Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
Ventricular tachycardia [keywords]
- Ischemic ventricular tachycardia presenting as a narrow complex tachycardia. [Journal Article]
- Indian Pacing Electrophysiol J 2014 Jul; 14(4):203-10.
This report describes a patient presenting with a narrow complex tachycardia in the context of prior myocardial infarction and impaired ventricular function. Electrophysiological studies confirmed ventricular tachycardia and activation and entrainment mapping demonstrated a critical isthmus within an area of scar involving the His-Purkinje system accounting for the narrow QRS morphology. This very rare case shares some similarities with upper septal ventricular tachycardia seen in patients with structurally normal hearts, but to our knowledge has not been seen previously in patients with ischemic heart disease.
- Increased Phosphorylation of Ca(2+) Handling Proteins as a Proarrhythmic Mechanism in Myocarditis. [JOURNAL ARTICLE]
- Circ J 2014 Jul 24.
Background:Because fatal arrhythmia is an important cause of death in patients with myocarditis, we investigated the proarrhythmic mechanisms of experimental autoimmune myocarditis.Methods and Results:Myocarditis was induced by injection of 2 mg porcine cardiac myosin into the footpads of adult Lewis rats on days 1 and 8 (Myo, n=15) and the results compared with Control rats (Control, n=15). In an additional 15 rats, 6 mg/kg prednisolone was injected into the gluteus muscle before the injection of porcine cardiac myosin on days 1 and 8 (MyoS, n=15). Hearts with myocarditis had longer action potential duration (APD), slower conduction velocity (CV; P<0.01 vs. Control), higher CV heterogeneity, greater fibrosis, higher levels of immunoblotting of high-mobility group protein B1, interleukin 6 and tumor necrosis factor-α proteins. Steroid treatment partially reversed the translations for myocarditis, CV heterogeneity, reduced APD at 90% recovery to baseline, increased CV (P<0.01), and reversed fibrosis (P<0.05). Programmed stimulation triggered sustained ventricular tachycardia in Myo rats (n=4/5), but not in controls (n=0/5) or Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) inhibitor (KN93) treated Myo rats (n=0/5, P=0.01). CaMKII autophosphorylation at Thr287 (201%), and RyR2 phosphorylation at Ser2808 (protein kinase A/CaMKII site, 126%) and Ser2814 (CaMKII site, 21%) were increased in rats with myocarditis and reversed by steroid.Conclusions:The myocarditis group had an increased incidence of arrhythmia caused by increased phosphorylation of Ca(2+)handling proteins. These changes were partially reversed by an antiinflammatory treatment and CaMKII inhibition.
- Detection of T-Wave Beat-By-Beat Variations prior to Ventricular Arrhythmias Onset in ICD-Stored Intracardiac Electrograms: The Endocardial T-Wave Alternans Study (ETWAS). [JOURNAL ARTICLE]
- Pacing Clin Electrophysiol 2014 Jul 23.
The aim of the Endocardial T-Wave Alternans Study was to prospectively assess the presence of T-wave alternans (TWA) or beat-to-beat repolarization changes on implantable cardioverter-defibrillator (ICD)-stored electrograms (EGMs) immediately preceding the onset of spontaneous ventricular tachycardia (VT) or fibrillation (VF).Thirty-seven VT/VF episodes were compared to 116 baseline reference EGMs from the same 57 patients. A Bayesian model was used to estimate the T-wave waveform in each cardiac beat and a set of 10 parameters was selected to segment each detected T wave. Beat-by-beat differences in each T-wave parameter were computed using the absolute value of the difference between each beat and the following one. Fisher criterion was used for determining the most discriminant T-wave parameters, then top-M ranked parameters yielding a normalized cumulative Fisher score > 95% were selected, and analysis was applied on these selected parameters. Simulated TWA EGMs were used to validate the algorithm.In the simulation study, TWA was detectable even in the case of the smallest simulated alternans of 25 μV. In 13 of the 37 episodes (35%) occurring in nine of 16 patients, significant larger beat-to-beat variations before arrhythmia onset were detected compared to their respective references (median one positive episode per patient). Parameters including the T-wave apex amplitude seem the more discriminant parameters.Detection of beat-by-beat repolarization variations in ICD-stored EGMs is feasible in a significant subset of cases and may be used for predicting the onset of ventricular arrhythmias.
- The Asymptomatic Wolff-Parkinson-White Patient: Time to be More Proactive? [JOURNAL ARTICLE]
- Circulation 2014 Jul 22.
