Novel insights into the substrate involved in maintenance of ventricular fibrillation: results from continuous multipolar mapping in a canine model.

BACKGROUND: While the triggers for ventricular fibrillation (VF) are well-known, the substrate required for its maintenance remains elusive. We have previously demonstrated dynamic spatiotemporal changes across VF from electrical induction of VF to asystole. Those data suggested that VF drivers seemed to reside in the distal RV and LV. However, signals from these areas were not recorded continuously. The aim of this study was to map these regions of significance with stationary basket electrodes from induction to asystole to provide further insights into the critical substrate for VF rhythm sustenance in canines. METHODS: In six healthy canines, three multipolar basket catheters were positioned in the distal right ventricle (RV), RV outflow tract, and distal left ventricle (LV), and remained in place throughout the study. VF was induced via direct current application from an electrophysiologic catheter. Surface and intracardiac electrograms were recorded simultaneously and continuously from baseline, throughout VF, and until asystole, in order to get a complete electrophysiologic analysis of VF. Focused data analysis was also performed via two defined stages of VF: early VF (immediately after induction of VF to 10 min) and late VF (after 10 min up to VF termination and asystole). RESULTS: VF was continuously mapped for a mean duration of 54 ± 9 min (range 42-70 min). Immediately after initiation of VF in the early phase, the distal LV region appeared to drive the maintenance of VF. Towards the terminal stage of VF, the distal RV region appeared to be responsible for VF persistence. In all canines, we noted local termination of VF in the LV, while VF on surface ECG continued; conversely, subsequent spontaneous termination of VF in the RV was associated with termination of VF on surface ECG into a ventricular escape rhythm. Continuous mapping of VF showed trends towards an increase in peak-to-peak ventricular electrogram cycle length (p = 0.06) and a decrease in the ventricular electrogram amplitude (p = 0.06) after 40 min. Once we could no longer discern surface QRS activity, we demonstrated local ventricular myocardial capture in both the RV and LV but could not reinitiate sustained VF despite aggressive ventricular burst pacing. CONCLUSIONS: This study describes the evolution of VF from electrical initiation to spontaneous VF termination without hemodynamic support in healthy canines. These data are hypothesis-generating and suggest that critical substrate for VF maintenance may reside in both the distal RV and LV depending on stage of VF. Further studies are needed to replicate these findings with hemodynamic support and to translate such findings into clinical practice. Ventricular fibrillation maintenance may be dependent on critical structures in the distal RV. ECG: electrocardiogram; LV: left ventricle; RV: right ventricle; RVOT: right ventricular outflow tract; VF: ventricular fibrillation.

Electrocardiographic markers of cardiac resynchronization therapy response: delayed time to intrinsicoid deflection onset in lateral leads.

Cardiac resynchronization therapy (CRT) has emerged as an important intervention for patients with heart failure (HF) with reduced ejection fraction and delayed ventricular activation. In these patients, CRT has demonstrated to improve quality of life, promote reverse left ventricular (LV) remodeling, reduce HF hospitalizations, and extend survival. However, despite advancements in our understanding of CRT, a significant number of patients do not respond to this therapy. Several invasive and non-invasive parameters have been assessed to predict response to CRT, but the electrocardiogram (ECG) has remained as the prevailing screening method albeit with limitations. Ideally, an accurate, simple, and reproducible ECG marker or set of markers would dramatically overcome the current limitations. We describe the clinical utility of an old ECG parameter that can estimate ventricular activation delay: the onset to intrinsicoid deflection (ID). Based on the concept of direct measurement of ventricular activation time (intrinsic deflection onset), time to ID onset measures on the surface ECG the time that the electrical activation time takes to reach the area subtended by the corresponding surface ECG lead. Based on this principle, the time to ID on the lateral leads can estimate the delay activation to the lateral LV wall and can be used as a predictor for CRT response, particularly in patients with non-specific intraventricular conduction delay or in patients with left bundle branch block and QRS < 150 ms. The aim of this review is to present the current evidence and potential use of this ECG parameter to estimate LV activation and predict CRT response.

Characteristics and long term outcomes of patients with acute coronary syndromes due to culprit left main coronary artery disease treated with percutaneous coronary intervention.

