Detectable serum cardiac troponin T as a marker of poor prognosis among patients with chronic precapillary pulmonary hypertension

Background-Right ventricular failure is a leading cause of death in patients with chronic pulmonary hypertension (PH). We checked whether detection of cardiac troponin T (cTnT), a specific marker of myocyte injury, could be useful in prognostic stratification of those patients. Methods and Results-Initial evaluation of 56 clinically stable patients (age 41+/-15 years) with pulmonary arterial (51 patients) or inoperable chronic thromboembolic (5 patients) PH (mean pulmonary arterial pressure 60+/-18 mm Hg) included cTnT test, allowing detection of its serum levels greater than or equal to0.01 ng/mL [cTnT(+)]. cTnT was detectable in 8 of 56 (14%) patients (mean+/-SD, 0.034+/-0.022; range, 0.010 to 0.077 ng/mL). Despite similar pulmonary hemodynamics, they had higher heart rate (92+/-15 versus 76+/-14 bpm, P=0.004), lower mixed venous oxygen saturation (50+/-10% versus 57+/-9%, P=0.04), and higher serum N-terminal pro-B-type natriuretic peptide (4528+/-3170 versus 2054+/-2168 pg/mL, P=0.03) and walked less during the 6-minute walk test (298+/-132 versus 396+/-101 m, P=0.02). Cumulative survival estimated by Kaplan-Meier curves was significantly worse at 24 months in cTnT(+) compared with cTnT(+) (29% versus 81%, respectively, log-rank test P=0.001). Multivariate analysis revealed cTnT status (hazard ratio, 4.89; 95% CI, 1.18 to 20.29; P=0.03), 6-minute walk test (hazard ratio, 0.93 for each 10 m; P=0.01), and pulmonary vascular resistance (hazard ratio, 1.13; P=0.01) as independent markers of mortality. All 3 cTnT(+) patients who survived the follow-up period converted to cTnT(-) during treatment. Conclusions-Detectable cTnT is a so-far ignored independent marker of increased mortality risk in patients with chronic precapillary PH, supporting the role of progressive myocyte injury in the vicious circle leading to hemodynamic destabilization.