Ventricular Cycle Length Research Articles

Efficacy of percutaneous stellate ganglion block according to ventricular arrhythmia cycle length: a post-hoc sub-analysis of the STAR study

Abstract Background Percutaneous stellate ganglion block (PSGB) is an effective treatment for patients with electrical storm (ES). However, literature is scarce about a possible relation between ventricular arrhythmias’ cycle length and the effectiveness extent of PSGB. Purpose To assess whether the PSGB efficacy is affected by the arrhythmias’ cycle length prior to the procedure. Methods This is a post-hoc sub-analysis of the STAR study (STellate ganglion block for Arrythmic stoRm), a multicentre observational study aimed to assess PSGB’s effectiveness and safety in ES patients [1]. According to both the type and the median cycle of the latest ventricular arrhythmia before PSGB we considered 3 groups: ventricular fibrillation (VF), fast ventricular tachycardia (VT) and slowVT. The primary outcome is the number of treated arrhythmic episodes (with ATPs and/or DC-shocks) in the hour immediately after the PSGB as compared to the hour immediately before. The secondary outcome was the extent of the reduction of the number of ATPs/DC-shocks delivered from the hour before to the hour immediately after the PSGB. Results The original study included 184 PSGBs performed on 131 patients. We excluded 32 PSGBs with a continuous infusion and 13 PSGBs with an unknown VT cycle. The median VT cycle was 375 msec, so the final dataset of 139 PSGBs from 112 patients was divided as follows: 51 VF; 44 fastVT (VT cycle <375 msec) and 44 slowVT (VT cycle ≥375 msec). The number of treated arrhythmic episodes in the first hour after every PSGB was significantly lower compared to the first hour before in all the three groups [VF: 0 (IQR, 0-1) vs 5 (IQR, 2-8), p<0.001; fastVT: 0 (IQR, 0-0) vs 1 (IQR, 0-6.5), p<0.001; slowVT: 0 (IQR, 0-0) vs 1 (IQR, 0-4.5), p=0.001] (Figure 1). The Hodges-Lehman median difference of treated arrhythmic episodes between the hour after and before the PSGB was significantly higher in VF group [-4 (-3 to -6)] than in the fast-VT [-2 (-1 to -4)] and slow-VT [-1 (0 to -2.5)] (Figure 2). Analysing the reduction (delta less than zero) of the number of ATPs/DC-shocks from the hour before to the hour immediately after the PSGB, a significant trend was observed across the three groups (Jonckheere-Terpstra trend p<0.001) and a significant difference was observed comparing slow-VT vs VF [0 (IQR, -3 to 0) vs -4 (IQR, -7 to -1)] and fast-VT versus VF [-1 (IQR, -4.5 to 0) vs -4 (IQR, -7 to -1)], but not comparing slow-VT versus fast-VT [0 (IQR, -3 to 0) vs -1 (IQR, -4.5 to 0)]. VF was a predictor of the reduction of treated arrhythmic episodes at univariable analysis and after correction for the number of treated arrhythmic episodes in the hour immediately before PSGB and of left ventricular ejection fraction (OR 7.8, 95%CI 2.1-28.6). Conclusion PSGB is an effective treatment for ES in patients with all type of ventricular arrhythmias. However, its effectiveness was more pronounced in patients with VF or rapid ventricular tachycardia.

Role of ventricular tachycardia cycle length in the outcomes after catheter ablation or antiarrhythmic drugs in the SURVIVE-VT trial

