CLINICAL IMPLICATIONS OF CARDIAC TROPONIN-I IN PATIENTS WITH HYPERTENSIVE CRISIS VISITING THE EMERGENCY DEPARTMENTS

Abstract

Objective: Cardiac troponin-I (cTnI) is the representative marker of myocardial injury. Elevation of cTnI is frequently accompanied in patients with hypertensive crisis, but there are few studies on its prognostic significance in hypertensive crisis. The aim of this study was to determine whether cTnI could predict the all-cause mortality in patients with hypertensive crisis visiting the emergency department (ED). Design and method: In this observational study, we enrolled patients aged > = 18 years who visited an ED between 2016 and 2019 for hypertensive crisis, which was defined as systolic blood pressure > = 180 mmHg and/or diastolic blood pressure > = 110 mmHg. Among the 6,467 patient, 3,938 patients who performed assay for cTnI were finally analyzed. Results: Among the 3,938 patients, 596 (15.1%) patients had cTnI levels above the 99th percentile upper reference limit (elevated cTnI, > 0.04 ng/mL) and 600 (15.2%) patients had cTnI levels between the detection limit (> = 0.01 ng/mL) and the 99th percentile upper reference limit (borderline cTnI). The 3-year all-cause mortality in elevated cTnI group, borderline cTnI groups, and normal cTnI groups were 41.6%, 36.5%, and 12.8%, respectively. After adjusting for confounding variables, patients with elevated cTnI (adjusted hazard ratio [HR] 2.01; 95% confidence interval [CI], 1.61–2.52) and patients with borderline cTnI (adjusted HR 1.64; 95% CI, 1.32–2.04) showed significantly higher risk of 3-year all-cause mortality than patients with normal cTnI. Conclusions: In patients with hypertensive crisis, cTnI levels provide useful prognostic information and permit the early identification of patients with an increased risk of death. Moreover, borderline cTnI was also significantly associated with higher risk of all-cause mortality. More intensive treatment and follow-up strategies are needed for patients with hypertensive crisis with elevated cTnI.