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Impaired atrial contraction in patients with atrial flutter and gradual recovery after cardioversion
N Kobayashi1, M Kasahara, H Kasahara
1Department of Internal Medicine, Yodakubo Hospital, Nagano, Japan.
Insights
Cardioversion for atrial flutter may require blood clot prevention due to potential blood stasis and impaired atrial function. Atrial enlargement and slow blood flow predict prolonged recovery of heart rhythm after the procedure.
Area of Science:
- Cardiology
- Echocardiography
- Thromboembolism Research
Background:
- The risk of thromboembolism following cardioversion of atrial flutter remains debated.
- Evidence suggests blood stasis in the atria of patients with atrial flutter.
Purpose of the Study:
- To investigate atrial thrombi and blood flow in the left atrial appendage in patients with atrial flutter.
- To assess the recovery of atrial contraction after cardioversion.
Main Methods:
- Transesophageal echocardiography was used to examine atrial thrombi and peak flow velocity in the left atrial appendage.
- Transmitral flow velocity was measured to evaluate atrial contraction recovery post-cardioversion.
Main Results:
- A thrombus was detected in one patient.
- Low peak flow velocity in the left atrial appendage correlated with left atrial dimension.
- Recovery of transmitral flow velocity after cardioversion was linked to pre-cardioversion flow velocity.
Conclusions:
- Some patients with atrial flutter exhibit impaired atrial contraction, which may persist after cardioversion.
- Atrial enlargement and reduced atrial appendage flow velocity are predictive factors for impaired recovery.
Abstract:
The risk of thromboembolism after cardioversion of atrial flutter is controversial. The present study provides evidence for blood stasis in the atria of patients with atrial flutter and for gradual recovery of atrial contraction after cardioversion, which justifies prophylactic treatment at cardioversion, as for atrial fibrillation. We examined atrial thrombi and peak flow velocity in the left atrial appendage as an index of blood stasis in 5 consecutive patients with atrial flutter. Transesophageal echocardiography revealed a thrombus in 1 patient, and peak flow velocity in the left atrial appendage was inversely correlated with left atrial dimension (r = -0.90, p < 0.05). After restoration of sinus rhythm, transmitral flow velocity in late diastole was also examined to evaluate the recovery of atrial contraction. The recovery of transmitral flow velocity the next day and 1 week after cardioversion was correlated with flow velocity in the left atrial appendage before cardioversion (r = 0.89, p < 0.05; r = 0.97, p < 0.01, respectively). These findings suggest that some patients with atrial flutter have impaired atrial contraction and that prolonged impairment after cardioversion is also possible. Atrial enlargement and low flow velocity in the atrial appendage were predictive factors for such patients.