Ventricular Premature Depolarizations Research Articles

Unusual responses of a short RP tachycardia to His-refractory ventricular premature depolarizations: What is the mechanism?

Unusual responses of a short RP tachycardia to His-refractory ventricular premature depolarizations: What is the mechanism?

Left Atrial Mechanical Function And Stiffness In Patients With Premature Ventricular Contraction: A Speckle Tracking Study.

Ventricular extrasystole (PVC) is characterized by premature ventricular depolarization and is associated with increased risk of arrhythmias and structural heart disease. This study aimed to investigate the association between the PVC burden and left atrial (LA) function in individuals without known cardiac disease. A cross-sectional study was conducted on 102 patients with PVCs who were admitted to a cardiology clinic. Transthoracic echocardiography was used to assess left ventricle (LV) parameters, including LV mass, LV ejection fraction (LVEF), LV global longitudinal strain (LVGLS), and LA function was evaluated using strain imaging. The PVC burden was categorized into three groups: <10 %, 10-20 %, and >20 %. Changes in LV dimensions and LV mass index were associated with the groups with the PVC burden with 10-20 %, and >20 %. but differences in LVEF and LVGSL were not significant. Mean E / e' increased as the PVC burden increased (p<0.001). The mean global LA peak strain decreased as the PVC burden increased (p<0.001), while other mean LA measurements increased as the PVC burden increased (p<0.001) A higher PVC burden was associated with impaired LA function, as indicated by decreased global LA peak strain (PVC burden <10 %=38.1±3.2 vs. PVC burden 10-20 %=32.4±3.2 vs. PVC burden >20 %=27.7±2.6, in all groups p<0.001) and with increased LA stiffness (PVC burden <10 %=18.6±3.2 vs. PVC burden 10-20 %=27.5±5.5 vs. PVC burden >20 %=39.0±7.9, in all groups p<0.001). A strong negative correlation was found between global LA peak strain and LA stiffness (r=-0.779, p<0.001). In individuals without known cardiac disease, a higher PVC burden was associated with impaired LA function, indicated by increased E / e', decreased LA strain, and increased LA stiffness. These findings suggest that PVC burden may contribute to LA dysfunction, potentially increasing the risk of cardiovascular events.

Catheter ablation of ventricular premature depolarizations originating from the mid interventricular septum: Significance of electrocardiographic morphology for predicting origin

Ventricular premature depolarizations (VPDs) originating from the mid interventricular septum (IVS) adjacent to the atrioventricular annulus between the His bundle and the coronary sinus ostium (mid IVS VPDs) have not been characterized. The aim of this study was to investigate the electrophysiological characteristics of mid IVS VPDs. Thirty-eight patients with mid IVS VPDs were enrolled. VPDs were divided into different types according to precordial transition of the electrocardiogram (ECG) and QRS morphology in lead V1. Four types of VPDs were divided. The precordial transition zone appeared earlier and earlier from types 1 to 4. The notch in lead V1 moved gradually backward, and its amplitude gradually became higher, resulting in the transition from left to right bundle branch block morphology in lead V1 from types 1 to 4. Based on activation and pace mapping, ablation response, and 3830 electrode pacing morphology in the mid IVS, the 4 types of ECG morphology corresponded to an origin in the right endocardial side, right/mid intramural region, left intramural region, and left endocardial side of the mid IVS, respectively. An intramural origin was identified for 50% of VPDs. Eighty-nine percent of mid IVS VPDs could be eliminated. Bilateral ablation (waiting for delayed efficacy) or bipolar ablation was sometimes needed for intramural VPDs. Mid IVS VPDs were found to have unique electrophysiological characteristics. The ECG characteristics of mid IVS VPDs were important in terms of prediction of its exact origin, the choice of ablation method, and the likelihood of treatment being successful.

