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Cytokeratin 18 as a Novel Biomarker in Patients with Hypertrophic Cardiomyopathy
Konstantinos Fragkiadakis1,2, Niki Ktena3, Aikaterini Kalantidou4
1Cardiology Department, Heraklion University General Hospital, 71110 Heraklion, Greece.
Insights
Hypertrophic cardiomyopathy (HCM) involves increased cell death. Elevated M30 and M65 antigens in HCM patients may serve as novel biomarkers for sudden cardiac death risk.
Area of Science:
- Cardiology
- Biochemistry
- Pathology
Background:
- Hypertrophic cardiomyopathy (HCM) is a genetic heart muscle disease.
- HCM increases the risk of sudden cardiac death (SCD).
- Cytokeratin 18 (CK18)-based proteins (M30, M65) are cell-death biomarkers.
Purpose of the Study:
- To investigate M30 and M65 antigen expression in HCM patients.
- To correlate antigen levels with SCD risk in HCM.
- To examine CK18 expression in HCM myocardium.
Main Methods:
- Measured M30 and M65 antigens in peripheral blood of 46 HCM patients and 27 controls.
- Assessed CK18 expression in postmortem HCM heart tissue.
- Analyzed M30/M65 ratio to differentiate cell death types.
Main Results:
- M30 and M65 antigens were significantly higher in HCM patients compared to controls.
- Elevated M30/M65 levels correlated with increased SCD risk.
- HCM myocardium showed increased CK18 expression.
- Necrosis was more prominent than apoptosis in HCM.
Conclusions:
- M30 and M65 antigens are elevated in HCM patients.
- These antigens may serve as novel biomarkers for HCM and SCD risk.
- Increased CK18 expression and cell death are features of HCM.
Abstract:
Hypertrophic cardiomyopathy (HCM) is a heart muscle disease associated with an increased risk for sudden cardiac death (SCD). Cytokeratin 18-based proteins, such as M30 and M65 antigens, are known cell-death biomarkers. M30 antigen is released from cells during apoptosis, and M65 antigen is released during cell death from any cause, such as apoptosis or necrosis. We aimed to study the expression of M30 and M65 antigens in peripheral blood obtained by 46 HCM patients and compare with 27 age- and sex-matched patients without HCM. We also investigated the CK18 expression in myocardium from postmortem HCM hearts. M30 and M65 antigens were significantly increased in the HCM vs. non-HCM group (Μ30: 338 ± 197 U/uL vs. 206 ± 166 U/uL, p = 0.003; M65: 428 ± 224 U/uL vs. 246 ± 214 U/uL, p = 0.001), and HCM patients with a higher expression of these markers (M30: 417 ± 208 vs. 271 ± 162 U/uL, p = 0.011; M65: 518 ± 242 vs. 351 ± 178 U/uL, p = 0.011) had a higher risk for SCD. In HCM, both apoptosis and necrosis are increased, but particularly necrosis (M30/M65 ratio: 0.75 ± 0.09 vs. 0.85 ± 0.02, p < 0.001). CK18 is expressed in the HCM myocardium (1.767 ± 0.412 vs. 0.537 ± 0.383, % of area, p = 0.0058). Therefore, M30 and M65 antigens may be novel biomarkers in HCM.
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