Nature of pulmonary hypertension in congestive heart failure. Effects of cardiac transplantation.

Abstract

Pulmonary hypertension associated with congestive heart failure carries a risk of right ventricular failure after cardiac transplantation. Few data, however, are available on the hemodynamic behavior of the pulmonary circulation in these patients. We therefore studied mean pulmonary artery pressure minus left atrial pressure (estimated by pulmonary artery occluded pressure) versus cardiac output relationships in 20 patients with congestive heart failure evaluated for orthotopic cardiac transplantation, and we repeated this study either within the first 3 days postoperatively (n = 10) or 1 month postoperatively (n = 11). Cardiac output was increased by physical exercise or (in the early postoperative period) by an infusion of dobutamine. Reversibility of pulmonary hypertension was tested by an infusion of prostaglandin E1. At preoperative evaluation, the extrapolated pressure intercept of pulmonary vascular pressure:flow plots was negative in 10 of the patients, suggesting active exercise-induced pulmonary vasoconstriction. In the other 10 patients, the extrapolated pressure intercept was positive, suggesting that an increased closing pressure contributed to pulmonary hypertension. However, transplantation was constantly associated with proportional decreases of pulmonary artery pressure and left atrial pressure. On the other hand, pulmonary vascular pressure:flow plots were displaced to equal or lower pressures and to higher flows by prostaglandin E1 before as well as after transplantation. We conclude that in patients with congestive heart failure evaluated for cardiac transplantation, an increased pulmonary venous pressure more than a reversible increase in closing pressure determines the severity of pulmonary hypertension.

Haemodynamic evaluation of pulmonary hypertension

“…Thus, in PH, both closing pressure and the capillary pressure determined from the analysis of the PAP decay curve after balloon occlusion are increased [86,88]. The main site of increased resistance may be at the periphery of the pulmonary arterial tree, and this is possibly a cause of increased closing pressure [86]. Greater venous involvement than previously assumed has also been suggested recently [88].…”

“…The first assumption appears valid in both normal and diseased pulmonary circulation over physiological ranges of flows [38,53,86,87] (fig. 4).…”

“…$: PCP=30 mmHg. more accurate insight into the nature of increased PVRI [38,53,[86][87][88][89]. Thus, in PH, both closing pressure and the capillary pressure determined from the analysis of the PAP decay curve after balloon occlusion are increased [86,88].…”

“…Greater venous involvement than previously assumed has also been suggested recently [88]. In patients with PH, recent data using two-point curves have suggested that exercise is associated with some pulmonary vasoconstrictive effect, while dobutamine at doses f10 mcg?kg -1 ?min -1 allows cardiac output to increase without affecting pulmonary vascular tone [86,89]. Finally, in patients with primary PH, mean PAP-flow plots have indicated that the improvement in exercise tolerance seen after 6 weeks of prostacyclin therapy may be ascribable to a decrease in incremental PVR during exercise through a vasodilator effect [87].…”

The transpulmonary pressure gradient for the diagnosis of pulmonary vascular disease

“…In patients with purely passive pulmonary hypertension, the mean Ppa would decrease along with decreased Pla, while in those with ''out of proportion'' pulmonary hypertension the mean Ppa would remain unchanged, or decrease proportionally less than Pla. This was examined in 20 previously reported patients with pre-and post-operative haemodynamic measurements [3]. Before transplantation the mean¡SE was: 43¡2 mmHg for Ppa; 29¡2 mmHg for Ppcw, 604¡60 dyn?s ?m -2 for PVRi; and 12¡1 mmHg for TPG.…”