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PubMed1989

Recent advances in therapy of congestive heart failure.

Approximately 3 million Americans are currently diagnosed as having congestive heart failure, and nearly 400,000 deaths occur per year in these patients. Fortunately, recent clinical investigations have made important contributions to the care of patients with congestive heart failure, allowing great improvement in the morbidity and mortality associated with this syndrome. Most patients presenting with signs and symptoms of heart failure suffer from systolic dysfunction. On objective testing, however, up to 30% of patients initially thought to have heart failure due to poor systolic function actually have abnormal diastolic performance. Since treatment that is beneficial for systolic dysfunction can be harmful if applied to patients with diastolic dysfunction, differentiation of these causes of pulmonary congestion is particularly important. Echocardiography has been shown to be particularly useful in making this distinction and is very useful in guiding therapy for patients with heart failure. Vasodilator therapy has been recently shown to both relieve symptoms and lessen long-term mortality for patients with heart failure. Additionally, vasodilators may be more effective than digitalis in relieving symptoms of heart failure for patients with mild-to-moderate symptoms. Thus it appears that vasodilators should play a prominent and early role in the treatment of most patients with heart failure due to systolic dysfunction. The value of digitalis for patients with heart failure related to uncontrolled atrial arrhythmias is well appreciated. Controversy exists, however, regarding the role of digitalis for patients who remain in normal sinus rhythm. A recent double-blind trial of digoxin, milrinone, both, or placebo has confirmed the beneficial effects of digoxin for these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

PubMedDate not supplied

Changes in the number of beta-adrenergic receptors of lymphocytes in patients with varying degrees of congestive heart failure.

This study was designed to determine changes in the number of beta-adrenergic receptors of circulating lymphocytes in patients with varying degrees of congestive heart failure. Thirty-seven patients with congestive heart failure were classified into four groups according to the functional classifications of the New York Heart Association (class I, 12 patients; class II, 12 patients; class III, eight patients; class IV, five patients). The control group consisted of 24 healthy volunteers. Binding assays of beta-adrenergic receptors in circulating lymphocytes and plasma norepinephrine concentrations were determined in each group. Compared with the control group, the number of beta-adrenergic receptors in patients of the class-III and class-IV groups was reduced by 37% and 36%, respectively, and plasma norepinephrine concentrations of class-III and class-IV patients were increased by 3.5 times and 5.9 times, respectively. No significant changes in the numbers of beta-adrenergic receptors or in plasma norepinephrine concentrations were observed in patients of the class-I and class-II groups. These findings show a decrease in the number of beta-adrenergic receptors in patients with high plasma norepinephrine concentrations. It is suggested that the chronically high concentration of norepinephrine, resulting from activation of the sympathetic nervous system associated with severe congestive heart failure, is linked with the down regulation of beta-adrenergic receptors. The action of sympathomimetic amines may therefore be altered in patients with congestive heart failure.

Heart Failure↗

PubMed1993

Triage practice guideline for patients hospitalized with congestive heart failure: improving the effectiveness of the coronary care unit.

