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Published on: July 29, 2011
Atrial structural remodeling in patients with atrial chronic fibrillations and in animal models
D Laky1, Liliana Parascan, V Cândea
1"Victor Babeş" National Institute, Bucharest, Romania.
Insights
Atrial fibrillation (AF) causes structural changes in the heart. This study suggests these changes are primarily an adaptive response, not purely degenerative, in patients and dogs with AF.
Area of Science:
- Cardiology
- Pathology
- Biomedical Engineering
Background:
- Atrial fibrillation (AF) is a common arrhythmia linked to increased mortality.
- Understanding structural changes in chronic AF is crucial for patient outcomes.
- Existing research often focuses on degenerative aspects of AF-related cardiac remodeling.
Purpose of the Study:
- To investigate the morphological changes in atrial biopsies from patients with chronic AF.
- To examine the structural adaptations in a canine model of induced atrial changes.
- To determine if observed structural changes represent an accommodative or degenerative response to AF.
Main Methods:
- Analysis of atrial biopsies from 175 patients undergoing surgery for sustained AF and cardiac diseases.
- Electrocardiogram (EKG) monitoring in 11 dogs with induced partial coronary obstructions.
- Morphological examination of cardiomyocyte dedifferentiation and fibrosis.
Main Results:
- Cardiomyocyte dedifferentiation (accommodation) was observed, particularly in the experimental model.
- Cell degeneration and fibrosis (mal-accommodation) were prominent in acquired valvular diseases.
- Structural changes were often a combination of accommodative and degenerative features.
Conclusions:
- The study supports the hypothesis that structural changes in AF are predominantly an accommodative response.
- These findings highlight the complex interplay between adaptation and degeneration in cardiac remodeling.
- Further research into the mechanisms of cardiomyocyte accommodation in AF is warranted.
Abstract:
Arrhythmia's atrium fibrillation (AF) is the most often met in clinical setting and it is associated with an increased in mortality risk. For profound the structural changes in chronic AF, we are studied the morphological changes of atrium biopsies to be effected at 175 patients. With sustained AF malformative and valvular acquired cardiac diseases operated under extracorporeal circulation. Similar studies we are effected to 11 dogs with partial coronary obstructions to a made periodical EKG investigations. The morphological changes mainly concern accommodation (dedifferentiation) of cardiomyocytes (particularly at experimental model) and mal-accommodation (degeneration of cells with fibrosis replacement features) particularly in acquired valvular diseases. These changes were often interfered. Over study, maintain the hypothesis that the structural changes to be an accommodation more than degenerative response to AF.
