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PubMed1990

Usefulness of bucindolol in congestive heart failure.

The sympathetic hyperactivity of congestive heart failure (CHF) may worsen cardiovascular function by down-regulation of myocardial beta-receptors. For this reason, beta blockade is proposed to be useful in CHF. Bucindolol is a new beta blocker that has intrinsic nonadrenergically-mediated vasodilation and may be valuable in treatment of CHF. To test this, 19 patients with CHF were randomized in a double-blind protocol to 3 months of treatment with bucindolol (n = 12) or placebo (n = 7). Significant improvement was seen in the bucindolol group using invasive and noninvasive tests; treadmill time increased from 445 to 530 seconds (p = 0.04), Minnesota Living With Heart Failure Questionnaire score improved from 61 to 40 (p = 0.0001), cardiac output increased from 4.0 to 4.7 (p = 0.02), and systemic vascular resistance decreased from 1,888 to 1,481 (p = 0.04). Also, peak exercise heart rate and pulmonary capillary wedge pressure decreased significantly with treatment. There were no changes in the placebo group. We conclude that bucindolol may be an effective treatment for CHF when administered chronically and that its nonadrenergic vasodilation may be an important feature.

Adrenergic beta-Antagonists↗

PubMed1991

Congestive heart failure in coronary artery disease.

Congestive heart failure (CHF) affects approximately 1% of the United States population and its incidence continues to increase. Next to hypertension, coronary artery disease (CAD) is the second most frequent cause of CHF. Important distinction should be made between systolic dysfunction and diastolic dysfunction in CAD. The diagnostic and therapeutic challenges posed by both have stimulated much investigation into the pathophysiologic mechanisms involved and have led to innovative pharmacologic interventions to forestall progression of the disease. The challenge in the 1990s is prevention. In the meantime, results of completed and ongoing randomized controlled trials will determine the most effective forms of therapy, which will not only improve symptoms but also hopefully extend survival.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2004

Intermittent outpatient ultrafiltration for the treatment of severe refractory congestive heart failure.

BACKGROUND: Patients with severe congestive heart failure (CHF) become refractory to conventional medical therapy, leading to recurrent rehospitalizations. We examined the impact of intermittent outpatient ultrafiltration (UF), using either peritoneal dialysis or hemofiltration, on long-term clinical outcomes in patients with refractory CHF. METHODS AND RESULTS: We analyzed clinical and hemodynamic data in 19 consecutive patients with refractory CHF who received intermittent outpatient UF for at least 1 year between July 1998 and November 2002. The mean left ventricular ejection fraction of all 19 patients was 30.2 +/- 19.0%. All patients (100.0%) were New York Heart Association (NYHA) class IV. Only 5 patients (26.3%) received peritoneal dialysis; the remaining 14 (73.7%) received hemofiltration. There were 6 patients with a normal left ventricular ejection fraction (45%). After UF was started, the number of patients that were considered inotrope-dependent was reduced from 86.4% to 36.8% (P < .005). Compared with the year before UF was initiated, the number of CHF hospitalizations during follow-up was reduced from 2.6 to 0.3 (P < .005), and the NYHA class was improved from 4 to 3.1 (P < .005). Among all patients, 2 deaths were related to complications of UF, and cumulative 1-year survival was 63.2%. CONCLUSION: Our study suggests that UF is a safe, feasible therapy, but it needs further evaluation in carefully designed, prospective, randomized clinical trials. UF has the potential for offering another important therapeutic option for patients with severe and refractory CHF.

Adult↗

PubMed1988

Direct and indirect assessment of skeletal muscle blood flow in chronic congestive heart failure.

