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PubMed1989

The use of levodopa, an oral dopamine precursor, in congestive heart failure.

The successful treatment of congestive heart failure with intravenous dopamine in the acute setting has prompted investigation into the development and use of oral dopamine analogs. The administration of dopamine can lead to an improvement in myocardial pump performance through a combination of afterload reduction and augmented contractile state. The ingestion of levodopa, an oral dopamine precursor, is associated with sustained hemodynamic and clinical improvement in patients with congestive heart failure. Improvements in hemodynamic performance correlated with the generation of substantial amounts of dopamine. Current research efforts are directed at developing oral dopamine analogs that exhibit improved bioavailability and do not traverse the blood-brain barrier.

Administration, Oral↗
PubMed2005

Combined effects of ramipril and angiotensin II receptor blocker TCV116 on rat congestive heart failure after myocardial infarction.

BACKGROUND: Congestive heart failure (CHF) is a major cause of morbidity and mortality worldwide and angiotensin converting-enzyme inhibitor (ACEI) is the cornerstone in its treatment. However, CHF continues to progress despite this therapy, perhaps because of production of angiotensin II (Ang II) by alternative pathways. The present study was conducted to examine the combined effects of a chronic ACEI, ramipril, and a chronic Ang II type 1 receptor blocker, TCV116, on rat CHF after myocardial infarction (MI). METHODS: Congestive heart failure was caused by MI in rats, which was induced by ligating the left anterior descending coronary artery. The experiment protocol included sham-operated rats (Sham), MI-control rats (MI-control), MI rats treated with ramipril 3 mg/kg (MI-ramipril) or TCV116 2 mg/kg (MI-TCV116) per day, half dosage (MI-1/2R&T) or full dosage (MI-R&T) combination of the two. At 22 weeks, cardiac hemodynamic parameters such as mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), maximal rate of left ventricule pressure development and decline (LV dP/dtmax) and left ventricular end diastolic pressure (LVEDP), and cardiac morphometric parameters such as heart weight (HW), left ventricular weight (LVW) and left ventricular cavity area (LVCA) were measured, mRNA expressions of cardiac molecule genes such as beta myosin heavy chain (betaMHC), B-type natriuretic peptide (BNP), transforming growth factor-beta1 (TGF-beta1), collagen I and III were quantified with reverse transcription polymerase chain reaction (RT-PCR) in the surviving septum myocardium, and survival rates were calculated. RESULTS: There were no significant differences in MI sizes (%) among each MI related experimental groups (33 +/- 13, 34 +/- 14, 33 +/- 13, 35 +/- 13 and 33 +/- 14 for MI-control, MI-ramipril, MI-TCV116, MI-1/2R&T and MI-R&T, respectively, no statistical significance for all). Compared with sham-operated rats, MI rats without therapy showed significant increases in morphometric parameters as well as in mRNA expressions of cardiac molecule genes (P < 0.01); while their hemodynamic parameters were significantly impaired (P < 0.01), and in terms of spontaneous deaths survival rate shortened (P < 0.05). Compared with MI rats without therapy, MI rats treated with each single drug showed significant attenuation of mRNA expressions of cardiac molecule genes (P < 0.01); while their hemodynamic parameters were significantly improved (P < 0.05 or P < 0.01), and in terms of spontaneous deaths survival rate prolonged (P < 0.05). Both half and full dosage combined treatments exerted more powerful effects on improvement of cardiac phenotypic changes and on attenuation of betaMHC, BNP mRNA expressions (P < 0.05 vs monotherapy); while LVEDP was further lowered (P < 0.05 vs monotherapy). However, the total death in MI rats with full dosage combined treatment was more though there were no significant differences when compared with other treatments. CONCLUSIONS: The results suggest that treatment with appropriate dosage combination of a chronic ACEI and a chronic ARB may further improve cardiac remodeling and cardiac function after MI.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Peripheral hemodynamic and humoral effects of oral zofenopril calcium (SQ. 26,991) in patients with congestive heart failure.

