Multimodal imaging shows fibrosis architecture and action potential dispersion are predictors of arrhythmic risk in spontaneous hypertensive rats

Abstract

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Cardiac fibrosis in three dimensions – mechanistic insights into arrhythmic risk due to hypertrophy

“…Studies in SHR model (also cited by the authors) show that the emergence of oxidative-stress induced early afterdepolarizations as a result of the source-sink mismatches caused by fibrosis, directly inducing spontaneous VT/VF (Nguyen et al, 2016). Thus, taken together, the data in Khwaounjoo et al (2022) provide a comprehensive picture of the well characterized SHR model. The emerging paradigm would be that ageing and Translational Perspective J Physiol 601.2 hypertrophy cause both fibrosis and dispersion of repolarization.…”

“…Thus, taken together, the data in Khwaounjoo et al. (2022) provide a comprehensive picture of the well characterized SHR model. The emerging paradigm would be that ageing and hypertrophy cause both fibrosis and dispersion of repolarization.…”

“…To conclude, Khwaounjoo et al. (2022) provide much needed data on the complex changes to the myocardial architecture in the setting of cardiac hypertrophy. Future studies should build on this framework to further elucidate the arrhythmic implications of fibrosis.…”

“…Complex fibrosis (as seen in cardiac hypertrophy) has been the subject of intense experimental investigation. In a recent issue of The Journal of Physiology, Khwaounjoo et al (2022) report the risk of VT/VF in the spontaneous hypertensive rat (SHR), a well-established model, characterizing the three-dimensional aspects of fibrosis and associated electrophysiological changes with mapping. They demonstrate proarrhythmic changes with increasing age and hypertensive heart disease in great detail, placing the structural and electrophysiological variables in context.…”

“…Neural remodelling is a key contributor to functional control of circuits and arrhythmogenesis in the setting of scars (Fukuda et al, 2015;Zhu et al, 2022). To conclude, Khwaounjoo et al (2022) provide much needed data on the complex changes to the myocardial architecture in the setting of cardiac hypertrophy. Future studies should build on this framework to further elucidate the arrhythmic implications of fibrosis.…”