In patients with chronic congestive heart failure (CHF), skeletal muscle blood flow can be measured directly by the continuous thermodilution technique and by the xenon133 clearance method. The continuous thermodilution technique requires retrograde catheterization of the femoral vein and, thus, cannot be repeated conveniently in patients during evaluation of pharmacologic interventions. The xenon133 clearance, which requires only an intramuscular injection, allows repeated determination of skeletal muscle blood flow. In patients with severe CHF, a fixed capacity of the skeletal muscle vasculature to dilate appears to limit maximal exercise performance. Moreover, the changes in peak skeletal muscle blood flow noted during long-term administration of captopril, an angiotensin-converting enzyme inhibitor, appears to correlate with the changes in aerobic capacity. In patients with CHF, resting supine deep femoral vein oxygen content can be used as an indirect measurement of resting skeletal muscle blood flow. The absence of a steady state complicates the determination of peak skeletal muscle blood flow reached during graded bicycle or treadmill exercise in patients with chronic CHF. Indirect assessments of skeletal muscle blood flow and metabolism during exercise performed at submaximal work loads are currently developed in patients with chronic CHF.

Captopril↗

PubMed1996

Detection and significance of a discrete very low frequency rhythm in RR interval variability in chronic congestive heart failure.

Although in advanced chronic congestive heart failure (CHF) very low frequency (< 0.04 Hz, VLF) oscillations are prominent, the clinical importance and the physiologic basis of these rhythms have not been elucidated. To investigate the physiologic determinants of the VLF rhythms in RR interval variability, we studied 36 patients with stable, moderate to severe CHF (33 men, age: 58 +/- 8 years, ejection fraction 25 +/- 10%, peak oxygen consumption 18.1 +/- 4.6 ml/kg/min) and 12 age- and sex-matched controls using autoregressive spectral analysis of RR interval, blood pressure, and respiratory signals during controlled conditions. We quantified low frequency (LF) (0.04 to 0.15 Hz), high frequency (HF) (0.15 to 0.40 Hz), VLF, and total power (0 to 0.5 Hz), and calculated the coherence between systolic blood pressure and RR interval variability within each band. Peripheral chemosensitivity was assessed by the ventilatory response to hypoxia using transient inhalation of pure nitrogen. The influence of transient inactivation of peripheral chemoreceptors on the VLF rhythm was investigated by exposing 6 patients to hyperoxic (60% oxygen) conditions for 20 minutes. Twenty-three patients (64%) with CHF, but no controls, had a discrete VLF rhythm (0.019 +/- 0.008 Hz) in RR variability. The presence of VLF rhythm was not related to any difference in clinical parameters (etiology, New York Heart Association class, ejection fraction, oxygen uptake) but rather to a different pattern in RR interval and blood pressure variability: lower LF power (2.8 +/- 1.6 ms2 natural logarithm [ln]) compared either to patients without VLF (4.0 +/- 1.3 ms2 ln) or to controls (5.9 +/- 0.7 ms2 ln), higher percentage of power within VLF band (86.3 +/- 8.3% vs 77.5 +/- 7.9% and 61.5 +/- 14.1%) and a markedly impaired coherence between RR interval and systolic blood pressure variability within the LF band (0.26 +/- 0.10 vs 0.42 +/- 0.18 and 0.63 +/- 0.15, in patients with vs without VLF peak and controls, respectively). Patients with VLF had significantly increased hypoxic chemosensitivity, and hyperoxic conditions were able to decrease VLF power and abolish the VLF rhythm in 5 of 6 patients with CHF. Discrete VLF oscillations in RR variability are common in patients with advanced CHF and appear to be related to severely impaired autonomic regulation and suppression of baroreceptor function, with enhancement of hypoxic chemosensitivity. We hypothesize that this rhythm represents an enhanced chemoreflex harmonic oscillation in CHF patients, which may have application for arrhythmogenesis.

Autonomic Nervous System↗

PubMed1998

Safety and hemodynamic effects of intravenous triiodothyronine in advanced congestive heart failure.