BACKGROUND: Decisions regarding the appropriate timing for transfer of patients hospitalized with congestive heart failure from the coronary care unit (CCU) to the medical ward are often not based on well-founded medical data. We investigated the potential safety and effectiveness of a practice guideline recommending early "step-down" transfer of low-risk patients with congestive heart failure. PATIENTS AND METHODS: We studied the use of a practice guideline for 384 patients hospitalized with congestive heart failure in a hypothetic experiment. The guideline stated that patients without any of the following conditions may be suitable for transfer to a nonmonitored bed 24 hours after admission: acute myocardial infarction or ischemia, complications, active or planned cardiac interventions, unstable comorbidity, worsening clinical status, or lack of response to diuretic therapy. Patients with any of the above conditions were classified as higher risk and potentially not suitable for early transfer. RESULTS: Life-threatening complications were 15.2 times more likely (95% confidence interval [CI] 2.2, 70, p = 0.001) and death 14.6 times more likely (95% CI 2.1, 68, p = 0.001) if the patient was classified as "high risk" rather than "low risk" by the guideline. The negative predictive value and sensitivity of the practice guideline for detecting patients who had life-threatening complications were 99.2% and 96.4%, respectively. Thirty-one percent of patients with congestive heart failure hospitalized in either the CCU or intermediate care unit were at low risk and potentially suitable for transfer to a nonmonitored bed 24 hours after admission. Use of the guideline would have reduced intermediate care unit lengths of stay from 2.91 days to 2.22 days and CCU length of stay from 2.06 to 2.04 days had it been used to triage patients with congestive heart failure. This reduction in length of stay would have resulted in 172 more intermediate care unit bed-days available per year to accommodate additional patients. On initial review, at least one cardiologist reviewer judged that use of the guideline may have adversely affected quality of care for 4% (95% CI 1%, 7%) of patients. After a consensus among the cardiologist reviewers, it was judged that the guideline may have adversely affected care for only 0.8% of patients (95% CI, 0%, 2.3%), and that no patient (95% CI 0%, 2.3%) would have had an unexpected life-threatening complication because of the guideline. CONCLUSIONS: Use of a practice guideline has the potential to reduce the intermediate care unit lengths of stay for selected low-risk patients with congestive heart failure.

Aged↗

PubMed1994

Apparent paradox of neurohumoral axis inhibition after body fluid volume depletion in patients with chronic congestive heart failure and water retention.

BACKGROUND: Hypovolaemia stimulates the sympathoadrenal and renin systems and water retention. It has been proposed that in congestive heart failure reduction of cardiac output and any associated decrease in blood pressure cause underfilling of the arterial compartment, which promotes and perpetuates neurohumoral activation and the retention of fluid. This study examined whether an intravascular volume deficit accounts for patterns that largely exceed the limits of a homoeostatic response, which are sometimes seen in advanced congestive heart failure. METHODS AND RESULTS: In 22 patients with congestive heart failure and water retention the body fluid mass was reduced by ultrafiltration and the neurohumoral reaction was monitored. A Diafilter, which was part of an external venous circuit was regulated to produce 500 ml/hour of ultrafiltrate (mean (SD) 3122 (1199) ml) until right atrial pressure was reduced to 50% of baseline. Haemodynamic variables, plasma renin activity, noradrenaline, and aldosterone were measured before and within 48 hours of ultrafiltration. After ultrafiltration, which produced a 20% reduction of plasma volume and a moderate decrease in cardiac output and blood pressure (consistent with a diminished degree of filling of the arterial compartment), there was an obvious decrease in noradrenaline, plasma renin activity, and aldosterone. In the next 48 hours plasma volume, cardiac output, and blood pressure recovered; the neurohumoral axis was depressed; and there was a striking enhancement of water and sodium excretion with resolution of the peripheral oedema and organ congestion. The neurohumoral changes and haemodynamic changes were not related. There were significant correlations between the neurohumoral changes and increase in urinary output and sodium excretion. CONCLUSIONS: In advanced congestive heart failure arterial underfilling was not the main mechanism for activating the neurohumoral axis and retaining fluid. Because a decrease in circulating hormones was associated with reabsorption of extravascular fluid it is likely that hypoperfusion and/or congestion of organs, such as the kidney and lung, reduce the clearance of circulating noradrenaline and help to keep plasma concentrations of renin and aldosterone raised. A positive feedback loop between fluid retention and plasma hormone concentrations may be responsible for progression of congestive heart failure.

Aged↗

PubMed1986

The relationship between atrial granularity and circulating atrial natriuretic peptide in hamsters with congestive heart failure.

