Mapping and ablation procedures for the treatment of ventricular tachycardia

<p><b>Introduction:</b> Ventricular tachycardia (VT) may occur in the presence or absence of structural heart disease. Given that the management of VT hinges on the presence of symptoms and risk of sudden cardiac death (SCD), the main treatment goals are elimination of symptoms (including frequent implantable cardioverter defibrillator [ICD] therapies) and prevention of SCD. Unfortunately, medical management is suboptimal in a significant proportion of patients. As such, ablative therapy plays a prominent role in the treatment of ventricular tachycardia.</p> <p><b>Areas covered:</b> In this review, we will discuss various VT disorders that are encountered in patients with and without structural heart disease. Further, we will highlight salient features regarding mapping and ablation of the various VT syndromes. Finally, we will discuss what lies on the horizon for VT ablation.</p> <p><b>Expert commentary:</b> Meticulous mapping should aim to find the region that is most likely to be successful and least likely to result in a complication. Although recognition of the various mechanisms of VT, familiarity with different methods to mapping and ablation, and awareness of potential limitations of current approaches is critical, a thorough understanding of the fundamental principles and nuances of each facet within EP is required to ensure optimal outcomes for our patients.</p

Pacemaker lead perforation causing hemopericardium eight years after implantation

The number of patients with intracardiac devices, including permanent pacemakers and implantable cardioverter-defibrillators is increasing. Lead perforation is a recognized complication which most often occurs during or shortly following pacemaker implantation. Late lead perforation occurring over 30 days after device insertion is a rare, potentially life-threatening complication. We present a case of late lead perforation unmasked greater than eight years after pacemaker implantation by initiation of anticoagulation

Effect of catheter ablation on the hemodynamics of the left atrium : Hemodynamics of ablation

BACKGROUND: This study aims to evaluate the impact of catheter ablation for atrial fibrillation (AF) on left atrial (LA) flow dynamics and geometrical changes. METHODS: This exploratory study included computational flow simulations from 10 patients who underwent catheter ablation for AF. Complete cardiac cycle dataset was simulated before and after ablation using computational fluid dynamics. The study main endpoints were the changes in LA volume, LA velocity, LA wall shear stress (WSS), circulation (Γ), vorticity, pulmonary vein (PV) ostia area, and LA vortices before and after ablation. RESULTS: There was an average decrease in LA volume (11.58 ± 15.17%) and PV ostia area (16.6 ± 21.41%) after ablation. A non-uniform trend of velocity and WSS changes were observed after ablation. Compared with pre-ablation, 4 patients exhibited lower velocities, WSS distributions, and a decreased Γ (\u3e 8.5%), while 6 developed higher velocities and WSS distributions. These geometrical changes dictated different flow mixing in the LA and distinct vortex patterns, characterized by different spinning velocities, vorticities, and rotational directions. Regions with q-criterion \u3e 0 were found to be dominant in the LA, indicating prevalent rotational vortex structures. CONCLUSION: Catheter ablation for AF induced different geometrical changes on the LA and the PVs, therefore influencing flow mixing and vortex patterns in the LA, in addition to overall velocity and WSS distribution. Further exploration of the impact of catheter ablation on intracardiac flow dynamics is warranted to discern patterns that may correlate with clinical outcomes

Mechanistic insights into transient severe mitral regurgitation

<p>Acute mitral regurgitation (AMR), a known complication of acute coronary syndromes, is usually associated with posterior papillary muscle dysfunction/rupture. In severe cases, management of AMR requires surgical intervention. Reversible severe AMR in patients in the absence of left ventricular systolic dysfunction and coronary artery stenosis may result from processes which cause transient subendocardial ischemia, such as intermittent episodes of hypotension or coronary artery vasospasm. We present two cases of reversible transient AMR due to subendocardial and/or endocardial ischemia, both of which offer insight into the mechanism of transient severe AMR.</p