Most patients with advanced congestive heart failure have altered thyroid hormone metabolism. A low triiodothyronine level is associated with impaired hemodynamics and is an independent predictor of poor survival. This study sought to evaluate safety and hemodynamic effects of short-term intravenous administration of triiodothyronine in patients with advanced heart failure. An intravenous bolus dose of triiodothyronine, with or without a 6- to 12-hour infusion (cumulative dose 0. 1 5 to 2.7 microg/kg), was administered to 23 patients with advanced heart failure (mean left ventricular ejection fraction 0.22 +/- 0.01). Cardiac rhythm and hemodynamic status were monitored for 12 hours, and basal metabolic rate by indirect calorimetry, echocardiographic parameters of systolic function and valvular regurgitation, thyroid hormone, and catecholamine levels were measured at baseline and at 4 to 6 hours. Triiodothyronine was well tolerated without episodes of ischemia or clinical arrhythmia. There was no significant change in heart rate or metabolic rate and there was minimal increase in core temperature. Cardiac output increased with a reduction in systemic vascular resistance in patients receiving the largest dose, consistent with a peripheral vasodilatory effect. Acute intravenous administration of triiodothyronine is well tolerated in patients with advanced heart failure, establishing the basis for further investigation into the safety and potential hemodynamic benefits of longer infusions, combined infusion with inotropic agents, oral triiodothyronine replacement therapy, and new triiodothyronine analogs.

Female↗

PubMed1998

Changes in L-type calcium channel abundance and function during the transition to pacing-induced congestive heart failure.

OBJECTIVE: The development of congestive heart failure (CHF) is accompanied by left ventricular (LV) and myocyte contractile dysfunction. However, time-dependent cellular and ionic events which contribute to the initiation and progression of CHF remain unclear. This study tested the central hypothesis that changes in L-type Ca2+ channel current (ICa) and abundance (Bmax) are early events in the transition to CHF. METHODS: LV fractional shortening by echocardiography, isolated LV myocyte shortening velocity by videomicroscopy, ICa by voltage-clamp, and Bmax by [3H]nitrendipine binding were determined at each week during the progression of pacing-induced CHF in pigs (240 bpm; n = 6/week for 3 weeks). Myocyte and L-type Ca2+ channel function were determined under basal conditions and after beta-adrenergic receptor stimulation with 25 nM isoproterenol. RESULTS: After 1 week of pacing, myocyte and L-type Ca2+ current responses to beta-adrenergic receptor stimulation were reduced by 20% from control values and was accompanied by over a 210% increase in plasma catecholamine levels. After 2 weeks of pacing, reductions in LV fractional shortening and myocyte shortening velocity from control values (20 +/- 1 vs. 34 +/- 2% and 36.7 +/- 2.9 vs. 50.6 +/- 2.4 microns/s, respectively, P < 0.05) were paralleled by decreased ICa (2.47 +/- 0.10 vs. 3.63 +/- 0.25 pA/pF, P < 0.02) and Bmax (149 +/- 16 vs. 180 +/- 12 fmol/mg, P < 0.03). After 3 weeks of pacing, LV fractional shortening was reduced by over 50%, myocyte shortening velocity by 37%, and ICa and Bmax were reduced by over 25% from control values. Furthermore, after 3 weeks of pacing, the ICa/Bmax ratio was reduced from control values (16.2 +/- 0.9 vs. 20.6 +/- 1.2 [fA/pF]/[fmol/mg], P < 0.03), which suggests functional defects in the remaining L-type Ca2+ channels. CONCLUSIONS: An early event during the transition to pacing-induced CHF was diminished beta-adrenergic receptor augmented L-type Ca2+ current, which was followed by an absolute loss of steady-state L-type Ca2+ current and channel abundance. The development of severe CHF was accompanied by a loss of Ca2+ carrying capacity through residual channels. These unique findings suggest that a contributory molecular mechanism for the initiation and progression of CHF is changes in the structure and function of the L-type Ca2+ channels.

Adrenergic beta-Agonists↗

PubMed1988

Neuro-endocrine changes as new targets in the drug treatment of congestive heart failure.