Sinus rhythm electrocardiographic abnormalities, sites of origin, and ablation outcomes of ventricular premature depolarizations initiating ventricular fibrillation

BackgroundVentricular fibrillation (VF) can be initiated by ventricular premature depolarizations (VPDs) in the absence of obvious structural abnormalities. ObjectiveThe purpose of this study was to determine the prevalence of 12-lead electrocardiographic (ECG) sinus rhythm reduced QRS amplitude, QRS fractionation (QRSf), and early repolarization (ER) pattern, and the outcome of catheter ablation and VPD anatomic distribution in patients with VPDs initiating VF. MethodsWe compared a cohort with no apparent structural heart disease and VPDs initiating VF (group 1; n = 42) to a reference cohort (group 2; n = 61) of patients with no structural heart disease and symptomatic unifocal VPDs. ResultsA reduced QRS amplitude (<0.55 mV) in aVF (59% vs 10%; P <.001), QRSf in ≥2 contiguous leads (50% vs 16%; P <.001), and ER pattern (21.4% vs 1.6%; P = .01) were more common in group 1 than in group 2. At least 1 abnormal ECG finding was present in 34 group 1 patients (81%) vs 17 group 2 patients (28%) (P <.001). VPD origin included right ventricular and left ventricular distal Purkinje system and moderator band/papillary muscles in 83% of group 1 patients vs 18% of group 2 patients (P <.001). VF was eliminated with a single ablation procedure in 77% of group 1 patients with at least 2 years of follow-up. ConclusionA reduced QRS amplitude (<0.55 mV) in aVF, QRSf in ≥2 contiguous leads, and/or an ER pattern are frequently observed in patients with VPDs initiating VF. VPDs initiating VF typically originate from the distal Purkinje system and papillary muscles and can be successfully eliminated with catheter ablation.

Para-Hisian pacing in a patient with a long RP tachycardia-What is the mechanism?

A 29-year-old man underwent a diagnostic electrophysiology study because of a recurrent symptomatic long RP supraventricular tachycardia (SVT). Twelve-lead electrocardiography and echocardiography were normal. Atrio-His (AH) and His-ventricular intervals measured 86 and 52 ms, respectively. The patient had retrograde ventriculoatrial (VA) activation that was midline and decremental. Para-Hisian pacing repeatedly induced his clinical SVT (Figure 1, top). The response to His-refractory ventricular premature depolarizations and entrainment from the ventricle are shown (Figure 1, middle and bottom).

Intramyocardial mapping of ventricular premature depolarizations via septal venous perforators: Differentiating the superior intraseptal region from left ventricular summit origins

The intramyocardial aspect of the left ventricular summit (LVS) can be mapped by advancing a unipolar guidewire into septal perforator branches of the anterior interventricular vein. The purpose of this study was to differentiate between ventricular premature depolarizations (VPDs) with a basal superior intraseptal (SIS) site of origin and those originating from the epicardial LVS using septal intramyocardial mapping. A retrospective cohort of patients with suspected LVS VPDs who underwent SIS unipolar mapping were reviewed for their clinical characteristics, mapping findings, and procedural outcomes. SIS mapping was successful in 44 of 47 cases (93.6%). VPD origin was SIS (defined as earliest activation from the intraseptal wire) in 20 patients (45.5%; median 23 ms pre-QRS). Procedure success was similar in patients with (group 1) and without (group 2) SIS origin (84% vs 87.5%, respectively; P = .842). Of the 10 patients in group 1 without presystolic endocardial activation, 5 (11.3% of all 44 cases) were successfully ablated from the left ventricular endocardium by using an anatomical approach targeting the endocardium closest to the earliest intraseptal activation site. A significant proportion (45.5%) of VPDs that appear to arise from the left ventricular summit can be demonstrated to have a SIS origin using septal perforator venous mapping. A significant minority (11.3%) of these can be ablated from the endocardium by targeting from an anatomic vantage point closest to the earliest intraseptal activation site. The described strategy may help differentiate true LVS VPDs from those with SIS sites of origin.

An Exploratory Study on Vectorcardiographic Identification of the Site of Origin of Focally Induced Premature Depolarizations in Horses, Part II: The Ventricles.

