered in use only if they were administered for at least 90% of follow-up time. Five hundred twenty-four patients were included with a mean follow-up after discharge of 31 +/- 18 months. Twenty percent used statins. In Cox multivariate regression analysis, the use of statins remained significantly associated with decreased mortality independent of the cause of CHF. However, there appeared no additional benefit of statins in patients using beta-blockers. Mortality rates were constant over time after discharge. Statins were as effective in ischemic as in nonischemic heart failure and in patients with depressed as well as preserved LVEF. CONCLUSION: Statins appear associated with improved survival in CHF independent of its etiology. No additional benefit was seen in patients treated with beta-blockers.

Adrenergic beta-Antagonists↗

PubMed1996

Bosentan improves renal regional blood flow in rats with experimental congestive heart failure.

The effects of the mixed endothelin receptor antagonist bosentan on renal regional haemodynamics were investigated in rats with aorto-caval fistula, an experimental model of congestive heart failure. A matched group of normal rats served as control. Injection of bosentan (10 mg/kg i.v.) to the rats with decompensated congestive heart failure produced an increase in cortical (+20%) and medullary (+12%) blood flow, and a decrease in vascular resistance in the cortex (-30%) and medulla (-23%), while reducing mean arterial pressure by approximately 10 mm Hg. In rats with compensated congestive heart failure and in normal animals, infusion of bosentan did not affect blood pressure and cortical perfusion. These findings indicate that 1) endothelin receptor blockade produces beneficial effects on renal haemodynamics in rats with experimental congestive heart failure and 2) endothelin-1 may be involved in the pathogenesis of renal hypoperfusion only in decompensated congestive heart failure.

Animals↗

PubMed2004

The role of anemia in congestive heart failure and chronic kidney insufficiency: the cardio renal anemia syndrome.

Anemia is a major problem in patients with chronic kidney insufficiency. The development of recombinant human erythropoietin has enabled physicians to correct this anemia. Although anemia has not been considered to be a common or important contributor to congestive heart failure, anemia of any cause can lead to cardiac damage and eventually congestive heart failure. Our joint renal-cardiac heart failure team found that anemia was indeed very common in congestive heart failure and was associated with severe, medication-resistant cardiac failure. Correction of the anemia with erythropoietin and intravenous iron led to a marked improvement in patients' functional status and their cardiac function, and to a marked fall in the need for hospitalization and for high-dose diuretics; renal function usually improved or at least stabilized. Subsequent investigations by others have confirmed many of our observations. We call this interrelationship between congestive heart failure, chronic kidney insufficiency, and anemia the Cardio-Renal Anemia syndrome. Treatment of the anemia in congestive heart failure may prove vital in preventing progression of both the heart failure and the associated renal disease.

Anemia↗

PubMed2006

Carvedilol can restore the multifractal properties of heart beat dynamics in patients with advanced congestive heart failure.

INTRODUCTION: Human heart beats in an extremely inhomogeneous and non-stationary manner. Recent study has demonstrated that it belongs to a class of signals called multifractal. Loss of multifractality was also uncovered in patients with congestive heart failure. We investigated whether carvedilol could restore the multifractal properties in a group of patients with advanced congestive heart failure. METHODS AND RESULTS: A Holter ECG recording was obtained before and 1 and 3 months after titrated addition of carvedilol therapy in 10 patients with advanced congestive heart failure. Multifractal spectrum, detrended fluctuation analysis (DFA) as well as the traditional time- and frequency-domain heart rate variability (HRV) parameters were compared before and after carvedilol therapy together with those in age and sex-matched normal control. The results showed that the multifractal spectrum tau(q) vs. q of N-N interval time series returned toward normal during carvedilol treatment. All the traditional HRV parameters and the short-term DFA improved significantly after 3 months of carvedilol therapy. CONCLUSION: We concluded that the deteriorated multifractal properties could be reversed by carvedilol treatment in patients with advanced congestive heart failure.

Adrenergic beta-Antagonists↗

PubMed1997

Soluble tumor necrosis factor receptors are elevated in relation to severity of congestive heart failure.

The level of tumor necrosis factor alpha (TNF-alpha) is increased in patients with congestive heart failure and may play an important role in the development and progression of heart failure. Two types of TNF receptor (TNF-RI and TNF-RII) are expressed in virtually every cell and have different biologic roles. Soluble forms of the two receptors (sTNF-RI and sTNF-RII) have been identified as extracellular domain fragments. Serum levels of TNF-alpha, sTNF-RI and sTNF-RII were measured in 66 patients with heart failure and 27 control subjects using an enzyme-linked immunosorbent assay (ELISA). Hemodynamic variables, norepinephrine, atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP) were evaluated. TNF-alpha was significantly higher in patients with heart failure than in controls subjects (9.4 +/- 1.4 vs 4.8 +/- 0.8 pg/ml; p < 0.05). sTNF-RI and -RII were significantly increased in relation to the severity of heart failure (control subjects, 0.66 +/- 0.04 and 1.97 +/- 0.15 ng/ml; NYHA class II, 1.10 +/- 0.08 and 2.28 +/- 0.12 ng/ml; NYHA class III, 1.63 +/- 0.22 and 3.00 +/- 0.24 ng/ml; NYHA class IV, 2.78 +/- 0.46 and 4.52 +/- 0.62 ng/ml, respectively). In 9 patients whose clinical symptoms improved after treatment, the levels of sTNF-RI and -RII decreased by 17.3 +/- 5.7% (p < 0.05) and 22.1 +/- 6.9% (p < 0.05), respectively. There were significant positive correlations between sTNF-RI and -RII and mean pulmonary pressure (r = 0.69 and r = 0.61; p < 0.001) and mean capillary wedge pressure (r = 0.65 and r = 0.54; p < 0.001 and p < 0.01, respectively), but not with left ventricular end-diastolic volume or ejection fraction (NS). sTNF-RI and -RII were also significantly positively correlated with plasma levels of norepinephrine (r = 0.75 and r = 0.50; p < 0.001 and p < 0.05), ANP (r = 0.72 and r = 0.70; p < 0.001), and BNP (r = 0.60 and r = 0.60; p < 0.001). In conclusion, soluble TNF receptors are increased in proportion to the severity of congestive heart failure and may reflect the current status of congestive heart failure rather than the level of left ventricular dysfunction.

Adult↗