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Compensated cardiac hypertrophy: arrhythmogenicity and the new myocardial phenotype. I. Fibrosis
P Assayag1, F Carré, B Chevalier
1U127-INSERM, Hôpital Lariboisière, Paris, France.
Insights
Cardiac hypertrophy and fibrosis independently contribute to arrhythmias. Fibrosis causes arrhythmias through uncoupling and re-entry, while triggered activity depends on cardiocyte membrane changes, worsened by myocardial heterogeneity.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
- Pathophysiology
Background:
- Compensated cardiac hypertrophy frequently leads to arrhythmias.
- Arrhythmias in this condition are linked to fibrosis and altered membrane proteins.
- Understanding these factors is crucial for managing cardiac conditions.
Purpose of the Study:
- To investigate the independent roles of cardiac hypertrophy and fibrosis in arrhythmia development.
- To analyze the mechanisms by which fibrosis contributes to arrhythmias.
- To explore the influence of membrane protein changes on triggered activity.
Main Methods:
- Studied regression of hypertensive cardiopathy in spontaneously hypertensive rats.
- Utilized an experimental model of myocardial infarction.
- Administered propranolol to assess its effect on arrhythmias and hypertrophy.
Main Results:
- Both cardiac hypertrophy and fibrosis independently correlate with arrhythmias.
- Fibrosis contributes to arrhythmias via anatomical uncoupling and re-entry mechanisms.
- Triggered activity and automaticity are linked to cardiocyte membrane phenotype and myocardial heterogeneity.
Conclusions:
- Cardiac hypertrophy and fibrosis are distinct contributors to arrhythmia genesis.
- Fibrosis plays a significant role in creating arrhythmogenic substrates.
- Modulating membrane phenotypes and addressing myocardial heterogeneity may be key to preventing arrhythmias.
Abstract:
The high incidence of arrhythmias in compensated cardiac hypertrophy is related to two independently regulated components-fibrosis and the adaptational phenotypic changes in membrane proteins linked to cardiac hypertrophy, and fibrosis. During the regression of hypertensive cardiopathy in middle-aged spontaneously hypertensive rats, the roles of cardiac hypertrophy and fibrosis can be analysed separately, revealing that both correlate independently with arrhythmias. In an experimental model of myocardial infarction it is possible to prevent arrhythmias with propranolol at the same time as cardiac hypertrophy, despite ventricular fibrosis. Fibrosis would appear to create arrhythmias both by anatomical uncoupling and by a re-entry mechanism generated by the zig-zag propagation of the transverse waveform. Triggered activity and automaticity depend on the membrane phenotype of the cardiocyte. They also play an important role, which is aggravated by myocardial heterogeneity.