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Differential Structural Remodeling of the Left‐Atrial Posterior Wall in Patients Affected by Mitral Regurgitation with or Without Persistent Atrial Fibrillation: A Morphological and Molecular Study
Author(s) -
CORRADI DOMENICO,
CALLEGARI SERGIO,
MAESTRI ROBERTA,
FERRARA DAVID,
MANGIERI DOMENICA,
ALINOVI ROSSELLA,
MOZZONI PAOLA,
PINELLI SILVANA,
GOLDONI MATTEO,
PRIVITERA YLENIA ADELAIDE,
BARTOLI VERONICA,
ASTORRI ETTORE,
MACCHI EMILIO,
VAGLIO AUGUSTO,
BENUSSI STEFANO,
ALFIERI OTTAVIO
Publication year - 2012
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2011.02187.x
Subject(s) - medicine , atrial fibrillation , sinus rhythm , cardiology , fibrosis , pathogenesis , myocyte , catheter ablation , mitral regurgitation , endocrinology , pathology
Structural Remodeling in Atrial Fibrillation . Introduction: Atrial fibrillation (AF) in mitral regurgitation (MR) is a complex disease where multiple factors may induce left‐atrial structural remodeling (SR). We explored the differential SR of the left‐atrial posterior wall (LAPW) of patients affected by MR with or without persistent AF, and the expression of key proteins involved in its pathogenesis. Methods and Results: Light microscopy of LAPW samples from 27 patients with MR and persistent AF (group 1), 33 with MR in sinus rhythm (group 2), and 15 autopsy controls (group 3) was used to measure myocyte diameter, percentage of myocytolytic myocytes, interstitial fibrosis, and capillary density; RT‐PCR and Western blotting were used to assess the mRNA and protein levels of SOD‐1, SOD‐2, HO‐1, calpain, MMP‐2, MMP‐9, TIMP‐1, TIMP‐2, and VEGF; immunofluorescence was used to locate these proteins. Myocyte diameter was similar in groups 1 and 2, but larger than controls. Compared to group 2, group 1 had more myocytolytic myocytes (20.8 ± 5.6% vs 14.7 ± 4.5%; P < 0.0001), increased interstitial fibrosis (10.4 ± 5.1% vs 7.5 ± 4.2%; P < 0.05), and decreased capillary density (923 ± 107 No/mm 2 vs 1,040 ± 100 No/mm 2 ; P < 0.0001). All of the proteins were more expressed in groups 1 and 2 than in controls. The protein and mRNA levels of SOD‐1, SOD‐2, MMP‐2, and MMP‐9 were higher in group 1 than in group 2. Conclusions: The LAPW of MR patients with or without AF shows considerable SR. The former has more severe histopathological changes and higher levels of proteins involved in SR, thereby reaching a threshold beyond which the sinus impulse cannot normally activate atrial myocardium. (J Cardiovasc Electrophysiol, Vol. 23 p. 271‐279, March 2012.)