Simple SummaryVentricular arrhythmias occur commonly in horses. Knowledge on the origin of ventricular arrhythmias is essential for proper treatment. Former studies in horses showed contradictory results regarding the diagnostic value of 12-lead electrocardiography and vectorcardiography due to the anatomical differences in horses compared to humans and small animals. As a consequence, no standardized approach is available for electrocardiography electrode configurations in horses. The current study investigated whether the anatomical origin of experimentally induced ventricular premature depolarizations in horses could be differentiated based upon spherical statistics of the vectorcardiography characteristics. Vectorcardiography shows the magnitude and direction of the cardiac electrical forces in three dimensions. The vectorcardiogram was recorded in seven horses under general anesthesia while right and left ventricular pacing was performed from inside the heart. Using spherical statistics, it could be shown that pacing induces significantly different initial and maximum electrical axes between different locations and between pacing and normal sinus rhythm. The current approach could be used in clinical patients to identify the origin of ventricular arrhythmias without the need for invasive studies. The technique could also be used in other species for which a standardized electrocardiogram electrode configuration is not available.In human cardiology, the anatomical origin of ventricular premature depolarizations (VPDs) is determined by the characteristics of a 12-lead electrocardiogram (ECG). Former studies in horses had contradictory results regarding the diagnostic value of the 12-lead ECG and vectorcardiography (VCG), which results were attributed to the different cardiac conduction system in this species. The objective of this study was to determine if the anatomical origin of pacing-induced VPDs could be differentiated in horses based upon VCG characteristics. A 12-lead ECG was recorded in seven horses under general anesthesia while right and left ventricular endomyocardial pacing was performed (800–1000 ms cycle length) at the apex, mid and high septum and mid and high free wall, and at the right ventricular outflow tract. Catheter positioning was guided by 3D electro-anatomical mapping and echocardiography. A median complex, obtained from four consecutive complexes, was calculated for each pacing location and sinus rhythm. The VCG was calculated from the 12-lead ECG-derived median complexes using custom-made algorithms and was used to determine the initial and maximum electrical axes of the QRS complex. An ANOVA for spherical data was used to test if VCGs between each paced location and between pacing and sinus rhythm were significantly (p < 0.05) different. The model included the radius, azimuth and elevation of each electrical axis. Pacing induced significantly different initial and maximum electrical axes between different locations and between pacing and sinus rhythm. The current results suggest that VCG is a useful technique to identify the anatomical origin of ventricular ectopy in horses.

An unusual incessant long RP tachycardia—What is the mechanism?

A 40-year-old man underwent a diagnostic electrophysiology study because of a slow incessant long RP supraventricular tachycardia (SVT). Echocardiography revealed an ejection fraction of 35%. Upon presentation to the electrophysiology laboratory, he was in SVT. His refractory ventricular premature depolarizations (VPDs) delivered from the right ventricular (RV) apex failed to affect the tachycardia; the responses to earlier VPDs and coronary sinus (CS) atrial premature depolarizations (APDs) are shown in Figure 1, top and bottom, respectively.

Non-invasive electroanatomic mapping to reduce mapping time during catheter ablation of outflow tract ventricular premature depolarizations.

Ventricular premature depolarizations (VPD) commonly arise from the septal anterior right ventricular outflow tract (sRVOT), the left coronary cusp (LCC), and the distal great cardiac vein (dGCV), and share common ECG characteristics. To assess the diagnostic accuracy of non-invasive electroanatomic mapping (NIEAM) in differentiating VPD origin between sRVOT, LCC and dGCV and quantify its clinical utility in eliminating unnecessary mapping and ablation. ECGs and NIEAMs (CardioInsight, Medtronic) from 32 patients (56.3 ± 15.2years) undergoing ablation for VPDs originating from sRVOT, LCC, or dGCV were blindly reviewed for their diagnostic accuracy in predicting the SOO. A 2-step algorithm using NIEAM-based activation timing of the superior basal septum of < 22.5ms and lateral mitral annulus of > 60.5ms was compared with subjective ECG evaluation, the maximum deflection index (MDI), and the V2 transitional ratio in predicting SOO. We calculated the mapping and ablation time that could have been avoided had the operators relied on activation timing by NIEAM in designing their mapping and ablation strategy. NIEAM was superior to subjective ECG evaluation, MDI, and V2 transition ratio in predicting the SOO yielding a sensitivity and specificity of 96.9% and 98.4% respectively. Using NIEAM in determining the SOO would have obviated 22 ± 4.5min of mapping in the wrong chamber and prevented unnecessary ablation of 4.5 ± 1.8min. NIEAM has high diagnostic accuracy in differentiating between sRVOT, LCC, and dGCV VPDs, and can significantly reduce mapping time, obviating the need for unnecessary access and ablation.

