Thorac Cardiovasc Surg 2003; 51(2): 111-112
DOI: 10.1055/s-2003-38989
Letter to the Editor
© Georg Thieme Verlag Stuttgart · New York

ICD Implantation With and Without Combined Myocardial Revascularization - Incidence of ICD Therapy and Late Survival

R.  Moosdorf1
  • 1Klinikum der Philipps-Universität, Marburg/Lahn, Germany
Further Information

Publication History

Received: January 28, 2003

Publication Date:
05 May 2003 (online)

We read with interest the recent publication by Brockes et al. concerning ICD implantation with and without combined myocardial revascularization [1]. The authors of this article conclude that even after revascularization, patients with ischemic heart disease are still prone to sudden cardiac death by ventricular tachycardia or fibrillation. This is undoubtedly true, but there are different underlying mechanisms in the development of ventricular arrhythmias in ischemic heart disease. To name only the important ones, ventricular fibrillation (VF) is often induced by acute ischemia or is associated with severely impaired ventricular function. In cases of sole ischemia, successful revascularization should also cure the risk of VF.

This should be confirmed by postoperative electrophysiological evaluation; otherwise an ICD should be implanted. In cases of diffuse coronary artery disease and significantly reduced ejection fraction, patients should be considered for ICD implantation according to the MADIT Trial without further electrophysiological testing, even after revascularization. The missing differentiation between VF and ventricular tachycardia (VT) is even more important. The latter is mostly based on an anatomical substrate in form of mixed scar leading to reentrant circuits. Not only the well-known larger aneurysms but also smaller scar formations after myocardial infarction may lead to such issues in the tissue areas bordering on normal myocardium and may serve as an origin of the VT. Our group has introduced a strict preoperative evaluation in those patients whose ventricular arrhythmias are suspicious for developing, or documented as having developed VT. As they may later degenerate to VF, it is important to look at the onset of the ventricular arrhythmia. In these cases, mapping guided surgical ablation of the VT origin is always intended as an adjunct to coronary revascularization. In cases of aneurysm, mapping and ablation are performed from the epi- and endocardium. In cases of smaller scar areas, we only perform epicardial mapping and ablation by laser to avoid a ventriculotomy. Even with this limited approach, about half of the patients can be cured of VT, while the cure rate using the more aggressive first approach is around 90 %.

In our experience, this differentiated approach to VT and VF has beneficial effects on the patients - and our healthcare system. Patients under high risk for recurrent VF are directly considered for ICD implantation without being submitted to the risks of an electrophysiological testing or consumption of laboratory resources. In contrast, patients with VT may be offered a curative therapy instead of palliation by ICD, so cost-intensive device therapy may be avoided.

In summary, we congratulate the authors on their study results, which again underline the high risk of sudden cardiac death in coronary artery disease patients. However, we would recommend further differentiation of underlying arrhythmias in preoperative evaluation and - even more importantly - in therapeutic strategy.


Prof. Dr. R. Moosdorf

Klinikum der Philipps-Universität, Klinik für Herz- und Thorakale Gefäßchirurgie


35043 Marburg/Lahn