Abstract Background It has been suggested that antiarrhythmic drugs (AAD) are less effective and safe in slow ventricular tachycardia (VT) due to their effect on conduction velocity, which could stabilize reentry. Conversely, catheter ablation aims to disrupt the VT circuit. Because of the distinct mechanisms of action of AAD and catheter ablation on the VT circuit, VT cycle length (VT-CL) may play a crucial role in determining their therapeutic efficacy. Therefore, VT-CL could be important in selecting VT treatment. Purpose The aim of this study was to assess the impact of VT-CL on outcomes following catheter ablation or antiarrhythmic drugs in AAD-naïve patients with ischemic cardiomyopathy presenting with VT. Methods This is a post hoc analysis of the previously published Substrate Ablation vs Antiarrhythmic Drug Therapy for Symptomatic Ventricular Tachycardia (SURVIVE-VT) trial. In summary, 144 patients with ischemic cardiomyopathy and symptomatic VT were randomized to receive either catheter ablation (N=71) or AAD (N=73) as first-line therapy. We analyzed VT recurrence, implantable cardioverter-defibrillator (ICD) therapies, and the incidence of slow/incessant VT/VT storm using Cox proportional hazard models, with treatment and VT-CL interaction terms, adjusted for age. Missing VT-CL data for five patients were imputed using the median value. Results In patients with chronic ischemic heart disease and VT treated with either AAD or catheter ablation, a significant interaction was observed between clinical VT-CL and treatment effect on VT recurrence (p=0.016 for the interaction). Specifically, slower VT cycle lengths were associated with higher rates of VT recurrence (hazard ratio per 10 ms [HR] 1.094, 95% confidence interval [CI] 1.015, 1.179; p=0.037) in patients treated with AAD, while no significant effect was observed in those undergoing catheter ablation (see Figure 1). Survival freedom from VT recurrence in patients with VT-CL ≥300ms was significantly higher in patients treated with catheter ablation (78.8% vs 58.1%, log-rank p=0.044, see Figure 2). As expected, VT-CL was significantly associated with a higher risk of slow/incessant VT/VT storm (HR per 10 ms 1.115, 95% CI 1.017-1.222, p=0.047) but was not associated with ICD therapies (HR per 10 ms 1.082, 95% CI 0.994-1.178, p=0.102). Conclusion VT-CL significantly influences treatment outcomes, with slower VT cycles associated with an increased risk of VT recurrence in patients treated with AAD, but not in those undergoing catheter ablation. Therefore, VT-CL should be taken into consideration when selecting the optimal therapy for patients with ischemic cardiomyopathy and VT.Figure 1Figure 2

Machine learning-derived cycle length variability metrics predict spontaneously terminating ventricular tachycardia in implantable cardioverter defibrillator recipients.

Implantable cardioverter defibrillator (ICD) therapies have been associated with increased mortality and should be minimized when safe to do so. We hypothesized that machine learning-derived ventricular tachycardia (VT) cycle length (CL) variability metrics could be used to discriminate between sustained and spontaneously terminating VT. In this single-centre retrospective study, we analysed data from 69 VT episodes stored on ICDs from 27 patients (36 spontaneously terminating VT, 33 sustained VT). Several VT CL parameters including heart rate variability metrics were calculated. Additionally, a first order auto-regression model was fitted using the first 10 CLs. Using features derived from the first 10 CLs, a random forest classifier was used to predict VT termination. Sustained VT episodes had more stable CLs. Using data from the first 10 CLs only, there was greater CL variability in the spontaneously terminating episodes (mean of standard deviation of first 10 CLs: 20.1 ± 8.9 vs. 11.5 ± 7.8 ms, P < 0.0001). The auto-regression coefficient was significantly greater in spontaneously terminating episodes (mean auto-regression coefficient 0.39 ± 0.32 vs. 0.14 ± 0.39, P < 0.005). A random forest classifier with six features yielded an accuracy of 0.77 (95% confidence interval 0.67 to 0.87) for prediction of VT termination. Ventricular tachycardia CL variability and instability are associated with spontaneously terminating VT and can be used to predict spontaneous VT termination. Given the harmful effects of unnecessary ICD shocks, this machine learning model could be incorporated into ICD algorithms to defer therapies for episodes of VT that are likely to self-terminate.

Site-specific effects of dobutamine on cardiac conduction and refractoriness.

Isoproterenol, a non-specific beta agonist, is commonly used during electrophysiology studies (EPS). However, with the significant increase in the price of isoproterenol in 2015 and the increasing number of catheter ablations performed, the cost implications cannot be ignored. Dobutamine is a less expensive synthetic compound developed from isoproterenol with a similar mechanism to enhance cardiac conduction and shorten refractoriness, thus making it a feasible substitute with a lower cost. However, the use of dobutamine for EPS has not been well-reported in the literature. To determine the site-specific effects of various doses of dobutamine on cardiac conduction and refractoriness and assess its safety during EPS. From February 2020 to October 2020, 40 non-consecutive patients scheduled for elective EPS, supraventricular tachycardia, atrial fibrillation, and premature ventricular contraction ablations at a single center were consented and prospectively enrolled to assess the effect of dobutamine on the cardiac conduction system. At the end of each ablation procedure, measures of cardiac conduction and refractoriness were recorded at baseline and with incremental doses of dobutamine at 5, 10, 15, and 20 mcg/kg/min. For the primary analysis, the change per dose of dobutamine from baseline to each dosing level of dobutamine received by the patients, comparing atrioventricular node block cycle length (AVNBCL), ventricular atrial block cycle length (VABCL) and sinus cycle length (SCL), was tested using mixed-effect regression. For the secondary analysis, dobutamine dose level was tested for association with relative changes from baseline of each electrophysiologic parameter (SCL, AVNBCL, VABCL, atrioventricular node effective refractory period (AVNERP), AH, QRS, QT, QTc, atrial effective refractory period (AERP), ventricular effective refractory period (VERP), using mixed-effect regression. Changes in systolic and diastolic blood pressures were also assessed. The Holm-Bonferroni method was used to adjust for multiple testing. For the primary analysis there was no statistically significant change of AVNBCL and VABCL relative to SCL from baseline to each dose level of dobutamine. The SCL, AVNBCL, VABCL, AVNERP, AERP, VERP and the AH, and QT intervals all demonstrated a statistically significant decrease from baseline to at least one dose level with incremental dobutamine dosing. Two patients (5%) developed hypotension during the study and one patient (2.5%) received a vasopressor. Two patients (5%) had induced arrhythmias but otherwise no major adverse events were noted. In this study, there was no statistically significant change of AVNBCL and VABCL relative to SCL from baseline to any dose level of dobutamine. As expected, the AH and QT intervals, and the VABCL, VERP, AERP and AVNERP all significantly decreased from baseline to at least one dose level with an escalation in dobutamine dose. Dobutamine was well-tolerated and safe to use during EPS.