The BIO 14.6 strain of hamster is a model of familial cardiomyopathy complicated by congestive heart failure, sodium retention, and edema. In previous studies, bioassay techniques have demonstrated that the cardiac content of atrial natriuretic peptide (ANP) is reduced in these animals. On the basis of this observation, the syndrome of congestive heart failure has been hypothesized to be due to a deficiency in ANP. The current study was designed to correlate the cardiac content of ANP (determined by immunohistochemical techniques) with plasma circulating ANP (determined by radioimmunoassay). alpha-ANP antibodies were used for both determinations. The content of ANP in the atria was based on the degree of immunoreactive staining present (1 = lowest; 5 = highest), as graded by two observers. The mean granularity score of the cardiomyopathic hamsters was decreased (2.1 +/- 0.3) in comparison with that of age- and sex-matched control animals (3.5 +/- 0.5; P less than 0.05). In contrast, circulating immunoreactive ANP was higher in the hamsters with congestive heart failure than in the control animals--185.5 +/- 27.2 pg/ml versus 77.7 +/- 10.8 pg/ml (P less than 0.005). This study demonstrates that an inverse relationship exists between ANP content in the atria and circulating ANP. Furthermore, this study suggests that these hamsters with congestive heart failure are not deficient in ANP; rather, secretion of ANP is stimulated and storage of the peptide, represented by atrial granularity, is reduced.

Animals↗

PubMed1998

Sympathetic control of circulation in hypertension and congestive heart failure.

Adrenergic overactivity is a common hallmark of both essential hypertension and congestive heart failure. Indirect and direct measures of sympathetic function have clearly shown that sympathetic activation characterizes essential hypertension. This adrenergic overactivity appears to be related to the severity of the hypertensive state, being detectable in its early stages and showing a progressive increase with the severity of the disease. Essential hypertension is also associated with an impaired baroreflex control of vagal activity, whereas baroreceptor modulation of sympathetic nerve traffic remains unaltered, although undergoing a resetting phenomenon. In contrast, secondary hypertension is not associated with an increased adrenergic activity, thus suggesting that an enhancement in efferent sympathetic outflow is a peculiar feature of essential hypertension. Congestive heart failure is a condition also characterized by sympathetic activation, whose degree is proportional to the clinical severity of the disease. This is paralleled by an impairment in arterial baroreceptor modulation of both vagal and sympathetic activity, thus suggesting that the adrenergic overactivity in congestive heart failure is triggered by a reduced afferent restraint on the vasomotor centre. Chronic angiotensin-converting enzyme inhibition reduces the degree of both sympathetic activation and baroreflex dysfunction occurring in heart failure patients, a finding which documents that the neurohumoral abnormalities can be at least partially reversed by pharmacologic treatment.

Adrenergic Fibers↗

PubMed2001

[Sleep-breathing disordered in stable chronic congestive heart failure].

OBJECTIVE: To determine the prevalence and effect of sleep-disordered breathing in patients with stable, optimally treated chronic congestive heart failure. METHODS: Patients with stable, optimally treated chronic congestive heart failure were monitored by polysomnography (Polywin 1000, Respironics Inc.). RESULTS: Patients were divided into two groups. Group I (n = 21) had a rate of apnea and hypopnea (apnea-hypopnea index) of 15 or less episodes per hour; group II (n = 15) had a rate of more than 15 episodes per hour. In group II, the rate varied from 16.8 to 78.8 episodes per hour 42.6 +/- 15.5, in which the obstructive apnea-hypopnea index was 11.1 +/- 8.4 and the central AHI was 31.5 +/- 9.6. Group II had significantly more arousals (36.8 +/- 21.3 compared with 19.4 +/- 11.2 in group I) that were directly attributable to episodes of apnea and hypopnea, lower arterial oxyhemoglobin saturation during sleep [(76.7 +/- 4.6)% compared with (86.5 +/- 2.8)%] and lower left ventricular ejection fraction [(24.2 +/- 8.8)% compared with (31.5 +/- 10.6)%]. CONCLUSIONS: The prevalence of sleep-disordered breathing (mainly periodic respiration or Cheyne-Stokes respiration with central sleep apnea) is high in patients with stable chronic congestive heart failure. The sleep-disordered breathing episodes are associated with severe nocturnal arterial blood oxyhemoglobin desaturation and excessive arousals. Severe untreated sleep-disordered breathing may affect left ventricular function and could contribute to death in patients with congestive heart failure.

