Van Wagoner David R
Department of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio 44195, USA.
Semin Thorac Cardiovasc Surg. 2007 Spring;19(1):9-15. doi: 10.1053/j.semtcvs.2007.01.006.
Although the problem of atrial fibrillation is now widely appreciated, the fundamental mechanisms that lead to arrhythmia onset and persistence have been difficult to elucidate. As a result, available pharmacologic therapies have focused more on modifying ion channel activity than on the underlying mechanisms. Recent studies suggest an important role for alterations in autonomic regulation, neurohormonal activation, and a systemic inflammatory state in the genesis and persistence of atrial fibrillation. The relative contributions of these distinct pathways to atrial fibrillation likely vary from patient to patient, and within a patient, as a function of age. Tailored therapies, together with patient-specific ablative interventions, may increase the success with which atrial fibrillation is treated and minimize the occurrence of life-threatening thromboembolic complications.
尽管心房颤动问题如今已广为人知，但导致心律失常发作和持续的根本机制却难以阐明。因此，现有的药物治疗更多地侧重于改变离子通道活性，而非潜在机制。最近的研究表明，自主神经调节改变、神经激素激活和全身炎症状态在心房颤动的发生和持续中起着重要作用。这些不同途径对心房颤动的相对贡献可能因患者而异，并且在同一患者体内，也会随年龄而变化。量身定制的治疗方法，以及针对患者的消融干预措施，可能会提高心房颤动的治疗成功率，并将危及生命的血栓栓塞并发症的发生率降至最低。