Evaluating subclinical left ventricular and left atrial dysfunction in idiopathic atrial fibrillation: A speckle-tracking based strain-analysis

ObjectiveA subset of patients with atrial fibrillation (AF) presents without established AF risk factors and normal left ventricular (LV) systolic function, called idiopathic AF (IAF). Traditionally, echocardiography derived LV dimensions and ejection fraction (EF) are used to exclude LV dysfunction in IAF, but their sensitivity is limited. Our objective is to evaluate the presence of subtle alterations in LV function despite normal LVEF in patients with IAF compared to healthy controls, using speckle-tracking echocardiography (STE) based global longitudinal strain (GLS). MethodsStandard transthoracic echocardiography was performed in 80 patients with IAF and 129 healthy controls. Patients with overt cardiac disease as well as known established AF risk factors were excluded. STE analysis was performed to assess GLS of the LV, and left atrial strain (LAS). ResultsLVEF was normal and comparable between patients with IAF and healthy controls (63 ± 4% for both groups; p = 0.801). Mean GLS was within normal limits for both groups but statistically significantly more negative in patients with IAF (−20.6 ± 2.5% vs. -19.7 ± 2.5%; p = 0.016), however not when indexed for ventricular cycle length (p = 0.784). No differences in LA volume or non-indexed LAS were seen in patients with IAF compared to healthy controls. ConclusionsIn this selected group of IAF patients, STE did not detect any overt LV or LA dysfunction compared to healthy controls. Thus, IAF occurred in these patients not only in the absence of established AF risk factors but also without evidence of ventricular or atrial dysfunction.

Abstract 15706: Non-Invasive 3D Electromechanical Cycle Length Mapping for Macroreentrant Atrial Flutter Characterization

Introduction: Arrhythmia localization prior to catheter ablation is critical for clinical decision making. The current standard of 12-lead EKG interpretation lacks spatial specificity and is anatomically limited. Electromechanical Cycle Length mapping (ECLM) is a high frame rate, echocardiography-based frequency analysis mapping technique, that can noninvasively map, localize and characterize cardiac activation frequencies in 3D. Hypothesis: Accurate localization prior to ablation may facilitate pre-op planning, reduce procedural times and fluoroscopic exposure. In this study we access ECLM feasibility for 3D mapping and quantifying macroreentrant atrial flutter (AFL) activation rates. Methods: Four patients (N = 4; 65 ± 9yo; 3 M) presented with AFL and were referred to RF ablation. Patients underwent pre-op transthoracic ECLM with simultaneous 3-lead EKG. 3D atrial ECLM cycle length (CL) maps were rendered and areas with arrhythmic CL were identified (100-330 ms). ECLM AFL and Ventricular CLs were defined as the dominant CL of the arrhythmic region and the region that remains synchronized with the ventricular activation respectively. ECLM findings were compared against identified origins and CLs on intracardiac electroanatomic mapping (EAM). Results: ECLM successfully identified and localized the presence of atrial typical CTI flutter in all four subjects when compared against successful RF ablation. An ECLM map in a CTI AFL case is shown on Fig. 1a with the CTI circuit in the right atrium. ECLM CLs exhibited excellent agreement with both the CL of the 3-lead EKG (Atrial CL: r 2 = 0.91, Ventricular CL r 2 = 0.99) and the EAM AFL CL (r 2 = 0.92). Conclusions: ECLM can localize, map and quantify the electromechanical CLs in AFL in excellent agreement with the clinical electrical CL rates and propagation patterns obtained by clinical albeit invasive procedures, providing thus a clinical noininvasive, non-ionizing mapping tool for RF ablation planning.

