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At least 19 recordsLinked to original sources
PubMed1977

[Systemic lupus erythematosus and congestive heart failure. Heart histological and ultrastructural study (author's transl)].

Histological and ultrastructural studies were performed on myocardial biopsies and aortic and mitral valve leaflets obtained during an operation on a patient with Systemic Lupus Erythematosus (S.L.E.). Congestive heart failure and valvular dysfunction appeared five years after the diagnosis of S.L.E. was made. On histological study, aortic and mitral valve leaflets are uniformly thickened by fibrous tissue with a nodular appearance. No active endocarditis was associated with the fibrous scarring. Atrial myocardium and papillary muscle countain a fibrous net-work discret in the former, extensive in the latter. The scattered foci of fibrosis in the papillary muscle surround vessels without obliteration or parietal necrosis. Ultrastructurally their lumina appears narrowed by prominent endothelial cells with cytoplasmic aggregates of tubuloreticular structures (T.R.S.). These tubules are also present in some endocardial endothelial cells but are rare in the normal intrapapillary or atrial vessels that are not associated with a scar. Myocardial fibrous foci enclose atrophic and severely degenerated cardiac muscle cells; other cells situated at the periphery of the foci are normal in size or hypertrophic and moderately degenerated. The most altered muscle cells show an important loss of myofibrils, a proliferation of sarcoplasmic reticulum in myofibril free spaces, or necrosis with macrophagic resorption. Focal changes with loss of myofilaments, Z material streaming and concentric lamellar bodies are found in moderately degenerate cardiac muscle cells. The remaining papillary muscle cells and the atrial cells are all hypertrophied without degeneration. These changes suggest that focal myocardial fibrosis and associated cardiac muscle cell degeneration may be responsible for impaired cardiac performance in some patients with S.L.E. According to the constant topographic relation between the narrowed vessels whose endothelial cells contain T.R.S. and the surrounding fibrous foci, we believe that the myocardial fibrous patches may correspond to scarring of microinfarcts related to active S.L.E. vascularitis.

Aortic Valve↗
PubMed1979

Postpartum cardiac failure--heart failure due to volume overload?

Ventricular function has been studied in 43 patients with the peripartum cardiac failure (PPCF) syndrome which occurs around Zaria. All patients had an echocardiogram on admission and 10 patients had right heart catheterization. Despite the gross edema, left ventricular function assessed by echocardiography and systolic time intervals was relatively good and the estimated cardiac output were high. At catheterization, although the pressures were high, the cardiac outputs were greater than normal in four out of six patients. No patient had a low cardiac output. These findings are not compatible with a severe heart muscle disorder, or cardiomyopathy. We suggest that the primary event in PPCF of Zaria is fluid retention which leads to a form of high output cardiac failure. The postpartum practices in this area (taking high sodium diets and lying on heated beds) almost certainly cause the fluid to accumulate initially, but the heart may be unable to meet the demands either because of preexisting heart muscle disease or, more likely, because of a rise of the peripheral resistance due to the volume expansion, overburdens such dilated hearts and leads to myocardial damage. Since there are similarities between this condition and PPCF in temperate climates, it is possible that there is a common mechanism which the traditional practices of this area have unveiled.

Adolescent↗
PubMed1990

Arterial baroreceptor control of peripheral vascular resistance in experimental heart failure.

Heart failure is known to impair arterial baroreceptor control of heart rate. To determine if baroreceptor control of peripheral vascular resistance is also impaired, heart rate and hind limb vascular responses to phenylephrine and nitroglycerin administration were compared in control dogs and in dogs with heart failure produced by chronic rapid ventricular pacing. Baroreflex control of the heart rate was depressed in the dogs with heart failure, as evidenced by a reduced slope of the blood pressure-to-heart rate relationship (controls: -2.5 +/- 0.3 beats/mm Hg versus heart failure: -1.5 +/- 0.2 beats/mm Hg [(p less than 0.04)]). Arterial blood pressure in the dogs with heart failure was also reduced (controls: 90 +/- 3 mm Hg versus heart failure: 75 +/- 3 mm Hg [(p less than 0.01)]). Nevertheless, dogs with heart failure exhibited normal slopes of the blood pressure versus hind limb vascular resistance relationship (controls: -2.4 +/- 0.4 units/mm Hg versus heart failure: -2.9 +/- 0.5 units/mm Hg [(p = NS)]), consistent with preserved baroreflex control of the peripheral vasculature. These data suggest that heart failure impairs arterial baroreflex control of heart rate and lowers the baroreflex pressure operating range but does not alter baroreflex control of peripheral resistance.

