Role of Biomarkers of Myocardial Injury to Predict Adverse Outcomes in Hypertrophic Cardiomyopathy

医学 心脏病学 内科学 肌钙蛋白I 危险系数 肌钙蛋白 心源性猝死 肥厚性心肌病 心力衰竭 猝死 心肌梗塞 置信区间
作者
Yu Zhang,Minghao Liu,Channa Zhang,Yubao Zou,Lianming Kang,Lei Song
出处
期刊:Circulation-cardiovascular Quality and Outcomes [Ovid Technologies (Wolters Kluwer)]
卷期号:17 (2): e010243-e010243 被引量:8
标识
DOI:10.1161/circoutcomes.123.010243
摘要

BACKGROUND: Serum troponins and CK-MB (creatine kinase-MB) are readily detectable and reliable cardiac-specific biomarkers of subclinical myocardial injury. This study explores the roles of cTnI (cardiac troponin I) and CK-MB in hypertrophic cardiomyopathy (HCM). METHODS: This study included 1045 patients with HCM who had baseline cTnI and CK-MB measurements at Fuwai Hospital between 1999 and 2019. Patients were excluded if they had undergone percutaneous coronary intervention or coronary artery bypass grafting, or had renal failure. Five end points were studied: all-cause death, cardiovascular death, noncardiovascular death, sudden cardiac death, and other cardiovascular death. Cox regression was used to assess the associations of cTnI and CK-MB levels with outcomes. RESULTS: Nine hundred seventy patients with available follow-up data were finally analyzed (mean age, 49.3 years; 36.4% female). During the median 4.3-year follow-up period, 87 patients reached the end points. Higher cTnI (per 0.05 ng/mL increase) and CK-MB (per 1 IU/L increase) levels were associated with increased risks of all-cause death (cTnI: adjusted hazard ratio [HR], 1.038, P <0.001; CK-MB: adjusted HR, 1.021, P =0.004), cardiovascular death (cTnI: adjusted HR, 1.040, P <0.001; CK-MB: adjusted HR, 1.025, P =0.006), and sudden cardiac death (cTnI: adjusted HR, 1.045, P <0.001; CK-MB: adjusted HR, 1.032, P =0.001). Patients with elevated levels of both cTnI and CK-MB had worse prognoses than patients with an elevated level of either biomarker alone and patients who did not have an elevated level of either biomarker. Addition of the binary indicator elevation of both cTnI and CK-MB significantly improved the discrimination and reclassification abilities of the standard HCM Risk- sudden cardiac death model (C statistics: P =0.002; net reclassification improvement, 0.652; integrated discrimination improvement, 0.064). CONCLUSIONS: Comprehensive evaluations of biomarkers of myocardial injury, cTnI and CK-MB, have considerable value for predicting adverse outcomes among patients with HCM. Routine cTnI and CK-MB assessments may help to guide implantable cardioverter defibrillator implantation for primary prevention in HCM.
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