Abstract
Aims
Heterogeneous tissue channels (HTCs) detected by late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) are related to ventricular arrhythmias, but there are few published ...data about their arrhythmogenic characteristics.
Methods and results
We enrolled 34 consecutive patients with ischaemic and non-ischaemic cardiomyopathy who were referred for ventricular tachycardia (VT) ablation. LGE-CMR was performed prior to ablation, and the HTCs were analyzed. Arrhythmogenic HTCs linked to induced VT were identified during the VT ablation procedure. The characteristics of arrhythmogenic HTCs were compared with those of non-arrhythmogenic HTCs. Three patients were excluded due to low-quality LGE-CMR images. A total of 87 HTCs were identified on LGE-CMR in 31 patients (age:63.8 ± 12.3 years; 96.8% male; left ventricular ejection fraction: 36.1 ± 10.7%). Of the 87 HTCs, only 31 were considered arrhythmogenic because of their relation to a VT isthmus. The HTCs related to a VT isthmus were longer 64.6 ± 49.4 vs. 32.9 ± 26.6 mm; OR: 1.02; 95% CI: (1.01–1.04); P < 0.001 and had greater mass 2.5 ± 2.2 vs. 1.2 ± 1.2 grams; OR: 1.62; 95% CI: (1.18–2.21); P < 0.001, a higher degree of protectedness 26.19 ± 19.2 vs. 10.74 ± 8.4; OR 1.09; 95% CI: (1.04–1.14); P < 0.001, higher transmurality number of wall layers with CCs: 3.8 ± 2.4 vs. 2.4 ± 2.0; OR: 1.31; 95% CI: (1.07–1.60); P = 0.008 and more ramifications 3.8 ± 2.0 vs. 2.7 ± 1.1; OR: 1.59; 95% CI: (1.15–2.19); P = 0.002 than non-arrhythmogenic HTCs. Multivariate logistic regression analysis revealed that protectedness was the strongest predictor of arrhythmogenicity.
Conclusion
The protectedness of an HTC identified by LGE-CMR is strongly related to its arrhythmogenicity during VT ablation.
Graphical Abstract
Graphical Abstract
Left bundle branch block (LBBB) is not just a simple electrocardiogram alteration. The intricacies of this general terminology go beyond simple conduction block. This review puts together current ...knowledge on the historical concept of LBBB, clinical significance, and recent insights into the pathophysiology of human LBBB. LBBB is an entity that affects patient diagnosis (primary conduction disease, secondary to underlying pathology or iatrogenic), treatment (cardiac resynchronization therapy or conduction system pacing for heart failure), and prognosis. Recruiting the left bundle branch with conduction system pacing depends on the complex interaction between anatomy, site of pathophysiology, and delivery tools.
Predicting sudden cardiac death risk in the first months after ST-segment elevation myocardial infarction (STEMI) remains challenging.
The purpose of this study was to investigate the ability of late ...gadolinium enhancement cardiac magnetic resonance (LGE-CMR) to identify the potentially arrhythmogenic substrate and its temporal evolution after STEMI.
One hundred consecutive patients with a first STEMI were included. Three-dimensional high-resolution LGE-CMR was obtained at 3 T on days 7 and 180. Left ventricular wall was segmented and characterized by pixel signal intensity algorithm in 5 layers from endocardium to epicardium. A 3-dimensional color-coded shell map was obtained for each layer, depicting scar core and border zone (BZ) distribution. Presence and characteristics of BZ channels were registered for each layer.
At 180 days, left ventricular ejection fraction had improved significantly (from 46.7% ± 10% to 51.5% ± 10%; P <.001) and scar mass was reduced (from 22.6 ± 20 g to 13.8 ± 12 g; P <.001). Most BZ channels (89%) were identified in the same myocardial layer and American Heart Association (AHA) segment, with the same orientation and morphology in both studies. Early LGE-CMR had 96% sensitivity and 90% specificity for predicting presence of BZ channels at 180 days. Greater presence was observed in patients with no-reflow phenomenon at baseline (P = .01).
Most BZ channels can be identified by LGE-CMR at day 7 post-STEMI and, despite scar mass reduction, remain unaltered at 6 months, suggesting that the potentially arrhythmogenic substrate is established within the first week post-STEMI.
