We analyzed the relationships among parameters of left ventricular (LV) early diastolic filling flow (EDF) obtained with pulsed Doppler echocardiography, mean pulmonary wedge pressure (PCWP) and the time constant of LV pressure fall calculated by either Weiss' (Tw) or Thompson's (Tb) method. PCWP correlated with the peak velocity (R) (r = 0.537, p less than 0.05), acceleration (Ac) (r = 0.545, p less than 0.05) and deceleration (Dc) (r = 0.606, p less than 0.01) of LVEDF. In contrast, Tb correlated only with the time to the peak of LVEDF (TPF) (r = 0.487, p less than 0.05), and Tw did not correlate with the Doppler-derived indices significantly. After correcting for the effect of PCWP, significant partial correlations between R and Tw (r = -0.535, p less than 0.05), and between Ac and both Tw (r = -0.606, p less than 0.01) and Tb (r = -0.569, p less than 0.05) were found. Dc did not correlate with Tw or Tb. These results suggest that the level of left atrial pressure may mask the relationship between parameters of LVEDF and LV relaxation, and that the relations among these variables vary with individual indices of LVEDF.
Alpha human atrial natriuretic polypeptide (α-hANP) was intravenously infused into 7 patients with ischemic heart disease who had almost normal cardiac function at a rate of 0.025 μg/kg/min for 15 min. During infusion of α-hANP, left ventricular (LV) systolic pressure decreased from 144 ± 19 (SD) to 129 ± 22 mmHg (p < 0.01), LV end diastolic pressure (EDP) from 15 ± 5 to 13 ± 4 mmHg (p < 0.05), mean aortic pressure from 102 ± 14 to 91 ± 14 mmHg (p < 0.01), time constant of LV pressure fall (T) from 100 ± 15 to 88 ± 13 msec (p < 0.05), systemic vascular resistance (SVR) from 1711 ± 206 to 1424 ± 340 dynes·sec·cm-5 (p < 0.05) and coronary vascular resistance (CVR) from 8.5 ± 1.2 to 7.4 ± 1.3 × 104 dynes·sec·cm-5 (p < 0.05). There was a linear correlation between percent changes in SVR and those of CVR (r=0.92, p < 0.01), and the fall in CVR was approximately 68% of that in SVR. Increases occurred in heart rate from 63 ± 7 to 66 ± 8 beats/min (p < 0.05), LV dp/dt from 1558 266 to 1627 238 mmHg/sec (p 0.05), LV dp/dt/p from 22.9 3.2 to 25.6 3.7/sec (p 0.01), and myocardial oxygen consumption (from 7.9 2.4 to 9.8 2.1 ml/min, p 0.05), while mean right atrial and mean pulmonary arterial pressures and pulmonary vascular resistance were unchanged. -hANP dilates the systemic and coronary resistance vessels, and increases myocardial shortening velocity and relaxation.
An animal experimental model which simulates human effort angina, especially in terms of diastolic abnormalities, was developted using isovolumically beating perfused rat hearts. Using this model, we studied the effects of nifedipine, a Ca2+ channel blocker. on diastolic properities during pacing-induced ischemia. When the preload of the left ventricle was set at a low level, low-flow ischemia (coronary perfusion pressure of 40mmHg) plus tachycardia (480 beats/min for 4 min) did not induce an increase in left ventricular end-diastolic pressure (LVEDP). However, with a high preload, low-flow ischemia plus pacing tachycardia indused an increase in LVEDP of 8.4±5.4mmHg (p<0.01) and a prolongation of the time constant of ventricular pressure decline (6.8±4.6msec, p<0.05) immediately after pacing tachycardia. Pretreatment with nifedipine (3×10-8M) prevented the rise in LVEDP induced by pacing tachycardia. Thus, in isolated perfused hearts, diastolic abnormalities similar to those seen in angina pectoris were obtained by low-flow ischemia plus pacing tachycardia. The response to nifedipine suggested that an alteration of Ca2+ movement may play an important role in the increase in left ventricular stiffness under these conditions.
The distensibility of the forearm veins in 24 patients with congestive heart failure was studied by occlusion plethysmography. Relationships between forearm venous distensibility and symptoms, hemodynamic data obtained by right heart catheterization and plasma levels of vasoactive hormones were evaluated. Forearm venous pressure (VP) and volume change (ΔV) were measured simultaneously by the venous occlusion technique with strain gauge plethysmography. The relationship between venous pressure and volume change was fitted by the equation VP=c∗exp.(k∗ΔV) (r=0.98±0.01) and the venous stiffness constant (k) was calculated. Venous volume change at a venous pressure of 20mmHg (V20) was also measured as another index of venous compliance. The pressure-volume curve of the peripheral veins shifted leftward on the volume axis and the stiffness constant (k) increased as the New York Heart Association functional class grade increased. Mean pulmonary arterial pressure and pulmonary vascular resistance were closely related to k (r=0.74, p<0.001; r=0.73, p<0.001, respectively), and less closely to V20 (r=-0.56, p<0.004; r=-0.59, p<0.002, respectively). K and V20 were also related to stroke index (r=-0.57, p<0.004; r=0.44, p<0.03, respectively) and stroke work index (r=-0.47, p<0.02; r=0.45, p<0.03, respectively). K was also related to heart rate (r=0.55, p<0.007), pulmonary capillary wedge pressure (r=0.54, p<0.02), right atrial pressure (r=0.51, p<0.02), cardiac index (r=-0.45, p<0.03), and systemic vascular resistance (r=0.45, p<0.03). Both indexes were related to the plasma level of norepinephrine (r=0.64, p
