Rate Of Ventricular Arrhythmias Research Articles

ICD shocks in LVAD patients are not associated with increased subsequent mortality risk.

Implantable cardioverter-defibrillator (ICD) shocks are associated with increased mortality risk in heart failure patients. Whether ICD shocks are associated with mortality in continuous flow LVAD (CF-LVAD) patients is unknown. We studied the relationship of ICD shocks and ventricular arrhythmias (VAs) to morbidity and mortality in CF-LVAD-supported patients in our institution. Single-center, retrospective study of prospectively collected ICD and LVAD databases. We analyzed data on VA which received ICD therapy in patients who underwent CF-LVAD implantation at Hartford Hospital between 2008 and 2018. A total of 157 patients were studied. During a median follow-up of 10months (interquartile range 5-20months), 48 patients (30.6%) experienced post-LVAD sustained VA. Thirty patients (19.1%) had appropriate shocks for VA and 5 patients (3.1%) had inappropriate shocks. Shocks for any arrhythmia were not associated with an increased risk of death (OR 0.836, 95% CI 0.224-3.115, p = 0.789). Neither post-LVAD VA nor the rate of VA was associated with an increased mortality risk (OR 0.662 [0.329-1.334], p = 0.248; OR 1.001 [0.989-1.014], p = 0.817, respectively). Cox multivariate regression analysis revealed pre-LVAD VA as a significant predictor of VA post LVAD implantation (OR 3.284 [1.584-6.808], p = 0.001). Symptoms with VA occurred in 22 (45.8%) patients, ranging from palpitations to near syncope/syncope. None of the variables including the rate of VA was associated with death or symptoms. VAs are common in CF-LVAD patients and occur with higher frequency in those with pre-LVAD VA and frequently cause symptoms. Neither VA nor ICD shocks are associated with mortality risk.

Clinical efficacy of open-irrigated electrode cooled with half-normal saline for initially failed radiofrequency ablation of idiopathic outflow tract ventricular arrhythmias.

Acute failure of radiofrequency ablation (RFA) of ventricular arrhythmias (VAs) occur in 10%-20% of patients and is partly attributed to inadequate lesion depth acquired with standard ablation protocols. Half-normal saline (HNS)-irrigation is a promising strategy to improve the success rate of VA ablation. This study investigated the efficacy of HNS-irrigated ablation after a failed standard plain normal saline solution (PNSS)-irrigated ablation on idiopathic outflow tract ventricular arrhythmia (OT-VA). This is a prospective observational study of consecutive patients undergoing RFA of idiopathic OT-VA comparing the efficacy of additional HNS-irrigated ablation for failed standard PNSS-irrigated ablation. Acute failure was defined as persistence of spontaneous VA or persistent inducibility of the clinical VA. Out of 160 OT-VA cases (51 ± 15-year-old, 62 males), 31 underwent HNS irrigation after a failed standard PNSS-irrigated ablation. The HNS group had a significantly longer procedure time (60.06 ± 43.83 vs 37.51 ± 33.40 minutes; P = .013) and higher radiation exposure (31.45 ± 20.24 vs 17.22 ± 15.25 minutes; P = .001) than the PNSS group but provided an additional acute success in 21 of 31 (67.7%) patients. Over a follow-up duration of 7.8 ± 4.6 months, 24 recurrences were identified, including 8 (25.8%) in the HNS and 16 (12.4%) in the PNSS group, with lower freedom from recurrence in the HNS group (log rank P = .009). No major complication was observed. HNS-irrigated ablation after failed standard PNSS-irrigated ablation is safe and additionally improves acute ablation success by 67.7% for idiopathic OT-VA but with a higher rate of recurrence on follow-up. Whether the application of HNS as initial irrigant could result in better outcome requires further investigation.

Prognostic Importance of Defibrillator-Appropriate Shocks and Antitachycardia Pacing in Patients With Mild Heart Failure.