Electrocardiographic features of the presence of occult myocardial disease in patients with VPD-induced cardiomyopathy.

BackgroundFrequent ventricular premature depolarizations (VPDs) can cause reversible cardiomyopathy (CMP). However, many patients maintain a normal left ventricular (LV) function with a high VPD burden. The electrocardiographic characteristics of VPD‐induced CMP have not been elucidated.MethodsOne hundred and eighty (91 men, age; 51 ± 15 years) patients with frequent idiopathic VPDs (>10% VPDs/day or >10 000 VPDs/day) were studied. All patients underwent successful ablation and were then divided into two groups according to the echocardiographic findings before and after the ablation procedure.ResultsGroup A (n = 139) had a normal LV function with VPD frequencies, and Group B (n = 41) had reversible LV dysfunction after ablation. The VPD QRS duration (QRSd) was wider in patients with CMP (Group A vs Group B; 137.2 ± 12.0 milliseconds vs 159.7 ± 5.3 milliseconds, P < .001). VPDs with a terminal QRS delay marked by a notch followed by a discrete lower amplitude signal after the peak R wave in any precordial lead were identified. The incidence of terminal signals was higher in the CMP group (Group A vs Group B; 2.1% vs 53.6%, P < .001).ConclusionsThe wider VPD QRSd and terminal QRS delay in patients with VPD‐induced CMP suggest subclinical cell‐to‐cell conduction abnormalities as a potential factor predisposing VPD‐induced CMP.

NON-INVASIVE ELECTROANATOMIC MAPPING TO PREDICT ORIGIN OF OUTFLOW TRACT VENTRICULAR PREMATURE DEPOLARIZATIONS

Ventricular premature depolarizations (VPD) commonly arise from the septal anterior right ventricular outflow tract (sRVOT), the left coronary cusp (LCC) and the distal great cardiac vein (dGCV). The use of non-invasive electroanatomic mapping (NIEAM) is superior to the 12 lead ECG alone in

Clinical and electrophysiological characteristics of idiopathic ventricular arrhythmias originating from the slow pathway region

The slow pathway region (SPR) is commonly targeted during ablation of atrioventricular nodal reentrant tachycardia. However, its role in idiopathic ventricular arrhythmias (IVAs) remains unknown. The purpose of this study was to describe the electrocardiographic and electrophysiological characteristics of IVAs that were successfully ablated from the SPR. Medical records of consecutive patients undergoing ablation of IVAs in the para-Hisian region between 2010 and 2018 were reviewed to identify subjects whose ventricular arrhythmias were targeted from the SPR. Among 63 patients with para-Hisian IVAs undergoing ablation, the SPR was targeted in 12 (20%; mean age 64 ± 7 years; 9 men). All patients presented with ventricular premature depolarizations manifesting left bundle branch block morphology with variable precordial transition (leads V2-V5) and a mean QRS duration of 131 ± 11 ms. In all cases, leads I and aVL had positive forces (R or Rs) and lead aVR had negative forces (QS or Qr). In the majority of cases, lead II had positive forces (R or Rs; n = 9 [75%]) and lead III had negative forces (rS or QS; n = 9 [75%]). Mean activation at the SPR was 31 ± 5 ms pre-QRS. All patients had initial ablation with radiofrequency, resulting in junctional rhythm in 9 (75%); 3 (25%) patients required additional cryoablation. Ablation was successful in 11 patients (92%). One patient required a permanent pacemaker for heart block but subsequently recovered intrinsic conduction. The SPR can be a source of IVAs, which can be safely and successfully ablated in most cases using radiofrequency energy. IVAs arising from this location manifest unique electrocardiographic features.

