Mapping and Ablation of Ventricular Fibrillation

Background

Sudden cardiac death (SCD; see Chapter 79 ) remains an important health problem globally, with nearly 350,000 victims per year in the United States and similar rates reported in Europe. Approximately half of SCDs are attributable to ventricular tachycardia (VT) or ventricular fibrillation (VF), with coronary artery disease and various cardiomyopathies as common etiologies. In younger patients, in whom ischemic heart disease is rare, conditions such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular (RV) dysplasia account for a substantial proportion of autopsy-positive SCDs, whereas inherited primary electrical disorders (e.g., idiopathic VF [see Chapter 100], J wave syndromes [see Chapter 99 ], long QT syndrome [see Chapter 96 ], catecholaminergic polymorphic ventricular tachycardia [see Chapter 91 ], and Wolff-Parkinson-White syndrome [see Chapter 74 ]) predominate in autopsy-negative cases. Unfortunately, for many affected individuals, SCD is the first clinical manifestation of their cardiac condition.

VF is believed to be initiated and maintained in several ways (see Chapter 46 ). Premature ventricular complexes (PVCs) are recognized as important triggers, likely by propagating erratically through variably refractory ventricular myocardium, potentially establishing reentrant circuits that give rise to rapid and chaotic ventricular depolarizations, thereby disrupting the coordinated contractile function of the ventricles. As these reentrant wavefronts break into an increasing number of small wavelets, the ventricles are subjected to high-frequency activation and rapidly lose coordinated mechanical function. As cardiac output is effectively lost, myocardial ischemia promptly ensues, establishing a vicious cycle of cardiac electrical instability and mechanical dysfunction that leads to death if not promptly corrected. On surface electrocardiograms (ECGs), VF manifests as a chaotic pattern of ventricular activation. At first, this pattern can be coarse, but it generally becomes finer as ventricular disorganization and metabolic derangements increase.

Current clinical practice guidelines recommend implantation of an implantable cardioverter-defibrillator (ICD) for secondary prevention of SCD and for primary prevention in selected patients deemed at high risk. ICDs, however, generally do not prevent but instead react to VF, thus patients remain at risk for recurrent VF, ICD shocks, and electrical storms. Therapeutic strategies to safely prevent VF initiation or maintenance are therefore preferable to therapies that solely terminate it once established. Ongoing advances in our understanding of the mechanisms and substrates of this arrhythmia, in part attributable to improvements in invasive and noninvasive electroanatomic mapping technologies, are rendering this prospect increasingly realistic.

In recent years, we and colleagues have identified and characterized VF triggers and drivers using noninvasive (see Chapter 68 ) and invasive mapping during sinus rhythm and VF in various patient populations at risk for arrhythmic SCD. Preliminary results demonstrate that VF drivers can be mapped using frequency, activation, and phase mapping, yielding insights into different VF phenotypes. We and others have shown that in patients with J wave syndromes (including early repolarization syndrome [ERS] and Brugada syndrome [BrS]), these drivers tend to cluster in distinct regions, suggesting that localized rather than widespread tissue abnormalities exist in this population. Similar findings were observed in patients with idiopathic VF. Detailed invasive mapping of the ventricular endocardium and epicardium have identified discrete areas with low-amplitude and fractionated electrograms (EGMs) in close proximity to these VF driver regions, suggesting that meaningful, albeit sometimes subtle, structural abnormalities exist in these regions and may play important roles in the genesis or maintenance of VF. Ablation of these sites has been associated with promising results. We herein review key mechanistic insights into VF gained from preclinical and early clinical mapping studies, present an overview of contemporary VF mapping and ablation strategies, and discuss VF mapping and ablation data specific to several cardiac conditions.

Mechanistic Insights from Ventricular Fibrillation Mapping