Brain Natriuretic Peptide: Effect on Left Ventricular Filling Patterns in Healthy Subjects

1995 ◽  
Vol 88 (2) ◽  
pp. 159-164 ◽  
Author(s):  
Peter B. M. Clarkson ◽  
Nigel M. Wheeldon ◽  
Catherine MacLeod ◽  
Wendy Coutie ◽  
Thomas M. MacDonald

1. Elevated plasma concentrations of brain natriuretic peptide are found in conditions associated with impaired left ventricular diastolic function. The purpose of this study was to determine whether this peptide actually plays a physiological role in improving myocardial performance in diastole. 2. Nine normal subjects received infusions of brain natriuretic peptide or placebo in a randomized, double-blind, crossover study. Brain natriuretic peptide infusion produced a significant reduction in isovolumic relaxation time (means and 95% confidence interval for difference−10.8 ms, −14.5 to −7.0 ms) (P < 0.01) and significantly increased both the peak E/A velocity (0.54, 0.14–0.94) (P < 0.05) and the E/A time velocity integral (1.09, 0.20–1.98) (P < 0.05). 3. These responses were evident at concentrations of brain natriuretic peptide that produced no associated effects on blood pressure, heart rate or stroke distance. 4. Brain natriuretic peptide infusion in normal subjects significantly reduces isovolumic relaxation time and improves transmitral Doppler flow profiles, suggesting that this peptide may be important in the control of left ventricular diastolic relaxation in man.

2004 ◽  
Vol 17 (4) ◽  
pp. 330-331 ◽  
Author(s):  
Antonio De Merulis ◽  
Giulio Calcagni ◽  
Paolo Versacci ◽  
Renato Lucchini ◽  
Flavia Ventriglia ◽  
...  

1999 ◽  
Vol 35 (4) ◽  
pp. 285-291 ◽  
Author(s):  
JM Bright ◽  
ME Herrtage ◽  
JF Schneider

Left ventricular (LV) diastolic function was evaluated in 16 cats with primary hypertrophic cardiomyopathy (HCM) using pulsed Doppler (PD) assessment of transmitral flow and isovolumic relaxation time. Data obtained was compared to data from 12 healthy, adult, research cats. Compared to normal cats, the HCM group showed significantly (p value less than 0.05) reduced early LV inflow velocities (mean +/- standard error [SE], peak velocity of 0.70+/-0.04 m/s versus 0.54+/-0.04 m/s and integrated velocity of 0.48+/-0.08 m/s versus 0.37+/-0.03 m/s); a reduced rate of deceleration of early inflow (mean+/-SE, -12.0+/-1.0 m/s2 versus -5.1+/-1.1 m/s2); prolonged isovolumic relaxation time (mean +/- SE, 45.7+/-3.3 ms versus 76.0+/-3.1 ms); and increased atrial systolic flow velocities (mean +/- SE, peak velocity of 0.29+/-0.04 m/s versus 0.48+/-0.04 m/s and integrated velocity of 0.21+/-0.03 m/s versus 0.34+/-0.03 m/s). The results suggest that PD provides a noninvasive method of identifying and quantifying functional diastolic impairment in cats with HCM.


1995 ◽  
Vol 89 (2) ◽  
pp. 165-169 ◽  
Author(s):  
Robert I. Cargill ◽  
David G. Kiely ◽  
Brian J. Lipworth

1. Abnormalities of myocardial relaxation may occur as a consequence of myocyte hypoxia. We have therefore examined the effects of hypoxaemia on right and left ventricular diastolic function in 10 healthy male subjects. 2. After resting to reach baseline haemodynamics, subjects were rendered hypoxaemic by breathing a variable nitrogen/oxygen mixture. Oxygen saturation (SaO2) was maintained at 85–90% for 20 min and then at 75–80% for a further 20 min. Haemodynamic and diastolic filling parameters were measured non-invasively at baseline and at the end of each period of hypoxaemia. 3. Diastolic filling of both ventricles was significantly impaired by hypoxaemia. In comparison with baseline, left ventricular isovolumic relaxation time and transmitral E-wave deceleration time corrected for heart rate were significantly prolonged at SaO2 75–80%: mean difference in corrected relaxation time, 9.8 ms (95% confidence interval 1–19); mean difference in corrected deceleration time, 34 ms (95% confidence interval 11–56). Similarly, right ventricular isovolumic relaxation time and transtricuspid E-wave deceleration time were significantly prolonged at SaO2 values of 75–80% compared with baseline: mean difference in relaxation time, 20.3 ms (95% confidence interval 3–38); mean difference in deceleration time, 33 ms (95% confidence interval 11–55). 4. During hypoxaemia there were dose-related increases in heart rate, cardiac output and mean pulmonary artery pressure, but no effects on mean arterial pressure. 5. Hypoxaemia significantly impairs relaxation of left and right ventricles in normal humans. These changes may reflect impairment of intracellular calcium transport secondary to the effects of myocyte hypoxia.


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