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Neurocrit Care. 2009;10(3):287-94. doi: 10.1007/s12028-009-9188-x. Epub 2009 Jan 28.

Ventricular arrhythmia risk after subarachnoid hemorrhage.

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Cardiovascular Institute, University of Pittsburgh Medical Center, S572 Scaife Hall, 200 Lothrop Street, Pittsburgh, PA 15213, USA.



Cardiac morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH) are attributable to myocardial injury, decreased ventricular function, and ventricular arrhythmia (VA). Our objective was to test the relationships between QTc prolongation, VA, and survival after SAH.


In 200 subjects with acute aneurysmal SAH, electrocardiograms, echocardiograms, and telemetry were evaluated. Serum electrolytes and troponin were also evaluated.


Initial QTc (mean 460 +/- 45 ms) was prolonged (> or = 470 ms) in 38% of subjects and decreased on follow-up (469 +/- 49 initial vs. 435 +/- 31 ms follow-up; N = 89; P < 0.0001). VA was present in 14% of subjects, 52% of subjects with VA had QTc > or = 470 ms, and initial QTc trended toward longer duration in subjects with VA (474 +/- 61 vs. 457 +/- 42 ms; P = 0.084). Multivariate analysis demonstrated significant predictors of VA after SAH were increasing age (OR 1.3/5 years; P = 0.025), increasing stroke severity (OR 1.8; P = 0.009), decreasing heart rate (OR 0.5/10 beats/min; P = 0.006), and the absence of angiotensin converting enzyme inhibitor or angiotensin II receptor antagonist use at SAH onset (OR 0.10; P = 0.027). All-cause mortality was 19% (25/135) at 3 months and subjects with VA had significantly higher mortality than those without VA (37% vs. 16%; P = 0.027).


These data demonstrate that QTc prolongation and arrhythmias are frequently noted after SAH, but arrhythmias are often not associated with QTc prolongation. In addition, the presence of VA identified subjects at greater risk of mortality following their SAH.

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