Atrial fibrillation (AF) is a frequent comorbidity in patients with pacemaker and is a recognized cause of mortality, morbidity, and quality-of-life impairment. The international MINimizE Right ...Ventricular pacing to prevent Atrial fibrillation and heart failure trial established that atrial preventive pacing and atrial antitachycardia pacing (DDDRP) in combination with managed ventricular pacing (MVP) reduce permanent AF occurrence in comparison with standard dual-chamber pacing (DDDR).
We aimed to determine the role of new-generation atrial antitachycardia pacing (Reactive ATP) in preventing AF disease progression.
Patients with dual-chamber pacemaker and with previous atrial tachyarrhythmias were randomly assigned to DDDR (n = 385 (33%)), MVP (n = 398 (34%)), or DDDRP+MVP (n = 383 (33%)) group. The incidence of permanent AF, as defined by the study investigator, or persistent AF, defined as ≥7 consecutive days with AF, was estimated using the Kaplan-Meier method, while its association with patients’ characteristics was evaluated via multivariable Cox regression.
At 2 years, the incidence of permanent or persistent AF was 26% (95% confidence interval CI 22%–31%) in the DDDR group, 25% (95% CI 21%–30%) in the MVP group, and 15% (95% CI 12%–20%) in the DDDRP+MVP group (P < .001 vs DDDR; P = .002 vs MVP). Generalized estimating equation–adjusted Reactive ATP efficacy was 44.4% (95% CI 41.3%–47.6%). Multivariate modeling identified high Reactive ATP efficacy (>44.4%) as a significant predictor of reduced permanent or persistent AF risk (hazard ratio 0.32; 95% CI 0.13–0.781; P = .012) and episodes’ characteristics, such as long atrial arrhythmia cycle length, regularity, and the number of rhythm transitions, as predictors of high ATP efficacy.
In patients with bradycardia, DDDRP+MVP delays AF disease progression, with Reactive ATP efficacy being an independent predictor of permanent or persistent AF reduction.
Purpose
This study was conducted to test, in mountain running route conditions, the accuracy of the Polar V800™ monitor as a suitable device for monitoring the heart rate variability (HRV) of ...runners.
Method
Eighteen healthy subjects ran a route that included a range of running slopes such as those encountered in trail and ultra-trail races. The comparative study of a V800 and a Holter SEER 12 ECG Recorder™ included the analysis of RR time series and short-term HRV analysis. A correction algorithm was designed to obtain the corrected Polar RR intervals. Six 5-min segments related to different running slopes were considered for each subject.
Results
The correlation between corrected V800 RR intervals and Holter RR intervals was very high (
r
= 0.99,
p
< 0.001), and the bias was less than 1 ms. The limits of agreement (LoA) obtained for SDNN and RMSSD were (− 0.25 to 0.32 ms) and (− 0.90 to 1.08 ms), respectively. The effect size (ES) obtained in the time domain HRV parameters was considered small (ES < 0.2). Frequency domain HRV parameters did not differ (
p
> 0.05) and were well correlated (
r
≥ 0.96,
p
< 0.001).
Conclusion
Narrow limits of agreement, high correlations and small effect size suggest that the Polar V800 is a valid tool for the analysis of heart rate variability in athletes while running high endurance events such as marathon, trail, and ultra-trail races.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Some ventricular tachycardias (VTs) originating from the epicardium are not suitable for endocardial radiofrequency ablation and require an epicardial approach. The aim of this study was to define ...the ECG characteristics that may identify an epicardial origin of VTs.
We analyzed the 12-lead ECG recordings during epicardial and endocardial left ventricular pacing in 9 patients to verify the hypothesis that the epicardial origin of the ventricular activation widens the initial part of the QRS complex. Then, we analyzed the ECG pattern in 14 VTs successfully ablated from the epicardium after a failed endocardial approach (group A), in 27 VTs successfully ablated from the endocardium (group B), and in 28 additional VTs that could not be ablated from the endocardium (group C). Four distinct intervals of ventricular activation were defined and measured: (1) the pseudodelta wave, (2) the intrinsicoid deflection time in V2, (3) the shortest RS complex, and (4) the QRS complex. VTs from groups A and C showed a significantly longer pseudodelta wave, intrinsicoid deflection time, and RS complex duration compared with VTs of group B. There was no difference between groups A and C. A pseudodelta wave of > or =34 ms has a sensitivity of 83% and a specificity of 95%, an intrinsicoid deflection time of > or =85 ms has a sensitivity of 87% and a specificity of 90%, and an RS complex duration of > or =121 ms has a sensitivity of 76% and a specificity of 85% in identifying an epicardial origin of the VTs.