The classical therapy of congestive heart failure (CHF) with inotropic agents (digitalis and newer inotropics) and diuretic agents remains unsatisfactory in many cases. More recently it is recognized, that some of the neuro-endocrine compensatory processes associated with CHF are detrimental in the long run, and therefore potentially targets for drug treatment. This holds for the following neuro-endocrine mechanisms: 1) increased activity of the sympathetic nervous system and high plasma catecholamines, accompanied by down-regulation of beta 1- but not beta 2-receptors in the heart; 2) stimulation of the renin-angiotensin-aldosterone system (RAAS), causing higher levels of renin, A II and aldosterone. The detrimental sequelae of both processes are even enhanced by their complex mutual interactions. Drug treatment aiming to reduce or suppress these processes and their negative results is potentially offered by: vasodilators, counteracting vasoconstriction, low dose selective beta 1-adrenoceptor blockers, which will not only impair tachycardia but also up-regulate cardiac beta 1-receptors and hence improve the inotropic response to catecholamines; aldosterone antagonists and ACE-inhibitors counteracting the activated RAAS. The beneficial effect of the ACE-inhibitors in CHF is well established and superior to that of classical vasodilators, since it additionally counteracts the enhanced RAAS activity.

Adrenergic alpha-Antagonists↗

PubMed2001

Blunted sympathetic response in diabetic patients with decompensated congestive heart failure.

BACKGROUND: The risk for congestive heart failure is strongly increased in diabetes, and the prognosis of diabetic patients with established heart failure is worse compared to nondiabetic patients. Heart failure entails complex alterations in autonomic and neurohormonal responses, which exert a direct deleterious effect on the heart and contribute to progressive circulatory failure. Altered neurohumoral physiology may underlie the poor prognosis of diabetic patients with heart failure. METHODS: We studied 88 patients (mean age 61+/-13 years) admitted for decompensated heart failure. Neurohormonal and cytokine profiles, including plasma renin activity, aldosterone, norepinephrine, endothelin-1, tumor necrosis factor-alpha, and interleukin-6, were obtained in all patients. In addition, a 24-h Holter recording was performed, and time and frequency domain heart rate variability indices were calculated. RESULTS: Of 88 patients, 48 were classified as having diabetes based on history, diet therapy, or use of oral hypoglycemic agents or insulin. The only difference in the neurohormonal and cytokine profile between the diabetic and nondiabetic groups was a significantly lower norepinephrine level in diabetic patients (668+/-64 vs. 489+/-50 pg/ml, P=0.009). Heart rate variability analysis revealed that the low-frequency power in normalized units (an index of sympathetic modulation) was significantly lower in diabetic patients (4.7+/-1.4 vs. 5.9+/-0.9, P=0.04). No significant differences occurred in any of the time (the percentage of RR intervals with >50 ms variation and the square root of mean squared differences of successive RR intervals) or frequency domain (high frequency power) indices of parasympathetic modulation between the two groups. CONCLUSIONS: Patients with diabetes mellitus exhibit a blunted sympathetic response during heart failure decompensation. Blunted sympathetic activation in the setting of symptomatic heart failure may impair the ability of the myocardium to compensate and contribute to the high incidence of symptomatic heart failure among diabetic patients.

Aged↗

PubMed1999

Abnormal renal vasodilation to an amino acid infusion in congestive heart failure: normalization by enalapril.

In congestive heart failure (CHF), the neurohormonal mechanisms that cause renal vasoconstriction, particularly those depending on the renin-angiotensin system, could interfere with renal vasodilating mechanisms. To elucidate this issue, we studied the kidney response to an amino acid infusion (known to cause renal vasodilation in healthy individuals) in eight patients with CHF. We found that the amino acid infusion (0.7 mL/kg/h of a 10% solution) elicited no renal hemodynamic response, in marked contrast to healthy subjects. We next hypothesized that the renin-angiotensin system (known to be activated in heart failure) has a role in the lack of response to the amino acid infusion. To test this hypothesis, we repeated the study after two 5-mg doses of enalapril, an inhibitor of the angiotensin-converting enzyme, administered 12 hours apart. After enalapril treatment, the amino acid infusion caused a 45% increase in mean renal blood flow (RBF) from 383 +/- 55 to 557 +/- 51 mL/min at the fifth hour (P < 0.05). This normalization of the renal response to the amino acid infusion occurred without changes in cardiac output or in systemic vascular resistance. Hence, the renal fraction of the cardiac output increased during the amino acid infusion. The recovery of the renal vascular response was not accompanied by an increase in glomerular filtration rate (GFR; filtration fraction decreased), suggesting a predominant efferent arteriole dilatation. Our study shows that, in heart failure, the kidney loses its ability to increase RBF in response to an amino acid load. This lack of renal vascular response can be restored by inhibiting the renin-angiotensin system and is unrelated to changes in systemic hemodynamics.

