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Levels of hs-cTn and Cardiac Outcomes
Study Questions:
What is the relationship between stable high-sensitivity cardiac troponin (hs-cTn) and outcomes in patients with chest pain, but without myocardial infarction (MI) or other causes for elevated hs-cTn?
Methods:
The authors conducted an observational cohort study including patients >25 years of age with a chief complaint of chest pain and ≥1 hs-cTn obtained in the emergency department at a single center. Patients with estimated glomerular filtration rate (eGFR) <15 ml/min/1.73 m2, MI, and any other cause for an increased hs-cTn were excluded, leaving 19,460 patients for analysis. The exposure was categorized as hs-cTn level of 5-9, 10-14, 15-29, 30-49, and ≥50 ng/L. The reference group had hs-cTn <5 ng/L. Outcomes included all-cause mortality, cardiovascular mortality, noncardiovascular mortality, MI, and heart failure. Models were conducted for covariates of age, sex, eGFR, prior MI, heart failure, stroke, chronic obstructive pulmonary disease, atrial fibrillation, hypertension, diabetes, and treatment with platelet inhibitors, beta-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and statins.
Results:
In the final study cohort, 62.0%, 21.0%, 8.6%, and 7.9% had hs-cTn of <5, 5-9, 10-14, and >14 ng/L, respectively. Higher hs-cTn levels were associated with older age, men, lower eGFR, and more comorbidities. Overall, 89% of the study population had minimal change in their hs-cTn level (0-2 ng/L). During a mean follow-up of 3.3 ± 1.2 years, 7% of the study cohort died. The yearly rate of death was 0.5% in patients with hs-cTn <5 ng/L compared to 2.1%, 5.1%, 12%, 23%, and 33% for patients with hs-cTn of 5-9, 10-14, 15-29, 30-49, and ≥50 ng/L, respectively. The adjusted risk of death was 2.0, 2.9, 4.1, 6.8, and 9.7 in patients with hs-cTn 5-9, 10-14, 15-29, 30-49, and ≥50 ng/L, respectively compared to patients with hs-cTn <5 ng/L. The adjusted risk of cardiovascular mortality was 3.6, 7.3, 9.1, 17.5, and 27.0 in patients with hs-cTn 5-9, 10-14, 15-29, 30-49, and ≥50 ng/L, respectively compared to patients with hs-cTn <5 ng/L. The adjusted risk of hospitalization for heart failure also consistently rose as a function of hs-cTn among all groups. Finally, the risk of MI was two-fold higher in patients with hs-cTn 10-14 and 15-29 ng/L, and almost three-fold higher in patients with hs-cTn 30-49 and ≥50 ng/L.
Conclusions:
Among patients with chest pain and stable hs-cTn levels, any detectable level of hs-cTn is associated with an increased risk of all-cause and cardiovascular mortality.
Perspective:
In this observational cohort study, the risk of death and cardiovascular outcomes was increased in patients with chest pain and elevated hs-cTn. Prior studies have reported that minimal elevations of hs-cTn are associated with adverse outcomes. The present study extends on these findings given that the authors evaluated for all potential causes of hs-cTn elevation and excluded these patients from their analysis. Elevated hs-cTn levels may be a reason to screen for undiagnosed heart disease in patients with no obvious cause for this abnormality. It may be beneficial to conduct studies to determine if preventive measures may reduce the risk of adverse outcomes in this population.
Keywords: Acute Coronary Syndrome, Adrenergic beta-Antagonists, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Atrial Fibrillation, Biomarkers, Chest Pain, Diabetes Mellitus, Emergency Service, Hospital, Heart Failure, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hypertension, Myocardial Infarction, Outcome Assessment, Health Care, Platelet Aggregation Inhibitors, Pulmonary Disease, Chronic Obstructive, Secondary Prevention, Stroke, Troponin T
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