In 14 patients with congestive heart failure (CHF) of various grade (NYHA class 2-4) the effects of zofenopril calcium (SQ 26,991) on blood pressure and forearm circulation were studied by venous occlusion plethysmography. Changes in plasma renin activity (PRA), aldosterone, Atrial natriuretic factor (ANF) and arginine-vasopressin (AVP) were also measured. Two hours after oral administration of 7.5 mg of zofenopril we observed a decrease in blood pressure, heart rate, and forearm vascular resistance along with an increase in venous distensibility. Zofenopril also decreased ANP levels in a manner directly related to peripheral venodilatation (r = .64; P less than .05) and modified arginine-vasopressin (AVP) proportionally to the fall in blood pressure observed in response to drug administration (%SBP/%AVP: r = .64, P less than .05; %DBP/%AVP: r = .67, P less than .05). Hemodynamic and humoral responses to zofenopril occurred without any significant unwanted adverse reaction, even in patients with greater pressor reduction. We conclude that oral acute zofenopril administration, in patients with congestive heart failure, causes an arterial and venous forearm vasodilatation which is probably involved in the acute changes in plasma levels of ANF and AVP observed after drug administration.

Administration, Oral↗
PubMed1980

Sustained effectiveness of converting-enzyme inhibition in patients with severe congestive heart failure.

Eight patients with severe congestive heart failure refractory to conventional therapy, including vasodilators, were given captopril (seven patients) or teprotide (one patient). All had dyspnea, edema, elevated pulmonary wedge pressure (28.0 +/- 2.6 mm Hg), low cardiac index (1.6 +/- 0.1 liters per minute per square meter), and elevated levels of serum creatinine (2.3 +/- 0.2 mg per deciliter [203.3 +/- 17.7 mumol per liter]), blood urea nitrogen (48 +/- 5 mg per deciliter [17.1 +/- 1.8 mmol of urea per liter]), plasma renin activity (21 +/- 7 ng of angiotensin I per milliliter per hour), plasma angiotensin II (271 +/- 51 pg per milliliter), and plasma aldosterone (65 +/- 14 ng per deciliter). After one week of therapy, all indexes improved. Creatinine and p-aminohippurate clearances were also increased (P less than 0.01). Improvement was sustained (more than six months) and was associated with a statistically significant increase in the cardiac ejection fraction (12 +/- 3 to 26 +/- 7 per cent). With a mean follow-up of seven months, the New York Heart Association Functional Class has been reduced from IV to II, and the number of days of hospitalization to less than 10 per cent of that before captopril therapy. We conclude that captopril reduces afterload in advanced congestive heart failure and induces sustained improvements in clinical status and renal function.

Adult↗
PubMed1980

Vasodilator therapy for congestive heart failure.

Six patients with severe congestive heart failure were treated with nitroprusside intravenously. Four of the six patients showed salutary responses and were successfully weaned from the NP with marked resolution of symptoms. No adverse side effects were observed. These four patients and one additional child (who did not receive NP) were treated with prazosin by mouth in addition to digoxin and diuretics daily. Two of these patients are entirely symptom free, and additional child is moderately improved, and the fourth patient has shown minimal symptomatic improvement. Despite the severity of their pretherapy symptoms, only one patient has died while receiving oral vasodilator therapy. This preliminary study suggests that afterload reduction may be life-saving in children who are virtually moribund because of congestive heart failure. This improvement can be maintained with oral vasodilator therapy and continuation of classic anticongestive therapy. However, afterload reduction has no effect on the underlying disease. Confirmatory studies are essential before this experimental mode of therapy is accepted for routine use in infants and children.

Adolescent↗
PubMed1998

Dissociation between muscle and skin sympathetic nerve activity in essential hypertension, obesity, and congestive heart failure.

