Abstract
Background: QT interval prolongation and risk of torsades de pointes have been associated with abrupt heart rate (HR) slowing after cardioversion from atrial fibrillation (AF) or AV nodal ablation. The degree to which the QT interval prolongs with abrupt changes in HR, and the underlying mechanisms, are poorly understood. We quantified ΔQT interval during cessation of rapid pacing and examined the relationship between QT and circulating neurohormonal and inflammatory markers. Methods: Eleven subjects with dual chamber pacemakers and intact AV conduction were atrially-paced at 90/min for 10 min, 60 min, and 1 week (Figure). Biomarkers were sampled during and after pacing. The relationships between QT, pacing stage, and biomarker levels were analyzed with a mixed effect model. QT intervals were compared for the 20 RR intervals before and 100 RR intervals after each pacing stage. Results: QT intervals prolonged after cessation of rapid pacing: 6.4 ms (95% confidence interval 4.9-7.8 ms) after 10 min (P<0.0001), 6.1ms (4.6-7.5 ms) after 60 min (P<0.0001), and 2.2ms (0.9-3.6 ms) after 1 week (P=0.002). QT interval was significantly associated with angiotensin II (P=0.002), epinephrine (P<0.0001), norepinephrine (P=0.03), dopamine (P<0.0001), C-reactive protein (P=0.0005), and interleukin-6 (P<0.0001), but not associated with atrial natriuretic peptide (P=0.26), B-type natriuretic peptide (P=0.08), renin (P=0.25), or aldosterone (P=0.42). There were no significant inter-individual differences in biomarker levels drawn before and after pacing (P>0.1 for all comparisons). Conclusion: Abrupt decreases in HR were associated with QT prolongation. QT interval changes correlated with several neuroendocrine and inflammatory biomarkers, though there were no inter-individual differences in biomarker levels before and after pacing. These findings may partially explain the increased risk of torsade de points after restoration of sinus rhythm from AF.
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