Animals↗
PubMed1989

Pharmacotherapeutic profile of ibopamine in heart failure.

Heart failure is a complex cardiovascular syndrome affording many pharmacotherapeutic targets. Ibopamine affords a unique pharmacological profile for the treatment of this complex syndrome by virtue of its ability to stimulate DA-1 and DA-2 receptors in the vasculature in combination with its beta 2-agonist activity. The drug has been shown to improve the Frank-Starling relationship in the failing heart and augment cardiac output and ejection fraction at the same time that cardiac filling pressure is reduced. Concomitantly, the drug has been shown to attenuate the activated neuroendocrine responses activated in heart failure. Clinically, ibopamine has been shown to improve exercise tolerance, reduce the patient's symptom score, and NYHA classification, and reduce the requirement for additional anti-heart failure drugs. The influence of ibopamine on survival in heart failure awaits pragmatic tests, but the results of open monitoring studies are promising in this respect. Ibopamine does not appear to have any substantial adverse reactions that would inhibit its use in patients in heart failure. The unique pharmacotherapeutic profile of ibopamine affords a new pharmacologic vista for the treatment of patients with chronic heart failure.

Adrenergic beta-Agonists↗
PubMed1992

Ventricular arrhythmias in heart failure.

Heart failure is an increasingly common disorder leading to reduced quality and expectancy of life. Asymptomatic and symptomatic ventricular arrhythmias are a frequent complication and have been found to be independent prognostic predictors for sudden cardiac death in patients with heart failure. Unfortunately, the positive predictive failure for this finding is low, but in patients with sustained ventricular arrhythmias, variables indicating impaired pump function are the most important predictors of sudden and of nonsudden cardiac death. Arrhythmias in heart failure may have many different underlying mechanisms. Indications for, and mode of treatment of, arrhythmias in heart failure depend on the symptoms and prognostic significance of the arrhythmia. Primarily, pump function should be optimized and antiarrhythmic drug therapy instituted only when the arrhythmia persists. In poorly tolerated and life-threatening arrhythmias, implantable devices allowing pacing and defibrillation must be considered. No data are presently available indicating a protective role of antiarrhythmic drugs in the prevention of sudden cardiac death in heart failure. Future directions should concentrate on the development of better stratification of risk for sudden death, better delineation of mechanisms of arrhythmias in heart failure (allowing the development of mechanism-specific antiarrhythmic drugs), and research into new nonpharmacologic techniques such as cardiomyoplasty and molecular biologic techniques to rebuild the failing heart muscles.

Arrhythmias, Cardiac↗
PubMed1989

Arrhythmias and their treatment in patients with heart failure.

Heart failure is almost without exception associated with arrhythmias, which may be either supraventricular or ventricular. Supraventricular arrhythmias include frequent supraventricular extrasystoles, and episodic or chronic atrial fibrillation. The absence of atrial contraction may further reduce cardiac output, as may impaired control of QRS frequency. Therefore, supraventricular arrhythmias may be markers of the degree of heart failure and these arrhythmias will respond to heart failure therapy including diuretics, nitrates and, possibly, angiotensin-converting enzyme (ACE) inhibitors. Ventricular rate will be controlled by cardiac glycosides and further rate reduction obtained by verapamil or diltiazem. The rationale for this therapy is to optimize heart rate without compromising contractility. Severe heart failure is generally accompanied by severe ventricular arrhythmias including repetitive forms. Improving left ventricular function by ACE inhibition is accompanied by a reduction in the number of ventricular premature complexes and also a reduction in the rate of ventricular tachycardia. ACE inhibition reduces mortality but does not seem to influence sudden death rate, and sudden death patients may have different neurohormonal responses compared with patients destined to die of progressive heart failure. Uncontrolled trials with class IA or class III antiarrhythmic drugs have suggested that prognosis may be improved, but other studies have pointed out the increased risk of proarrhythmic responses in patients with low ejection fraction.

