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Purpose To study the impact of genetic variants rs1739843, rs2290149 and rs10838692 in HSPB7 and MADD genes on myocardial remodeling in the patients with postinfarction cardiosclerosis. Methods and Results. The study included 252 men aged 30-65 y.o., who had MI more than 1 year ago. All patients had Q-MI of the anterior wall of the LV. Echocardiography was performed by the standard method (Vivid S6, GE, USA). Arterial hypertension (AH) was registered in more than 60% patients. Myocardial revascularization (CABG/PCI) was performed in more than in 50% of cases. Among 252 cases studies 156 patients had HFrEF (II–IV NYHA) LVEF (Sim)&amp;lt;40% (№1 group) and 96 patients had no clinical signs of HF and LVEF (Sim)&amp;gt;55% (№2 group). The groups were comparable in the AH prevalence and age. Patients all groups were on optimal drug therapy. Polymorphic genetic variants were studies using real-time-PCR. Eccentric types of LV remodeling prevailed in group 1 and concentric types of LV remodeling prevailed in group 2 (p &amp;lt; 0.001). The presence AH combined with CC genotype of rs1739843 in HSPB7 gene and TT genotype of rs2290149 in MADD and simultaneous carriage of the CC genotype of rs1739843 HSPB7 were associated with the presence of non-dilated ventricle (LV volume index ≤75 mL/m2) and relative wall thickness (RWT) &amp;gt;0.42 independently to LV mass index (p = 0.03). The T allele of rs1739843 HSPB7 (p = 0.006) and a combination of T allele of rs1739843 HSPB7 with the TT genotype of rs2290149 of the MADD gene were associated with the presence of dilated ventricles (p = 0.009) with LV hypertrophy (LV mass index &amp;gt;115 g/m2) independently to RWT. Conclusion Our preliminary data demonstrate that the genotype of HSPB7 (rs1739843) can modulated the association of AH and MADD rs2290149 with markers of ventricular hypertrophy and predispose to various types of post-MI remodeling of LV.

P195 Postinfarction myocardial remodelling according to 2D ECHO data and genetic predictors: effect of genetic common variants in HSPB7 and MADD genes