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Selected Publication:
Manninger-Wuenscher, M.
Impact of arterial hypertension on electrophysiological and structural arrhythmogenic atrial remodelling
PhD-Studium (Doctor of Philosophy); Humanmedizin; [ Dissertation ] Graz Medical University; 2018. pp.
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- Authors Med Uni Graz:
- Advisor:
- Heinzel Frank
- Scherr Daniel
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- Abstract:
- Atrial fibrillation (AF) is the most common sustained arrhythmia in humans and is associated with an increased risk of stroke, morbidity and death. Arterial hypertension (HT) is found in 60-80% of AF patients, is an independent predictor of new-onset AF and contributes to AF progression via unknown mechanisms. We aimed to investigate by which mechanisms HT facilitates AF development and favours AF progression. Methods: Two experimental series were conducted. First, landrace pigs with desoxycorticosterone acetate (DOCA) induced HT were compared to control animals. Transthoracic echocardiography, basic hemodynamic measurements, right atrial invasive electrophysiologic studies including AF inducibility testing as well as histological analyses were performed. In a second experimental series, landrace pigs with rapid atrial pacing (RAP) induced AF were either subjected to DOCA or used as controls. In these animals, transthoracic echocardiography, basic hemodynamic measurements, left and right atrial invasive electrophysiological studies, 3D electroanatomic mapping, high density epicardial multielectrode array mapping as well as histological stereological analyses were performed. Results: DOCA-induced HT leads to concentric left ventricular hypertrophy, atrial cardiomyocyte hypertrophy, impaired left atrial contractile function, each favouring AF inducibility. In animals subjected to AF+HT, longer AF durations were associated with atrial dilatation and fibrosis but not with an increased AF complexity. This finding could be verified in a computational model. Conclusion: DOCA-induced HT increases atrial susceptibility towards fibrillation at a state of impaired left atrial contractile function. In the presence of AF, DOCA-induced HT favours AF progression by increasing AF stability by early structural remodelling including atrial dilatation and fibrosis.