Various Forms Of Pulmonary Hypertension Research Articles

Morphological substrate for the reversibility and irreversibility of pulmonary hypertension.

The reversibility of pulmonary hypertension in hypertensive pulmonary vascular disease depends, in the first place, on the feasibility of eliminating the cause of the elevation of pressure. Equally important in this respect are the type, the severity, and the extent of the pulmonary vascular lesions. This implies that various forms of pulmonary hypertension have completely different tendencies for regression. In thrombotic arteriopathy, whether caused by primary thrombosis or by embolism, the chance of regression of pulmonary hypertension, and of the vascular lesions, is limited. On the other hand, in many patients pulmonary venous hypertension and the associated vasculopathy, even when severe, appear potentially reversible. Experimental evidence suggests that the same is true in cases of hypoxic pulmonary hypertension as long as prominent complicating vascular alterations, as often observed in chronic obstructive lung disease, are absent. In plexogenic arteriopathy regression of pulmonary hypertension, following elimination of its cause, is observed whenever the vascular lesions have not progressed beyond a certain stage that can be considered a point of no return. Thereafter, there is not only no regression but a distinct tendency to progression of pulmonary vascular disease.

The pulmonary capillary bed in various forms of pulmonary hypertension.

Pulmonary diffusing capacity for CO (D L ), membrane diffusing capacity (D M ), and pulmonary capillary blood volume (V c ) were measured in 44 patients with various forms and severity of pulmonary vascular disease, and these measurements were compared with hemodynamic data obtained at cardiac catheterization, with clinical disability, and, in 27 patients, with the results of corrective cardiac surgery. In 11 of these patients, D L , D M , and V c were remeasured up to 8 months after cardiac surgery. In general, the diffusing characteristics and pressure-volume relationships in this larger group confirmed the previously reported findings in mitral valve disease. 1 D M was impaired in almost all cases regardless of etiology or severity. Most of the 11 patients restudied showed no change in D L , D M , or V c up to 8 months after surgery. Reduction in V c correlated well both with clinical disability and with surgical results. Two patients with primary pulmonary hypertension and three of the four patients with equally severe pulmonary hypertension due to mitral valve disease had high V c relative to pulmonary vascular resistance. If the measurements of V c are not falsely high, then it appears that the capillary bed makes relatively and absolutely less contribution to the total rise in pulmonary vascular resistance in these patients. This could be explained by intense precapillary vasoconstriction in the presence of a relatively normal pulmonary capillary bed.