Atrial fibrillation ( AF ) is a common tachyarrhythmia and may cause seriouscomplications, such as stroke. When atrial pressure was elevated, the effect refraction period (ERP)was shortened and the conductivity in atr...Atrial fibrillation ( AF ) is a common tachyarrhythmia and may cause seriouscomplications, such as stroke. When atrial pressure was elevated, the effect refraction period (ERP)was shortened and the conductivity in atria was slowed and the heterogeneity of different parts ofatria was increased These changes facilitate the occurrence and maintenance of AF. Recent researchesdemonstrated that pulmonary veins (PVs) are important sources of ectopic beats in the initiation ofparoxysmal AF. In patients with drug-resistant chronic AF and structural heart disease, afterelectrical cardioversion, the PVs are also the dominant trigger in reinitiating AF. Yamane et alreported that, AF patients were often with dilated PVs if the AF was initiated by focal activity inPVs. Atrial myocardial fibers wrap around the PVs entering the left atrium to form PV myocardialsleeves (PVMSs), and this structure is the origin of focal activity. Little is known about theeffects of elevated atrial pressure on PV electrophysiology. In the present study, we found that,spontaneous activity in PVMSs could be induced by elevated atrial pressure and it could affect theatrial rhythm.展开更多
Atrial fibrillation (AF) is the most common sustained arrhythmia encounteredin clinical practice.1 Its incidence increases with age and the presence of structural heartdisease. It is a major cause of stroke, especiall...Atrial fibrillation (AF) is the most common sustained arrhythmia encounteredin clinical practice.1 Its incidence increases with age and the presence of structural heartdisease. It is a major cause of stroke, especially in the elderly. It has been shown thatangiotensin converting enzyme inhibitor (ACEI) can reduce the incidence of AF after acute myocardialinfarction.2 Several studies have shown that activation of the rennin-angiotensin system isassociated with the mechanisms of AF. Irbesartan is a long-acting angiotensin II type 1 receptorantagonist used widely in the treatment of hypertension.3 In recent years, it has been demonstratedthat patients treated with amiodarone plus irbesartan had a lower rate of recurrence of atrialfibrillation than did patients treated with amiodarone alone.4 These findings suggest that theinhibition of angiotensin II may prevent AF, but its underlying electrophysiological mechanisms areobscure. The purpose of this study is to investigate the effects of irbesartan on atrial cellelectrophysiology.展开更多
文摘Atrial fibrillation ( AF ) is a common tachyarrhythmia and may cause seriouscomplications, such as stroke. When atrial pressure was elevated, the effect refraction period (ERP)was shortened and the conductivity in atria was slowed and the heterogeneity of different parts ofatria was increased These changes facilitate the occurrence and maintenance of AF. Recent researchesdemonstrated that pulmonary veins (PVs) are important sources of ectopic beats in the initiation ofparoxysmal AF. In patients with drug-resistant chronic AF and structural heart disease, afterelectrical cardioversion, the PVs are also the dominant trigger in reinitiating AF. Yamane et alreported that, AF patients were often with dilated PVs if the AF was initiated by focal activity inPVs. Atrial myocardial fibers wrap around the PVs entering the left atrium to form PV myocardialsleeves (PVMSs), and this structure is the origin of focal activity. Little is known about theeffects of elevated atrial pressure on PV electrophysiology. In the present study, we found that,spontaneous activity in PVMSs could be induced by elevated atrial pressure and it could affect theatrial rhythm.
文摘Atrial fibrillation (AF) is the most common sustained arrhythmia encounteredin clinical practice.1 Its incidence increases with age and the presence of structural heartdisease. It is a major cause of stroke, especially in the elderly. It has been shown thatangiotensin converting enzyme inhibitor (ACEI) can reduce the incidence of AF after acute myocardialinfarction.2 Several studies have shown that activation of the rennin-angiotensin system isassociated with the mechanisms of AF. Irbesartan is a long-acting angiotensin II type 1 receptorantagonist used widely in the treatment of hypertension.3 In recent years, it has been demonstratedthat patients treated with amiodarone plus irbesartan had a lower rate of recurrence of atrialfibrillation than did patients treated with amiodarone alone.4 These findings suggest that theinhibition of angiotensin II may prevent AF, but its underlying electrophysiological mechanisms areobscure. The purpose of this study is to investigate the effects of irbesartan on atrial cellelectrophysiology.