The Association of Clustered Ventricular Arrhythmia and Cycle Length With ScarBurden in Cardiomyopathy.

Patients with≥2 ventricular arrhythmia (VA) events within 3months (clustered VA) have increased risk for mortality. The aim of this study was to examine the association of risk factors including scar characteristics on cardiovascular magnetic resonance imaging with clustered VA and VA cycle length in nonischemic cardiomyopathy (NICM) and ischemic cardiomyopathy (ICM). Data from 329 primary prevention implantable cardioverter-defibrillator recipients (mean age 57 years, 26% women) were analyzed from the Left Ventricular Structural Predictors of Sudden Cardiac Death study. Twenty-one patients developed clustered VA (median time 2.7 years after implantable cardioverter-defibrillator placement). Men had the greatest risk for recurrent VA. Patients with NICM and scar had the highest incidence rate of clustered VA. In patients with NICM, each 1-g increase in core scar correlated with greater clustered VA risk (HR: 1.19; 95%CI: 1.07-1.32). Gray scar was similar among subgroups. Patients with NICM with clustered VA had the longest mean VA cycle length (297 ± 40 milliseconds). Higher core scar burden correlated with longer VA cycle length inpatients with NICM (P = 0.002), and higher body mass index correlated with shorter VA cycle length in those with ICM (P = 0.02). Type of VA was similar between cardiomyopathy subgroups, and no scar pattern predominated. Clustered VA was most common in patients with NICM and scar, with greatest risk among those with larger core scar. Core scar correlated with slower VA in patients with NICM, and higher body mass index correlated with faster VA in those with ICM. Type of VA was similar by cardiomyopathy etiology, and no dominant scar pattern was associated with clustered VA.

"Irregular" tachycardia atrial cycle length and activation sequence with relatively constant ventricular cycle length: What is the mechanism?

"Irregular" tachycardia atrial cycle length and activation sequence with relatively constant ventricular cycle length: What is the mechanism?

Regional and Temporal Variation of Ventricular and Conduction Tissue Activity During Ventricular Fibrillation in Canines.

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915ATP efficacy on terminating ventricular tachycardia by device type, indication, and ventricular median cycle length

Abstract Funding Acknowledgements Medtronic OnBehalf PainFree SST Background Anti-tachycardia Pacing (ATP) is an established therapy that terminates VT without the need for painful ICD shocks. Here we use the data from PainFree SST clinical trial to evaluate the ATP success rate by device type, indication and MCL. Methods Spontaneous episodes that were detected by ICD or CRT-D devices in the VT, fast VT and VF zones were included in the analysis. Episodes successfully terminated by ATP were deemed as having ATP success. Using the GEE method, ATP success rate and its 95% CI were calculated for device types, indications and ventricular MCL. Results Of the 2770 enrolled patients (79% male, average age 65 years), 1699 (61%) were implanted with an ICD and 1071 (39%) with a CRT-D system; 1917 (69%) were reported as primary prevention and 847 (31%) were secondary prevention patients. For all MVT episodes, the ATP success rate was similar between ICD and CRT-D devices (82.3% vs 80.3%, p = 0.74). Patients with secondary prevention had a higher ATP success rate compared to those with primary prevention but the difference was not statistically significant (84.4% vs 76.8%, p = 0.16). Regardless of device type and indication, ATP success rate was significantly higher in the slower VTs (MCL ≥ 320 ms) compared to the faster VTs (MCL ≥ 240 to &amp;lt; 320 ms) (89.2% vs 73.7%, p &amp;lt; 0.0001). Conclusion We found that ATP had a greater than 80% rate of success for terminating ventricular tachycardias overall. Slower VTs was significantly associated with a higher ATP success rate regardless of device type and indication compared to faster VTs. For faster VTs with a MCL ≥ 240 to &amp;lt; 320 ms, the ATP success rate was still successful at terminating VT more than 70% of the time. Table 1. ATP Success Rates - No. of Enrolled Subjects (% of total) No. of Episodes Analyzed for ATP Success (No. of Subjects) GEE-estimated ATP Success Rate (95% CI) P-value* Overall 2770 (100%) 2277 (376) 81.5% (78.4%, 84.2%) - Device Type - - - 0.7440 ICD 1699 (61.3%) 1484 (229) 82.3% (78.3%, 85.6%) - CRT-D 1071 (38.7%) 793 (147) 80.3% (75.0%, 84.6%) - Indication - - - 0.1609 Primary Prevention 1917 (69.2%) 631 (160) 76.8% (71.2%, 81.6%) - Secondary Prevention 847 (30.6%) 1615 (212) 84.4% (80.7%, 87.6%) - Median Cycle Length - - - &amp;lt;0.0001 (&amp;gt;/=) 240 ms and &amp;lt; 320 ms - 861 (257) 73.7% (69.2%, 77.7%) - (&amp;gt;/=) 320 ms - 1416 (209) 89.2% (85.7%, 91.9%) - * Per a GEE main effect model for all episodes where device type, indication and median cycle length were considered.

