Management of ventricular arrhythmias in heart failure: Current perspectives

Figures

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  Figure 1. Substrate mapping using a multipolar catheter in a patient after previous anterior myocardial infarction. A: Bipolar voltage map of the left ventricle in the right anterior oblique view. Voltage is color-coded, with violet representing healthy tissue and gray color dense scar. B: Activation map during sinus rhythm. Blue color corresponds to the late activated regions and areas of late potentials (arrow). A set of ablation lesions encircling the anterior scar led to the elimination of late potentials and suppressed ventricular tachycardia inducibility.

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  Figure 2. Ablation of an electrical storm caused by recurrent episodes of polymorphic ventricular tachycardia/ventricular fibrillation (pVT/VF) in a patient after inferior myocardial infarction. A: Multiple episodes of pVT/VF requiring repeated shocks. All episodes were triggered by monomorphic premature ventricular contractions (triggering beat). B: The electrocardiogram morphology of the triggering beat. C: An electroanatomical voltage map of the left ventricle in the right anterior oblique view. The map shows localized scar in the posteroseptal region of the left ventricle; sites with conduction system were marked by yellow tags. The triggering ectopy was localized to the border zone of the scar area (arrow). Elimination of the triggering ectopy suppressed the episodes of pVT/VF.

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  Figure 3. Epicardial mapping and ablation in a patient with nonischemic cardiomyopathy. A: Cardiac magnetic resonance image with late gadolinium enhancement located dominantly in the epicardial circumference of the left ventricle (LV). The endocardium is spared. B: Puncture of the epicardial space using percutaneous subxiphoid access. Tenting of the parietal pericardium is marked by a small amount of contrast media. C: Electroanatomical voltage map in the inferior view. Large areas of late potentials (arrow) were located and abolished by radiofrequency ablation (red dots). RV = right ventricle.

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  Figure 4. Stereotactic body radioablation for refractory ventricular tachycardia (VT) in patient with nonischemic cardiomyopathy. A: Electroanatomical voltage map of the left ventricle in the left lateral view. Despite endo-epicardial radiofrequency ablation, VTs were still inducible. B: Integration of the electroanatomical map with planning computed tomography image with highlighted target for radioablation (red color). C: Prescribed radiotherapy doses.

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  Figure 5. A: Ventricular bigeminy interfering with cardiac resynchronization therapy. The ectopic focus was successfully eliminated by catheter ablation on the basal left ventricular septum, which restored biventricular pacing to 100% (B) and led to improvement of left ventricular ejection fraction.

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  Figure 6. Resting electrocardiogram in a patient with multifocal ectopic Purkinje-related premature ventricular contractions (PVCs). The typical feature of multifocal ectopic Purkinje-related PVCs is that the PVCs are very “narrow” and may be mistaken for aberrant conduction of premature atrial beats. The underlying mechanism is pathogenic mutations in the SCN5A gene, which leads to a gain of function of the sodium channel and hyperexcitability of the fascicular-Purkinje system. The high burden of ventricular ectopy led to PVC-induced cardiomyopathy. The treatment with hydroquinidine suppressed the ectopy and improved left ventricular ejection fraction.

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  Figure 7. Catheter ablation of recurrent ventricular tachycardia in a patient after implantation of the left ventricular assist device. A: Electroanatomical map of the left ventricle in the right oblique view. Arrow marks the location of the inflow cannula. B: Fluoroscopic image with an ablation catheter inserted transseptally in the left ventricle close to the inflow cannula. C: Position of the ablation catheter close to the inflow cannula shown by intracardiac echocardiography.