Elevated troponin predicts long-term adverse cardiovascular outcomes in hypertensive crisis: a retrospective study
Deepak J Pattanshetty1, Pradeep K Bhat, Ashish Aneja
1The Heart and Vascular Center, MetroHealth Campus of Case Western Reserve University, Cleveland, Ohio 44109-1998, USA.
Insights
Elevated cardiac troponin I (cTnI) in hypertensive crisis patients indicates a higher risk of major adverse cardiac or cerebrovascular events (MACCE) and predicts obstructive coronary artery disease (CAD). This finding is crucial for managing patients with hypertensive crisis.
Area of Science:
- Cardiology
- Emergency Medicine
- Clinical Outcomes Research
Background:
- Hypertensive crisis is linked to adverse clinical outcomes.
- Elevated troponin in hypertensive crisis may stem from supply-demand mismatch or coronary artery disease (CAD).
- The prevalence of CAD and long-term outcomes in hypertensive crisis patients with elevated troponin are not well-defined.
Purpose of the Study:
- To determine the impact of elevated troponin on cardiovascular outcomes in hypertensive crisis.
- To assess troponin's predictive value for obstructive CAD in hypertensive crisis.
Main Methods:
- Retrospective analysis of 171 patients with hypertensive crisis and cardiac Troponin I (cTnI) assay.
- Comparison of major adverse cardiac or cerebrovascular events (MACCE) at 2 years between patients with elevated cTnI (≥ 0.12 ng/ml) and normal cTnI (< 0.12 ng/ml).
- Evaluation of obstructive CAD prevalence based on cTnI levels.
Main Results:
- Patients with elevated cTnI had a significantly higher rate of MACCE at 2 years (71.4% vs. 38.3%).
- Elevated cTnI was associated with a substantially increased risk of MACCE (Hazard Ratio: 2.77).
- Elevated cTnI strongly predicted the presence of obstructive CAD (Odds Ratio: 8.97).
Conclusions:
- Elevated cTnI in hypertensive crisis patients signifies a greater risk of long-term MACCE.
- Cardiac troponin I is a potent predictor of obstructive CAD in this patient population.
- These findings aid in risk stratification and management of hypertensive crisis.
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.
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