Aged↗

PubMed1987

Pharmacokinetic-hemodynamic studies of transdermal nitroglycerin in congestive heart failure.

Ten patients with chronic congestive heart failure were studied to assess the hemodynamic effects and bioavailability of a transdermal nitroglycerin delivery system. Nitrate sensitivity was defined by a prior 20 minute infusion of nitroglycerin, 21 micrograms/min. Five patients with a satisfactory hemodynamic response to intravenous nitroglycerin received two nitroglycerin patches of 10 cm2 each and five patients who did not achieve a satisfactory response to intravenous nitroglycerin (that is, greater than or equal to 25% reduction in left ventricular filling pressure) received larger doses of transdermal nitroglycerin. In the five nitrate-sensitive patients who received 20 cm2 of transdermal nitroglycerin, one study was terminated at 90 minutes, at which point there was no detectable hemodynamic response or arterial plasma nitroglycerin evident. Two patients had a minimal hemodynamic response and a peak plasma concentration of 1 ng/ml. A fourth patient had a short-lived hemodynamic response at 60 and 120 minutes and a plasma nitroglycerin concentration of 1 ng/ml at 60 minutes. A fifth patient had a hemodynamic response persisting for 24 hours and plasma concentrations between 0.6 and 1.1 ng/ml. The remaining five patients showed little or no hemodynamic response despite doses of transdermal nitroglycerin from 40 to 60 cm2. The highest plasma concentration achieved in these patients was 2 ng/ml and there was no relation between dose administered and plasma concentration achieved. In 4 of the 10 patients who subsequently received nitroglycerin ointment, there were a greater decrease in left- and right-sided filling pressures and greater increase in plasma nitroglycerin concentrations (from 1.6 to 4.8 ng/ml) than those that occurred with transdermal nitroglycerin.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗

PubMed2006

Risk factors for acute renal insufficiency induced by diuretics in patients with congestive heart failure.

BACKGROUND: In patients with congestive heart failure (CHF), continuous diuretic therapy may result in acute renal insufficiency (ARI). This study examines factors contributing to this complication. METHODS: We analyzed clinical data from 318 consecutive patients who were hospitalized for CHF. All were treated with diuretics and had echocardiography performed within 4 days of hospitalization. Systolic left ventricular (LV) dysfunction is defined as an ejection fraction less than 50%, and diastolic LV dysfunction, as an ejection fraction of 50% or greater in the presence of LV hypertrophy and a reversed E/A ratio. RESULTS: ARI, defined as a 25% increase in serum creatinine level, occurred in 110 patients (35%) after diuretic therapy. Risk factors for ARI on univariate analyses were older age, higher baseline serum creatinine level, lower baseline serum sodium level, lower mean arterial pressure (MAP) during diuretic therapy, and greater doses and longer duration of diuretic therapy. In multivariate analyses, ARI occurred more frequently in patients with systolic (40%) than diastolic dysfunction (28%). The use of digoxin in patients with systolic LV dysfunction was observed to decrease the risk for ARI by 61%, independent of other agents used for the treatment of patients with CHF. CONCLUSION: Age, baseline renal function and serum sodium concentration, MAP, and intensity of diuretic therapy can identify individuals at risk for ARI while receiving diuretic therapy for CHF. This complication is observed more often in individuals with systolic dysfunction, and its risk may be decreased with the use of digoxin.

Acute Kidney Injury↗

PubMedDate not supplied

[Congestive heart failure in infancy and childhood].

