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Hyperlipidemia in patients with apolipoprotein E 2/2 phenotype: apolipoprotein A5 S19W mutation as a cofactor

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Even if the strong genetic component of EOFAD is recognized, its pathophysiology and etiology are not fully known (Lepara et al

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Gidekel Friedlander SY, Chu GC, Snyder EL, Girnius N, Dibelius G, et al

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The resultant myocardial cell damage and electrophysiological alterations are strongly predisposed to triggering arrhythmias, particularly ventricular arrhythmias such as premature ventricular beats, ventricular tachycardia, and ventricular fibrillation

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