Conduction patterns of idiopathic arrhythmias from the endocardium and epicardium of outflow tracts: New insights with noninvasive electroanatomic mapping

Idiopathic arrhythmias commonly arise from the septal right ventricular outflow tract (RVOT), sinuses of Valsalva (SoV), and great cardiac vein (GCV). Predicting the exact site of origin is important for preparation for catheter ablation. The purpose of this study was to examine the diagnostic value of noninvasive electroanatomic mapping (NIEAM) to differentiate between septal RVOT, SoV, and GCV origin and compare it to that of 12-lead electrocardiography (ECG). NIEAM maps (CardioInsight, Medtronic) were generated during spontaneous ventricular premature depolarizations (VPDs) and threshold pacing from septal RVOT, SoV, and GCV. Origin prediction using NIEAM was compared to algorithmic ECG criteria (maximal deflection index; V2 transition ratio) and subjective ECG evaluation. Sixty NIEAMs (18 spontaneous VPDs and 42 pace-maps) from 31 patients (age 56 ± 16 years) were analyzed. NIEAM showed distinct conduction patterns, best visualized at the base of the heart: septal RVOT VPDs propagate toward the tricuspid annulus, depolarizing the septum from inferior to superior; SoV VPDs engage the superior septum early; and GCV VPDs move laterally along the mitral annulus, depolarizing the heart from left to right. Activation of the lateral mitral annulus >60.50 ms and the superior basal septum <22.5 ms from onset predicts RVOT and SoV origin, respectively, in 100% of cases. NIEAM was superior to maximum deflection index in predicting GCV origin (100% vs 42.2% accuracy) and superior to V2 transition ratio in predicting SoV origin (100% vs 75.9% accuracy). Arrhythmias arising from the outflow tracts follow distinct propagation patterns depending on the origin. A 2-step algorithm using activation timing by NIEAM yields 100% diagnostic accuracy in predicting origin.

Accuracy of smartphone-based ECG for the diagnosis of various cardiac arrhythmias

Diagnosis of cardiac arrhythmias can be challenging due to their frequent transient nature. Smartphone-based ECG has previously been studied for atrial fibrillation (AF) diagnosis. However, data is lacking regarding diagnostic accuracy of smartphone-based ECGs for other frequent arrhythmias. To assess the accuracy of Alivecor smartphone-based ECG (AECG) device for the diagnosis of various bradyarrhythmias or tachyarrhythmias. Hospitalized patients were eligible for inclusion if they had any of the following arrhythmias: AF, atrial tachycardia/flutter (AT), sinus rhythm with frequent atrial premature depolarizations (APD), sinus rhythm with frequent ventricular premature depolarizations (VPD), sinus tachycardia > 120 beats/min, sinus bradycardia < 40 beats/min, high-degree atrioventricular (AV) block, atrioventricular node reentrant tachycardia (AVNRT) and ventricular tachycardia (VT). Reference twelve-lead ECG were recorded, and the corresponding one-lead AECG was independently interpreted by four blinded electrophysiologists. Seventy-three patients (57 men; aged 72 ± 14 years) were included. For the diagnosis of bradyarrhythmias, AECG had a sensitivity and specificity of 75%–95% for sinus bradycardia, and 52%–98% for AV block. For atrial tachyarrhythmias, sensitivites and specificites were good for APD (83%–97%), AF (82%–87%), and sinus tachycardia (86%–98%), whereas sensitivity was poor for AT (49%–93%) and AVNRT (10%–99%), with very frequent confusion between them. For ventricular tachyarrhythmias, sensitivities and specificities were 70%–95% for VPD, and 89%–100% for VT ( Table 1 , Fig. 1 ). AECG is accurate for the diagnosis of sinus bradycardia, sinus tachycardia, APD, VPD, AF and VT. However, AV block, AT and AVNRT were poorly diagnosed by AECG, with a low sensitivity and very frequent confusion between AT and AVRNT.

