Muhammad S Khan1, Matthias Lange1, Ravi Ranjan2, Vikas Sharma3, Jason P Glotzbach3, Craig Selzman4, Derek J Dosdall5. 1. Nora Eccles Harrison Cardiovascular Research and Training Institute, The University of Utah - Health, Salt Lake City, UT 84112, USA. 2. Nora Eccles Harrison Cardiovascular Research and Training Institute, The University of Utah - Health, Salt Lake City, UT 84112, USA; Division of Cardiovascular Medicine, Department of Internal Medicine, The University of Utah - Health, Salt Lake City, UT 84112, USA; Department of Bioengineering, The University of Utah - Health, Salt Lake City, UT 84112, USA. 3. Division of Cardiothoracic Surgery, Department of Surgery, The University of Utah - Health, Salt Lake City, UT 84112, USA. 4. Nora Eccles Harrison Cardiovascular Research and Training Institute, The University of Utah - Health, Salt Lake City, UT 84112, USA; Division of Cardiothoracic Surgery, Department of Surgery, The University of Utah - Health, Salt Lake City, UT 84112, USA. 5. Nora Eccles Harrison Cardiovascular Research and Training Institute, The University of Utah - Health, Salt Lake City, UT 84112, USA; Division of Cardiovascular Medicine, Department of Internal Medicine, The University of Utah - Health, Salt Lake City, UT 84112, USA; Department of Bioengineering, The University of Utah - Health, Salt Lake City, UT 84112, USA; Division of Cardiothoracic Surgery, Department of Surgery, The University of Utah - Health, Salt Lake City, UT 84112, USA. Electronic address: derek.dosdall@utah.edu.
Abstract
BACKGROUND: postoperative atrial fibrillation (POAF) is a common cardiac surgery complication that is associated with increased complications and negative outcomes, but the association between presurgical atrial conduction abnormalities and POAF has not been investigated clinically during premature atrial S1S2 stimulation. This clinical study sought to examine whether intraoperative premature atrial stimulation reveals increased areas of slowed and/or blocked conduction in patients that develop POAF. METHODS: High-density intraoperative epicardial left atrial mapping was conducted in 20 cardiac surgery patients with no prior history of atrial fibrillation (AF). In 20 patients, 6 (30%) developed POAF. A flexible-array of 240-electrodes was placed on the posterior left atrial wall in between the pulmonary veins. Activation maps were generated for sinus and premature atrial S1S2 stimulated beats. The area of conduction block (CB), conduction delay (CD) and the combination of both (CDCB) for conduction velocity < 0.1, 0.1 ≤ x < 0.2 and < 0.2 m/s, respectively were quantified. RESULTS: For a premature atrial S2 beat with shortest cycle length captured, conduction velocity maps revealed a significantly higher area for CD (13.19 ± 6.59 versus 6.06 ± 4.22 mm2, p = 0.028) and CDCB (17.36 ± 8.75 versus 7.41 ± 6.39 mm2, p = 0.034), and a trend toward a larger area for CB (4.17 ± 3.66 versus 1.34 ± 2.86 mm2, p = 0.063) in patients who developed POAF in comparison to those that remained in the sinus. Sinus and S1 paced beats did not show substantial differences in abnormal conduction areas between patients with and without POAF. CONCLUSION: In comparison to sinus and S1 beats, premature atrial S2 beats accentuate conduction abnormalities in the posterior left atrial wall of cardiac surgery patients that developed POAF.
BACKGROUND: postoperative atrial fibrillation (POAF) is a common cardiac surgery complication that is associated with increased complications and negative outcomes, but the association between presurgical atrial conduction abnormalities and POAF has not been investigated clinically during premature atrial S1S2 stimulation. This clinical study sought to examine whether intraoperative premature atrial stimulation reveals increased areas of slowed and/or blocked conduction in patients that develop POAF. METHODS: High-density intraoperative epicardial left atrial mapping was conducted in 20 cardiac surgery patients with no prior history of atrial fibrillation (AF). In 20 patients, 6 (30%) developed POAF. A flexible-array of 240-electrodes was placed on the posterior left atrial wall in between the pulmonary veins. Activation maps were generated for sinus and premature atrial S1S2 stimulated beats. The area of conduction block (CB), conduction delay (CD) and the combination of both (CDCB) for conduction velocity < 0.1, 0.1 ≤ x < 0.2 and < 0.2 m/s, respectively were quantified. RESULTS: For a premature atrial S2 beat with shortest cycle length captured, conduction velocity maps revealed a significantly higher area for CD (13.19 ± 6.59 versus 6.06 ± 4.22 mm2, p = 0.028) and CDCB (17.36 ± 8.75 versus 7.41 ± 6.39 mm2, p = 0.034), and a trend toward a larger area for CB (4.17 ± 3.66 versus 1.34 ± 2.86 mm2, p = 0.063) in patients who developed POAF in comparison to those that remained in the sinus. Sinus and S1 paced beats did not show substantial differences in abnormal conduction areas between patients with and without POAF. CONCLUSION: In comparison to sinus and S1 beats, premature atrial S2 beats accentuate conduction abnormalities in the posterior left atrial wall of cardiac surgery patients that developed POAF.
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