Essential hypertension, obesity, and congestive heart failure are characterized by an increase in muscle sympathetic nerve activity. Whether in these conditions skin sympathetic nerve activity is also increased has never been systematically examined, however. In 10 untreated mild essential hypertensive, 12 untreated normotensive obese, 10 mild (New York Heart Association class II) heart failure, and 10 normotensive lean healthy control subjects, we measured beat-to-beat arterial blood pressure (Finapres technique), body mass index, and postganglionic sympathetic nerve activity in skeletal muscle and skin areas (microneurographic technique, peroneal nerve). The muscle and skin nerve measurements were made in a randomized sequence. All data were obtained with the subject supine in a quiet, semidark environment at constant temperature over two periods of 30 minutes each, separated by a 20- to 30-minute interval. Blood pressure was increased only in hypertensive and body mass index only in obese subjects. Muscle sympathetic nerve activity quantified as bursts/min was markedly and significantly (P<.01) greater in essential hypertensive (33.3+/-1.7), obese (42.2+/-2.8), and congestive heart failure subjects (55.8+/-4.3) in comparison with control subjects (23.9+/-1.6). This was the case also for muscle sympathetic nerve activity, quantified as bursts per 100 heart beats. In contrast, skin sympathetic nerve activity (bursts per minute) was superimposable in hypertensive, obese, heart failure, and control subjects, its ability to increase being documented in all four groups by the marked response to an acoustic stimulus. Thus, in various diseases, muscle but not skin sympathetic activity is increased, with the sympathetic activation not being uniformly distributed over the whole cardiovascular system.

Adult↗
PubMed1991

Acute and chronic efficacy of felodipine in congestive heart failure.

In 13 patients with congestive heart failure we tested the acute hemodynamic effects of 5 vs. 10 mg felodipine tablets, in a double-blind, cross-over study. One hour after felodipine 5 mg, echocardiographic ejection fraction (%), cardiac index (thermodilution-ml/min/m2), and pulmonary wedge pressure (mm Hg) significantly changed (from 21 +/- 2 to 26 +/- 2, 2350 +/- 150 to 2790 +/- 160, 24 +/- 4 to 17 +/- 4) while they remained steady after felodipine 10 mg. The greatest stroke index increases were associated with felodipine 5 mg in 12 patients and 10 mg in 1 patient. Therefore we evaluated (open study) the long-term (2 months- 1 year) clinical and hemodynamic efficacy following the treatment with the acutely most effective dose (twice daily). After 2 months ejection fraction, cardiac index and pulmonary wedge pressure were respectively 24 +/- 2, 2550 +/- 150, and 18 +/- 4 (12 hours after the last drug administration, n = 11, P less than 0.02 from baseline). These parameters further increased one to two hours after the following administration of felodipine. Clinical improvement (reduction of 1 functional class, according to the New York Heart Association) was observed in 8/13 patients. These 8 patients participated to the one year follow-up. In 5 patients follow-up was interrupted because of acute cardiovascular events. However, before study interruption (5 patients) or ending (3 patients) clinical status did not worsen and ejection fraction remained higher than in the pretreatment period. Therefore, low dose felodipine might be used in the treatment of congestive heart failure.

Double-Blind Method↗
PubMed1993

Downregulation of cardiac guanosine 5'-triphosphate-binding proteins in right atrium and left ventricle in pacing-induced congestive heart failure.

The extent to which congestive heart failure (CHF) is dependent upon increased levels of the cardiac inhibitory GTP-binding protein (Gi), and the impact of CHF on the cardiac stimulatory GTP-binding protein (Gs) and mechanisms by which Gs may change remain unexplored. We have addressed these unsettled issues using pacing-induced CHF in pigs to examine physiological, biochemical, and molecular features of the right atrium (RA) and left ventricle (LV). CHF was associated with an 85 +/- 20% decrease in LV segment shortening (P < 0.001) and a 3.5-fold increase (P = 0.006) in the ED50 for isoproterenol-stimulated heart rate responsiveness. Myocardial beta-adrenergic receptor number was decreased 54% in RA (P = 0.004) and 57% in LV (P < 0.001), and multiple measures of adenylyl cyclase activity were depressed 49 +/- 8% in RA (P < 0.005), and 44 +/- 9% in LV (P < 0.001). Quantitative immunoblotting established that Gi and Gs were decreased in RA (Gi: 59% reduction; P < 0.0001; Gs: 28% reduction; P < 0.007) and LV (Gi: 35% reduction; P < 0.008; Gs: 28% reduction; P < 0.01) after onset of CHF. Reduced levels of Gi and Gs were confirmed by ADP ribosylation studies, and diminished function of Gs was established in reconstitution studies. Steady state levels for Gs alpha mRNA were increased in RA and unchanged in LV, and significantly more GS alpha was found in the supernatant (presumably cytosolic) fraction in RA and LV membrane homogenates after CHF, suggesting that increased Gs degradation, rather than decreased Gs synthesis, is the mechanism by which Gs is downregulated. We conclude that cardiac Gi content poorly predicts adrenergic responsiveness or contractile function, that decreased Gs is caused by increased degradation rather than decreased synthesis, and that alterations in beta-adrenergic receptors, adenylyl cyclase, and GTP-binding proteins are uniform in RA and LV in this model of congestive heart failure.

