Left ventricular dynamic geometry and diastolic mechanics in a model of chronic cyanosis and right ventricular pressure overload.
Left ventricular (LV) mechanics and dynamic geometry were studied in eight dogs 1 to 151 days after creation of a model of cyanosis and increased right ventricular (RV) pressure. In each dog, an 8 mm conduit was interposed between the main pulmonary artery and left atrium; the pulmonary artery was then banded distal to this shunt. Ultrasonic dimension transducers were subsequently implanted for the measurement of LV equatorial minor axis and wall thickness. Catheter-tipped micromanometers were used to measure LV and pleural pressures; RV pressure was measured with a fluid-filled catheter and an external transducer. Eight control animals were similarly instrumented. At the time of study, the cyanotic dogs had significantly decreased arterial oxygen saturations (66% +/- 7% versus controls: 96% +/- 5%), significantly elevated peak RV pressures, (55 +/- 7 mm Hg versus controls: 30 +/- 5 mm Hg) and significantly elevated ratios of RV to LV mass (0.52 +/- 0.05 versus controls: 0.36 +/- 0.05). Diastolic pressure-dimension curves were generated and time constant for LV relaxation were calculated for each animal. The diastolic curves obtained from the cyanotic dogs were not significantly different from those of the control animals, and LV relaxation was not prolonged in the cyanotic dogs. In the three dogs that were cyanotic for 4 months or longer, there was a profound abnormality in the geometric pattern of LV contraction, manifested by asynchronous shortening of the anteroposterior equatorial minor axis. In two of these three dogs, inotropic reserves were assessed by means of postextrasystolic potentiation and were found to be normal. The results of this study indicate that short-term mild cyanosis and RV pressure overload do not alter diastolic compliance nor prolong relaxation of the LV. LV dynamic geometry may become abnormal after 4 months, with preservation of global LV inotropic reserves.
D000818:Animals; D003490:Cyanosis / Q000503:physiopathology*; D003971:Diastole; D004195:Disease Models, Animal; D004285:Dogs; D006330:Heart Defects, Congenital / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D009200:Myocardial Contraction; D010100:Oxygen / Q000097:blood; D013997:Time Factors
D010100:Oxygen