Biomedical subjects

B Czerska

Publications and source records attributed to B Czerska.

4 recordsLinked to original sources

PubMed1994

Congestive heart failure. Current and future strategies to decrease mortality.

The prevalence of and mortality from congestive heart failure increase with advancing age. The most important prognostic indicators are exercise tolerance and left ventricular function. Currently, drug treatment consists of digitalis, diuretics, and ACe inhibitors. Future management may include medications to modulate the extracardiac mechanisms of decompensation and newer surgical techniques to assist or replace the failing heart.

Age Factors↗

PubMed1991

Hypertension and left ventricular hypertrophy in black vs white heart transplant patients 1 year after surgery.

To evaluate the impact of race on the prevalence of systemic hypertension and its effects on left ventricular function, structure, and allograft survival after cardiac transplantation, 31 heart transplant recipients (7 blacks and 24 whites) were studied at 1 year after surgery. Echocardiographic and hemodynamic evaluation of the allografts was performed in addition to clinical follow-up and estimation of patients' survival. There was no difference in the demographic and clinical data between black and white patients. No differences between black and white cardiac transplant recipients were detected with regard to the prevalence of systemic hypertension, left ventricular hypertrophy, left ventricular function, renal function, or patients' survival. Moreover, racial mismatch did not predispose to allograft rejection. However, black patients had significantly higher resting systolic blood pressure and lower heart rates. We conclude that the race of heart recipients is not a detrimental factor in the early outcome after cardiac transplantation. The long-term cardiovascular consequences of these findings should be explored.

Adult↗

PubMed1990

Inotropic effects of angiotensin II on human cardiac muscle in vitro.

The direct effects of angiotensin II (Ang II) on human cardiac muscle were investigated using isolated trabecular muscles from failing and functionally normal hearts. Atrial and ventricular trabeculae were studied. Results demonstrated a positive inotropic effect of Ang II on human cardiac muscle. Comparison of the effects of Ang II among groups indicated that the responsiveness tended to be greater in atrial and normal muscle compared with failing muscle. Results of this study also demonstrated heterogeneity in the responsiveness to Ang II among human muscles, which was not correlated with patient age, sex, diagnosis, prior treatment with angiotensin converting enzyme inhibitor, or heart function. A significant correlation between response to Ang II and response to isoproterenol was demonstrated in failing ventricular trabeculae, which may suggest that defects in beta-adrenergic responsiveness in the failing human ventricle are accompanied by a loss of responsiveness to Ang II. Studies were extended to the Syrian cardiomyopathic hamster and its control. A dose-dependent inotropic response occurred in normal hamster ventricular muscle but was significantly diminished in cardiomyopathic muscle. Ang II did not shorten the timing of contraction, and pretreatment with adrenergic-blocking agents did not shift the dose-response curve, indicating that the response was not cyclic AMP mediated. This study demonstrates for the first time that Ang II can exert an inotropic effect directly on human cardiac muscle and confirms that there is a direct effect of Ang II on hamster cardiac muscle. The study further suggests, however, that the inotropic response to Ang II in cardiac muscle is heterogeneous and may be diminished by heart failure.

Angiotensin II↗

PubMed1987

Changes in hemodynamics and myocardial contractility during chronic sodium depletion in conscious dogs.

Chronic sodium depletion has been reported to decrease ejection fraction in anesthetized dogs. We tested the hypothesis that this reduction in cardiac performance is due to either hemodynamic or humoral factors. Seven mongrel dogs were fed a low sodium diet (less than 2 mEq Na+ per day) for 5 weeks. Echocardiographic and radionuclide techniques were used to monitor cardiac function. There was a gradual but significant (p less than 0.01) decrease in ejection fraction from 61 +/- 7% (SD) at baseline to 47 +/- 8% after 5 weeks of sodium depletion in association with a fall in left ventricular end-diastolic volume. Ejection fraction did not change in five control dogs fed 55 mEq Na+ per day throughout the 5-week follow-up period. Myocardial contractility did not change in either salt-depleted or control dogs. Plasma norepinephrine levels in the coronary sinus were twice as high in salt-depleted as in control dogs, but there were no significant differences in arterial norepinephrine concentration between the two groups. Therefore, we concluded that reduced ejection fraction during sodium depletion resulted from hemodynamic changes (decreased preload). The excess available norepinephrine failed to increase myocardial contractility, suggesting a dysfunction at the cardiac adrenergic neuroeffector junction.

Animals↗