INTRODUCTION: 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. METHODS: In 200 subjects with acute aneurysmal SAH, electrocardiograms, echocardiograms, and telemetry were evaluated. Serum electrolytes and troponin were also evaluated. RESULTS: 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). CONCLUSIONS: 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.
INTRODUCTION: 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. METHODS: In 200 subjects with acute aneurysmalSAH, electrocardiograms, echocardiograms, and telemetry were evaluated. Serum electrolytes and troponin were also evaluated. RESULTS: 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). CONCLUSIONS: 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.
Authors: S R Spielman; A M Greenspan; H R Kay; K F Discigil; C R Webb; N M Sokoloff; A P Rae; J Morganroth; L N Horowitz Journal: J Am Coll Cardiol Date: 1985-07 Impact factor: 24.094
Authors: Amber McAteer; Marilyn Hravnak; Yuefang Chang; Elizabeth A Crago; Matthew J Gallek; Khalil M Yousef Journal: Biol Res Nurs Date: 2017-06-19 Impact factor: 2.522
Authors: Elizabeth Crago; Kelly Kerris; Chien-Wen J Kuo; Paula Sherwood; Marilyn Hravnak; David Crippen; Michael Horowitz Journal: Am J Crit Care Date: 2014-01 Impact factor: 2.228