Dose-Dependent Effects of Ranolazine on Reentrant Ventricular Arrhythmias Induced After Subacute Myocardial Infarction in Rabbits.

Ranolazine has been found to prevent ventricular arrhythmias (VAs) during acute myocardial infarction (AMI). This study aimed to investigate its efficacy on VAs induced several days post-MI. For this purpose, 13 anesthetized rabbits underwent coronary artery ligation. Ten of these animals that survived AMI were reanesthetized 3 to 7 days later for electrophysiologic testing. An endocardial monophasic action potential combination catheter was placed in the right ventricle for simultaneous pacing and recording. Monophasic action potential duration, ventricular effective refractory period (VERP), and VAs induced by programmed stimulation were assessed. Measurements were performed during control pacing, and following an intravenous infusion of either a low-dose ranolazine (2.4 mg/kg, R1) or a higher dose ranolazine (4.8 mg/kg cumulative dose, R2). During control stimulation, 2 animals developed primary ventricular fibrillation (VF), 6 sustained ventricular tachycardia (sVT), and 2 nonsustained VT (nsVT). R1 did not prevent the appearance of VAs in any of the experiments; in contrast, it aggravated nsVT into sVT and complicated sVT termination in 2 of 6 animals. Sustained ventricular tachycardia cycle length and VERP were only slightly decreased after R1 (112 ± 5 vs 110 ± 6 ms and 101 ± 11 vs 98 ± 10 ms, respectively). R2 suppressed inducibility of control nsVT, VF, and sVT in 2 animals. In 4 animals with still inducible sVT, R2 significantly prolonged VT cycle length by 150 ± 23 ms (P < .01), and VERP by 120 ± 7 ms (P < .001) versus control. In conclusion, R2 exerted antiarrhythmic efficacy against subacute-MI VAs, whereas R1 rather aggravated than prevented these arrhythmias. Ventricular effective refractory period prolongation could partially explain the antiarrhythmic action of R2 in this rabbit model.

Association left ventricular lead and ventricular arrhythmias after upgrade to cardiac resynchronization therapy in patients with implantable cardioverter defibrillators.

BackgroundThere are some controversial reports related to the pro‐arrhythmic or anti‐arrhythmic potential of cardiac resynchronization therapy (CRT) and little is known about the relationship between ventricular arrhythmia (VA) and left ventricular (LV)‐lead threshold.HypothesisUpgrade CRT is anti‐arrhythmic effect of VA with implantable cardioverter‐defibrillator (ICD) patients and has a relationship with the incident of VA and LV‐lead threshold.MethodsAmong 384 patients with the implantation of CRT‐defibrillator (CRT‐D), 102 patients underwent an upgrade from ICD to CRT‐D. We divided patients into three groups; anti‐arrhythmic effect after upgrade (n = 22), pro‐arrhythmic effect (n = 14), and unchanging‐VA events (n = 66). The VA event was determined by device reports. We described the electrocardiography parameters, LV‐lead characteristics, and clinical outcomes.ResultsBefore upgrade, the numbers of VA were 305 episodes and the numbers of ICD therapy were 157 episodes. While after upgrade, the numbers of VA were 193 episodes and the number of ICD therapy were 74 episodes. Ventricular tachycardia cycle length (VT‐CL) after upgrade was significantly slower as compared to those with before upgrade. Pro‐arrhythmic group was significantly higher with delta LV‐lead threshold (after 1 month—baseline) as compared to those with anti‐arrhythmic group (0.74 vs −0.21 V). Furthermore, pro‐arrhythmic group was significantly bigger with delta VT‐CL (after 3 months—before 3 months) as compared to those with anti‐arrhythmic group (P = .03).ConclusionsWe described upgrade‐CRT was associated with reduction of VA, ICD therapies and VT‐CL. While 14 patients had a pro‐arrhythmic effect and LV lead threshold might be associated with VA‐incidents.

