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Left intra ventricular filling was studied by colour M-mode Doppler ultrasound to determine whether the flow pattern can be assessed visually, and explore its relation to left ventricular (LV) function. Patients with coronary artery disease (CAD) or dilated cardiomyopathy (DCM) were divided into three groups according to angiographically evaluated LV function. The groups were compared with a control group of 54 healthy volunteers. The mitral to apical delay of early diastolic flow was qualitatively assessed from printed colour M-mode images, twice by four independent observers blinded to the subject's status. The repeatability of the assessments as determined by the kappa statistic was good intra observer (kappa = 0.75) and moderate inter observer (kappa = 0.53). The CAD-group with angiographically normal LV function (n = 25) had flow patterns resembling those observed in the control group. The group with ejection fraction (EF) < 50% (n = 19) had flow patterns clearly different from the control group. Patients with regional wall motion abnormality (RWMA) but EF > 50% (n = 16) exhibited flow patterns intermediate between the control and the low EF group. Among the 50 CAD patients there was a negative correlation between EF and the presence of delay of apical peak velocity (Spearman's rs = -0.62, p < 0.0001). A visible delay of apical peak velocity had a sensitivity towards DCM of 83% and specificity of 75%. The sensitivity towards CAD with either RWMA or low EF was 55% and the specificity 75%. In conclusion, visual assessment of intra ventricular flow patterns was feasible and allowed discrimination between normal and diseased ventricles.

Background: This study investigates the effects of sodium nitroprusside on regional vascular capacitance in eight patients with severe congestive heart failure (New York Heart Association class IV) and pulmonary hypertension., Methods and Results: Regional relative blood volumes in the splanchnic and pulmonary region were determined by equilibrium blood pool scintigraphy. Hepatic venous wedge pressure and the mean of pulmonary artery and pulmonary capillary wedge pressure were used to represent the distending pressures of the splanchnic and pulmonary capacitance vessels, respectively. The dose of sodium nitroprusside was increased stepwise until systolic pulmonary artery pressure decreased below 50 mm Hg. This caused reductions in mean aortic pressure from 89 +/- 5 to 66 +/- 3 mm Hg (p less than 0.005), in pulmonary capillary wedge pressure from 31 +/- 1 to 16 +/- 2 mm Hg (p less than 0.001), and in hepatic venous wedge pressure from 10.0 +/- 1.0 to 5.9 +/- 0.6 mm Hg (p less than 0.005). Intestinal blood volume increased by 26 +/- 7% (p less than 0.005), whereas hepatic blood volume decreased by 9 +/- 3% (p less than 0.02). Pulmonary blood volume was unchanged. Analysis of intestinal and pulmonary vascular pressure-volume relations showed larger or equal blood volumes contained at lower distending pressures, indicating that sodium nitroprusside reduced smooth muscle tone of the capacitance vessels in these regions. The reduction of hepatic blood volume was compatible with passive expulsion of blood subsequent to reduced venous pressure. There was no change in the count rate from the spleen., Conclusions: Nitroprusside reduced venous pressure in patients with congestive heart failure by active relaxation of intestinal and pulmonary capacitance vessels. Hepatic vascular volume was probably reduced by a passive mechanism.

We investigated 1) the effects of HCl-mediated acute left lung injury on regional juxtacardiac pressures and 2) the haemodynamic effects of different modes of ventilation before and after induction of left lung injury. The study was done in 7 mechanically ventilated, anaesthetized dogs. Juxtacardiac pressures and haemodynamic variables were recorded during 1) differential ventilation (DV) with zero positive end-expiratory pressure (PEEP = 0) and 2) DV with general (G) PEEP and selective right (R) and left (L) lung PEEP. Left lung injury increased left, but not right pleural pressure of pericardial pressure. Pulmonary vascular resistance (PVR) and pulmonary artery pressure (PAP) were increased moderately. Cardiac output (CO) did not change. GPEEP reduced LV filling and cardiac output markedly and by approximately the same degree before and after lung injury. The haemodynamic effects of LPEEP were minor before as well as after the induction of lung injury. RPEEP, which had only moderate haemodynamic effects during control, caused a marked reduction in cardiac function after the induction of left lung injury. The transmission of airway pressure to the pleura was reduced in the diseased lung. These results suggest that serious haemodynamic side effects may be avoided by applying PEEP selectively to the diseased lung.

The aim of the present study was to determine the effect of i.v. inosine on myocardial substrate uptake and function in the in situ dog heart. Inosine was infused i.v. at a rate of 5 mg kg min-1 in eight closed-chest pentobarbital anaesthetized dogs. Inosine caused a 46% decrease (P less than 0.01) in plasma free fatty acids (FFA), a 15% decrease (P less than 0.05) in plasma glycerol, an 18% decrease (P less than 0.05) in plasma glucose and a 46% increase (P less than 0.01) in blood lactate. This was associated with a 55% decrease (P less than 0.01) in myocardial FFA uptake and a 72% increase in lactate uptake, while glucose uptake remained unchanged. These metabolic changes were associated with a five-fold increase (P less than 0.05) in arterial insulin. Inosine caused an 18% increase (P less than 0.01) in myocardial blood flow without changing MVO2. There was a 33% increase (P less than 0.01) in LV dP/dtmax, a decrease in LVEDP from 4.9 +/- 0.9 (mean +/- SEM) to 0.9 +/- 0.3 mmHg (P less than 0.05) and a 24% decrease (P less than 0.01) in systemic vascular resistance. Inosine caused a transient 38% increase (P less than 0.05) in pulmonary vascular resistance. In conclusion, in addition to a positive inotropic effect and vascular effects inosine was found to cause release of insulin and to shift myocardial metabolism towards increased uptake of carbohydrates relative to FFA.