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PubMed1995

Early left ventricular dysfunction elicits activation of sympathetic drive and attenuation of parasympathetic tone in the paced canine model of congestive heart failure.

BACKGROUND: Although autonomic imbalance is known to be characteristics of patients with clinically overt symptomatic congestive heart failure, it is currently unknown whether this autonomic response arises early in the course of left ventricular dysfunction or is restricted to the later stages of circulatory failure. METHODS AND RESULTS: This investigation utilized the technique of spectral analysis of heart rate variability in a paced canine model of congestive heart failure that permits an examination of autonomic activity at the earliest stages of ventricular dysfunction to determine whether early systolic dysfunction in congestive heart failure is characterized by autonomic imbalance, which may contribute to subsequent myocardial and vascular dysfunction. The results indicate that autonomic imbalance as reflected in an abnormal pattern of heart rate variability evolves early in the course of ventricular systolic dysfunction consisting of both a significant increase in sympathetically influenced low-frequency heart rate variability and a significant reduction of parasympathetically mediated high-frequency variability. This was quantified by a marked and significant increase in the area under the low-frequency region from 0.053 +/- 0.037 (beats per minute)2 at baseline to 0.182 +/- 0.143 (beats per minute)2 at 48 hours to 0.253 +/- 0.202 (beats per minute)2 after 7 days of pacing (ANOVA, P < .04). The area under the high-frequency region of the curve showed a decrease from a baseline value of 0.945 +/- 0.037 (beats per minute)2 to 0.811 +/- 0.152 (beats per minute)2 at 48 hours to 0.733 +/- 0.197 (beats per minute)2 after 7 days of pacing (ANOVA, P < .03). This resulted in a shift in autonomic balance away from parasympathetic tone and toward augmented sympathetic drive as reflected by the ratio of high- to low-frequency areas from a baseline value of 15.2 +/- 9.6 to 10.1 +/- 6.89 at 48 hours and 0.004 +/- 0.001 at 7 days (ANOVA, P < .01). CONCLUSIONS: The results indicate that autonomic imbalance as reflected in an abnormal pattern of heart rate variability evolves early in the course of ventricular systolic dysfunction consisting of both a significant increase in sympathetically influenced low-frequency heart rate variability and a significant reduction of parasympathetically mediated high-frequency variability. The early appearance of these autonomic abnormalities suggests that autonomic imbalance plays a significant role in promoting the progression of circulatory failure.

Animals↗

PubMed1992

Current status of phosphodiesterase inhibitors in the treatment of congestive heart failure.

The phosphodiesterase inhibitors have been recognised as potent inotropic and vasodilating drugs. In acute congestive heart failure they increase cardiac output, decrease left pulmonary capillary wedge pressure, and reduce total peripheral resistance with an improvement in loading conditions of the failing heart. Their potency in reversal of symptoms of acute congestive heart failure is quite similar to, or even better than, treatment with intravenous catecholamines and sodium nitroprusside. In chronic congestive heart failure, however, these agents increase mortality and have deleterious effects in the outcome of patients with severe left ventricular dysfunction.

Acute Disease↗

PubMed1998

Temporal trends in pharmacotherapy for congestive heart failure at an academic medical center: 1990-1995.

