Human atrial repolarization: effects of sinus rate, pacing and drugs on the surface electrocardiogram
Nadia M. G. Debbas, MD, PhD, FESC, FACCa,
Steve H. D. Jackson, MD ,
Daniel de Jonghe, MDa,
Annie Robert and
A. John Camm, MD, PhD, FESC, FACC
a Department of Cardiology, Cliniques Universitaires St Luc, UCL, Brussels, Belgium
Department of Epidemiology, Cliniques Universitaires St Luc, UCL, Brussels, Belgium
Department of Cardiological Sciences, St Georges Hospital Medical School, London, England, United Kingdom

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Figure 1 Lead I of the surface electrocardiogram as recorded (top panel), with further amplification (middle panel) and with further amplification and filtration (bottom panel).
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Figure 2 Correlation between PTa and atrial paced cycle length (PP) in 20 patients (n = 103 points); rho = 0.76, p < 0.001, slope = 0.24, intercept = 243 ms.
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Figure 3 Correlation between Ta and atrial paced cycle length (PP) in 20 patients (n = 103 points); rho = 0.62, p < 0.001, slope = 0.24, intercept = 124 ms.
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Figure 4 Correlation between P and atrial paced cycle length (PP) in 20 patients (n = 103 points); rho = 0, p = NS.
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Figure 5 Effect of intravenous propranolol (0.1 mg/kg) on the atrial surface electrocardiogram. Before propranolol: P = 106 ms, Ta = 289 ms. On propranolol: P = 102 ms, Ta = 319 ms. C = corrected.
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Figure 6 Effect of propranolol, atropine, disopyramide and flecainide on the atrial cycle length (PP).
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Figure 7 Effect of propranolol, atropine, disopyramide and flecainide on the atrial surface electrocardiographic intervals, PTa, P and Ta.
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Figure 8 Effect of propranolol, atropine, disopyramide and flecainide on the PTa interval corrected for rate using the linear regression equation (top panel) and Bazetts hyperbolic formula adapted to the atrium (bottom panel).
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