It is well known by now that sudden cardiac death (SCD) may occur even in the asymptomatic individual with Wolff-Parkinson-White (WPW) pattern(1). This is related to the occurrence of atrial fibrillation (AF) with a rapid ventricular response leading to ventricular fibrillation (VF). The essential and critical risk factor is the presence of an accessory pathway(s) (AP) with critically short antegrade refractoriness. The most common numeric in the literature reflecting this is shortest RR interval between pre-excited cycles <250 ms (SPRRI) in AF. The risk of SCD in the individual with asymptomatic WPW has been estimated to be low, in the range of 0.05-0.2% per year(1), a risk that can obviously be eliminated with successful, uncomplicated catheter ablation. These facts are not in dispute. The controversy that remains is related simply to the fact that population wide electrophysiological assessment and ablation cannot be carried out without risk of complications and even mortality that can mitigate the benefit and broad screening and electrophysiologically based management would be very costly(2). Current guidelines reflect this(3) by suggesting that electrophysiological assessment with a view to ablation is reasonable when a well-informed patient chooses the small risk of ablation over a small risk due to the natural history (2A recommendation) depending on their individual circumstances. Further, there is little advocacy in the guidelines for large-scale population screening. Do we now have evidence to support improved clinical outcomes for electrophysiological assessment with a view to ablation in all individuals with the WPW pattern in the general population?
- CMR-Based Identification of Critical Isthmus Sites of Ischemic and Nonischemic Ventricular Tachycardia. [JOURNAL ARTICLE]
- JACC Cardiovasc Imaging 2014 Jul 9.
This study evaluates whether contrast-enhanced (CE) cardiac magnetic resonance (CMR) can be used to identify critical isthmus sites for ventricular tachycardia (VT) in ischemic and nonischemic heart disease.Fibrosis interspersed with viable myocytes may cause re-entrant VT. CE-CMR has the ability to accurately delineate fibrosis.Patients who underwent VT ablation with CE-CMR integration were included. After the procedure, critical isthmus sites (defined as sites with a ≥11 of 12 pacemap, concealed entrainment, or VT termination during ablation) were projected on CMR-derived 3-dimensional (3D) scar reconstructions. The scar transmurality and signal intensity at all critical isthmus, central isthmus, and exit sites were compared to the average of the entire scar. The distance to >75% transmural scar and to the core-border zone (BZ) transition was calculated. The area within 5 mm of both >75% transmural scar and the core-BZ transition was calculated.In 44 patients (23 ischemic and 21 nonischemic, left ventricular ejection fraction 44 ± 12%), a total of 110 VTs were induced (cycle length 290 ± 67 ms). Critical isthmus sites were identified for 78 VTs (71%) based on ≥11 of 12 pacemaps (67 VTs), concealed entrainment (10 VTs), and/or termination (30 VTs). The critical isthmus sites, and in particular central isthmus sites, had high scar transmurality and signal intensity compared with the average of the entire scar. Of the pacemap, concealed entrainment, and termination sites, 74%, 100%, and 84% were within 5 mm of >75% transmural scar, and 67%, 100%, and 94% were within 5 mm of the core-BZ transition, respectively. The areas within 5 mm of both >75% transmural scar and the core-BZ transition (median 13% of LV) contained all concealed entrainment sites and 77% of termination sites.Both in ischemic and nonischemic VT, critical isthmus sites are typically located in close proximity to the CMR-derived core-BZ transition and to >75% transmural scar. These findings suggest that CMR-derived scar characteristics may guide to critical isthmus sites during VT ablation.
- Complications in the clinical course of tako-tsubo cardiomyopathy. [JOURNAL ARTICLE]
- Int J Cardiol 2014 Jul 11.
This study evaluated the frequency, severity and outcome of complications in the clinical course of tako-tsubo cardiomyopathy (TTC).TTC is regarded as a benign disease since left ventricular (LV) function returns to normal within a short time. However, severe complications have been reported in selected patients.From 37 hospitals, 209 patients (189 female, age 69±12years) were prospectively included in a TTC registry.Complications developed in 108/209 patients (52%); 23 (11%) had >2 complications. Complications occurred median 1day after symptom onset, and 77% were seen within 3days. Arrhythmias were documented in 45/209 patients (22%) including atrial fibrillation in 32 (15%) and ventricular tachycardia in 17 (8%). Of 8 patients resuscitated (4%), 6 survived. Additional complications were right ventricular involvement (24%), pulmonary edema (13%), cardiogenic shock (7%), transient intraventricular pressure gradients (5%), LV thrombi (3%) and stroke (1%). During hospitalization, 5/209 patients (2.5%) died. Patients with complications were older (70±13 vs 67±10years, p=0.012), had a higher heart rate (91±26 vs 83±19/min, p=0.025), more frequently Q\ waves on the admission ECG (36% vs 21%, p=0.019) and a lower LV ejection fraction (47±15 vs 54±14%, p=0.002). Multivariate regression analysis identified Q-waves on admission (OR 2.49, 95% CI 1.23-5.05, p=0.021) and ejection fraction ≤30% (OR 4.03, 95% CI 1.04-15.67, p=0.022) as independent predictors for complications.TTC may be associated with severe complications in half of the patients. Since the majority of complications occur up to day 3, monitoring is advisable for this time period.