The objectives of this study were to assess current practice patterns in pharmacotherapy for congestive heart failure at an academic medical center and to analyze temporal trends in management of congestive heart failure from 1990 to 1995. Records of all patients discharged from the hospital in 1990 or 1995 with a primary diagnosis of congestive heart failure who also underwent echocardiography were found by a search of the hospital's medical records database. All charts were reviewed, and relevant clinical data, including all discharge medications, were recorded. On the basis of echocardiograms, patients were classified as having preserved or impaired left ventricular systolic function (estimated ejection fraction > or =45% versus <45%). The use of digoxin, diuretics, angiotensin-converting enzyme (ACE) inhibitors, calcium and beta-blockers, nitrates, and hydralazine in 1990 and 1995 were compared in subgroups according to left ventricular function. A total of 297 patients were identified who fulfilled study criteria and for whom all pertinent data were available (1990, n = 109; 1995, n = 188). The median age was 74 years; 37.3% of the patients were men, and 45.1% were white. Among patients with impaired systolic function, the proportion receiving either an ACE inhibitor or the combination of nitrates and hydralazine increased from 80.9% in 1990 to 95.4% in 1995 (p = 0.009). In addition, among patients treated with an ACE inhibitor, the proportion receiving an optimal dose increased from 24.3% in 1990 to 61.5% in 1995 (p < 0.001). The use of beta-blockers also increased significantly during this time period (2.1% versus 15.7%; p = 0.031 ). Among patients with preserved ventricular function, the use of ACE inhibitors and beta-blockers increased from 1990 to 1995 (both p < 0.05). The use of other medications did not change for either subgroup. Current use of appropriate vasodilator therapy at an academic medical center is very high and is in accordance with published guidelines for the management of congestive heart failure. The use of vasodilators and beta-blockers has increased significantly since 1990 among patients with congestive heart failure with either impaired or preserved left ventricular contractility.

Academic Medical Centers↗

PubMed2003

Reversal of refractory congestive heart failure after thiamine supplementation: report of a case and review of literature.

Patients with refractory heart failure comprise a very important subgroup of patients with congestive heart failure. Before assuming that this condition simply reflects advanced, perhaps terminal, myocardial dysfunction, potentially reversible factors should be sought carefully. We describe a 58-year-old Hispanic man with a diagnosis of idiopathic dilated cardiomyopathy who presented with symptoms of severe congestive heart failure, glossitis, and peripheral neuropathy. His hemodynamic profile was characterized by refractory low-output cardiac failure and decreased vascular resistance. Thiamine deficiency was documented by a high thiamine pyrophosphate effect. His clinical condition was quickly reversed with thiamine administration. This response to thiamine administration supports the diagnosis and indicates that thiamine deficiency may play an important etiologic role in the deterioration of cardiac function in some patients with congestive heart failure.

Cardiac Output, Low↗

PubMed1989

Neurohumoral activation in congestive heart failure: a double-edged sword?

The search for the basic mechanism(s) responsible for the progressive and frequently irreversible deterioration of left ventricular pump function in congestive heart failure has been quite extensive; nonetheless, no single explanation has been forthcoming. Indeed, given the complexity of this disease process, it is becoming increasingly unlikely that a single pathogenetic mechanism will ever be uncovered for congestive heart failure. This review will examine recent experimental and clinical evidence which suggests that excessive adrenergic stimulation of the heart is double-edged. That is, while increased adrenergic input to the heart may initially enable the failing myocardium to function adequately for a period of months to years, continued excessive adrenergic stimulation of the heart through both local neural and circulating catecholamines may lead to frank myopathic effects on the heart, with resultant worsening of left ventricular function and the development of intractable congestive heart failure. While we do not mean to suggest that excessive sympathetic stimulation of the heart is the only, or even the major mechanism responsible for the development of irreversible congestive heart failure, the data reviewed herein do suggest that adrenergic stimulation may play a primary role in the pathogenesis of congestive heart failure.

Adrenergic beta-Antagonists↗

PubMed1993

Medical advances in the treatment of congestive heart failure.

