Journal of hypertension · 2012
Elevated troponin predicts long-term adverse cardiovascular outcomes in hypertensive crisis: a retrospective study.
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Pattanshetty Deepak J, Bhat Pradeep K, Aneja Ashish, Pillai Dilip P
Аннотация
BACKGROUND: Hypertensive crisis is associated with poor clinical outcomes. Elevated troponin, frequently observed in hypertensive crisis, may be attributed to myocardial supply-demand mismatch or obstructive coronary artery disease (CAD). However, in patients presenting with hypertensive crisis and an elevated troponin, the prevalence of CAD and the long-term adverse cardiovascular outcomes are unknown.
OBJECTIVE: We sought to assess the impact of elevated troponin on cardiovascular outcomes and evaluate the role of troponin as a predictor of obstructive CAD in patients with hypertensive crisis.
METHODS: Patients who presented with hypertensive crisis (n = 236) were screened retrospectively. Baseline and follow-up data including the event rates were obtained using electronic patient records. Those without an assay for cardiac Troponin I (cTnI) (n = 65) were excluded. Of the remaining 171 patients, those with elevated cTnI (cTnI ≥ 0.12 ng/ml) (n = 56) were compared with those with normal cTnI (cTnI < 0.12 ng/ml) (n = 115) at 2 years for the occurrence of major adverse cardiac or cerebrovascular events (MACCE) (composite of myocardial infarction, unstable angina, hypertensive crisis, pulmonary edema, stroke or transient ischemic attack).
RESULTS: At 2 years, MACCE occurred in 40 (71.4%) patients with elevated cTnI compared with 44 (38.3%) patients with normal cTnI [hazard ratio: 2.77; 95% confidence interval (CI): 1.79-4.27; P < 0.001]. Also, patients with elevated cTnI were significantly more likely to have underlying obstructive CAD (odds ratio: 8.97; 95% CI: 1.4-55.9; P < 0.01).
CONCLUSION: In patients with hypertensive crisis, elevated cTnI confers a significantly greater risk of long-term MACCE, and is a strong predictor of obstructive CAD.
OBJECTIVE: We sought to assess the impact of elevated troponin on cardiovascular outcomes and evaluate the role of troponin as a predictor of obstructive CAD in patients with hypertensive crisis.
METHODS: Patients who presented with hypertensive crisis (n = 236) were screened retrospectively. Baseline and follow-up data including the event rates were obtained using electronic patient records. Those without an assay for cardiac Troponin I (cTnI) (n = 65) were excluded. Of the remaining 171 patients, those with elevated cTnI (cTnI ≥ 0.12 ng/ml) (n = 56) were compared with those with normal cTnI (cTnI < 0.12 ng/ml) (n = 115) at 2 years for the occurrence of major adverse cardiac or cerebrovascular events (MACCE) (composite of myocardial infarction, unstable angina, hypertensive crisis, pulmonary edema, stroke or transient ischemic attack).
RESULTS: At 2 years, MACCE occurred in 40 (71.4%) patients with elevated cTnI compared with 44 (38.3%) patients with normal cTnI [hazard ratio: 2.77; 95% confidence interval (CI): 1.79-4.27; P < 0.001]. Also, patients with elevated cTnI were significantly more likely to have underlying obstructive CAD (odds ratio: 8.97; 95% CI: 1.4-55.9; P < 0.01).
CONCLUSION: In patients with hypertensive crisis, elevated cTnI confers a significantly greater risk of long-term MACCE, and is a strong predictor of obstructive CAD.