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At least 1,423 records · Page 79Linked to original sources
PubMed1990

Beta, partial agonists to treat heart failure: effects of xamoterol upon cardiac function and clinical status.

The presence of systolic dysfunction, diastolic dysfunction, or both is an important consideration in selecting the optimal pharmacologic approach to the treatment of congestive heart failure in an individual patient. Cardiac glycosides and arterial vasodilators act only on systolic function, whereas beta 1-adrenoceptor-stimulating agents, such as beta 1 full and partial agonists, have both inotropic and lusitropic activity. Acute and chronic administration of xamoterol, a new beta 1 partial agonist, to patients with congestive heart failure has been shown to improve myocardial contractility, as indicated by increases in the peak rate of rise in left ventricular pressure, left ventricular ejection fraction, and cardiac output. Improvement in ventricular relaxation and filling, reflected by increases in the peak rate of decline in left ventricular pressure, reductions in the time constant of the decrease in isovolumic pressure, improved left ventricular compliance, and increases in the atrial contribution to diastolic filling, are other beneficial effects of xamoterol on diastolic function. Exercise capacity increases in response to xamoterol therapy, while heart rate at maximum exercise declines. Relief of the signs and symptoms of congestive heart failure and improvement in functional status have also been demonstrated in xamoterol-treated patients. The undesirable effects of beta 1 full agonists, such as tachycardia, arrhythmias, increased myocardial oxygen consumption, and effects on the peripheral vasculature, are not seen with xamoterol. The beta 1 partial agonist also causes no beta-adrenoreceptor down-regulation, a finding that may account for its sustained effectiveness with long-term therapy.

Adrenergic beta-Agonists↗
PubMed1988

Echocardiographic assessment of cardiac function during respiratory syncytial virus infection.

Respiratory syncytial virus infection has been associated with increased morbidity and mortality in infants with underlying cardiac and pulmonary disease. To understand better the cardiopulmonary interaction in patients with acute respiratory syncytial virus bronchiolitis, we performed M-mode echocardiograms and pulsed Doppler assessment of pulmonary arterial flow in 19 patients with structurally normal hearts during acute illness. Studies were repeated in 11 of these patients following complete recovery. Based on severity of respiratory compromise, patients were grouped into those with severe illness (ten patients) or mild illness (nine patients). Left ventricular dimensions and shortening fraction were used to assess left ventricular function. Right ventricular systolic time intervals and specific Doppler flow velocity measurements were used to assess right ventricular function and elevation of pulmonary artery pressure. Comparisons were made between patients with severe and mild illness and between acute and follow-up studies. No statistically significant differences in left ventricular function, right ventricular systolic time intervals, or Doppler flow measurements were observed. We conclude that in patients with structurally normal hearts, respiratory syncytial virus bronchiolitis is not associated with significant depression of cardiac performance or elevation in pulmonary resistance.

Bronchiolitis, Viral↗
PubMed1995

One-day hypothermic preservation of isolated hearts with halothane improves cardiac function better than low calcium.

BACKGROUND: Halothane exerts a potent negative inotropic effect on the heart and mimics many of the cardiac effects of lowered extracellular CaCl2. Reduced slow inward Ca2+ current and sarcoplasmic reticular effects on intracellular Ca2+ are likely involved. The authors reported previously that halothane protects against hypoxic and ischemia reperfusion injury in isolated hearts. The aim of this isolated heart study was to compare protective effects of halothane and low CaCl2 (0.5 mM) administered during 1 day of hypothermic perfusion on return of normothermic perfusion. METHODS: Guinea pig hearts (n = 66) were isolated and perfused at 37 degrees C with a Krebs' solution, gassed with 96% O2, 4% CO2, and containing 2.5 mM Ca2+, and 4.5 mM K+. Heart rate, isovolumetric left ventricular pressure, coronary flow, %O2 extraction, O2 consumption rate, and relative cardiac efficiency (EFF = heart rate.left ventricular pressure/O2 consumption rate) were measured in five groups of hearts: time controls (no hypothermia); 1.5, and 3% halothane delivered by vaporizer; cold controls (hypothermia only); and 0.5 mM CaCl2. Halothane was administered, or CaCl2 was decreased 0.5 h before hypothermia at 3.8 +/- 0.1 degrees C, during hypothermia for 22 h, and for 0.5 h after rewarming to 37.0 +/- 0.1 degrees C. Hearts were perfused at 25% of initial coronary flow during hypothermia. RESULTS: All groups had similar ventricular function and vasodilator responses before hypothermia. During normothermic reperfusion after hypothermia, both concentrations of halothane protected better than low CaCl2. Values, expressed as a percent of initial values in the five groups (time control, 3% halothane, 1.5% halothane, cold control, and 0.5 mM CaCl2, were respectively: 90 +/- 6, 54 +/- 6*, 48 +/- 5*, 27 +/- 8, 27 +/- 4% for left ventricular pressure; 84 +/- 5, 61 +/- 4*, 62 +/- 6*, 40 +/- 5, 34 +/- 5% for EFF; and 102 +/- 3, 63 +/- 3*, 66 +/- 3*, 55 +/- 2, 42 +/- 2% for coronary flow (*P < 0.05 halothane vs. 0.5 mM CaCl2). The coronary flow response to endothelium-dependent (acetylcholine) and endothelium-independent (nitroprusside) vasodilators was also greater after halothane than after 0.5 mM CaCl2. CONCLUSIONS: Halothane administered during hypothermia restores left ventricular pressure, cardiac efficiency, basal coronary flow, and flow responses better than low CaCl2. Although halothane and low CaCl2 both reduce intracellular Ca2+, contractile force, and metabolic demand, the better protective effect of halothane is not likely simply due to a reduction in contractile function and metabolic rate before or initially after hypothermia because these were reduced much more by low CaCl2 than by halothane.

