Cardiology Medical News about Ventricular Fibrillation

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Increased Susceptibility of Aged Hearts to Ventricular Fibrillation During Oxidative Stress
Heart And Circulatory Physiology, 09/25/09

Morita N et al. – In aged ventricles exposed to oxidative stress, fibrosis facilitates the ability of cellular EADs to emerge and generate TA, VT and VF at the tissue level.

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Hrayr S. Karagueuzian, 09/25/09

The major finding of this study is that aged fibrotic hearts are notorious for their stable normal sinus rhythm and do not die of VF. However, when these hearts otherwise in stable normal rhythm are exposed to oxidative stress, suddenly develop VF without prior acceleration of heart rate. Such levels of oxidative stress and even levels as high as 20 times consistently fail to promote VF in adult, non fibrotic hearts putting the role of cardiac fibrosis as the major culprit as all other electrophysiological parameter are not much different in the two aged groups. Aged hearts have structural features (fibrosis) that are not unlike heart failure and cardiac hypertrophy are therefore like a “timed bomb” any elevation in the level of stress (oxidative in our case) promote EADs and generated TA causing VT and VF. While reducing and/or reversing cardiac fibrosis may be a highly desirable therapeutic intervention in the long run, preventing elevation of the level of oxidative stress could be an immediate and effective therapeutic measure to prevent VF and sudden cardiac death in patients with cardiac fibrosis.

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