Congestive heart failure is the inability of the heart to provide a sufficient output at a sufficient arterial pressure for the metabolic needs of the organism. Having presented the physiologic mechanisms of the contraction of the heart and its regulatory mechanisms the different aspects of classification of heart failure and its neurohormonal modulation are described. The epidemiology of heart failure in childhood is largely unknown, the causes vary considerably, symptoms are age-dependent. Main diagnostic tools for etiologic clarification are echocardiography and chest-x-ray. Focus of therapy is to eliminate the causes, but general recommendations may not be forgotten. Medical treatment of acute severe heart failure is use of catecholamines, ino- and vasodilators in the intensive care unit. Therapy of chronic heart failure is performed with diuretics, digitalis and ACE-inhibitors. Their pharmacologic effect, therapeutic trials in adults and children and peculiarities of pharmacology and side effects in childhood are reported. Low dose beta-blockers are a new therapeutic strategy still not established in children.

Animals↗

PubMed2001

Medical and socioenvironmental predictors of hospital readmission in patients with congestive heart failure.

BACKGROUND: Patients with chronic congestive heart failure (CHF) require frequent rehospitalization because of the exacerbation of CHF. It is of clinical importance to determine predicting factors for readmission to reduce this likelihood. Previous studies have focused primarily on the demographic and medical characteristics in selected subsets of patients. Therefore, within a broad cohort of consecutively hospitalized patients, we sought to identify not only demographic and medical predictors but also socioenvironmental factors associated with readmission. METHODS: We assessed demographic (age, sex), medical (etiology of CHF, New York Heart Association functional class, left ventricular ejection fraction, previous admission for CHF, length of hospital stay, comorbidity, and medications), and socioenvironmental variables (occupation, financial resources, living alone, and follow-up visits) in 230 patients discharged with a diagnosis of CHF and recorded hospital readmission. RESULTS: Within 1 year after discharge, 81 patients (35%) were readmitted. Five variables, including poor follow-up visits (odds ratio [OR] 4.9, 95% CI 2.0-11.8), previous admission for CHF (OR 3.3, 95% CI 1.8-6.1), no occupation (OR 2.6, 95% CI 1.2-5.5), longer hospital stay (OR 3.2, 95% CI 1.2-8.5), and hypertension (OR 2.0, 95% CI 1.1-3.7), were identified as significant independent predictors for readmission by multivariate logistic regression analysis. CONCLUSIONS: Our independent predictors of readmission support the importance of medical and socioenvironmental factors in the deterioration of CHF. Therefore interventions to decrease readmission should also target social management in all hospitalized patients.

Acute Disease↗

PubMed2007

Inhalation of the phosphodiesterase-3 inhibitor milrinone attenuates pulmonary hypertension in a rat model of congestive heart failure.

BACKGROUND: Most patients with congestive heart failure (CHF) develop pulmonary venous hypertension, but right ventricular afterload is frequently further elevated by increased pulmonary vascular resistance. To investigate whether inhalation of a vasodilatory phosphodiesterase-3 inhibitor may reverse this potentially detrimental process, the authors studied the effects of inhaled or intravenous milrinone on pulmonary and systemic hemodynamics in a rat model of CHF. METHODS: In male Sprague-Dawley rats, CHF was induced by supracoronary aortic banding, whereas sham-operated rats served as controls. Milrinone was administered as an intravenous infusion (0.2-1 microg.kg body weight.min) or by inhalation (0.2-5 mg/ml), and effects on pulmonary and systemic hemodynamics and lung water content were measured. RESULTS: In CHF rats, intravenous infusion of milrinone reduced both pulmonary and systemic arterial blood pressure. In contrast, inhalation of milrinone predominantly dilated pulmonary blood vessels, resulting in a reduced pulmonary-to-systemic vascular resistance ratio. Repeated milrinone inhalations in 20-min intervals caused a stable reduction of pulmonary artery pressure. No hemodynamic effects were detected when 0.9% NaCl was administered instead of milrinone or when milrinone was inhaled in sham-operated rats. No indications of potentially adverse effects of milrinone inhalation in CHF, such as left ventricular volume overload, were detected. Moreover, lung edema was significantly reduced by repeated milrinone inhalation. CONCLUSION: If these results can be confirmed in humans, inhalation of nebulized milrinone may present a novel, effective, safe, and pulmonary selective strategy for the treatment of pulmonary venous hypertension in CHF.

