Assessment of left ventricular systolic function in hypertrophic cardiomyopathy patients with myocardial injury: a study based on layer-specific speckle tracking echocardiaography

Wen, Lei; Zhang, Yanfen; Liu, Yan; Ma, Chao; Jun, Yang; Sun, Dandan

doi:10.1007/s10554-020-01921-6

Cited by 1 publication

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“…We found that patients with elevated levels of cTnI and CK-MB had more severe clinical phenotypes, consistent with previous reports. [8][9][10][11][12] The elevated levels of cTnI and CK-MB were associated with greater LV wall thickness, presumably because thicker myocardium causes more severe intimal hyperplasia and luminal reduction within coronary arteries, triggering microvascular dysfunction. 22,23 Consequently, the coronary arterial supply is insufficient.…”

Section: Discussionmentioning

confidence: 99%

“…The results of small-scale studies have suggested associations between troponins/CK-MB and the extents of hypertrophy, 8 myocardial strain, 9,10 cardiac fibrosis, 11 arrhythmia, 12 and mortality 13 among patients with HCM. However, the existing evidence is insufficient to warrant the inclusion of troponins and CK-MB in the risk stratification strategies for HCM.…”

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confidence: 99%

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

Zhang,

Liu,

Zhang

et al. 2024

Circ: Cardiovascular Quality and Outcomes

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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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