Haemodynamic and metabolic effects of the new antiarrhythmic drug melperone were studied during acute ischaemic left ventricular failure in closed-chest anaesthetized dogs. Embolisation of the left main coronary artery with 50 micrometer plastic microspheres induced severe depression of left ventricular performance as evidenced by a marked increase in left ventricular end-diastolic pressure and a marked reduction in the maximum rate of left ventricular pressure rise (LVdP/dtmax), cardiac output, and stroke volume. Six dogs received intravenous melperone 1.0 and 2.5 mg . kg-1 (cumulative dose) 90 and 115 min after the embolisation, respectively. Six other dogs received no treatment and served as controls. Melperone effected a marked reduction in left ventricular end-diastolic pressure, a slight but transient increase in LVdP/dtmax, a moderate reduction in heart rate, a moderate reduction in mean aortic blood pressure and total peripheral resistance and a moderate increase in stroke volume. Melperone moderately decreased myocardial O2-consumption, while myocardial lactate uptake remained unchanged. In conclusion, in contrast to commonly used antiarrhythmic drugs which may all induce cardiodepression, melperone improved left ventricular function in dogs with acute ischaemic left ventricular failure.

The effects of the beta-adrenergic receptor agonist pirbuterol on left ventricular (LV) performance were examined during acute ischaemic LV failure in anaesthetized dogs. Plastic microspheres (50 microns) were injected into the left main coronary artery, and the dogs developed severe LV failure. The stability of the heart failure model was demonstrated in a group of untreated control dogs (n = 5). Administration of pirbuterol 7 micrograms X kg-1 i.v. during failure caused an increase in cardiac output from 1.52 +/- 0.14 (mean +/- S.E.M., n = 7) to 2.56 +/- 0.32 1 X min-1 (P less than 0.01) at 30 min after drug administration. The LV end-diastolic pressure (LVEDP) decreased from 24.6 +/- 1.1 to 21.0 +/- 1.9 mmHg (P less than 0.05), and maximum LV dP/dt was increased from 2012 +/- 124 to 2602 +/- 119 mmHg X s-1 (P less than 0.01). The LVEDP-stroke work relation (n = 2) shifted markedly upward. Heart rate was not significantly changed by pirbuterol. Mean aortic blood pressure and total peripheral resistance decreased from 103 +/- 3 to 85 +/- 5 mmHg (P less than 0.05) and from 68 +/- 6 to 34 +/- 4 mmHg X 1(-1) X min (P less than 0.01), respectively. Pirbuterol increased plasma free fatty acid concentrations from 264 +/- 45 (n = 4) to a maximum value of 956 +/- 169 mumol X 1(-1). In conclusion, by a combination of inotropic stimulation and systemic vasodilation, pirbuterol markedly improved cardiac performance in dogs with acute ischaemic LV failure.

Haemodynamic and metabolic effects of elevated plasma concentrations of free fatty acids (FFA) were studied during acute ischaemic left ventricular failure in closed-chest anaesthetized dogs. Embolization of the left main coronary artery with 50 micron plastic microspheres induced severe depression of left ventricular performance as indicated by a marked increase in left ventricular end-diastolic pressure (LVEDP), and marked reductions in LVdP/dtmax, cardiac output and myocardial oxygen consumption (MVO2). When stable conditions were reached, eight dogs received a triglyceride emulsion and heparin to raise plasma FFA. This was associated with increased MVO2 and further elevation of LVEDP. In two dogs receiving the triglyceride emulsion but no heparin, plasma FFA was not elevated, and MVO2 and LVEDP were unchanged. In conclusion, elevation of plasma FFA was associated with increased myocardial oxygen requirement and further depression of LV function in dogs with acute ischaemic LV failure.

ABSTRACT Objectives To evaluate maternal left ventricular ( LV) systolic and diastolic function during normal pregnancy by non-invasive measures of LV contractility incorporating loading conditions. METHODS Sixty-five women were examined using echocardiography, including tissue Doppler and two-dimensional speckle tracking, and subclavian artery pulse trace recordings at gestational weeks 14-16, 22-24 and 36, and at 6 months postpartum. Results The mean ± SD age of the women was 32.0 ± 4.6 years. Cardiac output and LV end-diastolic volume were on average 20% and 23% higher, respectively, during pregnancy, compared to that at 6 months postpartum (both, P < 0.01). LV ejection fraction, global peak systolic strain and rate-corrected LV velocity of circumferential fiber shortening (Vcfc) were 11%, 6% and 6% lower, respectively, at 36 weeks' gestation compared to at 6 months postpartum (all, P < 0.01). Afterload, measured as LV end-systolic wall stress ( ESWS) increased by 10% between 14-16 and 36 weeks' gestation ( P < 0.01). Analysis of the relationship between Vcfc and ESWS revealed that LV contractility was lower during pregnancy than at 6 months postpartum. Changes in diastolic function were demonstrated by 11% lower mitral early diastolic (E) wave velocity, 8% lower tissue Doppler early diastolic velocity (e′) and 13% higher left atrial area (all P < 0.01) during pregnancy. Tissue Doppler E/e′ remained unaltered ( P = 0.78). Conclusions During normal pregnancy, LV contractility is lower than it is at 6 months postpartum. This is associated with increased LV and left atrial area, whereas filling pressures are unchanged. These findings suggest that pregnancy exerts a larger load on the cardiovascular system than previously assumed. Copyright © 2012 ISUOG. Published by John Wiley & Sons Ltd. [ABSTRACT FROM AUTHOR]