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Abstract: PO2077

Troponin Level in Relation to Angiographic Coronary Artery Disease in CKD Patients

Session Information

Category: Hypertension and CVD

  • 1401 Hypertension and CVD: Epidemiology, Risk Factors, and Prevention


  • Batra, Sachin, James J Peters VA Medical Center, Bronx, New York, United States
  • Chokshi, Bhavin, Wayne State University School of Medicine, Detroit, Michigan, United States
  • Hanumanthu, Balaram krishna J., Mount Sinai Beth Israel Hospital, New York, New York, United States
  • Jim, Belinda, Jacobi Medical Center, Bronx, New York, United States

An association between cardiac troponin I (cTI) in the diagnosis of angiographic coronary artery disease(CAD) is unclear in the CKD population. We evaluated the association between cTI to findings of angiographic significant CAD in CKD patients with traditional risk factors.


Data was collected from left cardiac catheterizations (LCHs) performed between 2006 -2017 at Jacobi Medical Center. CAD outcomes were defined as:none, mild(<50% stenosis), moderate(50-69% stenosis), severe (>70% stenosis of any major epicardial artery). ROC characteristics of cTI as biomarker for severe CAD was performed in patients with CKD stages 3-5. C-Statistic/AUC were used to compare pretest probabilities for severe CAD based on CAD risk factors (age, race, HTN, HLD, DM, smoking), abnormalities on ECHO and ECG, cTI level, and CKD stage.


798 LHCs were included. Fig1a shows that cTI level is only significantly higher in severe CAD as compared to no CAD among CKD 1-2 patients. ROC showed cTI >0.3ng/mL displayed peak sensitivity (59%), specificity (62%). Multivariate analysis for predictors of severe CAD among 223 CKD patients was stratified by cTI >0.3 and cTI <0.3. Among cTI <0.3 subgroup, age >65(OR 4.6, 95% CI 1.55-13.9, p=0.006), segmental wall motion abnormalities(OR 6.46; 95% CI 1.49-27.9, p=0.012) and eGFR<30(OR 2.92; 95% CI 0.94-9.00; p=0.06) were associated with severe CAD. Among cTI>0.3 subgroup, none of the clinical factors were significantly associated with severe CAD. Fig1b shows that the addition of dichotomized cTI > or < 0.3 to CAD risk factors did not significantly change the AUC value.


cTI levels are not associated with different levels of CAD in patients with eGFR <=60. The addition of cTI>0.3 does not alter the predictive value of severe CAD when other cardiac risk factors are considered. It will be important to study if the change in cTI during a cardiac event would be more predictive in the CKD population.