Anti-Arrhythmia Agents↗
PubMed1990

Regional blood flow supply and demand in heart failure.

Heart failure results not only in a fall in cardiac output but also in a redistribution of blood flow favoring some regional beds (the brain and the heart) at the expense of others (the kidney and working skeletal muscle). The chronic resting hypoperfusion of striated muscle is further compromised with exercise. Maladaptive vasoconstrictor control mechanisms prevent the redirection of blood flow from nonworking muscle and liver to working muscle. This inappropriate preservation of nonworking organ perfusion further compromises the functional capacity of working muscle and is associated with evidence for metabolic deconditioning with reduced oxygen extraction and impaired oxidative phosphorylation. It is becoming increasingly clear that the clinical response to the inotropic and vasodilator therapy used in heart failure is in part dependent on the differing regional blood flow profiles of the various agents studied. The ability of the angiotensin-converting enzyme inhibitors to redirect blood flow away from nonworking regional beds to exercising muscle, and thereby to reestablish an appropriate physiologic response to changing metabolic needs, may be the overriding reason for their long-term efficacy. Certainly in the future the comprehensive therapy of heart failure will have to take into consideration not only central hemodynamic but also regional blood flow/supply and demand issues.

Heart Failure↗
PubMed1992

Clinical, hemodynamic and sympathetic neural correlates of heart rate variability in congestive heart failure.

Heart rate (HR) variability has long been recognized as a sign of cardiac health. In the presence of heart disease, HR variability decreases, an observation that has been associated with poor prognosis in a number of recent studies. HR variability is particularly altered in congestive heart failure (CHF), a condition associated with a number of typical functional hemodynamic and neurohumoral alterations. The relation of measurements of HR variability to these abnormalities in patients with heart failure has not been carefully examined. Twenty-three patients (19 men, 4 women, mean age 49 years) with New York Heart Association class II to IV CHF were studied prospectively without cardiac medications; radionuclide ventriculography, right-sided heart catheterization, peroneal microneurography, plasma norepinephrine and 24- to 48-hour ambulatory electrocardiography were performed. Average RR interval and its standard deviation, and HR power spectrum (0 to 0.5, 0.05 to 0.15 and 0.2 to 0.5 Hz) were derived from the ambulatory electrocardiographic recordings and compared with left ventricular ejection fraction, thermodilution cardiac output, pulmonary arterial wedge pressure, New York Heart Association class, age, muscle sympathetic nerve activity (peroneal nerve) and norepinephrine level by linear regression. None of the measures of HR variability were significantly related to age, left ventricular ejection fraction, cardiac output or functional classification, whereas the 0.05 to 0.15 and 0.20 to 0.50 Hz components were weakly but significantly related to cardiac output (r = 0.49 and 0.42, p = 0.02 and 0.045, respectively). In contrast, a generally stronger and negative relation was demonstrated between spectral and nonspectral measurements of HR variability, and indicators of sympathoexcitation, muscle sympathetic nerve activity and plasma norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Changes in pulmonary vascular reactivity to adrenergic stimuli in congestive heart failure].

Heart failure is associated with increased activity of sympathetic nervous system. As to the latter's effector organs, attention has been mainly drawn by heart and systemic circulation. In this study we investigated whether and how the neurogenic vasomotility of the lesser circulation is modified. Therefore, we compared 12 patients with heart failure in III NYHA functional class, with 10 subjects, undergoing hemodynamic study for diagnostic reasons and found to be normal. The neurogenic reactivity of pulmonary vessels was assayed by means of 2 sympathetic stimuli: arithmetic test (AT) and cold pressor test (CPT), performed both with and without obstruction to right heart venous return. This was obtained by expanding a balloon in inferior vena cava, in order to rid the neurogenic component of pulmonary vasomotility of the interference of the normally prevailing mechanical component (consisting in adaptations to flow variations). AT caused pulmonary vasodilation in normal subjects, as a passive consequence of the increase of cardiac output and, therefore, of pulmonary flow. Caval obstruction, by simply restraining this increase, induced a clearly neurogenic vasoconstrictor response. On the contrary, in failing patients, a slight vasodilation, independently from the condition of venous return, was observed. This took place in spite of the constant absence of any variations of cardiac output, which both indicates the reduction of myocardial function and helps to show the diminished nervous influence on pulmonary circulation. On the other hand, CPT had a vasoconstrictor effect in both groups, though potentiated by the reduction of transpulmonary flow in normal subjects only.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

The heart rate slowing effect of pindolol in patients with digitalis resistant atrial fibrillation and heart failure.

