Fibrosis of the left atria during progression of heart failure is associated with increased matrix metalloproteinases in the rat

Abstract

Hemodynamic overload of the atria is an important pathogenic factor of fibrosis; MMP-7 appears to be involved in the early stage of this tissue remodeling process.

Matrix metalloproteinase‐1 and its inhibitor, TIMP‐1, in systolic heart failure: relation to functional data and prognosis

“…The results of the present study are in accordance with those from a previous study of our group, where found a decreased level of MMP-1 and an increased level of TIMP-1 in plasma samples from patients suffering from AF compared with a control group in sinus rhythm [19]. Our findings [19] and others [20] suggest that increased interstitial fibrosis in atrial tissue are more likely to be due to underlying comorbidities, like hypertension, ischaemic heart disease or uncontrolled heart failure (circumstances associated with high risk to develop AF) than the presence of arrhythmia itself. Moreover, experimental data suggest that underlying diseases promote AF by causing atrial interstitial fibrosis [21].…”

Reduced Phosphoinositide 3-Kinase (p110α) Activation Increases the Susceptibility to Atrial Fibrillation

“…To explore the possibility that changes in components of the blood may activate pro-MMPs to MMPs and contribute to atrial and LV structural disarrangement with increased deposition of collagen, we assessed latent and active forms of two MMPs in ventricular tissue (inadequate protein available from mouse atria) that have been associated with marked structural abnormalities in the atria in a setting of heart failure ie, MMP2 and MMP9. 44,45 By gelatin zymography we found no changes in latent or active MMP9 (data not shown). However, both latent and active MMP2 were increased in ventricles of DCM and dnPI3K-DCM compared with NTg and dnPI3K ( Figure 3C), although there were no differences between DCM and dnPI3K-DCM.…”

Atrial Flutter Versus Atrial Fibrillation in a General Population: Differences in Comorbidities Associated With Their Respective Onset

“…[15][16][17] We postulated that COPD may predispose patients to cardiac arrhythmia either by the direct effects on the right heart through pulmonary hypertension, right ventricular strain, and stretching of the right atrium or as a result of therapeutic modalities used to treat COPD. The effect of metabolic changes (hypoxia and acidosis) could be significant.…”