The increased incidence and prevalence of congestive heart failure place a high priority on novel treatment strategies. Left ventricular ejection fraction remains the single most valuable measurement providing both diagnostic and prognostic insights. The most systematic approach to heart failure involves an objective assessment of functional disability, to include exercise tests such as a 6-minute walk under standardized conditions. Left ventricular dysfunction incites a host of neurohumoral compensations that are of fundamental importance in the heart failure syndrome expression. Both vasoconstrictor and vasodilator neurohormones are stimulated and provide new therapeutic opportunities. The therapeutic approach to heart failure begins with a strong emphasis on prevention, patient education, and self-participation in therapy with respect to both its monitoring and adjustment. Diuretics remain a mainstay of therapy but, in the face of severe heart failure, may become ineffectual, requiring constant infusion of loop-active diuretics, combination diuretics, or diuretics in association with concomitant low-dose dopamine infusion. Vasodilator therapy has been an important advance: combination hydralazine and nitrate therapy was initially shown to be efficacious in improving survival, and more recently, angiotensin-converting enzyme (ACE) inhibitors, in the form of enalapril, have shown incremental benefit on survival over this combination. Interestingly, there is now evidence from both SOLVD and SAVE to demonstrate an unexpected and, as yet, unexplained reduction in the frequency of both unstable angina and myocardial infarction. Although, on balance, the weight of evidence concerning the long-term efficacy of inotropic agents has been disappointing, especially as it relates to their unfavorable effects on survival, recent information on vesnarinone, an agent with a complex and diversified mechanism of action, suggests that with appropriate doses, improved symptoms and survival are possible. A substantial amount of new information from randomized placebo-controlled trials attests to the symptomatic relief, hemodynamic improvement, and gain in exercise performance achieved by digoxin. A long-term survival study is ongoing to assess its effects on mortality. beta-Blockers, especially metoprolol, appear beneficial in some patients with heart failure, possibly related to their reduction in sympathetic nervous activity and restoration of beta-receptor population, with resultant improved contractile performance, enhanced myocardial relaxation, and overall increase in cardiac efficiency. Based on available evidence, the best contemporary approach to treatment involves the use of ACE inhibitors coupled with diuretic therapy, either continuous or intermittent, to relieve central or peripheral congestion. The addition of digoxin or a hydralazine nitrate combination is a logical next step, with commencement of low-dose beta-blocker a reasonable option.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗

PubMed1996

Exercise-induced vasodilation in forearm circulation of normal subjects and patients with congestive heart failure: role of endothelium-derived nitric oxide.

OBJECTIVES: This study was undertaken to investigate the role of endothelium-derived nitric oxide in the regulation of forearm blood flow during exercise in normal subjects and patients with congestive heart failure. BACKGROUND: Nitric oxide-mediated vasodilation in response to muscarinic stimulation is impaired in the peripheral circulation of patients with congestive heart failure. Whether nitric oxide-mediated vasodilation during exercise is also impaired in patients with congestive heart failure is unknown. METHODS: Forearm blood flows (ml/min per 100 ml) were determined during rhythmic hand grip exercise at 15%, 30% and 45% of maximal voluntary contraction by venous occlusion plethysmography before and after regional inhibition of nitric oxide synthesis with administration of L-NG-monomethylarginine (L-NMMA) in the brachial artery of 17 patients with congestive heart failure (mean age 49 years, mean left ventricular ejection fraction 0.22) and 10 age-matched normal subjects. RESULTS: Before administration of L-NMMA in the brachial artery, forearm blood flows in patients with congestive heart failure during rhythmic hand grip exercise at 15%, 30% and 45% of maximal voluntary contraction were slightly but not significantly lower than that of normal subjects ([mean +/- SE] 6.8 +/- 1.0, 8.5 +/- 1.0 and 12.9 +/- 1.7 ml/min per 100 ml, respectively, in patients with congestive heart failure vs. 6.6 +/- 1.2, 11.6 +/- 1.9 and 16.2 +/- 1.9 ml/min per 100 ml, respectively, in normal subjects, p = NS). After administration of L-NMMA in the brachial artery, forearm blood flows in normal subjects significantly decreased by 10% to 21% during hand grip exercise but did not change during exercise in patients with congestive heart failure. CONCLUSIONS: Regional inhibition of nitric oxide synthase with administration of L-NMMA in the brachial artery significantly decreased forearm blood flows during rhythmic hand grip exercise in normal subjects but not in patients with congestive heart failure. These findings suggest that nitric oxide-mediated vasodilation during submaximal exercise is impaired in the forearm circulation of patients with congestive heart failure.