Heart rate (HR) slowing action and the possible negative inotropic effect of pindolol (P) (daily dose +/- standard error of the means (SEM): 14.7 +/- 1.6 mg) were studied in 12 patients with heart failure and with rapid atrial fibrillation (AF) resistant to effective beta-methyl dioxin (BMD) doses (mean plasma digoxin concentration +/- SEM: 2.05 +/- 0.17 ng/ml). Mild bicycle ergometer exercise test with the same work load was performed under both BMD and combined BMD--P therapy. Rest exercise and 5 minute recovery HR were significantly lower under combined BMD--P therapy than under BMD alone (80.8 +/- 3 vs. 101 +/- 4.5 beats/min, 123.8 +/- 3.9 vs. 155.8 +/- 7.6 beats/min and 84.9 +/- 2.6 vs. 105.1 +/- 4.5 beats min respectively, p less than 0.001, paired t test). Differences in cardiac volume were not significant (1.131 +/- 76 vs. 1.116 +/- 92 ml). Although all patients were clinically improved under combined BMD--P therapy the 13 to 14% increase in cardiac volume noted in 3 cases could be related to some negative inotropic effect of P. It is concluded that in patients with heart failure and with rapid AF resistant to digitalis, the association of P to digitalis is effective in rest- and mild-exercise HR control without a clinically expressed negative inotropic effect.

Adult↗
PubMed1992

An overview of survival studies in patients with heart failure.

Heart failure is associated with poor prognosis, but recent large-scale investigations have generated valuable and practical information to help improve clinical management and patient survival. This review presents an overview of the findings of recent heart failure survival studies and how these may affect therapeutic strategy for patients with this condition.

Double-Blind Method↗
PubMed1989

Heart transplantation may not improve quality of life for patients with stable heart failure.

Heart transplantation is a therapeutic option for many patients with end-stage heart failure. Vigorous medical therapy has evolved so that many patients eligible for heart transplantation can now be discharged and stabilized with medical therapy. Heart transplantation improves survival, but it has not been compared previously with sustained medical therapy with regard to quality of life. We compared quality of life for 24 patients who survived at least 6 months after heart transplantation with that for 20 patients clinically similar at baseline who survived at least 6 months with sustained medical therapy. Quality of life was assessed by using three questionnaires. Both groups were similar in psychosocial functioning, with patients receiving medical therapy reporting greater dysfunction in social activities, as compared with those who underwent heart transplantation. No differences were seen in 6-minute walking distances and employment status. Survival benefits are expected with heart transplantation; however, quality of life for survivors may not be different than that for patients who survive with sustained medical therapy.

Female↗
PubMed1992

Problems in measuring heart rate variability of patients with congestive heart failure.

Heart rate variability (HRV) has become an important noninvasive measure of the integrity of the autonomic nervous system in various disease states. The power spectrum of HRV is a means to separate the instability oscillations of the various feedback mechanisms that contribute to cardiovascular homeostasis. The reliability of HRV data is largely unexplored. The day-to-day correlations in the low and mid-frequency components of HRV spectra average 91%, and that of the high-frequency component averages 81%. The correlations among spectral and nonspectral measures of HRV (SD) for the same data segment average 50-60%, suggesting that they encode similar information. Heart rate variability spectra exhibit diurnal variation consistent with physiologic expectation: respiratory sinus arrhythmia (thought to be mediated by parasympathetic tone) and to a lesser extent, the low-frequency spectral component (thought to be of mixed sympathetic-parasympathetic origin) are higher at night than in the daytime; the mid-frequency component (associated with the baroreflex, which is more excited when the patient is upright) is slightly higher during the daytime. Increased frequency of ectopic beats, such as occurs in congestive heart failure, reduces the reliability of the power spectrum since the number of usable data segments falls off rapidly with even small increases in rate of ectopy, and the variance of the estimate (in the method of averaged periodograms) is inversely proportional to the square root of the number of data segments. Using shorter data segments increases the number of segments available, but reduces resolution. Interpolation over ectopic beats (by either linear or cubic splint interpolation) increases the apparent power in low frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗
PubMed1989

Decreased spontaneous heart rate variability in congestive heart failure.

