Serum biomarker release patterns following alcohol septal ablation for treatment of hypertrophic cardiomyopathy

Abstract:

Alcohol septal ablation (ASA) is employed to relieve the pressure gradient associated with symptomatic hypertrophic cardiomyopathy. Serum concentrations of cardiac troponin I, creatine kinase MB band, brain natriuretic protein, matrix metalloproteinase-9, myoglobin, C-reactive protein, tumor necrosis factor-alpha, soluble CD40 ligand, interleukin-6, adiponectin, interleukin-1β, myeloperoxidase, and soluble intercellular adhesion molecule-1 were determined at baseline and at 8, 16, 24, and 48 hours in patients with hypertrophic cardiomyopathy presenting for ASA. Comparisons were made with 107 healthy control subjects. Sixteen hours following ASA, serum levels rose over 800-fold for cardiac troponin I, 70-fold for creatine kinase MB band, and 11-fold for myoglobin (P<0.001). C-reactive protein and interleukin-6 both rose slowly and became significantly elevated at 16 and 48 hours, respectively. Matrix metalloprotease-9 rapidly increased two-fold at 8 hours, but returned to baseline thereafter. Other biomarkers evaluated either trended downward or showed little change from baseline. Among the ASA patients, baseline serum concentration of all biomarkers, except for matrix metalloproteinase-9, soluble intercellular adhesion molecule-1, and myeloperoxidase, were elevated in the ASA group compared with the controls. These findings suggest that hypertrophic cardiomyopathy is a proinflammatory and prothrombotic state. The time-dependent changes in these biomarkers suggest they may be useful in predicting the success of ASA and could potentially offer insight into biochemical events during the time course of acute myocardial ischemia.

Keywords::

• alcohol septal ablation
• cardiac biomarkers
• hypertrophic cardiomyopathy
• inflammation
• acute myocardial infarction

Acknowledgments

This study was supported by grants from the National Institute of Health (P20 RR020145 and M01-RR02602) and the University of Kentucky General Clinical Research Core, and was partially supported by a Clinical Translational Science Award (UL1RR033173). We thank Dawn G Dawson, Justin R Kolasa, and Jason Stevens from the Department of Oral Health Practice, College of Dentistry, University of Kentucky, Lexington, KY, USA. Additionally, we thank the University of Kentucky Clinical Chemistry Laboratory.

Disclosure

The authors report no conflicts of interest in this work.