Thorac Cardiovasc Surg 2020; 68(S 01): S1-S72
DOI: 10.1055/s-0040-1705469
Short Presentations
Sunday, March 1st, 2020
Cardiovascular Basic Sciences
Georg Thieme Verlag KG Stuttgart · New York

MYBPHL Plasma Levels Are Increased after Induced Atrial Damage

H. Lahm
1   München, Germany
,
M. Dreßen
1   München, Germany
,
N. Beck
1   München, Germany
,
S. Doppler
1   München, Germany
,
R. Lange
1   München, Germany
,
M. Krane
1   München, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
13 February 2020 (online)

Objectives: In cardiovascular research, troponin has been established as a highly sensitive biomarker for acute myocardial infarction. In contrast, at present no reliable biomarkers exist which monitor an atrial damage. We have investigated whether MYBPHL could serve as a biomarker for that purpose.

Methods: Blood samples from healthy controls and patients were collected prior to operation and at five different later time points up to 24 hours. Samples were centrifuged for 10 minutes at 2,000 × g and plasma was aliquoted and stored at −80°C until further use. MYBPHL concentration in plasma was determined by a commercial ELISA (Mybiosource.com). To analyze gene expression in different tissues, frozen biopsies were minced, total RNA was extracted, reverse-transcribed into cDNA, and relative gene expression was evaluated by qRT-PCR.

Results: MYBPHL is expressed predominantly in the atria and occurs in two different isoforms with identical sequences except a 23 amino acid deletion in isoform 2. The expression of isoform 2 is almost exclusively confined to atrial tissue and hardly detectable in ventricles, arteria mammaria interna, and skeletal muscle. In patients with atrial fibrillation, preoperative MYBPHL plasma concentrations were similar to those of healthy controls (9.66 ± 1.66 ng/mL vs. 12.32 ± 3.33 ng/mL). After an intended atrial damage by endo- or epicardial ablation during surgical intervention, MYBPHL plasma concentrations were threefold elevated at the arrival at the intensive care unit (31.19 ± 8.56 ng/mL, p < 0.05) and remained significantly increased for 1 day. Ablation also provokes elevated levels of the established biomarkers CK-MB and troponin T. Interestingly, MYBPHL concentrations correlated with those of CK-MB (R 2 = 0.9908) but not with those of troponin T (R 2 = 0.0675). To confirm the specificity of the MYBPHL increase as a consequence of atrial damage but not due to the surgical intervention, we investigated two further groups of surgical patients undergoing aortic valve replacement or transcatheter aortic valve implantation. In both groups, we did not see an increase of postoperative MYBPHL concentrations in the plasma and the values remained comparable to those measured in healthy controls.

Conclusion: Our results identify MYBPHL as a novel and reliable biomarker to assess atrial damage.