Background

Myeloperoxidase (MPO), a polymorphonuclear neutrophil (PMN)-released heme-enzyme, has been linked to arrhythmogenic ventricular remodeling and ventricular arrhythmias (VT) in animal models. A link between MPO levels chronic heart failure (CHF), history of VT and impaired left ventricular function (LVEF) has been proven earlier in humans after myocardial ischemia. However, so far only retrospective human data exit on vulnerability for VT. Furthermore, no data exist on the extend of LV scar tissue, as a surrogate for arrhythmogenic substrate and MPO levels in patients (pts) undergoing VT ablation.

Objective

This explorative data collection was conducted to evaluate a potential correlation of MPO levels and LV low voltage area extend in patients undergoing catheter ablation (CA) for VT. It remains unclear, whether this may also play a role in pts with structural heart disease and VT.   

Methods

We investigates 10 consecutive pts (9 men, age 64±11 years) undergoing CA for VT. Prior to CA blood samples were collected and MPO levels were analyzed out of heparinized plasma. In all pts an 3D-electro-anatomic map was created using either the CARTO3 (Biosense-Webster^®) or the Ensite-Precision- (Abbott^®) mapping system. The extend of scar area was obtained by analyzing the 3D-maps. Scar was defined as a voltage amplitude of <1.5mV dense scar as < 0.5mV. Plasma levels of MPO and scar area were correlated with Spearman’s rho due to not normally distributed MPO values.

Results

All 10 pts underwent successful VT ablation. Seven (70%) pts suffered from ischemic cardiomyopathy (ICM) and 3 (30%) pts from non-ischemic cardiomyopathy. Left ventricular ejection fraction (LVEF) was 32±7%. The majority underwent de novo CA for VT, whereas 3 pts had previous VT ablation.

Evaluation of obtained electro-anatomical maps revealed an average LV scar area of 44.6±28.0cm² while the total left ventricular area was 187.6±53.8 cm². In proportion to the total LV this led to a mean relative LV scar extend of 23.7±11.7%.

Analysis of blood samples showed a median MPO plasma level of 75ng/ml with an interquartile range of 40ng/ml to 223ng/ml. In comparison to the extent of LV scar there is a positive correlation between relative scared LV area (relative to LV extend) and MPO level with a spearman’s rho of 0.6 (p=0.05).

Conclusion

In this explorative cohort of pts with structural heart disease undergoing CA for VT a positive correlation of plasma MPO levels and extent of LV scar area (spearman’s rho: 0.6) was shown. These findings in humans are in line with data from previous animal studies showing MPO derives VT-inducibility in mice.

Our results form the basis for further investigation to develop inflammation markers as potential surrogates for ventricular scar extend and outcome stratification.