- Sudden Death in Adult Congenital Heart Disease: Risk Stratification in 2014. [JOURNAL ARTICLE]
- Heart Rhythm 2014 Jul 18.
Arrhythmias and sudden death continue to plague a subset of adult patients with congenital heart disease. Despite investigative efforts spanning many decades, accurate identification of the high-risk patient remains challenging owing to a limited population size, relatively low event rate, and constantly evolving surgical approaches to the various malformations. Furthermore, until recently, most studies of the subject involved single center formats with limited statistical power. The number of adult survivors has now reached a critical size where larger collaborative projects are beginning to generate more objective criteria for assessing risk. This review will provide an update on risk-stratification for several of the major congenital cardiac lesions, and outline the current recommendations for surveillance and management.
- Interatrial differences of basal molecular set-up and changes in tachycardia-induced heart failure-a proteomic profiling study. [JOURNAL ARTICLE]
- Eur J Heart Fail 2014 Jul 12.
Left and right atria show compelling differences regarding organogenesis and specific clinical diseases. In congestive heart failure (CHF), remodelling of the atria occurs leading to increased arrhythmogenic susceptibility and deterioration of clinical symptoms. We aimed to assess the basal left and right atrial molecular set-up and different chamber-specific atrial changes in heart failure.We combined an animal model of rapid ventricular pacing induced heart failure in the rabbit and a gel-based proteomic screening of left and right atrial specimen. A gene ontology over-representation analysis was performed for biological function. Ultrastructural adaptations were evaluated using transmission electron microscopy. Comparing left and right atria of healthy control animals (CTRL), 39 proteins displayed significant expression differences involving various biological functions. Upon further statistical analyses, four pathways of energy metabolism were confirmed to be significantly over-represented beneath the other biological processes. Rapid ventricular pacing induced severe left ventricular systolic dysfunction, symptomatic heart failure and a macroscopic atrial remodelling. In CHF versus CTRL, metabolic and antioxidative enzymes were differentially expressed and showed chamber-specific bidirectional alterations. Transmission electron microscopy visualized a remarkable and again chamber-specific ultrastructural disturbance of mitochondrial morphology.Our data indicate a diverging basal left and right atrial molecular set-up in the adult healthy heart. In addition, metabolic and antioxidative enzymes are profoundly and chamber-specifically altered during atrial remodelling in progressive heart failure.
- Prevalence and Significance of Rare Ryr2 Variants in Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia: Results of a Systematic Screening. [JOURNAL ARTICLE]
- Heart Rhythm 2014 Jul 17.
Arrhythmogenic right ventricular Cardiomyopathy/Dysplasia (ARVC/D) is a genetic disease predominantly caused by desmosomal gene mutations that account for only ~50% of cases. RYR2 gene mutations usually cause Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) but have been associated with peculiar phenotype named ARVC2.We aim to determine the prevalence and phenotype associated with RYR2 mutations in a large ARVC/D population.We analyzed the whole RYR2 coding sequence by Sanger sequencing in 64 ARVC/D probands without desmosomal gene mutations.We have identified six rare missense variants p.P1583S, p.A2213S, p.G2367R, p.Y2932H, p.V3219M and p.L4670V. It corresponds to a prevalence of 9% of rare RYR2 variants in ARVC/D population (6 probands/64) that is significantly higher than the estimated rate of rare RYR2 variants in control (Fisher test, p=0.03). Phenotypes associated with RYR2 variants were similar to desmosome-related ARVC/D, associating typical ECG abnormalities at rest, frequent monomorphic ventricular tachycardia, right ventricular dilatation, wall motion abnormalities and fibro-fatty replacement when histopathological examination was available.In this first systematic screening of the whole coding region of the RYR2 gene in a large ARVC/D cohort without mutation in desmosomal genes, we show that putative RYR2 mutations are frequent (9% of ARVC/D probands) and are associated with a conventional phenotype of ARVC/D, in contrast with previous findings. The results support the role of RYR2 gene in conventional ARVC/D.