BACKGROUND: Patients with acute coronary syndrome (ACS) due to unprotected culprit left main coronary artery disease (LMCAD) treated with percutaneous coronary intervention (PCI) are rare, high-risk, and not represented in trials. Data regarding long term outcome after PCI are limited. METHODS: Between January 2000 and December 2014, there were 8,794 patients hospitalized with unstable angina/non-ST elevation myocardial infarction (UA/NSTEMI) or ST-elevation myocardial infarction (STEMI) treated with PCI at our institution; of these, 83 (0.94%) patients were identified as having culprit LMCAD ACS. RESULTS: Of the 83 patients with unprotected LMCAD ACS, 40 patients presented with STEMI and 43 patients presented with UA/NSTEMI. As compared to LM UA/NSTEMI, LM STEMI patients were younger and had less hypertension, with a trend towards greater frequency of cardiogenic shock. Distal LM involvement was common in both groups and did not differ by ACS type. In-hospital mortality was 33% in LM STEMI and 9% in LM UA/NSTEMI (P = .009). Over median follow up of 6.3 years, long term survival rates in both groups were similar (46% for STEMI vs 51% for UA/NSTEMI; P = .50 by log-rank). CONCLUSIONS: Unprotected culprit LMCAD ACS necessitating PCI is uncommon, occurring in <1% of cases, but is associated with reduced survival, with long term follow-up noting continued and similar risk of death regardless of index ACS type.

ST-Segment Elevation Myocardial Infarction and Normal Coronary Arteries after Consuming Energy Drinks.

The use of energy drinks, which often contain stimulants, is common among young persons, yet there have been few reports of adverse cardiac events. We report the case of a 27-year-old man who was admitted to our facility with an acute ST-segment elevation myocardial infarction in the setting of using energy drinks. Angiography revealed no obstructive coronary disease. The patient had elevation of cardiac troponin. Noninvasive testing with echocardiography and cardiac magnetic resonance imaging demonstrated both abnormalities in resting wall motion at the anterior apex along with late gadolinium enhancement of the anterior wall, respectively. The patient also underwent formal invasive evaluation with an intracoronary Doppler study demonstrating normal coronary flow reserve and acetylcholine provocation that excluded endothelial dysfunction and microvascular disease. The patient recovered and has abstained from consuming additional energy drinks with no reoccurrence of symptoms. A review of some of the potential cardiac risks associated with consuming energy drinks is presented.

Outflow tract ventricular tachycardia mapped to the coronary arteries: anatomical correlates and management strategies.

BACKGROUND: The coronary cusps have been well described as a successful site for ablation in patients with symptomatic outflow tract ventricular tachycardia. The earliest site of activation is rarely found at the ostia or into the main coronary arteries. The exact anatomic substrate, diagnostic characteristics, and therapeutic approaches for such instances are poorly understood. METHODS: We retrospectively reviewed outflow tract ventricular arrhythmia (OTVA) ablations done at Mayo Clinic Rochester from 2003 to 2011 (total VT: 414; outflow tract VT: 106). Three cases were identified where the earliest site of activation was not within the cusp but rather at or within the coronary ostia (3/414 for all VT: 0.7%; 3/106 for all OTVT: 2.8%). RESULTS: In 1 patient, the left main coronary artery (LMCA) was found to have electrograms (EGMs) recorded with bipolar mapping that preceded activation in the cusps or the left ventricular outflow tract. In 2 cases, the right coronary ostium and proximal right coronary artery recorded the earliest signals. Intracardiac echocardiographic guidance was used to successfully ablate these arrhythmias targeting the aortic route (1 patient) or the right coronary cusp (2 patients), and essentially isolated the focus of origin from the ventricular outflow tracts. Detailed mapping of surrounding structures, including the atrial appendages, the contralateral outflow tract, and the coronary venous system excluded far-field mapping in the artery as a cause for early activation at the ostial location. Local EGM characteristics suggested an unusually lengthy supravalvar myocardial extension as the likely arrhythmogenic substrate. Ablation was successful without coronary arterial or valvular injury and without valvular or root stenosis. CONCLUSIONS: Endocardial ablation isolating foci of origin in the vicinity of the coronary ostia is a challenging procedure but can be performed safely with appropriate visualization and is effective in the treatment of OTVA.

Left-sided intraventricular conduction delay concealed by right bundle branch block.

The electrocardiograms of a 69-year-old woman with severe heart failure showed a left-sided nonspecific intraventricular conduction delay (QRS duration, 0.13 seconds) characterized by notches and slurrings in the descending part of the R waves in the left precordial leads and in the ascending parts of the S waves in the right precordial leads. Subsequently, a complete right bundle branch block with wider QRS complexes (0.17 seconds) appeared. It is possible to consider that the left-sided nonspecific intraventricular conduction delay was concealed by the greater conduction delay occurring when the complete right bundle branch block was present. This would be in keeping with a previous study using Doppler tissue imaging in which this was postulated but where the corresponding electrocardiograms were not shown.