Elevated Pulmonary Artery Pressure* An Independent Predictor of Mortality Richard Cooper, M .D.;t ]alaI ChoU, M.D., F.C.C .P.; Brian E. Simmons, M.D., F.C.C.P.;:f: and Angel Castanet; M.D.
Analyses in this study were based on hemodynamic and angiographic data obtained in a cohort of 1,371 predominantly black patients during right and left heart catheterization. All patients were followed up prospectively for a mean of 117 weeks, and 103 fatal events were recorded. In Cox survival analysis, three variables were found to be independently related to survival: pulmonary artery mean pressure (PAMP), number of stenosed vessels, and left ventricular (LV) ejection fraction (p70 percent stenosis.
was thus entirely independent of the effect of increasing severity of LVH. To assess further the relative contribution of PAMP in relation to the level of LV systolic function, Cox regression analysis was performed separately in patients with and without depressed LV function (Table 4). In patients with normal LVfunction (ie, LVEF>50), PAMP was confirmed as a powerful predictor of outcome along with ejection fraction, followed by number of stenosed vessels. Similarly, in patients with a reduced ejection fraction, PAMP provided the most explanatory information regarding outcome, followed by the number of stenosed vessels; the contribution ofejection fraction did not reach statistical significance in this subgroup. Todetermine whether the predictive value of PAM P was relevant in patients with normal coronary arteriograms, further Cox regression analyses were carried out in this subgroup. (At baseline, 629 patients had normal coronary arteries and 23 fatal events were recorded during the follow-up period.) Pulmonary artery mean pressure was found to be the only hemodynamic variable among those described above that retained its predictive value (p=0.016) in these patients. In this analysis, number of vessels was not included in the model, ofcourse, while LVEDp, LVEF, and right atrial pressure contributed no statistically significant information regarding prognosis. Toestimate the magnitude of the effect of increased pulmonary pressure on survival, Kaplan-Meir product limit survival curves were constructed to compare patients with and without pulmonary pressures above 20 mm Hg (Fig 1). Survival differences for these two groups appeared early in the course of the follow-up and were highly significant (p :J III
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Mean PA pressure < 20 mmHg Mean PA pressure
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Analyses in this study were based on hemodynamic and angiographic data obtained in a cohort of 1,371 predominantly black patients during right and left heart catheterization. All patients were followed up prospectively for a mean of 117 weeks, and 103 fatal events were recorded. In Cox survival analysis, three variables were found to be independently related to survival: pulmonary artery mean pressure (PAMP), number of stenosed vessels, and left ventricular (LV) ejection fraction (p70 percent stenosis.
was thus entirely independent of the effect of increasing severity of LVH. To assess further the relative contribution of PAMP in relation to the level of LV systolic function, Cox regression analysis was performed separately in patients with and without depressed LV function (Table 4). In patients with normal LVfunction (ie, LVEF>50), PAMP was confirmed as a powerful predictor of outcome along with ejection fraction, followed by number of stenosed vessels. Similarly, in patients with a reduced ejection fraction, PAMP provided the most explanatory information regarding outcome, followed by the number of stenosed vessels; the contribution ofejection fraction did not reach statistical significance in this subgroup. Todetermine whether the predictive value of PAM P was relevant in patients with normal coronary arteriograms, further Cox regression analyses were carried out in this subgroup. (At baseline, 629 patients had normal coronary arteries and 23 fatal events were recorded during the follow-up period.) Pulmonary artery mean pressure was found to be the only hemodynamic variable among those described above that retained its predictive value (p=0.016) in these patients. In this analysis, number of vessels was not included in the model, ofcourse, while LVEDp, LVEF, and right atrial pressure contributed no statistically significant information regarding prognosis. Toestimate the magnitude of the effect of increased pulmonary pressure on survival, Kaplan-Meir product limit survival curves were constructed to compare patients with and without pulmonary pressures above 20 mm Hg (Fig 1). Survival differences for these two groups appeared early in the course of the follow-up and were highly significant (p :J III
c
L __
-I--1 I
.80
.2 .o.. Q. o... Q.
Q)
>
.60
Mean PA pressure < 20 mmHg Mean PA pressure
IV
:J
E E
20 mmHg
P
