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Cardiac Troponin I Detected with a Highly Sensitive Assay Predicts Mortality Risk in Patients with Different Types of Pulmonary Hypertension

Mariella Velez-Martinez

Fernando Torres


C. Ayers

M. H. Drazner

A. T. Turer

J. A. de Lemos

Kelly Chin


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Conference: 2012 International PHA Conference and Scientific Sessions

Release Date: 06.22.2012

Presentation Type: Abstracts

Velez-Martinez M, Torres F, Ayers C, Drazner MH, Turer AT, de Lemos JA, Chin KM

UT Southwestern Medical Center at Dallas, Texas, USA 

BACKGROUNDPulmonary Hypertension (PH) is a heterogeneous group of diseases that includes pulmonary arterial hypertension (PAH). The latter commonly progresses to right heart failure and eventually death. Although several biomarkers, including cardiac troponin I (cTnI) have recently been shown to stratify risk for adverse outcomes in patients with PAH, no data are available regarding highly sensitive (hs) cTnI assays in PAH and PH in general. Novel hs assays can detect cTnI levels ten-fold lower than currently available assays, allowing detection of very small amounts of myocardial damage from the left or right ventricle. The purpose of this study was to evaluate the association between cTnI measured by a new hs assay with clinical outcomes (death and/or lung transplantation) among patients with different types of PH.

METHODScTnI was measured in 255 PH patients that had been enrolled in one of two single center registries using a new highly sensitive assay (hs-cTnI ARCHITECT, Abbott Diagnostics). Individuals were divided into quartiles based on hs-cTnI levels. Death and/or lung transplantation follow-up was complete through February 2012. The association between hs-cTnI and outcomes was assessed using Kaplan-Meier analysis and Cox regression models adjusting for glomerular filtration rate (GFR), right atrial pressure (RAP), mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), and cardiac index (CI).

RESULTS66% of the patients had PAH (WHO Group 1), 15% had PH due to left heart disease (WHO Group 2), 10% had PH due to lung disease (WHO Group 3), 5% had CTEPH (WHO Group 4), and 4% had miscellaneous PH (WHO Group 5). Hs-cTnI was detectable (≥1.2 pg/ml) in 95% of the patients with a median level of 6.9 pg/ml (IQR 2.7-12.6 pg/ml). During a median follow-up of 3.5 years, there were 68 deaths. Rates of death and transplantation increased in a stepwise fashion across higher cTnI quartiles (Figure). After adjusting for GFR, RAP, mPAP, PVR, and CI, individuals in quartiles 3 and 4 remained at increased risk for all-cause mortality and for transplantation (adjusted HR 3.4, 95% CI 1.4-8.1 and adjusted HR 4.5, 95% CI 1.8-10.9, respectively). This finding also remained significant among the subgroup of patients with PAH (WHO group 1).

CONCLUSIONS: Hs-cTnI is detectable with a hs assay in almost all patients with PH. Higher hs-cTnI levels associate with subsequent risk for all-cause death and lung transplantation in a cohort of patients with different types of PH, including those with PAH WHO group 1. This assay has the potential to improve current risk-stratification algorithms.

Cardiac Troponin I Detected with a Highly Sensitive Assay Predicts Mortality Risk in Patients with D