Adult↗

PubMed1993

Effect of enalapril, hydralazine plus isosorbide dinitrate, and prazosin on hospitalization in patients with chronic congestive heart failure. The V-HeFT VA Cooperative Studies Group.

BACKGROUND: Hospitalization of persons with congestive heart failure for recurrent heart failure or other complications is common. METHODS AND RESULTS: Male patients aged 18-75 with chronic heart failure were randomized in two sequential trials designed to study the efficacy of vasodilator therapy. Patients were evaluated every 3 months, and information regarding hospitalizations between visits was obtained from the patient, his family, and/or hospital records. Hospitalization data also were obtained for patients who had died between scheduled clinic visits. Hospitalizations were not recorded if a patient died during transit to the hospital or in the hospital emergency department before admission. In Vasodilator-Heart Failure Trial (V-HeFT) I, no significant difference in number of patients hospitalized or number of hospitalizations was noted among the treatment groups, although there was a trend for fewer and delayed cardiac hospitalizations in the hydralazine plus isosorbide dinitrate arm in which the survival was greater. In V-HeFT II, no difference in hospitalizations was apparent between the enalapril and hydralazine plus isosorbide dinitrate arms. Univariate predictors of hospitalization for all causes were reduced peak oxygen consumption (VO2) during exercise (p < 0.0001), reduced exercise duration (p < 0.0001), increased cardiothoracic ratio on chest radiograph (p < 0.0001), increased age (p < 0.03), and use of antiarrhythmic drugs (p < 0.013), whereas multivariate predictors were reduced peak VO2 (p < 0.0001), use of antiarrhythmic drugs (p < 0.015), and increased cardiothoracic ratio (p < 0.03). Univariate predictors of hospitalization for heart failure were peak VO2 (p < 0.0001), LVEF (p < 0.0001), reduced exercise duration (p < 0.0001), elevated cardiothoracic ratio (p < 0.0001), and elevated plasma norepinephrine (p < 0.0001). Multivariate predictors were exercise duration (p < 0.0001), LVEF (p < 0.04), elevated cardiothoracic ratio (p < 0.03), plasma norepinephrine (p < 0.0005), and coronary artery disease (p < 0.02). Time to first hospitalization, cause specific or overall, was considerably shorter for patients with baseline peak VO2 < 10 mL.kg-1 x min-1 compared with those with peak VO2 > 15 mL.kg-1 x min-1. CONCLUSIONS: Despite better survival in patients randomized to hydralazine plus isosorbide dinitrate compared with placebo and better survival in patients randomized to enalapril compared with hydralazine plus isosorbide dinitrate, no significant differences between the treatment groups were apparent in the incidence of hospitalization or time to first hospitalization for congestive heart failure, for cardiac reasons other than congestive heart failure, or for other causes. V-HeFT I and V-HeFT II data demonstrate no treatment effect on hospitalization, perhaps reflecting in part the effectiveness of the Veterans Affairs special heart failure clinics in dealing with worsening heart failure on an outpatient basis. Identification of predictors of hospitalization were similar in both studies.

Drug Therapy, Combination↗

PubMed1981

Increase in plasma norepinephrine during prazosin therapy for chronic congestive heart failure.

