The review highlights that altered membrane currents and calcium handling in hypertrophied and failing myocardium create a proarrhythmic substrate leading to sudden cardiac death.
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Alerts clinicians to SCD risk in HF; leaves open targeted ion channel/Ca therapies pending trials.
Tomaselli et al. (2000) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: