The role of polymorphonuclear neutrophils (PMN) in myocardial ischemia and reperfusion (I/R) is controversially discussed. The PMN surface protein CD11b/CD18 plays a critical role for PMN activation and adhesion. Using CD11b/CD18 deficient (CD11b-/-) mice we herein sought to further elucidate the effects of infiltrating PMN on ventricular remodeling and arrhythmogenesis in the context of myocardial I/R. Wildtype (WT) and CD11b-deficient (CD11b-/-) mice of C57BL/6J background were subjected to 40 minutes of myocardial ischemia by ligation of the left anterior descending artery following 6- or 48 hours of reperfusion (I/R). CD11b-/- resulted in significantly less myocardial myeloperoxidase release (MPO+ cells / field of view: WT: 308.4 ± 22.2 vs. CD11b-/-: 178.3 ± 13.1, p < 0.05) and tyrosin chlorination (fluorescence intensity / AU: WT: 0.5 ± 0.07 vs. CD11b-/-: 0.18 ± 0.04, p < 0.01) after ischemia following 6 hours of reperfusion. Immunohistochemical Ly6g staining revealed a significant decrease in PMN infiltration in CD11b-/- hearts after 48 hours of reperfusion (Ly6g+ cells / field of view: WT: 84.07±2.74 vs. CD11b-/-: 64.72 ± 2.53, p < 0.03). Infarct size, as analysed by Triphenyl-tetrazolium chloride / Evans-Blue dye staining of myocardial sections was markedly reduced in CD11b-/- compared to WT mice (infarct area / area at risk: WT: 37.26 ± 7.72% vs. CD11b-/-: 21.8 ± 6.73%; p < 0.001). Standardized right ventricular stimulation in vivo indicated a significantly reduced susceptibility of CD11b-/- animals to ventricular tachycardias (VT) (WT: 8.11±2.85 vs. CD11b-/-: 4.75±1.5, p = 0.009) and a reduced VT length (WT: 8.11±2.85 vs. CD11b-/-: 4.75±1.5, p = 0.009) as compared to WT mice after ischemia followed by 2 days of reperfusion (WT: 8.11±2.85 vs. CD11b-/-: 4.75±1.5, p < 0.01). Decreased myocardial PMN infiltration and oxidative protein modifactions caused by the absence of CD11b/CD18 suggests a clear role of PMN infiltration for maldadaptive left ventricular remodelling and arrhythmogenesis following myocardial I/R.