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Myeloperoxidase-deficiency protects from ventricular tachycardia in a murine model of ischemic cardiomyopathy

Session Poster session 2

Speaker Volker Rudolph

Congress : ESC Congress 2014

  • Topic : arrhythmias and device therapy
  • Sub-topic : Arrhythmias, General - Pathophysiology and Mechanisms
  • Session type : Poster Session
  • FP Number : P1445

Authors : V Rudolph (Cologne,DE), M Mollenhauer (Cologne,DE), A Klinke (Cologne,DE), L Remane (Cologne,DE), K Friedrichs (Cologne,DE), TK Rudolph (Cologne,DE), S Baldus (Cologne,DE)


V. Rudolph1 , M. Mollenhauer1 , A. Klinke1 , L. Remane1 , K. Friedrichs1 , T.K. Rudolph1 , S. Baldus1 , 1Cologne University Hospital - Heart Center - Cologne - Germany ,

European Heart Journal ( 2014 ) 35 ( Abstract Supplement ), 258

Background: Leukocytes have emerged as important mediators of adverse myocardial remodeling following myocardial infarction. Myeloperoxidase (MPO), a heme enzyme abundantly expressed and released by polymorphonuclear neutrophils (PMN), exerts pro-inflammatory and pro-fibrotic properties and has been identified to be causally linked to the formation and propagation of various cardiovascular disorders. We disclosed recently, that MPO critically promotes atrial fibrosis and arrhythmias. Thus, we sought to investigate whether MPO might also influence structural and electrical remodelling in ventricular myocardium.

Methods and results: Wild-type C57bl/6J (WT) and MPO-deficient (Mpo−/−) mice underwent either sham surgery (n=7, 6) or ligation of the left descending coronary artery (LAD) (n=7, 5). Right ventricular electrophysiological investigations 3 weeks after LAD ligation disclosed profoundly increased vulnerability for ventricular tachycardia (VT) in infarcted WT as compared to Mpo−/− mice (number of VT episodes: 6.7±1.3 vs. 1.8±0.9, p<0.01, sham: 2.0±0.4 vs. 1.7±0.8, p=0.79; total time of VT episodes: 3.67±0.88 vs. 0.88±0.36 sec, p<0.05, sham: 0.70±0.18 vs. 1.07±0.75 sec, p=0.67). Epicardial mapping analyses indicated a delayed velocity and enhanced heterogeneity of electrical conduction in WT as compared to Mpo−/− mice. No differences were observed in infarct size between WT and Mpo−/− mice, as assessed by hematoxylin/eosin stain of myocardial sections.

Conclusions: The current data demonstrate, that MPO increases the vulnerability for ventricular arrhythmias in a murine model of ischemic cardiomyopathy. Whereas no differences were observed in infarct size, characteristics of electrical conduction pointed to aggravated adverse electrical or structural remodeling in WT as compared to Mpo−/− mice. While the underlying mechanisms still have to be elucidated, the results underline the important role of inflammatory processes in cardiac remodeling upon myocardial infarction and identify MPO as a potential therapeutic target to prevent ventricular arrhythmias in ischemic cardiomyopathy.

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