Abstract

Background: Subarachnoid hemorrhage (SAH) leads to significant death and disability. Cardiac abnormalities after SAH include atrial arrhythmias (AAs). The MinK (KCNE1) G38S polymorphism has been associated with atrial fibrillation, with the G38 allele being linked to increased action potential duration in heterologous expression systems. The relationship of AAs and ion channel polymorphisms after SAH is not known. Methods: In 148 patients admitted for acute, aneurysmal SAH, EKG parameters, 24-hour Holter monitors, serum troponin (TnI), potassium (K), magnesium (Mg), and echocardiograms (ejection fraction [EF] and left atrial diameter [LA D]) were examined. MinK G38S was genotyped using fluorescent primers and analyzed with an ABI Prism 7000. Results: No patient had AAs on presentation, but AAs developed in 101 (68%) patients: SVT (95; 64%); fibrillation (9; 6%); flutter (4; 3%); idioventricular rhythm (2; 1%); and 3° block (1; 1%). AAs were not associated with PR or QTc intervals, TnI, K, Mg, EF, LA D, or stroke severity. AAs were associated with older age (58±9 vs 51±10yrs; p<0.001), lower heart rate (HR; 80±10 vs 84±14bpm; p=0.02), and higher HR variability (SDNN; 97±34 vs 85±32; p=0.05). The MinK S38 allele was associated with AAs (Figure ; GS & SS 70% vs GG 51%; p=0.02), but not LA D. Conclusions: Atrial arrhythmias are common following SAH and the MinK S38 allele is associated with an increased frequency of atrial arrhythmias. The SAH-induced catecholamine surge, followed by increased parasympathetic activity, may enhance the shortening of the atrial effective refractory period in patients carrying the MinK S38 allele and increase susceptibility to atrial arrhythmias.

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