Anesthetics↗
PubMed2004

Abnormal maternal cardiac function precedes the clinical manifestation of fetal growth restriction.

OBJECTIVE: To compare maternal hemodynamics in women whose fetuses are small-for-gestational age (SGA) with those in women with fetal growth restriction (FGR) before manifestation of the clinical disease. METHODS: Thirty-five normotensive pregnant women with fetal abdominal circumference < 10th centile, normal fetal anatomy and normal umbilical artery pulsatility index (PI) underwent maternal echocardiographic examinations between 27 and 30 weeks of gestation. Pregnancies were followed until delivery and fetuses were retrospectively classified as either SGA or FGR and the maternal hemodynamic data were compared. RESULTS: Nineteen SGA and 16 FGR patients were retrospectively identified after delivery. Heart rate, stroke volume, cardiac output, left atrial function and left ventricular mass index were higher, while mean blood pressure and total vascular resistance were lower in the SGA group compared with the FGR group. A significant inverse linear correlation was found between total vascular resistance and weight centile (r = 0.83; P < 0.0001). CONCLUSIONS: Mothers of SGA fetuses show hemodynamic features similar to those with physiological pregnancies suggesting that their fetuses are likely to be constitutionally small and not pathologically growth-restricted.

Adult↗
PubMed1991

Effect of L-thyroxine (LT4) and D-thyroxine (DT4) on cardiac function and high-energy phosphate metabolism: a 31P NMR study.

31P NMR spectroscopy was used to monitor the cardiac energy metabolism in hypothyroid rat hearts. Differential alterations in phosphocreatine and inorganic phosphate levels were observed upon treatment of hypothyroid animals with DT4 and LT4, while both agents were equipotent in reducing cholesterol. These results show potential for NMR spectroscopy as a technique to determine therapeutic selectivity.

Adenosine Triphosphate↗
PubMed1998

The interrelation between renal and cardiac function. Physiology and pathophysiology with a focus on congestive heart failure.

The inter-relationship between the renal and cardiac systems is complex, but once understood it provides the critical care nurse with a wealth of knowledge to analyze and assess clinical situations. Being able to determine when the neurohumoral response is compensating for or complicating a disease process is an essential skill for the critical care nurse in his or her daily decision making processes.

Aged↗
PubMed1993

Effects of flecainide and propafenone on systolic performance in subjects with normal cardiac function.

