Author + information
- Paolo Della Bella, MD∗ ( and )
- Antonio Frontera, MD
- ↵∗Address for correspondence:
Dr. Paolo Della Bella, Arrhythmia Unit and Electrophysiology Laboratories, Ospedale San Raffaele, Via Olgettina 60, Milan 20132, Italy.
In the history of interventional cardiology, chronic total occlusion (CTO) angioplasty has encountered some barriers, which have included lack of dedicated expertise, risk of procedural complications, and long and technically difficult procedures. In the last 10 years, technical advances have been made, and new revascularization opportunities that were previously unattainable could be offered in the vast majority of centers to more and more patients.
Growing evidence supports that recanalization of coronary artery CTO provides substantial benefits. This includes improved left ventricular systolic function in selected patients with ischemic myocardial dysfunction (1) and, possibly, enhanced long-term survival (2). Also, symptom control and quality of life improve significantly with successful percutaneous revascularization: all these factors have reignited interest in percutaneous modalities. The improved outcome might be the consequence of the reduced incidence of ventricular arrhythmias (VAs), resulting from modifications of the hibernating myocardium in a CTO region.
In the last 5 years, several groups have reported on the favorable link between VAs in the field of CTO. The VACTO (Ventricular arrhythmias among implantable cardioverter-defibrillator recipients for primary prevention: impact of chronic total coronary occlusion) study (3), among 162 patients with ischemic cardiomyopathy who received an implantable cardioverter-defibrillator (ICD), assessed the prognostic importance of CTO in the incidence of appropriate ICD therapy for VAs in a population with ischemic cardiomyopathy. The main finding was that presence of a CTO had a negative impact on the incidence of VAs at long-term follow-up. More than 30% of the patients with CTO had arrhythmic events after 3 years of follow-up, which put them in a high-risk subgroup for receiving ICD discharges. On the contrary, 90% of the patients without CTO with primary prevention indication for an ICD remained free from VA at 2 years follow-up.
In this issue of JACC: Clinical Electrophysiology, Chi et al. (4) provide a study on the relationship between CTO status and the occurrence of ventricular tachycardia (VT) or ventricular fibrillation (VF), or appropriate ICD therapy. This large meta-analysis included a total number of 54,365 patients, with a mean follow-up of 38 ± 16 months. Major findings were that presence of CTO was associated with a significant increase in the risk of VT or VF, or appropriate ICD therapy, but not with cardiac mortality or all-cause mortality. Furthermore, CTOs of an infarct-related coronary artery had higher risk of VT or VF, or appropriate therapy, and all-cause mortality, but not in cardiac mortality, than those with non–infarct-related CTOs.
Should then a CTO be actively looked for, and possibly corrected, as part of the treatment protocol in patients undergoing electrophysiologic evaluation of recurrent post-infarct VT?
Recurrent monomorphic VT, the leading cause for appropriate ICD intervention in patient with a prior myocardial infarction, is currently thought to result from stable reentry due to the abnormal electrophysiological environment around and within the scar. The current view is also reflected by the recommendations expressed in the recent American Heart Association/American College of Cardiology/Heart Rhythm Society guidelines (5), where revascularization alone is a Class III (no benefit) indication for the treatment of recurrent monomorphic post-infarct VT. This recommendation is mainly based on the manuscript published in year 2001 by Brugada et al. (6). In the Brugada et al. (6) study, the authors have prospectively studied 64 patients with prior myocardial infarction and spontaneous VAs not related to an acute ischemic event (55 VT, 9 VF). Each patient underwent revascularization (coronary artery bypass grafting or percutaneous coronary intervention). The study tried to answer the question, “do coronary artery revascularizations modify the electrophysiological substrate?” The study indicated that, despite effective revascularization, VT was persistently and uniformly inducible in the study population, supporting the hypothesis that scar-related re-entry occurs independently of ischemic triggers. As electrophysiologists, we retain a strong belief to this view.
According to a retrospective study on patients who underwent VT ablation at our institution (7), CTO of an infarct-related artery was proven as an independent predictor of VT recurrence after ablation, identifying a subgroup of patients with high recurrence rate despite a successful procedure. Greater scar extension and increased heterogeneity of the border zone area are hallmark features of CTO and go along with increased vulnerability to recurrent VT.
Whether the treatment of a CTO, and through which mechanism, might affect the tendency of VT to recur, should probably be addressed by a purposely designed mechanistic trial. Revascularization will determine an electrophysiological change of the substrate along the circuit as well as outside in the “not involved” remaining part of the ventricular tissue.
On the other hand, electrical storm may seldom occur after surgical revascularization (8). VAs are aggravated by the surgical procedure due to revascularization of chronically hibernating myocardial region. As described by Steinberg et al. (9), a specific subset of patients (mainly characterized by low ejection fraction, severe congestive heart failure, and extensive prior myocardial infarction) appear to be more vulnerable to reperfusion VF. Resumption of blood flow to areas previously poorly perfused may trigger abnormal automaticity of cells at the borders of myocardial scar.
Several questions need to be answered, such as: how will the revascularization modify the electrophysiological properties of the substrate along the circuit, or in neighboring areas? Not every revascularization of CTOs, especially of nonvital tissue, could really favorably affect an arrhythmia substrate. There are consistent data that do show improved outcome after revascularization in patients with left ventricular dysfunction and viable myocardium, but not in the absence of viability (10). Someone could point out that myocardium subtended by a CTO is sustained by microvascular connections from adjacent myocardial vascular zones.
An additional question could be: is this described decreased incidence of VAs represented by VT or VF episodes?
Limitations of current studies available in published data are mainly represented by the small numbers of patients enrolled and by their retrospective nature. Another limitation is represented by the heterogeneity of the population: left ventricular ejection fraction percentage ranged significantly in the patients enrolled in those studies and may have influenced the outcome. Also, noninvasive functional tests were not systematically performed in all the patients, and information about viability and ischemia extension are limited.
Although guidelines do not recommend revascularization (alone) as a treatment for VT, more recent studies on revascularization of CTOs prove that this might actually be the case, with a better outcome and a significant reduction of VA burden.
We need additional knowledge.
↵∗ Editorials published in JACC: Clinical Electrophysiology reflect the views of the authors and do not necessarily represent the views of JACC: Clinical Electrophysiology or the American College of Cardiology.
Dr. Della Bella has served as a consultant for Abbott and Biosense; and has received research grant support from Abbott, Biosense, Boston Scientific, and Biotronik. Dr. Frontera has reported that he has no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
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