Adenylyl Cyclases↗
PubMed1993

Effects of histamine type 2-receptor antagonists cimetidine and famotidine on left ventricular systolic function in chronic congestive heart failure.

Twelve patients with stable congestive heart failure and left ventricular dysfunction were enrolled in a double-blind, randomized crossover trial of famotidine, cimetidine and placebo to determine whether histamine type 2 (H2) antagonists adversely affect left ventricular systolic performance. Two-dimensional echocardiograms were obtained at baseline, after 4 days of oral treatment with standard doses of famotidine and cimetidine, and placebo, and at the conclusion of the trial. The baseline mean ejection fraction was 19 +/- 7%. The changes in ejection fraction were +2 +/- 11% (95% confidence interval [CI] -5 to 9%) with famotidine, +3 +/- 10% (95% CI -3 to 10%) with cimetidine, and -3 +/- 7% (95% CI -8 to 2%) with placebo. There were no significant differences in changes in ejection fraction among the 3 experimental treatments (p = 0.22; analysis of variance). The changes in end-systolic wall stress/volume ratios from baseline were +6 +/- 21% (95% CI -6 to 18%) for famotidine, +8 +/- 29% (95% CI -8 to 25%) for cimetidine, and +2% +/- 29% (95% CI -15 to 18%) for placebo (p = 0.69; analysis of variance). No patient had a worsening of symptoms during therapy. Despite previous reports that H2 antagonists may depress left ventricular systolic function, at standard doses these agents result in no decrease in left ventricular systolic function in patients with chronic congestive heart failure.

Aged↗
PubMedDate not supplied

Management of the patient with congestive heart failure using outpatient, home, and palliative care.

Congestive heart failure is a chronic, debilitating illness, with increasing prevalence in the elderly. It is one of the most common causes for hospital admission, and associated treatment costs are estimated at $20.2 billion. Despite improved survival with medical therapy, beneficial effects on quality of life have not been consistently reported. In addition, optimum medical therapy, as recommended by evidence-based guidelines, are not always implemented. Counseling and education involving dietary modifications, activity recommendations, medication management, self-monitoring, prognosis, coping skills, social support, caregiver stress, and spiritual needs are critical components in the management of heart failure through initial diagnosis to end of life. Within the last decade, close follow-up for congestive heart failure has been associated with decreased hospitalizations, reduced hospital length of stay, improved functional status, better compliance, lower costs, and improved survival. Research trials have mainly been observational and small, and they have used different interventions. Little has been written regarding outpatient management of the patient with advanced congestive heart failure, and none of the current published guidelines addresses recommendations for the New York Heart Association class IV (other than for transplant candidacy). New models of close follow-up for chronic and advanced congestive heart failure should be investigated. These models could be implemented in urban and rural settings and be supported by private insurance or Medicare.

Ambulatory Care↗
PubMed1990

Marked spontaneous improvement in ejection fraction in patients with congestive heart failure.