Flecainide and propafenone are effective in suppressing both ventricular and supraventricular tachyarrhythmias, but their efficacy is often limited by dose-related side effects. This study was performed to evaluate noninvasively the effects of intravenous flecainide and propafenone on left ventricular systolic function indices in a selected population of 40 subjects (28 men and 12 women; mean age, 25 years) with normal cardiac structure and performance. Echocardiographic indexes of global systolic pump function (ejection fraction [EF] and percentage of fractional shortening [percent FS]) as well as monodimensional parameters of the intraventricular septum (IVS) and left ventricular posterior wall (PW) contractility (percent systolic thickening [percent th] and systolic excursion [ex]) were assessed in all subjects at baseline, immediately after, and in the early recovery (15 min) after randomized injection of either flecainide or propafenone. Heart rate and blood pressure did not significantly change after both drugs. A significant increase (p < 0.001) in left ventricular systolic internal diameter was observed after both flecainide and propafenone; simultaneously a significant decrease of percent FS (p < 0.001), EF (p < 0.001), PW percent thickening (th) (p < 0.001), and PWex (p < 0.001 after flecainide and p < 0.01 after propafenone) was recorded. These changes were comparable and promptly reversible. In analyzing individual data, a marked systolic dysfunction was observed in two patients after intravenous flecainide (percent FS from 37 percent to 17 percent and from 42 percent to 13 percent; EF from 55 percent to 40 percent and from 65 percent to 35 percent, respectively) and in one patient after intravenous propafenone (percent FS from 30 percent to 15 percent; EF from 58 percent to 35 percent). We conclude that both intravenous flecainide and propafenone exhibit mild negative inotropic effects leading to a moderate and reversible reduction of left ventricular systolic performance; however, in some cases, a dramatic impairment of systolic pump function may occur, suggesting careful use of both drugs as first-line agents also in normal subjects; finally, the true incidence of this deleterious effect is still unknown.

Adolescent↗
PubMed2004

Exercise training improves cardiac function postinfarction: special emphasis on recent controversies on na+/ca2+ exchanger.

Exercise training instituted after myocardial infarction improves many steps involved in cardiac excitation-contraction coupling. Focusing on Na/Caexchange, current controversies regarding whether it mediates Cainflux during an action potential, whether it is increased or decreased in disease models, whether protein kinase A alters its activity, and whether exercise training affects its function are reviewed. Finally, a novel target for exercise training in the heart is suggested.

Animals↗
PubMed1997

Doppler flow and echocardiography in functional cardiac insufficiency: assessment of nisoldipine therapy. Results of the DEFIANT-II Study. The DEFIANT-II Research Group.

AIMS: A multicentre, double-blind, placebo-controlled trial was conducted in 542 patients, randomized 7-10 days after myocardial infarction, to study the effect of nisoldipine coat-core (nisoldipine-CC) on exercise after 6 months. Secondary endpoints included exercise-induced ischaemia, left ventricular function measured by Doppler echocardiography, adverse cardiac events and clinical outcome. METHODS AND RESULTS: Patients had reduced left ventricular ejection fraction between 25 and 50%, but no heart failure. Exercise time was not different in the two groups. Nisoldipine-CC prolonged time to 1 mm ST deviation (P = 0.03). There was an effect of nisoldipine-CC of +3.6 cm.s-1 on early peak velocity (P = 0.01) and of -6.2 ms on isovolumic relaxation time (P = 0.005), but no effects on left ventricular volumes or ejection fraction. There was a trend towards reduced mortality (one death in the nisoldipine-CC group vs seven in the placebo group. P < 0.07) and the combined end-point of mortality and cardiac events (P = 0.09). Peripheral oedema occurred in 49 patients assigned to nisoldipine-CC and two assigned to placebo (P < 0.001). There were no differences in non-cardiac events. CONCLUSIONS: Nisoldipine-CC did not improve exercise time but increased time to 1 mm ST deviation, and improved diastolic left ventricular function. It is safe and well tolerated in post-infarction patients with impaired left ventricular function.

Adult↗
PubMed1984

Reversal of left ventricular hypertrophy and improvement of cardiac function in man by nifedipine.

The effects of long-term (mean 3.9 months) pharmacotherapy of hypertensive and normotensive hypertrophy (hypertensive heart disease, hypertrophic non-obstructive cardiomyopathy) as well as of advanced cardiac disease due to coronary artery disease and dilatative cardiomyopathy by large doses of nifedipine (mean 120 mg/day-1) were analyzed with regard to systolic blood pressure, to left ventricular function and to the hypertrophy degree of the ventricle. Nifedipine, in addition to conventional and maintained antihypertensive and cardiac therapy, lowers blood pressure in hypertensive patients, whereas hypotensive effects in the normotensive patients were absent. Nifedipine enhances left ventricular function in all patient groups significantly, i.e. in normotensive hypertrophic non-obstructive cardiomyopathy, in hypertensive heart disease and especially in heart disease due to coronary artery disease and dilatative cardiomyopathy. Significant regression of septal and of global hypertrophy was found in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease. These results indicate, that long-term nifedipine treatment may be beneficial for left ventricular function in all patient groups and for hypertrophy regression in established left ventricular hypertrophy due to hypertrophic, non-obstructive cardiomyopathy and due to hypertensive left ventricular hypertrophy. It is concluded that long-term nifedipine treatment improves left ventricular function and leads to regression of established ventricular wall hypertrophy in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease.

Adult↗