Heart rate (HR) variability is a noninvasive index of the neural activity of the heart. Although also dependent on the sympathetic activity of the heart, HR variability is mainly determined by the vagal outflow of the heart. Several HR abnormalities have been described in patients with congestive heart failure (CHF); however, there are no data on HR variability in CHF patients. In the present study HR variability was assessed in 20 CHF patients and 20 control subjects from 24-hour Holter tapes. HR variability was evaluated by calculating the mean hourly HR standard deviation and by analyzing the 24-hour RR histogram. Mean hourly HR standard deviation was markedly and significantly reduced in CHF patients both over the 24-hour period (97.5 +/- 41 vs 233.2 +/- 26 ms, p less than 0.001) as well as during most of the individual hours examined. The 24-hour RR histogram of CHF patients had a different shape and had a decreased variation compared to control subjects (total variability 356 +/- 102 vs 757 +/- 156 ms, p less than 0.001). Thus, CHF patients with depressed ejection fraction (less than 30%) have a low HR variability compared to normal individuals. This result can be interpreted as adjunctive evidence for decreased parasympathetic activity to the heart during CHF.

Adult↗
PubMed1988

Delayed reversal of impaired vasodilation in congestive heart failure after heart transplantation.

The effects of changes in central cardiovascular function on peripheral vasodilation were investigated. Strain gauge plethysmography was used to measure the maximal blood flow response following release of forearm arterial occlusion and the peak reactive hyperemic blood flow response (ml/min.100 ml) before and twice after orthotopic heart transplantation in 10 subjects with severe congestive heart failure. The 2 posttransplantation studies were done before hospital discharge (mean 18 days after transplantation) and again after discharge (mean 114 days after transplantation). Transplantation led to a significant but delayed increase in maximal vasodilation (reactive hyperemic blood flow: pretransplant 21 +/- 3; predischarge 25 +/- 2; postdischarge 43 +/- 5) and a concurrent significant reduction in minimal forearm resistance. Although the improvement in peripheral vasodilator function may be linked to improvement in cardiac function, this linkage is not direct, nor is it immediate. If the normalization of maximal metabolic blood flow is related to resumption of normal physical activity postdischarge, then much of the basic abnormality in vasodilator capacity in congestive heart failure may be related to physical deconditioning.

Adult↗
PubMed1988

Assessment of autonomic regulation in chronic congestive heart failure by heart rate spectral analysis.

Neurohumoral modulation of cardiovascular function is an important component of the hemodynamic alterations in patients with chronic congestive heart failure (CHF). Analysis of heart rate (HR) variability is a noninvasive means of investigating the autonomic control of the heart. The variability of HR and respiratory signals, both derived from ambulatory electrocardiographic recordings, were analyzed with power spectral analysis to evaluate autonomic control in 25 patients with chronic stable CHF (class III or IV) and 21 normal control subjects. In the patients with CHF, HR spectral power was markedly reduced (p less than 0.0001) at all frequencies examined (0.01 to 1.0 Hz, period 1 to 100 seconds) and virtually absent at frequencies greater than 0.04 Hz. Heart rate fluctuations at very low frequencies (0.01 to 0.04 Hz) less effectively differentiated CHF patients from control subjects, due to discrete (about 65 seconds, 0.015 Hz) oscillation in HR, which was associated with a similar pattern in respiratory activity in many of the patients with CHF. These findings demonstrate a marked derangement of HR modulation in patients with severe CHF. The frequency characteristics of HR fluctuations in these patients are consistent with abnormal baroreflex responsiveness to physiologic stimuli, and suggest that there is diminished vagal, but relatively preserved sympathetic, modulation of HR.

Adult↗