Effect of selective His bundle pacing on ventricular fibrillation activation rates in rabbit hearts

Background/significanceThe His‐Purkinje system is electrically active and influences activation patterns and rates during ventricular fibrillation (VF). Purkinje system is involved in maintaining VF and may contribute to defibrillation shock failure. This study investigates if the His‐Purkinje system could be paced to modulate rate or patterns of activation during VF.MethodSeven New Zealand rabbit hearts were explanted and perfused in a Langendorff setup. The His bundle (HB) was accessed from the right atrial septal wall by opening the right atrium. An 8×8 Ag/AgCL electrode array was placed by the anterior vertex of Koch's triangle. The HB was identified using a custom real‐time stimulation‐recording and signal processing system. The system used spatial derivatives to identify electrodes specifically over the HB. A separate silver wire was inserted in the ventricular myocardium (VM) of the right septal wall to stimulate the VM and detect ventricular cycle lengths. A 64‐channel basket catheter (Orion catheter, Boston Scientific Inc) was inserted through an opening made in left atrium through the mitral valve and into the left ventricle. VF was induced by 50 Hz pacing on the left ventricular free wall. During VF, the HB was paced at 80 and 95% of intrinsic HB cycle lengths. Both the HB and VM were paced at 80 and 95% of the intrinsic VM cycle lengths. Both HB and VM were stimulated during VF at 10× the amplitude of the diastolic stimulation threshold. While the VM and HB were being stimulated, left ventricular endocardial activations were recorded from the basket catheter electrodes.The left ventricular endocardial recordings were analyzed using a custom graphical user interface developed in MATLAB (Mathworks, Inc., MA, USA). Broken channels or channels not in contact with the endocardial wall were excluded from the analysis.ResultsData from 2 out of 7 animals were excluded from analysis as pacing at electrodes with HB potentials did not lead to capture of the HB. HB pacing at 80% or 95% of HB CL did not affect the VF. In 4 animals, when the HB was paced at 95% of VM cycle lengths, the left ventricular endocardial activation rate was higher than when VM was paced at 95% of VM cycle lengths. In 3 animals, when HB was paced at 80% of VM cycle length, the left ventricular endocardial activation rate was higher than when the VM was paced at 80% of VM cycle length.Conclusion and discussionHB paced at 80 or 95% of HB cycle length did not affect the underlying VF. HB paced at 80% or 95% of VM cycle length affected the underlying VF activation rate more than when VM was paced at 80% or 95% VM CL. The increase in ventricular activation rate suggests ventricular tissue is activated at the Purkinje endpoints of the His‐Purkinje system as a result of His bundle pacing.Support or Funding InformationNational Institutes of Health award number R01HL128752 to Dr. Derek DosdallThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Insecticide pyriproxyfen (Dragón®) damage biotransformation, thyroid hormones, heart rate, and swimming performance of Odontophrynus americanus tadpoles

Odontoprynus americanus tadpoles were used to determine the safety concentration of pyriproxyfen (PPF) insecticide by acute and sublethal toxicity tests (nominal range tested 0.01 to 10 [± 15%] PPF mg/L). Median lethal concentration (LC50) and no, and lowest-observed-effect concentrations (NOEC and LOEC, respectively) were calculated. We also assessed the effect on the activities of glutathione S-transferse (GST), acetylcholinesterase (AChE), and carboxylesterase (CbE) and compared to control (CO) tadpoles. Based on the 48-h NOEC value, two sublethal concentrations of PPF (0.01 and 0.1 mg/L) were assayed to detect effects on enzymes activities (GST and CbE), thyroid hormone's levels (triiodothyronine; T3 and thyroxine; T4), heart function, and tadpoles swimming behaviour. The results showed that the LC50 values of O. americanus tadpoles were 3.73 PPF mg/L and 2.51 PPF mg/L at 24-h and 48-h, respectively (NOEC = 0.1 mg/L; LOEC = 1 mg/L, for both times). PPF concentrations at 48 h, induced enzymatic activities such as GST (212.98%–242.94%), AChE (142.15%–165.08%), and CbE (141.86%–87.14%) significantly respect to COs. During the 22 days of chronic PPF exposure, GST (0.01 mg/L 88%–153% NOEC), AChE (177.82% NOEC), and T4 (70% NOEC) also significantly increased respect to COs. Similarly, heart rate (fH) and ventricular cycle length (VV interval) in CO tadpoles were significantly higher than PPF treated. Finally, at NOEC tadpoles exhibited significant effects on the behavioral endpoint (swimming distance, mean speed, and global activity; P < 0.05).