ECG suggests VTs originating from the epicardium and those with an unsuccessful radiofrequency ablation from the endocardium.
Ventricular tachycardia (VT) substrate-based ablation has become the gold standard treatment for patients with structural heart disease–related VT. VT is linked to re-entry in relation to myocardial ...scarring, with areas of conduction block (core scar) and of slow conduction (border zone). Slow conduction areas can be detected in sinus rhythm as late potentials (LPs). LP abolition has been shown to be the best end point to avoid long-term recurrences. Our study aimed to analyze the challenges of LP abolition and the predictors of failure. We analyzed 169 consecutive patients with structural heart disease (61% ischemic cardiomyopathy, left ventricular ejection fraction: 37 ± 13%) who underwent VT ablation between 2013 and 2018. A preprocedural clinical evaluation, including cardiac magnetic resonance, was done in 66% of patients. Electroanatomical mapping with the identification of LPs was performed in all patients. Noninducibility was achieved in 71% (119), and complete LP abolition was achieved in 61% (103) of patients. Incomplete LP abolition was a powerful predictor of VT recurrence (67% vs 33%, hazard ratio 3.19 2.1 to 4.7; p <0.001). Lack of use of a high-density mapping catheter (odds ratio 6.2, 1.2 to 38.1; p = 0.028), the septal substrate (odds ratio 9.34, 2.27 to 38.4; p = 0.002), and larger left ventricular mass (190 ± 58 g vs 156 ± 46 g, p = 0.002) were predictors of incomplete LP abolition. The main reasons that contributed to unsuccessful LP abolition were anatomic obstacles (such as the conduction system) and large extension of the LP area. In conclusion, incomplete LP abolition is related to VT recurrence. Lack of use of a high-density mapping catheter, the septal substrate, and larger left ventricular mass are related to incomplete LP abolition.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Arrhythmogenic right ventricular (RV) remodeling has been reported in response to regular training, but it remains unclear how exercise intensity affects the presence and extent of such remodeling. ...We aimed to assess the relationship between RV remodeling and exercise load in a long-term endurance training model. Wistar rats were conditioned to run at moderate (MOD; 45 min, 30 cm/s) or intense (INT; 60 min, 60 cm/s) workloads for 16 wk; sedentary rats served as controls. Cardiac remodeling was assessed with standard echocardiographic and tissue Doppler techniques, sensor-tip pressure catheters, and pressure-volume loop analyses. After MOD training, both ventricles similarly dilated (~16%); the RV apical segment deformation, but not the basal segment deformation, was increased apical strain rate (SR): -2.9 ± 0.5 vs. -3.3 ± 0.6 s
, SED vs. MOD. INT training prompted marked RV dilatation (~26%) but did not further dilate the left ventricle (LV). A reduction in both RV segments' deformation in INT rats (apical SR: -3.3 ± 0.6 vs. -3.0 ± 0.4 s
and basal SR: -3.3 ± 0.7 vs. -2.7 ± 0.6 s
, MOD vs. INT) led to decreased global contractile function (maximal rate of rise of LV pressure: 2.53 ± 0.15 vs. 2.17 ± 0.116 mmHg/ms, MOD vs. INT). Echocardiography and hemodynamics consistently pointed to impaired RV diastolic function in INT rats. LV systolic and diastolic functions remained unchanged in all groups. In conclusion, we showed a biphasic, unbalanced RV remodeling response with increasing doses of exercise: physiological adaptation after MOD training turns adverse with INT training, involving disproportionate RV dilatation, decreased contractility, and impaired diastolic function. Our findings support the existence of an exercise load threshold beyond which cardiac remodeling becomes maladaptive.
Exercise promotes left ventricular eccentric hypertrophy with no changes in systolic or diastolic function in healthy rats. Conversely, right ventricular adaptation to physical activity follows a biphasic, dose-dependent, and segmentary pattern. Moderate exercise promotes a mild systolic function enhancement at the right ventricular apex and more intense exercise impairs systolic and diastolic function.
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