Inflammation and myocardial fibrosis: is there a relation with left bundle branch block

Author:

Rimskaya Elena M.ORCID,Stukalova Olga V.ORCID,Aparina Olga P.ORCID,Mironova Nataliia A.ORCID,Kuznetsova Tatiana V.ORCID,Chumachenko Petr V.,Golitsyn Sergey P.ORCID

Abstract

Aim. To assess myocardial changes during left bundle branch block (LBBB) in patients with dilated cardiomyopathy (DCM) and in structurally normal hearts. Materials and methods. Seventy three patients with clinic-instrumental signs of DCM, were divided into 2 groups with LBBB (group 1; n=41) and without LBBB (group 2; n=32). Moreover, 15 patients with LBBB with no signs of structural heart diseases (group 3) and 10 healthy subjects were included in the study. Fibrosis assessment and the inflammation detection was performed by cardiovascular magnetic resonance (CMR). The inflammation in 15 patients from group 1 and 16 patients from group 2 was confirmed by endomyocardial biopsy (EMB). Moreover, the level of transforming growing factor β1was assessed in serum of all patients and healthy subjects (TGF-β1). Results. The diffuse inflammatory process was defined in 46.7% cases of group 1 according to EMB data. The frequency of inflammation detection in groups 1 and 2 was comparable in EMB analyses (p=0,64) and CMR analyses (12,2% positive cases in group 1 vs 50% in group 2; p=0,18). The frequency of focal left ventricular fibrosis and intramural scar in the interventricular septum (“stria”) was also comparable in groups 1 and 2: 16 (39%) positive cases with focal fibrosis in group 1 versus 17 (53%) cases in group 2; p=0,35 and 6 (14,6%) cases with intramural scar in group 1 versus 7 (22%) in group 2; p=0,12. Patients from group 3 demonstrated no late gadolinium enhancement on CMR images but increased TGF-β1 level in the serum. Conclusion. Focal myocardial fibrosis is not related to the LBBB. Patients with idiopathic LBBB are characterized by increased TGF-β1 level with no myocardial fibrosis. Diffuse inflammation in LBBB-DCM patients may contribute to the progression of systolic dysfunction but is not the reason for LBBB formation.

Publisher

Consilium Medicum

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