Radiofrequency Ablation of Focal Atrial Tachycardia from Coronary Sinus

Focal atrial tachycardia (AT) is defined as atrial activation originating from a discrete focus with centrifugal spread. Available information suggests that focal activity can be caused by automaticity, triggered activity, or microreentry. Generally, AT response poorly to medication but can be treated by radiofrequency ablation with high long-term success. Focal AT represents approximately 3% to 17% of the patients referred for supraventricular tachycardia (SVT) radiofrequency ablation (RFA). Electrophysiology study is important to correctly diagnose the mechanism of the SVT before RFA is performed. Observation and several pacing maneuver could be done to identify the mechanism of SVT.A 54 year old female came with chief complaint of palpitation. During palpitation her ECG showed narrow complex regular tachycardia with the P-wave that was difficult to ascertain clearly. Electrophysiology study showed VA interval 130 ms, differences between VA interval during tachycardia and VA interval during RV pacing was 55 ms, no advanced in atrial activation, difference between ventricular post pacing interval (PPI) and tachycardia cycle length (TCL) was 130 ms, ventricular pacing during tachycardia results in V-A-A-V response before tachycardia resumes, and showed concentric atrial activation with earliest point at CS 9-10, indicating an AT from coronary sinus origin. AT was terminated during the RFA.Electrophysiology study is important to correctly diagnose AT, especially when P-wave during tachycardia in the surface ECG is uncertain. Several pacing maneuver during electrophysiology study can be very helpful to verify the diagnosis of AT.

Formation of reentrant circuits in the mid-myocardial infarct border zone

IntroductionIn this study, the mechanisms for onset and maintenance of mid-myocardial (intramural) reentrant circuits are considered, based upon anatomical structure. MethodA model of electrical activation wavefront curvature in the mid-myocardial postinfarction border zone is developed. Two arrhythmogenic structures are considered: 1. a constrained slab of viable tissue, and 2. a strand of surviving myocardial fibers with distal expansion. Equations are formulated to estimate activation coupling intervals, and ranges in taper and circuit dimensions, that will support functional conduction block during premature stimulation and reentrant ventricular tachycardia. ResultsFor onset and maintenance of reentry, the arrhythmogenic regions forming both slab and strand circuits are in the range of 50–600µm at their thinnest dimension. For constrained slabs, unidirectional block leading to reentry forms in the thin-to-thick direction during premature stimulation, and functional block at lateral boundaries enable formation of a double-loop circuit. The activation wavefront proceeds around the impediment and then curves in the opposite direction through the slab, reentering the previously excited tissue. For strands, unidirectional block forms at a distal expansion in response to premature stimulation. The strand reentrant circuit is bounded by infarcted tissue causing anatomical block, and can be single-loop or coaxial. For all architectures, circuit dimensions ranging from 1.6×1.6mm to 3.5×3.5mm support functional block when premature stimulus coupling intervals are 117–150ms and ventricular tachycardia cycle lengths are 160–350ms. ConclusionsFor slab and strand mid-myocardial arrhythmogenic structures, taper and circuit dimensions govern ranges in premature excitation coupling intervals and tachycardia cycle lengths necessary to support functional block.

Determining the Site of Accessory Pathways in Orthodromic Reciprocating Tachycardia by Using the Response to Right Ventricular Pacing

Postpacing interval (PPI) after right ventricular (RV) pacing entrainment minus tachycardia cycle length (TCL) with a correction for atrioventricular (AV) node delay (corrected PPI-TCL) was useful to differentiate atrioventricular node reentrant tachycardia (AVNRT) from orthodromic reciprocating tachycardia (ORT). However, the value of corrected PPI-TCL in determining the site of the accessory pathway (AP) in ORT has not been investigated. The purpose of this study was to assess whether the corrected PPI-TCL is useful in differentiating ORT using a left-sided AP from a right-sided AP. We studied 52 patients with ORT using a left-sided AP and 13 patients with a right-sided AP. The PPI was measured upon cessation of the RV pacing at a cycle length 10-40 ms shorter than the TCL. The corrected PPI-TCL was calculated from the subtraction of the increment in AV nodal conduction time of the first PPI from the PPI-TCL. The mean corrected PPI-TCL was 83 ± 20 ms in patients with ORT using a left-sided AP and 27 ± 19 ms in patients with a right-sided AP (P ≤ 0.001). All patients with ORT using a left-sided AP except three patients with left septal AP and none of the patients with ORT using a right-sided AP had a corrected PPI-TCL > 55 ms. The corrected PPI-TCL after the RV pacing entrainment is useful to guide differentiating ORT using a left-sided AP from a right-sided AP.

