Kalıcı Kalp Pili, İmplante Edilebilen Kardiyoverter-Defibrilatör ve Kardiyak Resenkronizasyon Tedavisinin Triküspit Kapak ve Sağ Boşluklar Üzerinde Etkisinin 2-Boyutlu Transtorasik Ekokardiyografi Yöntemi ile Değerlendirilmesi
Özet
Endocardial lead–induced tricuspid regurgitation has not been well recognized, either clinically or echocardiographically, and yet it is likely a preventable iatrogenic disease. In severe cases, it can lead to right ventricular failure and require tricuspid valve surgery. This complication will become increasingly important, because the numbers of permanent pacemakers and implantable cardioverter-defibrillators are expected to increase due to the aging population and the expanding capabilities of these devices. The mechanism may be mechanical perforation or laceration of leaflets, scarring and restriction of leaflets, or asynchronized activation of the right ventricle. Pacemaker-related TR might cause severe heart failure on the right side, but data regarding associated with mortality is lacking. The aim of this study was to assess the effect of trans-tricuspid placement of permanent pacemaker (PPM), implantable cardioverter defibrillator (ICD) and cardiac resynchronization therapy (CRT) leads on tricuspid valve and right sided heart function by two-dimensional echocardiography. Patients who required dual-chamber pacemakers, ICD and CRT were enrolled in the study. Initial echocardiography was performed before PPM/ICD and CRT implantation and re-evaluation by echocardiography was performed in 1'th ,6'th and 12'th month after implant. A total of 41 patients (31 male,10 female; mean age: 63.6 ±12.2 years) were included in the study, and patients were followed up for an average of 9 months. Echocardiography results demonstrated an absent of tricuspid regurgitation (TR) in 8 (19.5%), mild in 23 (56.1%) and moderate in 10 (24.4%) patients before PPM/ICD and CRT implantation. Patients with baseline absent TR of 8 (19.5% ) developed abnormal TR (9.8% mild , 9.8% moderate) after implant. Patients with baseline mild TR of 23 (56.1%) developed abnormal TR ( 41.5% moderate, 7.3% severe) after implant. Patients with baseline moderate TR of 10 (24.4%) developed abnormal TR (19.5% severe) after implant. TR worsened by 1 grade in 70.8% and 2 grade in 17.1% after implant. After lead implantation, abnormal TR developed in 68.3% and severe TR developed in 7.3% of patients with baseline mild TR or less. In overall, there is no significant difference in the TR worsening between PPMs/ICDs and CRTs groups (P˃0.05). Our results show that implantation of permanent transvenous right ventricular electrodes is not in general associated with an acute worsening of TR. The presence of new significant TR shortly after electrode implantation have not been observed in our patients; However, worsening of TR is observed following first month. The dysfunction the right side of the heart was considered but none of the patients developed symptoms of right ventricular failure related to pacing effect on the tricuspid valves. Transvenous right ventricular electrodes are associated with left ventricular dysfunction and mitral regurgitation.