Administration, Inhalation↗

PubMed1996

Congestive heart failure: a continuum of care.

Congestive heart failure is the nation's most rapidly growing category of cardiovascular disorders. As more and more people are surviving cardiac insults, health care providers are called upon to improve the health status of this population. The article describes a program at Advocate Health Care that follows the patient beyond the four walls of the hospital after discharge and into the most appropriate care environment for him or her. The evolution of a clinical quality improvement project aimed at partnering with patients in the care of this chronic illness is discussed.

Aftercare↗

PubMed2003

Effectiveness of the clinical pathway in the management of congestive heart failure.

BACKGROUND: The prevalence of congestive heart failure (CHF) in the United States is approximately 4 million, with associated annual health care expenditures exceeding dollar 8 billion. Clinical pathways for CHF have been developed, but they have not been rigorously evaluated regarding efficacy and improvement in the quality of care. We sought to evaluate the effect of a CHF clinical pathway on hospital charges, length of stay, and use of angiotensin-converting enzyme (ACE) inhibitors in patients with CHF in a retrospective cohort study. METHODS: We studied 371 patients (age range, 44-92 yr) with discharge diagnoses of CHF in a 376-bed community hospital between July 1996 and December 1997. We conducted chart reviews to determine length of stay, hospital charges, and use of ACE inhibitors. RESULTS: Of the 371 patients, 174 were assigned to the clinical pathway and 197 were not. Baseline characteristics of the two groups were similar. The benchmark of less than 4 days' in-hospital stay was achieved in 65% of patients on the pathway and 42% who were not on the pathway (odds ratio, 2.6; 95% confidence interval, 1.67-4.05; P < 0.001). The median hospital charges were lower in the group on the clinical pathway (dollar 3,000 versus dollar 5,500, P < 0.001). In addition, 81% of the patients on the clinical pathway were administered ACE inhibitors, compared with 48% of equally eligible patients from the nonpathway group (odds ratio, 4.68; 95% confidence interval, 2.85-7.72; P < 0.001). CONCLUSION: The clinical pathway for CHF was associated with increased use of ACE inhibitors as well as reduced length of stay and hospital charges.

Adult↗

PubMedDate not supplied

Epidemiology of congestive heart failure in three ethnic groups.

Congestive heart failure (CHF) is a leading cause of morbidity, disability, and mortality in old age, but little is known about the epidemiology of this condition in free-living minority populations. To determine the prevalence of CHF and associated risk factors in a multiethnic community, a population sample of 2759 elderly (i.e., 65 years of age and older) African American (AA), Hispanic-Cuban (HC), and white non-Hispanic (WNH) men and women from Miami-Dade County, Florida, were examined. There were 153 (5.6%) cases of self-reported CHF in the sample. The unadjusted prevalence rate of CHF was virtually identical among elderly AA (4.8%) and WNH (4.9%) but was significantly (p=0.04) lower than the rate among HC (6.8%). Sex- and ethnic-specific analyses showed that the highest prevalence rate of CHF was among HC women (8.2%). A multiple logistic analysis was used to calculate the odds ratio (OR) and 95% confidence interval (CI) of CHF in relation to age, sex, ethnicity, medical history, and smoking and alcohol drinking habits. Age (65-74 vs. 75-84; OR 1.7; CI 1.2-2.4; p=0.01), HC ethnic group (OR 1.5; CI 1.0-2.4; p=0.05), history of hypertension (OR 1.5; CI 1.1-2.1; p=0.02), history of myocardial infarction (OR 2.3; CI 1.5-3.5; p=0.0001), and history of diabetes mellitus (OR 1.9; CI 1.3-2.8; p=0.001) were directly, significantly, and independently associated with the prevalence of self-reported CHF. The findings here confirm those of prior studies in elderly white US residents, which indicate that heart attack, hypertension, and diabetes mellitus are major risk factors for CHF. The results also show that elderly AA and WNH have similar CHF prevalence rates. The higher CHF prevalence in elderly HC women found in this study requires further investigation. (c)2001 by CHF, Inc.

Journal Article↗