Ventricular cycle length irregularity affects the correlation between ventricular rate and coronary flow in isolated, Langendorff perfused guinea pig hearts

IntroductionHeart rate affects coronary flow, but the mechanism is complex. The relationship between rhythm and flow is unclear, especially in experimental settings used for determining drug actions. The present study examined whether ventricular irregularity influences coronary flow independently of heart rate. MethodsGuinea pig hearts were perfused (Langendorff mode) at constant pressure. Hypokalemic Krebs solution facilitated spontaneous development of arrhythmias. The ECG, left ventricular and perfusion pressures were recorded, and the coronary flow was measured. Beat-to-beat ventricular cycle length variability was quantified. Hearts were retrospectively allocated to arbitrary ‘Low’ or ‘High’ RR variability groups. ResultsA positive linear correlation was found between mean ventricular rate and coronary flow. The slope of the regression line was significantly greater in the ‘High’ versus ‘Low’ RR variability group, with greater coronary flow values in the ‘High’ RR variability group in the physiological heart rate range. During regular rhythm, left ventricular pressure exceeded perfusion pressure and prevented coronary perfusion at peak systole. However, ventricular irregularity significantly increased the number of beats in which left ventricular pressure remained below perfusion pressure, facilitating coronary perfusion. DiscussionIn isolated hearts, cycle length irregularity increases the slope of the positive linear correlation between mean ventricular rate and coronary flow via producing beats in which left ventricular pressure remains below perfusion pressure. This means that changes in rhythm have the capacity to influence coronary flow independently of heart rate in isolated hearts perfused at constant pressure, which should be noted in drug studies on arrhythmias performed in Langendorff hearts.

Shortness of breath in a patient with complete heart block and permanent pacemaker: A case of effective pacemaker reprogramming

An 82-year-old frail woman with a prior history of hypertension, complete heart block, and dual permanent pacemaker (Sensia DR SEDR01, Medtronic Inc., Minneapolis, MN) presented to pacemaker clinic with symptoms of shortness of breath (SOB), dizziness, and “low pulse rate”. Pacemaker interrogation showed underlying normal sinus rhythm, sinus rate of around 74 beats/ min with atrial sensed events, and ventricular paced rhythm with frequent symptomatic premature ventricular complexes (PVC). Pacemaker parameters were DDD, lower rate limit (LRL) of 60 beats/min, and maximum tracking rate of 120 beats/min, along with paced/sensed AV delay of 300/250 ms. Also noted was high pacing threshold of 3.5 V at 1 ms in the atrial lead with normal sensing parameters. In view of these, the pacemaker mode was reprogrammed to VDD mode and the patient was given betablocker therapy for frequent PVCs. She presented to arrhythmia clinic a few weeks later because of worsening SOB, light-headedness, and transient ischemic attacklike symptoms. Electrocardiography (ECG) performed in the clinic showed ventricular paced rhythmwith retrograde P waves (Fig. 1). What was the underlying arrhythmia mechanism? What treatment options are available? 2. Discussion

Troubleshooting implantable cardioverter-defibrillator sensing problems II.

Accurate atrial sensing during tachycardia is essential for reliable determination of atrial rate, which is a critical component of interval-based dual-chamber supraventricular tachycardia (SVT)–VT discrimination algorithms.1 Thus, atrial sensing in dual-chamber implantable cardioverter-defibrillators (ICDs) must be reliable at fast ventricular rates, a technically challenging requirement. Determining the atrial rate during rapidly conducted atrial flutter (AF) requires accurate sensing of low-amplitude signals (Figure I in the Data Supplement). The required high atrial sensitivity increases the risk of atrial oversensing, especially of far-field R waves. Pacemakers rely on a long postventricular atrial blanking period (PVAB) to prevent oversensing of far-field R waves, but ICDs cannot: for a fixed PVAB, the blanked fraction of the cardiac cycle increases with the ventricular rate. For example, a 100-ms PVAB blanks 10% of the cycle at a bradycardia pacing cycle length of 1000 ms, but 33% during rapidly conducted AF with ventricular cycle length of 300 ms. PVABs longer than ≈80 ms produce clinically significant, functional atrial undersensing in rapidly conducted AF,2 and any PVAB may cause undersensing of alternate atrial electrograms in AF with 2:1 atrioventricular conduction. The inherent trade-off between atrial oversensing and undersensing is problematic. Both cause errors in dual-chamber SVT–VT discrimination algorithms.2–6 In contemporary ICDs, ventricular electrogram morphology algorithms mitigate this problem but do not eliminate it. ### Determinants of Far-Field R Waves #### General Considerations In the absence of atrial lead dislodgement, the amplitude of far-field R wave depends on 4 variables. The first is the amplitude of the ventricular electrogram in ventricular myocardium. Thus, there is a correlation between far-field R–wave oversensing and left ventricular hypertrophy.7 The second is interelectrode spacing.8 Closely spaced electrodes (1.1 mm) minimize far-field R waves in comparison with conventional 10-mm spacing, but they also reduce the amplitude of atrial electrograms during short-term follow-up9,10 and …