Author + information
- Received June 28, 2009
- Revision received October 22, 2009
- Accepted October 26, 2009
- Published online March 23, 2010.
- Bobby John, MD, PhD⁎,†,
- Martin K. Stiles, MBChB, PhD⁎,
- Pawel Kuklik, PhD⁎,
- Anthony G. Brooks, PhD⁎,
- Sunil T. Chandy, MD†,
- Jonathan M. Kalman, MBBS, PhD‡ and
- Prashanthan Sanders, MBBS, PhD⁎,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Prashanthan Sanders, Cardiovascular Research Centre, Department of Cardiology, Level 5, McEwin Building, Royal Adelaide Hospital, Adelaide, SA 5000, Australia
Objectives The aim of this report was to study the effect of chronic stretch reversal on the electrophysiological characteristics of the atria in humans.
Background Atrial stretch is an important determinant for atrial fibrillation. Whether relief of stretch reverses the substrate predisposed to atrial fibrillation is unknown.
Methods Twenty-one patients with mitral stenosis undergoing mitral commissurotomy (MC) were studied before and after intervention. Catheters were placed at multiple sites in the right atrium (RA) and sequentially within the left atrium (LA) to determine: effective refractory period (ERP) at 10 sites (600 and 450 ms) and P-wave duration (PWD). Bi-atrial electroanatomic maps determined conduction velocity (CV) and voltage. In 14 patients, RA studies were repeated ≥6 months after MC.
Results Immediately after MC, there was significant increase in mitral valve area (2.1 ± 0.2 cm2, p < 0.0001) with decrease in LA (23 ± 7 mm Hg to 10 ± 4 mm Hg, p < 0.0001) and pulmonary arterial pressures (38 ± 16 mm Hg to 27 ± 12 mm Hg, p < 0.0001) and LA volume (75 ± 20 ml to 52 ± 18 ml, p < 0.0001). This was associated with reduction in PWD (139 ± 19 ms to 135 ± 20 ms, p = 0.047), increase in CV (LA: 1.3 ± 0.3 mm/ms to 1.7 ± 0.2 mm/ms, p = 0.006; and RA: 1.0 ± 0.1 mm/ms to 1.3 ± 0.3 mm/ms, p = 0.002) and voltage (LA: 1.7 ± 0.6 mV to 2.5 ± 1.0 mV, p = 0.005; and RA: 1.8 ± 0.6 mV to 2.2 ± 0.7 mV, p = 0.09), and no change in ERP. Late after MC, mitral valve area remained at 2.1 ± 0.3 cm2 (p = 0.7) but with further decrease in PWD (113 ± 19 ms, p = 0.04) and RA ERP (at 600 ms, p < 0.0001), with increase in CV (1.0 ± 0.1 mm/ms to 1.3 ± 0.2 mm/ms, p = 0.006) and voltage (1.8 ± 0.7 mV to 2.8 ± 0.6 mV, p = 0.002).
Conclusions The atrial electrophysiologic and electroanatomic abnormalities that result from chronic stretch due to MS reverses after MC. These observations suggest that the substrate predisposing to atrial arrhythmias might be reversed.
This work was supported in part by a Grant-in-Aid (G 08A 3646) from the National Heart Foundation of Australia and by the Australia-India Strategic Research Fund. Dr. John is supported by the Biosense-Webster Electrophysiology Scholarship, University of Adelaide. Dr. Stiles is supported by the National Heart Foundation of New Zealand and the Dawes Scholarship, Royal Adelaide Hospital. Drs. Brooks and Sanders are supported by the National Heart Foundation of Australia. Dr. Sanders reports having served on the advisory board of and having received lecture fees and research funding from St. Jude Medical, Bard Electrophysiology, Biosense-Webster, and Medtronic.
This work was presented in part by Dr. John, who received the Young Investigator Award, at the 3rd Asia-Pacific AF Symposium, October 2007, Taipei, Taiwan; and at the Annual Scientific Sessions of the American Heart Association, November 2007, Orlando, Florida; and published in abstract form (Circulation 2007;116:II438).
- Received June 28, 2009.
- Revision received October 22, 2009.
- Accepted October 26, 2009.
- American College of Cardiology Foundation