An increase in the pulmonary capillary wedge pressure (PAWP) has been shown to impact on the inherent relationship between the pulmonary arterial compliance (PAC) and pulmonary vascular resistance (PVR), thus augmenting the pulsatile relative to the resistive load of the right ventricle. However, the PAWP comprises the integration of both the steady and the pulsatile pressure components. We sought to address the differential impact of the these distinct PAWP components on the PAC–PVR relationship in a cohort of patients with heart failure. The study population consisted of 192 patients with hemodynamic findings diagnostic for heart failure. Off-line analysis was performed using the MATLAB software. The steady and pulsatile PAWP components were calculated as mid-A pressure and mean pressure during the V-wave oscillation, respectively. The PAC and PVR were hyperbolically and inversely associated and the subgroup of patients with PAWP above the median (>18 mm Hg) displayed a significant left and downward shift of the curve fit (P < .001). The shift in the PAC–PVR fit between patients with higher versus low steady PAWP was not significant (P = .43). In contrast, there was a significant downward and leftward shift of the PVR–PAC curve fit for the subgroup with a higher pulsatile PAWP (P < .001). Furthermore, only the pulsatile PAWP was significantly associated with the time-constant of the pulmonary circulation, assessed as the PAC × PVR product (P < .001).In patients with heart failure, the pulsatile rather than the steady PAWP component stands for the previously documented shift of the PAC–PVR relationship occurring at an elevated PAWP.

The relationship of left atrial contraction to ventricular filling was studied in 24 patients. Eight patients had aortic stenosis, eight had mitral stenosis, and eight others served as a control group. All had normal sinus rhythm. Cineangiocardiographic volumetric determinations of the left ventricle were done throughout the cardiac cycle, and the rate of left ventricular filling before and during left atrial contraction was calculated.In the group with aortic stenosis 39% of the left ventricular stroke volume entered the ventricle during left atrial contraction; in the group with mitral stenosis 24% was contributed during left atrial contraction, and in the control patients, 26%.The rate of left ventricular filling more than doubled during left atrial contraction in aortic stenosis, while no consistent change in the rate of filling occurred during left atrial contraction in mitral stenosis and in the control group.The character of the resistance to left ventricular filling in aortic stenosis and mitral stenosis is discussed. An important contribution by left atrial contraction to left ventricular performance in aortic stenosis is suggested.