Left atrial function and blood coagulation in non valvular atrial fibrillation

2000 Fiscal Year Final Research Report Summary

• Project/Area Number: 11672305
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Laboratory medicine
• Research Institution: Keio University
• Principal Investigator: IWANAGA Shiro Keio Univerity, School of Medicine, Assistant, 医学部, 助手 (70213303)
• Project Period (FY): 1999 – 2000
• Keywords: Atrial fibrillation / Left atrial function / Cerebral embolism / Left atrial thrombus / Transesophageal echocardiography / Electrical defibrillation / Anti-coagulation therapy / Left atrial appendage

Research Abstract

Atrial fibrillation (AF) is an important cause of cerebral embolism. This study investigated time sequence of recovery from left atrial (LA) dysfunction after electrical defibrillation of paroxysmal AF and risk factors of thromboembolism in patients with chronic AF.
Forty-five patients with paroxysmal AF who had transesophageal echocardiography (TEE) before electrical defibrillation (DC) were followed with serial TEE after DC.Flow velocity in the LA appendage and A wave height of transmitral flow velocity, measured as indexes of LA systolic function, recovered within 1 month after DC, and there was no difference in these parameters between 1 and 3 month after DC.An anatomical index of LA size, area of LA appendage on a vertical image, gradually decreased in size over the period of 3 month. Atrial functional recovery delayed in patients with long term AF over 5 months, and LA appendage flow velocity, A wave, and LA appendage area required more than 3 month after DC for atrial functional recovery.
To clarify risk factors of thromboembolism in chronic AF, 75 patients with non valvular AF were evaluated with TEE and followed up for 3 years. Thirty-nine patients had a history of cerebral infarction, and 14 suffered from new episodes of symptomatic thromboembolism during the follow-up period. Logistic regression analysis revealed non-significant risk for the following factors : anti-coagulation therapy, anti-platelet agents, high blood pressure, diabetes mellitus, LA dilation, and left ventricular systolic dysfunction. Four factors, LA thrombus, atherosclerosis in thoracic aorta, low velocity in LA appendage flow, and age, were found to be significant risk for thromboembolism. In these factors, only one factor, LA appendage flow velocity less than 20 cm/sec, was the independent risk factor for symptomatic thromboembolism.
I concluded that immediate defibrillation after onset of paroxysmal AF prevent from sustained LA dysfunction after DC and from embolism due to LA thrombus. LA dysfunction is a major cause of thromboembolism in patients with chronic AF.