Right ventricle apex pacing identifies the presence of ventricular premature depolarizations-induced cardiomyopathy.

A high burden of ventricular premature depolarizations (VPDs) has been associated with potentially reversible left ventricular (LV) dysfunction, termed as VPD-induced cardiomyopathy (CMP). However, many patients maintain normal LV function despite a high VPD burden. The purpose of this study was to identify CMP by right ventricle apex (RVa) pacing method in patients with high VPD burden. A total of 62 patients (28 male; mean age=50±15years) with idiopathic VPDs undergoing ablation were enrolled. RVa pacing was recorded in all patients during the procedure. The paced QRS duration (QRSd) during RV pacing was measured from the pacing spike to the latest QRS deflection on any surface electrocardiogram lead. Patients were divided into two groups: reversible VPD-induced CMP (Group R; n =15, 14 males, mean age=54±14 years) and normal LV function (Group N; n=47, 23 males, mean age=54±15 years). The LV ejection fraction (%) was significantly lower in Group R as compared with Group N (Group R, Group N=36±6, 58±4; P<0.001); however, LV end-diastolic dimension mm was not significantly different between the two study groups (Group R, Group N=54±5, 50±6; P=0.06). Similarly, sinus QRS width (P=0.10), VPD-burden (P=0.36), and body surface area (P=0.75) were not significantly different between Group R and Group N. The QRSd was significantly longer in Group R compared with Group N (177±8vs 150±14; P<0.001). Using a QRSd cut-off value of 170.1ms, VPD-induced CMP was identified with a sensitivity of 73% and a specificity of 97%. RVa pacing with transmyocardial conduction time assessment was a useful method for identifying idiopathic VPD-induced CMP. Using a QRSd cut-off value of 170.1ms, VPD-induced CMP was identified with a sensitivity of 73% and a specificity of 97%.

MOLECULAR STUDY OF FMD INFECTED EGYPTIAN BUFFALO CALVES WITH REFERENCE TO ELECTROCARDIOGRAPHY AND CARDIAC BIOMARKERS AS PROGNOSTIC TOOLS

A total of 200 Egyptian buffalo calves aging between 9-11 months previously vaccinated with local trivalent oil inactivated vaccine (O, A and SAT-2), in different locations at Menufyia Governorate showing typical clinical signs of FMD were examined for molecular characterization of FMD virus, electrocardiographic picture (ECG) and cardiac biomarkers. The results of serological tests revealed that incidence of non-structural proteins against natural infection with FMDV was 31.5% in serum samples collected from vaccinated buffalo calves. Moreover, 51.5 % of the samples showed detection of structural proteins against trivalent vaccination. On the other hand, there were no protective antibodies against FMDV in 17 % of the examined samples. ECG of FMD infected calves showed ventricular premature depolarization with flattening of P- wave and increased QRS duration with decrease in its amplitude compared with healthy calves. In FMD infected buffalo calves, there were significant (P < 0.01) increases in (cTnI), (CK-MB), urea, CL and K and there was significant (P < 0.01) decrease in Na levels than that of healthy ones. The identified strains in FMD infected Egyptian buffalo calves were unique and different from the vaccinal and other Egyptian strains as well as they were clustered with Topotype ME-SA. Cardiac enzymes along with ECG can be used as useful prognostic tools in FMD infected Egyptian buffalo calves.

A narrow complex tachycardia with atrioventricular dissociation: What is the mechanism?

A 74-year-old woman underwent diagnostic electrophysiologic study because of recurrent, symptomatic supraventricular tachycardia. Baseline atrio-His and His-ventricular intervals measured 75 ms and 50 ms, respectively. Programmed atrial extrastimulation elicited dual atrioventricular (AV) nodal physiology and ventricular pacing showed no ventriculoatrial conduction despite isoproterenol. Figure 1 shows her clinical tachycardia. The response of tachycardia to a His-refractory ventricular premature depolarization (VPD) is shown in the top section of Figure 2, while its induction twice by rapid ventricular pacing (340 ms) is shown in the middle and bottom sections of Figure 2. Based on these observations, what is the mechanism of tachycardia? Figure 2Top: Response of tachycardia to a His-refractory ventricular premature depolarization. Middle, Bottom: Induction of tachycardia by rapid ventricular pacing (340 ms). View Large Image Figure Viewer Download Hi-res image

