Yoshiaki Tamada

Effect of left ventricular volume on right ventricular end-systolic pressure-volume relation. Resetting of regional preload in right ventricular free wall.

Effect of left ventricular (LV) volume on right ventricular (RV) end-systolic pressure-volume relation (ESPVR) was investigated, and the mechanism was examined from a standpoint of the alteration of RV free wall mean fiber length. Twelve cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were controlled independently were used, and RV-ESPVR was determined at three different LV volume levels. At small (10.2 ± 0.6 ml), middle (IS J ± 1.0 ml), and large (20.5 ± 1.4 ml) LV volume, the slope of the RV-ESPVR was 2.63 ± 0.13, 2.74 ± 0.13, and 2.89 ± 0.12 mm Hg/ml, respectively, and each value was significantly different from the others (p <0.01). The volume intercept (V0) of the relation (RV-V0) was significantly decreased with the increment of LV volume (RV-V0 in small, middle, and large LV volume; 3.92 ± 0.68, 3.39 ± 0.67, and 2.87 ± 0.71 ml, respectively; p <0.01). In nine hearts, RV free wall lengths in latitudinal and meridional direction were measured at three LV volume levels when RV volume was held constant (16.1 ± 1.1 ml). RV latitudinal end-diastolic length was significantly augmented with increasing LV volume (latitudinal length in small, middle, and large LV volume; 9.68 ± 0.55, 9.81 ± 0.56, and 9.92 ± 0.55 mm, respectively). RV meridional end-diastolic length also increased significantly with increasing LV volume. We concluded that RV-ESPVR showed upward-leftward shift with increasing LV volume and that this shift could be, at least in part, explained by the alteration of end-diastolic length in RV free wall that occurred with constant RV volume (resetting of regional preload), probably due to the deformation of RV becoming more crescent.

Coronary Artery Aneurysm Without Stenosis in Association with Osler-Weber-Rendu Disease—A Case Report:

A fifty-three-year-old woman presented with coronary artery aneurysm in association with Osler-Weber-Rendu disease (hereditary hemorrhagic telangiec tasia) manifested also by large pulmonary arteriovenous fistulas. The arterial dye dilution curves were unusually distorted owing to the right-to-left shunts. The coronary artery aneurysm was located in multiple sites but was not accom panied by stenotic lesions. Coronary artery aneurysm without stenosis is a rare pathologic state and has not been previously reported in association with heredi tary telangiectasia.

Increasing coronary perfusion pressure on diastolic and systolic performance is less pronounced in right ventricle than in left ventricle.

OBJECTIVE Little is known as to whether an increase in coronary perfusion pressure can alter the right ventricular (RV) distensibility and the contractile function as it does in the case of the LV. METHODS In eight isolated isovolumically contracting canine hearts, RV and LV volumes and coronary perfusion were independently controlled. Effects of an increase in coronary perfusion pressure (from 73 +/- 1 to 152 +/- 6 mmHg) on the end-diastolic and end-systolic pressure-volume relations in both RV and LV were assessed. RESULTS Following an increase in coronary perfusion, and at a similar volume of the ventricles, end-diastolic pressure was elevated by 2.8 +/- 0.8 mmHg in RV and 8.9 +/- 2.0 mmHg in LV (P < 0.01; RV vs LV), and the slope of RV end-systolic pressure-volume relation, Ees, increased by 11 +/- 6% (P < 0.05) and that of the LV Ees by 21 +/- 5% (P < 0.01). The percent change of RV pressure-volume area (PVA) was less than that in LV-PVA (26 +/- 9 vs 48 +/- 11%; P < 0.05). CONCLUSIONS Accordingly, increases in coronary perfusion pressure and/or flow decreased the RV distensibility and enhanced the RV contractile function, the extent of which, however, was less than that in the LV.