PURPOSE: The overall prognosis for patients with congestive heart failure is poor. Defining specific populations that might demonstrate improved survival has been difficult. We therefore examined our patient database for patients with congestive heart failure who demonstrated sustained improvement in left ventricular function and associated resolution of signs and symptoms of congestive heart failure. PATIENTS AND METHODS: We identified 11 patients with severe congestive heart failure (average ejection fraction 21.9 +/- 4.23% (+/- SD) who developed spontaneous, marked improvement over a period of follow-up lasting 4.25 +/- 1.49 years. All 11 patients were initially symptomatic with exertional dyspnea and fatigue for a minimum duration of 3 months. They form a subset of a larger group of 97 patients with chronic congestive heart failure that we have followed with sequential ejection fraction measurements. All 11 patients were treated with digitalis diuretics, and either converting-enzyme inhibitors or a combination of isosorbide dinitrate and hydralazine. Ten of the 11 patients had a history consistent with chronic alcoholism, and each reportedly abstained from alcohol during follow-up. RESULTS: During the follow-up period, the average ejection fraction improved in 11 patients from 21.9 +/- 4.23% to 56.64 +/- 10.22%. Late follow-up indicates an average ejection fraction of 52.6 +/- 8.55% for the group. Congestive heart failure resolved in each case. CONCLUSIONS: We conclude that selected patients with severe congestive heart failure can markedly improve their left ventricular function in association with complete resolution of heart failure. This appears to be particularly evident in those patients with chronic alcoholism who subsequently abstain.

Aged↗
PubMed1990

Cardiodynamic improvement following PGE1 administration in sheep with congestive heart failure.

The cardiodynamic effects of Prostaglandin E1 were studied in sheep with congestive heart failure. Six Merino ewes were equipped surgically with high fidelity micromanometers and left ventricular pressures measured. Heart rate, left ventricular systolic and end-diastolic pressures, [+dP/dt]max and a single-exponential time constant (T) were calculated on a computer from the recorded pressure curves and the Wilcoxon signed rank test used to determine the statistical significance of the differences. Prostaglandin E1 (20 micrograms.kg-1) significantly improved left ventricular contractility and relaxation rate as seen respectively from [+dP/dt]max and the single-exponential time-constant and reduced the afterload conditions under which the heart operated, during various stages of congestive heat failure, without significant tachycardia during the more advanced stages of the disease. The results show that [+dP/dt]max increased between 16% (stage 4) and 38% (stage 1); T shortened between 14% (stage 4) and 25% (stage 1) and left ventricular systolic pressure decreased between 14% (stage 4) and 21% (stage 1) when prostaglandin E1 was administered during four stages of left ventricular pump failure, which ranged from a 20% decrease in [+dP/dt]max (congestive heart failure stage 1) to a 50% decrease in [+dP/dt]max (congestive heart failure stage 4). In contrast to normal animals, prostaglandin E1 caused an increase in left ventricular end-diastolic pressure during the more advanced stages of pump failure. Nevertheless the favourable cardiodynamic changes brought about by prostaglandin E1 administration might contribute, together with afterload reduction, to a general haemodynamic improvement during congestive heart failure.

Alprostadil↗
PubMed2006

The impact of peritoneal dialysis upon quality of life and mortality of patients with end-stage congestive heart failure.

BACKGROUND: Aged patients affected by congestive heart failure refractory to pharmacologic therapy, coupled with severe comorbidities that preclude heart transplantation have a gloomy prognosis. Use of automated peritoneal dialysis resulted in a significantly improved quality of life and survival. METHODS: Twenty patients (mean age: 65.7 +/- 7.7 years) with severe congestive heart failure (Class IV-NYHA) and a high Charlson comorbidity index (7.8 +/- 1.8) were treated by means of automated peritoneal dialysis (3 sessions/week, 8 h each). The period of follow-up ranged between 7 and 35 months (19.8 +/- 7.4 months). RESULTS: After 1 year of follow-up, all patients showed functional (Class I-NYHA) and hemodynamic improvement: left cardiac work index increased from 2.33 +/- 0.69 to 2.59 +/- 0.47 kg/min/m(2) (p < 0.01); systolic times ratio was significantly reduced (from 61.14 +/- 12.57 to 39.18 +/- 13.44%, p < 0.01); and the thoracic fluid contents was substantially reduced (from 0.04 +/- 0.005 to 0.003 +/- 0.0001 Omega). A marked drop of hospitalization days was observed. CONCLUSIONS: Automated peritoneal dialysis appears as a promising tool for treating patients suffering from refractory, end stage congestive heart failure. Improvement of cardiac function may result from clearing the blood from middle molecular weight myocardial depressant substances, including atrial natriuretic peptide. Results of this investigation are a call for a prospective multicenter study in order to confirm these promising observations.