BackgroundPatients with heart failure and an implantable cardioverter‐defibrillator (ICD) for primary prevention are at increased mortality risk after receiving shock therapy. We sought to determine the prognostic significance of ICD therapies, both shock and antitachycardia pacing, delivered for different ventricular arrhythmia (VA) rates.Methods and ResultsWe evaluated mortality risk among 1790 ICD‐implanted patients from MADIT‐CRT (Multicenter Automatic Defibrillator Implantation Trial With Cardiac Resynchronization Therapy). For the first analysis, patients were divided into mutually exclusive groups by the rate of treated VA only: slow VA (<200 beats per minute) and fast VA (≥200 beats per minute or ventricular fibrillation). In a secondary analysis, both the type of ICD therapy and VA rate were used. The reference group was always patients who had no ICD therapy. ICD therapy for fast VA was associated with increased mortality risk (hazard ratio [HR], 2.27; 95% CI, 1.48–3.48; P<0.001). However, mortality risk after ICD therapy for slow VA was similar to the risk related to no ICD therapy (HR, 1.45; 95% CI, 0.86–2.44; P=0.162). Consistently, shocks (HR, 2.96; 95% CI, 1.91–4.60; P<0.001) and antitachycardia pacing (HR, 2.22; 95% CI, 0.96–5.14; P=0.063) for fast VA were both associated with increased mortality risk. Shocks and antitachycardia pacing for slow VA were not significantly associated with increased mortality risk (HR, 1.43 [95% CI, 0.52–3.92; P=0.489]; and HR, 1.43 [95% CI, 0.80–2.56; P=0.232], respectively).ConclusionsIn patients with mild heart failure receiving ICD for primary prevention, mortality is associated with the rate of underlying VA rather than the type of therapy. These findings suggest that fast VA is a marker for increased mortality rather than shock therapy directly contributing to increased risk.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00180271.

Predictors and Clinical Impact of Late Ventricular Arrhythmias in Patients WithContinuous-Flow Left Ventricular Assist Devices.

This study aimed to evaluate the incidence, clinical impact, and predictors of late ventricular arrhythmias (VAs) in left ventricular assist device (LVAD) recipients aiming to clarify implantable cardioverter-defibrillator (ICD) indications. The arrhythmic risk and need for ICD in patients implanted with an LVAD are not very well known. This observational study was conducted in 19 centers between 2006 and 2016. Late VAs were defined as sustained ventricular tachycardia or fibrillation occurring >30 days post-LVAD implantation, without acute reversible cause and requiring appropriate ICD therapy, external electrical shock, or medical therapy. Among 659 LVAD recipients, 494 (median 58.9 years of age; mean left ventricular ejection fraction 20.7 ± 7.4%; 73.1% HeartMate II, 18.6% HeartWare, 8.3% Jarvik 2000) were discharged alive from hospital and included in the final analysis. Late VAs occurred in 133 (26.9%) patients. Multivariable analysis identified 6 independent predictors of late VAs: VAs before LVAD implantation, atrial fibrillation before LVAD implantation, idiopathic etiology of the cardiomyopathy, heart failure duration >12 months, early VAs (<30 days post-LVAD), and no angiotensin-converting enzyme inhibitors during follow-up. The "VT-LVAD score" was created, identifying 4 risk groups: low (score 0 to 1), intermediate (score 2 to 4), high (score 5 to 6), and very high (score 7 to 10). The rates of VAs at 1 year were 0.0%, 8.0%, 31.0% and 55.0%, respectively. Late VAs are common after LVAD implantation. The VT-LVAD score may help to identify patients at risk of late VAs and guide ICD indications in previously nonimplanted patients. (Determination of Risk Factors of Ventricular Arrhythmias [VAs] after implantation of continuous flow left ventricular assist device with continuous flow left ventricularassist device [CF-LVAD] [ASSIST-ICD]; NCT02873169).

Cardiac resynchronization is pro-arrhythmic in the absence of reverse ventricular remodelling: a systematic review and meta-analysis.

Cardiac resynchronization therapy (CRT) has been shown to reduce mortality and heart failure (HF) hospitalization but its effects on the rate of ventricular arrhythmias (VAs) appears to be neutral. We hypothesize that CRT with LV epicardial stimulation is inherently pro-arrhythmic and increases VA rates in the absence of reverse ventricular remodelling while conferring an anti-arrhythmic effect in mechanical responders. In this systematic review and meta-analysis, we considered retrospective cohort, prospective cohort, and randomized controlled trials comparing VA rates between cardiac resynchronization therapy-defibrillator (CRT-D) non-responders, CRT-D responders and those with implantable cardioverter-defibrillator (ICD) only. Studies were eligible if they defined CRT-D responders using a discrete left ventricular volumetric value as assessed by any imaging modality. Studies were identified through searching electronic databases from their inception to July 2017. We identified 2579 citations, of which 23 full-text articles were eligible for final analysis. Our results demonstrated that CRT-D responders were less likely to experience VA than CRT-D non-responders, relative risk (RR) 0.49 [95% confidence interval (CI) 0.41-0.58, P < 0.01] and also less than patients with ICD only: RR 0.59 (95% CI 0.50-0.69, P < 0.01). However, CRT-D mechanical non-responders had a greater likelihood of VA compared with ICD only, RR 0.76 (95% CI 0.63-0.92, P = 0.004). CRT-D non-responders experienced more VA than CRT-D responders and also more than those with ICD only, suggesting that CRT with LV epicardial stimulation may be inherently pro-arrhythmic in the absence of reverse remodelling.

