Comparison of the Association Between High-Sensitivity Troponin I and Adverse Cardiovascular Outcomes in Patients With Versus Without Chronic Kidney Disease.

MedStar author(s):
Citation: American Journal of Cardiology. 121(12):1461-1466, 2018 06 15.PMID: 29628129Institution: MedStar Health Research InstituteForm of publication: Journal ArticleMedline article type(s): Journal ArticleYear: 2018Local holdings: Available online from MWHC library: 1995 - present, Available in print through MWHC library: 1999 - 2006ISSN:
  • 0002-9149
Name of journal: The American journal of cardiologyAbstract: Copyright (c) 2018 Elsevier Inc. All rights reserved.It is unknown whether the association of high-sensitivity troponin I (hs-TnI) with adverse cardiovascular outcomes varies by the presence of chronic kidney disease (CKD). We examined the association of hs-TnI with adverse cardiovascular outcomes in those with and without CKD in 4,107 (mean age, 64 years; 63% men; 20% black) patients from the Emory Cardiovascular Biobank who underwent coronary angiography. CKD (n=1,073) was defined as estimated glomerular filtration rate <60ml/min/1.73m<sup>2</sup> or urine albumin/creatinine ratio >30mg/g at baseline. Cox regression was used to compute hazard ratios (HR) for the association between hs-TnI levels (per doubling of hs-TnI: log<sub>2</sub>[hs-TnI]+1) and death, cardiovascular death, and major adverse cardiac events (MACE), separately. Hs-TnI was a stronger predictor of death (CKD: HR 1.23, 95% confidence interval [CI] 1.15 to 1.31; no CKD: HR 1.11, 95% CI 1.05 to 1.17, p-interaction=0.023), cardiovascular death (CKD: HR 1.24, 95% CI 1.14 to 1.34; no CKD: HR 1.15, 95% CI 1.07 to 1.22, p-interaction=0.12), and MACE (CKD: HR 1.18, 95% CI 1.11 to 1.25; no CKD: HR 1.11, 95% CI 1.06 to 1.16, p-interaction=0.095) in CKD compared with non-CKD. The association between hs-TnI and death in patients with CKD was stronger for patients without obstructive coronary artery disease (no obstructive coronary artery disease: HR 1.60, 95% CI 1.27 to 2.01; obstructive coronary artery disease: HR 1.19, 95% CI 1.11 to 1.27, p-interaction=0.041). In conclusion, hs-TnI is a stronger predictor of adverse cardiovascular events in patients who have CKD than those without, even in the absence of obstructive coronary artery disease. Hs-TnI may identify CKD patients who are high risk for adverse cardiovascular outcomes in whom aggressive risk factor modification strategies are warranted.All authors: Alkhoder A, Beshiri A, Epstein SE, Gafeer MM, Hammadah M, Hayek SS, Khambhati J, Kim JH, Ko YA, Lee SK, Murtagh G, O'Neal WT, Quyyumi AA, Sandesara PB, Shaw L, Sperling LS, Tahhan AS, Topel ML, Wilson PFiscal year: FY2018Digital Object Identifier: Date added to catalog: 2018-05-08
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Item type Current library Collection Call number Status Date due Barcode
Journal Article MedStar Authors Catalog Article 29628129 Available 29628129

Available online from MWHC library: 1995 - present, Available in print through MWHC library: 1999 - 2006

Copyright (c) 2018 Elsevier Inc. All rights reserved.

It is unknown whether the association of high-sensitivity troponin I (hs-TnI) with adverse cardiovascular outcomes varies by the presence of chronic kidney disease (CKD). We examined the association of hs-TnI with adverse cardiovascular outcomes in those with and without CKD in 4,107 (mean age, 64 years; 63% men; 20% black) patients from the Emory Cardiovascular Biobank who underwent coronary angiography. CKD (n=1,073) was defined as estimated glomerular filtration rate <60ml/min/1.73m<sup>2</sup> or urine albumin/creatinine ratio >30mg/g at baseline. Cox regression was used to compute hazard ratios (HR) for the association between hs-TnI levels (per doubling of hs-TnI: log<sub>2</sub>[hs-TnI]+1) and death, cardiovascular death, and major adverse cardiac events (MACE), separately. Hs-TnI was a stronger predictor of death (CKD: HR 1.23, 95% confidence interval [CI] 1.15 to 1.31; no CKD: HR 1.11, 95% CI 1.05 to 1.17, p-interaction=0.023), cardiovascular death (CKD: HR 1.24, 95% CI 1.14 to 1.34; no CKD: HR 1.15, 95% CI 1.07 to 1.22, p-interaction=0.12), and MACE (CKD: HR 1.18, 95% CI 1.11 to 1.25; no CKD: HR 1.11, 95% CI 1.06 to 1.16, p-interaction=0.095) in CKD compared with non-CKD. The association between hs-TnI and death in patients with CKD was stronger for patients without obstructive coronary artery disease (no obstructive coronary artery disease: HR 1.60, 95% CI 1.27 to 2.01; obstructive coronary artery disease: HR 1.19, 95% CI 1.11 to 1.27, p-interaction=0.041). In conclusion, hs-TnI is a stronger predictor of adverse cardiovascular events in patients who have CKD than those without, even in the absence of obstructive coronary artery disease. Hs-TnI may identify CKD patients who are high risk for adverse cardiovascular outcomes in whom aggressive risk factor modification strategies are warranted.

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