Aged↗
PubMedDate not supplied

The brain in congestive heart failure.

In the present paper we discuss two issues about relationships between congestive heart failure and the brain. First, major acute cerebrovascular events are very frequent among elderly people, but stroke does not appear to be frequently associated with congestive heart failure. Second, some cardiovascular conditions may determine progressive damage of cerebral tissue, with consequent impairment of cognitive functions. The association of cognitive impairment and cardiovascular diseases may dramatically increase morbility and mortality risks in the elderly. Recent studies seem to show that hypotension and congestive heart failure are risk factors for dementia in elderly people. In view of this data, an Italian multicentric study on congestive heart failure in hospitalized elderly patients (CHF Italian Study I) included a brief screening of cognitive abilities (MMSE). The presence of congestive heart failure induced a significant decrease of MMSE scores: mean MMSE score after statistical adjustment for the other variables was about one point lower in patients with congestive heart failure respect to elderly patients affected by heart disease but without congestive heart failure. A novel multicentric study (CHF Italian Study II) has been performed to identify cognitive functions more specifically impaired during congestive heart failure in the elderly. Preliminary data relative to 385 patients, confirmed that congestive heart failure may induce a generalized impairment of cognitive functions. These data have relevant clinical implications because they demonstrate that a multidisciplinary approach is necessary in these patients, both for prevention and rehabilitation therapy.

Journal Article↗
PubMed1980

The management of congestive heart failure.

The symptoms and physical findings of congestive heart failure are learned during the early stages of medical education. They are considered prominently in physical diagnosis courses even before a medical student's clinical clerkships begin. Yet, the diagnosis and proper management of congestive heart failure may still represent a challenge even for the most experienced clinician. Obviously, there is more to this syndrome than a collection of symptoms and signs. In fact, it is probably best to reject entirely the concept of congestive heart failure as a syndrome and consider it merely a descriptive term that requires an application of knowledge and skills learned in physiology, pharmacology and clinical medicine if the patient is to receive proper care. Many fine monographs and textbooks have been written about congestive heart failure, from the standpoint of myocardial mechanics, pathophysiology, cardiovascular pharmacology and biochemistry. It is our aim in this monograph to provide clinical insights into the management of congestive heart failure, including such factors as myocardial mechanics and cardiovascular pharmacology only when applicable in a clinical sense. Several cases recently encountered are included to underscore certain concepts.

Diet, Sodium-Restricted↗
PubMed1994

Response of plasma neuropeptide Y and noradrenaline to dynamic exercise and ramipril treatment in patients with congestive heart failure.

Forty-two patients with congestive heart failure were studied in order to clarify whether the plasma level of neuropeptide Y-like immunoreactivity (NPY-LI) rises in parallel with plasma noradrenaline (NA) during physical exercise in congestive heart failure (CHF). All patients were studied in a randomized placebo-controlled trial with the ACE-inhibitor ramipril during 12 weeks to determine whether ACE-inhibition alters the response of plasma NPY-LI to exercise. The patients were treated with diuretics and had stable congestive heart failure (NYHA classes II-III). Plasma NPY-LI was 50 +/- 5 pmol l-1 (mean +/- standard error of the mean) at rest and 60 +/- 6 pmol l-1 at the end of exercise at baseline (P < 0.01). The corresponding values for plasma NA were 2.8 +/- 0.2 nmol l-1 and 15.3 +/- 1.2 nmol l-1 (P < 0.001). Before ACE-inhibition, there was a correlation between high NPY-LI and NA values after exercise. After treatment with ramipril or placebo for 12 weeks, there was no difference in plasma NPY-LI and NA at rest or after exercise between the two treatment groups. The maximal exercise time was unchanged. It is concluded that plasma NPY-LI and NA were elevated at rest in CHF. The additional rise of plasma NPY-LI and NA after exercise was attenuated in CHF compared to healthy individuals. ACE-inhibition with ramipril did not alter plasma NPY-LI or NA at rest or after exercise compared to placebo.

Aged↗