To investigate the mechanism of pharmacodynamic tolerance reported to occur during prazosin therapy of chronic congestive heart failure, we measured plasma norepinephrine, plasma epinephrine, plasma renin activity (PRA) and plasma aldosterone, as well as hemodynamics in eight patients with chronic congestive heart failure, functional class III and IV (NYHA), before and during 10 weeks of prazosin therapy. Initially, prazosin therapy produced significant hemodynamic improvement, but no significant changes were noted in norepinephrine, epinephrine, plasma renin activity or aldosterone. During ambulatory therapy, fluid retention developed in four patients, and three of them had symptoms or clinical evidence of congestive heart failure for which they required an increase in diuretic or prazosin therapy. Plasma norepinephrine levels for the whole group were significantly higher after four weeks of therapy (p less than 0.01). Repeat inpatient studies after 10 weeks showed a persistent hemodynamic response to prazosin in seven patients. One patient demonstrated complete hemodynamic tolerance whereas three others showed partial tolerance. In these four patients the cardiac output increased only to 3.78 +/ 1.17 liters/min compared to 5.04 +/- 2.11 liters/min during initial prazosin therapy. Plasma norepinephrine increased further and levels were significantly higher for the whole group than before prazosin therapy (p less than 0.05). No significant changes in epinephrine, plasma renin activity or aldosterone were demonstrated. This increase in plasma norepinephrine suggests that the sympathetic nervous system could be involved in the pharmacodynamic tolerance to prazosin therapy in congestive heart failure. Further studies are necessary to extend these results.

Aged↗

PubMed1995

Clinical Spectrum of Congestive Heart Failure in the Elderly Population.

One hundred and fifty-two patients with congestive heart failure above 65 years of age were treated at The Mercy Hospital of Pittsburgh in the calendar year 1992, forming 38% of the total number of inpatients with this condition for that year. Hypertension, ischemic heart disease, and valvular diseases were the common etiological factors. Evidence for diastolic dysfunction was seen in 34% of patients by echocardiographic Doppler study. Atrial fibrillation was the most common arrhythmia. Acute or subacute dyspnea was the most common presenting symptom. Response to conventional treatment was excellent but readmissions for recurrence of congestive heart failure were very common. The in-hospital mortality of these patients in that year was 6%. The possible precipitating factors for recurrent admissions are discussed. In order to favorably control precipitating factors and reduce readmissions, a multicenter registry of congestive heart failure in the elderly is suggested.

Journal Article↗

PubMed2004

Importance of chronic obstructive pulmonary disease for prognosis and diagnosis of congestive heart failure in patients with acute myocardial infarction.

AIMS: To evaluate the importance of chronic obstructive pulmonary disease for prognosis and diagnosis of congestive heart failure in patients with acute myocardial infarction. METHOD AND RESULTS: Prospective registration of 6669 consecutive patients admitted with infarction and screened for a randomised controlled trial. A history of COPD was present in 765 (11.5%) patients. Thirty-day and 5-year survival in patients with chronic obstructive pulmonary disease was 86.3 and 42.9%. In patients without pulmonary disease the figures were 87.7 and 57.5%, respectively, giving a relative risk of 1.49 (1.35-1.65). In multivariate analysis the relative risk was 1.15 (1.04-1.28). The prevalence of congestive heart failure was 65.9% in patients with chronic obstructive pulmonary disease and 52.0% in patients without. This difference was most distinct in patients with normal or only slightly decreased left ventricular systolic function. In patients without congestive heart failure, chronic obstructive pulmonary disease was of prognostic importance [RR=1.44 (1.17-1.78)], but not in patients with congestive heart failure [RR=1.09 (0.96-1.23)]. CONCLUSION: Chronic obstructive pulmonary disease is a predictor of long-term mortality in patients with acute myocardial infarction without congestive heart failure, but is also a confounding factor for the diagnosis of congestive heart failure.

Aged↗