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. 2018 Mar 7;34(4):336-346.
doi: 10.1002/joa3.12028. eCollection 2018 Aug.

Ventricular arrhythmias in nonischemic cardiomyopathy

Affiliations

Ventricular arrhythmias in nonischemic cardiomyopathy

Fa-Po Chung et al. J Arrhythm. .

Abstract

Nonischemic cardiomyopathies (NICMs) are composed of variable disease entities, including primary and secondary cardiomyopathies. Determining the etiology of NICM provides pivotal roles of not only the understanding of the individual pathogenesis, but also the clinical management, such as risk stratification, pharmacological treatment, and intervention therapies. Despite the diverse causes of NICM, these cases mostly require clinical attention owing to progressive myocardial injury, resulting in ventricular dysfunction and heart failure. The interaction between the diseased ventricular substrates and systemic/neurophysiological factors contributes to the cornerstones responsible for ventricular arrhythmogenesis and sudden cardiac death (SCD). Prevention of SCD and diminishing ventricular tachyarrhythmias are the important mainstays for the management of NICM patients. Given the understanding of the abnormal ventricular substrates and advancement of navigation systems, radiofrequency catheter ablation (RFCA) has become an adjunctive or alternative strategy for NICM patients who experience drug-refractory ventricular tachycardias (VTs). Successful ablation can frequently be achieved at the expense of an epicardial intervention. A recent study has proven the survival benefits for NICM patients who are free from recurrent VTs after a successful RFCA, regardless of the New York Heart Association (NYHA) functional class status or left ventricular ejection fraction. Additionally, recent evidence has highlighted the better delineation of a diseased myocardium through the incorporation of cardiovascular magnetic resonance imaging (CMRI) and 3D mapping systems, which can facilitate the identification of critical ventricular arrhythmogenic substrates in NICM patients.

Keywords: arrhythmogenic substrate; cardiovascular magnetic resonance imaging; catheter ablation; implantable cardioverter‐defibrillator; sudden cardiac death.

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Figures

Figure 1
Figure 1
Classification of nonischemic cardiomyopathies. The figure was modified from the 2006 contemporary classification of NICM proposed by the AHA, including primary and secondary cardiomyopathies
Figure 2
Figure 2
Delayed enhancement in a patient with DCM. A 62‐year‐old woman with idiopathic dilated cardiomyopathy who experienced syncope and several episodes of nonsustained VT. The CMRI demonstrated dilated LV with a decreased LVEF of 34% and patchy delayed myocardial enhancement at mid‐wall of the basal anteroseptal, basal anterior, and basal anterolateral regions, as well as the subepicardial part of the mid‐anteroseptal region of the LV, which was compatible with the origin of VAs
Figure 3
Figure 3
Integration of a 3D reconstruction of a cardiac CT and electroanatomic mapping to prevent potential injuries to coronary arteries during an epicardial catheter ablation. A, A diagnostic catheter in conjunction with a coronary angiogram (gray) was used to confirm the accuracy of the 3D reconstruction of the cardiac CT (yellow). B, Two white lines represent the safe margin at a distance of 1 cm from the coronary arteries (yellow). Late potentials were recorded in the area close to the left circumflex and right coronary arteries. Preprocedural detailed image processing helps to prevent incidental coronary artery injury
Figure 4
Figure 4
Endocardial and epicardial substrates in a patient with DCM. Endocardial bipolar voltage mapping demonstrated a limited scar/low voltage zone (LVZ) surrounding the peri‐mitral and aortic valve region, whereas unipolar voltage mapping showed an extensive scar/LVZ. The unipolar scar/LVZ area was compatible with the epicardial bipolar substrates. Several very late potentials were recorded at the epicardial peri‐mitral region (green dashed circle) using a multi‐electrode catheter (Pentaray)
Figure 5
Figure 5
Stepwise approaches of localization and ablation of VTs in patients with NICM in our laboratory. For hemodynamically stable VTs, both activation mapping and entrainment provide an accurate identification of the critical isthmus, whereas substrate mapping based on the complete elimination of any abnormal electrograms is the most acceptable strategy for those with nontolerable VT. Single and a combination of substrate modification strategies are used to achieve complete elimination of abnormal electrograms

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