Horse: anaesthetic management for open castration of a Belgian draught horse with interventricular septum defect, aortic regurgitation and ventricular premature depolarisations

A 2 years and 11 months old Belgian draught horse stallion with a membranous ventricular septal defect, severe aortic regurgitation, mild left ventricular enlargement and ventricular premature depolarisations was anaesthetised...

Recovery of renal dysfunction after catheter ablation of outflow tract ventricular arrhythmias in patients with ventricular premature depolarization-mediated cardiomyopathy.

Frequent ventricular premature depolarizations (VPDs) may cause cardiomyopathy (VPDCM), which often improves after VPD suppression. This study aimed to evaluate whether ablation of outflow tract ventricular arrhythmias (OT VAs) in patients with VPDCM improves renal in addition to left ventricular (LV) function. We retrospectively evaluated 153 patients with OT VAs and examined VPD burden and LV ejection fraction (LVEF), as well as estimated glomerular filtration rate (eGFR) pre- and post-ablation. LV dysfunction was defined as LVEF <50% and impaired renal function was defined as eGFR of <60mL/min/1.73m2. Fifty-five patients had VPDCM. During mean follow-up of 14months, 140 (92%) were free from arrhythmia. In patients with VPDCM, patients with baseline LVEF 40-50% had greater improvement in the post-ablation LVEF compared to patients with baseline LVEF <40% (p < 0.01). At baseline, 36 (72%) patients had renal dysfunction, 29 (81%) of whom had improvement in eGFR from baseline after successful ablation from eGFR 51 to 57mL/min/1.73m2. There was a significant association between cardiac (ΔLVEF ≥10%) and renal (ΔeGFR ≥10%) improvement (r = 0.54, p = 0.04). Using logistic regression analysis, procedural success was an independent predictor of improvement of cardiac (odds ratio [OR] = 13.7, p = 0.03) and renal function (OR = 21.0, p = 0.047). Successful catheter ablation of OT VA reduces VPD burden and is associated with improved cardiac and renal function in patients with VPDCM.

Atrial Premature Depolarization-Induced Changes in QRS and T Wave Morphology on Resting Electrocardiograms in Horses.

BackgroundThe electrocardiographic differentiation between atrial (APDs) and ventricular (VPDs) premature depolarizations is important. P wave prematurity and normal QRS and T wave morphology generally are used as discriminating criteria for APDs.Hypothesis/ObjectivesThe aim of this study was to determine whether P, Q, R, S, and T wave amplitude, PQ interval, QRS and P wave duration and P and T wave morphology differ between APDs and sinus beats. To determine the relationship between the RR coupling interval and the change in S wave amplitude between sinus beats and APDs.MethodsCase–control study. From a modified base‐apex configuration of 30 horses with APDs at rest, sinus beat and APD associated preceding RR interval, P, PQ and QRS duration and P, R, S, and T wave amplitudes were measured. Linear mixed models and logistic regression were used to determine the effect of APDs on the ECG variables studied.ResultsIn comparison to sinus beats, APDs were associated with a significant (P < .001) change in P amplitude (−0.03 ± 0.01 mV) and increase in S (0.20 ± 0.02 mV) and T (0.08 ± 0.03 mV) amplitude. PQ (−20.3 ± 5.2 ms) and RR (−519 ± 14 ms) interval and P duration (−21.1 ± 3.0 ms) decreased (P < .001). APDs were significantly associated with a singular positive P wave (OR: 11.0, P < .001) and were more likely to have a monophasic positive T wave (OR: 9.2, P < .001). A smaller RR coupling interval was associated with an increased relative difference in S amplitude (P < .01).ConclusionsAtrial premature depolarizations may lead to changes in QRS and T wave morphology. Knowledge of these changes is important to avoid interpreting certain APDs as VPDs.