BACKGROUND: Cardioversion by direct current (DC) and other methods can cause atrial "stunning." There are case reports of acute pulmonary edema after DC cardioversion, but whether acute ventricular dysfunction is a general consequence of DC cardioversion is unknown. We have investigated whether DC cardioversion acutely affects myocardial velocity assessed by Doppler tissue imaging. METHODS: 40 patients (30 with atrial fibrillation and 10 with atrial flutter) undergoing elective DC cardioversion underwent transthoracic echocardiography with Doppler tissue imaging before and immediately after cardioversion, and after follow-up. Peak systolic velocity was derived for 6 ventricular segments using Doppler tissue imaging. RESULTS: Immediately after DC cardioversion of atrial fibrillation, peak systolic velocity decreased in basal lateral (4.3 +/- 2.0-3.3 +/- 1.7 cm/s, P <.001), mitral annulus-septal (3.8 +/- 1.0-3.5 +/- 0.9, P <.05), mitral annulus-lateral (4.9 +/- 1.6-4.1 +/- 1.7, P <.001), and tricuspid annular (7.8 +/- 2.0-7.0 +/- 1.2, P <.03) segments, even though left ventricular ejection fraction was unchanged. In contrast, for the atrial flutter group there were no significant changes in peak systolic velocity in any segment post-DC cardioversion. Follow up studies were performed after sustained in sinus rhythm in both atrial fibrillation and atrial flutter groups. For both groups, increased peak systolic velocity was found in all 6 segments on follow-up (all P <.05). CONCLUSIONS: DC cardioversion causes subclinical, acute reversible reduction in left ventricular peak systolic velocity in patients with atrial fibrillation. The causes of this reduction in myocardial contractile velocity and the circumstances in which acute dysfunction become clinically significant warrant further investigation.
BACKGROUND: Cardioversion by direct current (DC) and other methods can cause atrial "stunning." There are case reports of acute pulmonary edema after DC cardioversion, but whether acute ventricular dysfunction is a general consequence of DC cardioversion is unknown. We have investigated whether DC cardioversion acutely affects myocardial velocity assessed by Doppler tissue imaging. METHODS: 40 patients (30 with atrial fibrillation and 10 with atrial flutter) undergoing elective DC cardioversion underwent transthoracic echocardiography with Doppler tissue imaging before and immediately after cardioversion, and after follow-up. Peak systolic velocity was derived for 6 ventricular segments using Doppler tissue imaging. RESULTS: Immediately after DC cardioversion of atrial fibrillation, peak systolic velocity decreased in basal lateral (4.3 +/- 2.0-3.3 +/- 1.7 cm/s, P <.001), mitral annulus-septal (3.8 +/- 1.0-3.5 +/- 0.9, P <.05), mitral annulus-lateral (4.9 +/- 1.6-4.1 +/- 1.7, P <.001), and tricuspid annular (7.8 +/- 2.0-7.0 +/- 1.2, P <.03) segments, even though left ventricular ejection fraction was unchanged. In contrast, for the atrial flutter group there were no significant changes in peak systolic velocity in any segment post-DC cardioversion. Follow up studies were performed after sustained in sinus rhythm in both atrial fibrillation and atrial flutter groups. For both groups, increased peak systolic velocity was found in all 6 segments on follow-up (all P <.05). CONCLUSIONS:DC cardioversion causes subclinical, acute reversible reduction in left ventricular peak systolic velocity in patients with atrial fibrillation. The causes of this reduction in myocardial contractile velocity and the circumstances in which acute dysfunction become clinically significant warrant further investigation.