Bursts of reperfusion arrhythmias occur independently of area at risk size and are the first marker of reperfusion injury

BackgroundThe presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger infarct size (IS). However it is unclear whether the initial area at risk (AAR), also a determining factor for IS, is responsible for this correlation. We hypothesized that IS would be significantly larger in the presence of VA, while AAR would not differ. Methods68 STEMI patients from the MAST study with 24-hour, continuous, 12‑lead Holter monitoring initiated prior to primary percutaneous coronary intervention (PCI) resulting in TIMI 3 flow post PCI were included. VA bursts were identified against subject-specific background VA rates using a previously validated statistical outlier method. IS, and infarct endocardial surface area (ESA) were obtained using CMR at mean 4.9 days after admission. Holter and CMR results were determined in core laboratories blinded to all other data. ResultsVA bursts were present in 69% (45/65) of patients. No significant differences were found for demographic characteristics, comorbidities, infarct location, number of diseased coronary vessels, or duration of ischemia between groups with and without VA burst. IS was significantly smaller in the group without VA bursts (median 9.3% vs 17.0%; p = 0.025). Infarct ESA did not significantly differ between the population with and without VA burst; median 24.3% vs 20.0%; p = 0.15. ConclusionVA bursts are a marker for larger IS independent of AAR, assessed by surrogate markers. These findings support the hypothesis that VA bursts are a marker of reperfusion damage occurring downstream at myocellular level.

Ventricular Arrhythmia Occurrence and Compliance in Patients Treated With the Wearable Cardioverter Defibrillator Following Percutaneous Coronary Intervention

The wearable cardioverter defibrillator (WCD) is a life-saving therapy in patients with high risk of arrhythmic death. We aimed to evaluate ventricular arrhythmia (VA) occurrence rate and compliance with the WCD during the first 90 days following myocardial revascularisation with percutaneous coronary intervention (PCI) in patients with left ventricular ejection fraction (LVEF) <30%. From September 2015 to November 2016, clinical characteristics, WCD recordings and compliance data of the aforementioned subset of patients were prospectively collected. Twenty-four patients (men=20, 80%) were included in this analysis. Mean age was 56±10 years and mean LVEF at enrolment was 26.6±4.3%. During a mean wearing period of 3.0±1.3 months, two episodes of VA occurred in two patients (8.3%): one successfully treated with WCD shock and one with spontaneous termination. The mean and median daily use of the WCD was 21.5hours and 23.5hours a day, respectively. Eighteen patients (75%) wore the WCD more than 22hours a day. The rate of VA, during the WCD period use after myocardial revascularisation with PCI, was high in our study. Otherwise it underlined that patient compliance is critical during the WCD period use. Remote monitoring and patient education are keys to achieve good compliance.

A real world wearable cardioverter defibrillator experience – Very high appropriate shock rate in ischemic cardiomyopathy patients at a European single-center

BackgroundThe wearable cardioverter defibrillator (WCD) has emerged as a valuable tool to protect patients with increased risk of sudden cardiac death (SCD). We sought to characterize WCD patients and to analyze predictors of ventricular arrhythmia (VA) occurrence and WCD shock delivery. Methods and resultsOne hundred fourteen patients with WCD use were included in the study. Indications were mainly ischemic cardiomyopathy (ICM; 31.6%), non-ICM (45.6%) and explantation of implantable cardioverter defibrillator due to device infection (11.4%). We observed sustained VA in 9.6% of the study population and 6.1% received an appropriate shock. VA occurred in 16.7% of ICM, 3.8% of non-ICM and 15.4% of patients with device infection. ConclusionsOur data demonstrate a very high rate of sustained VA in patients at risk for SCD during WCD use. ICM patients, including those with recent MI, bore the highest risk.

Reperfusion ventricular arrhythmia bursts identify larger infarct size in spite of optimal epicardial and microvascular reperfusion using cardiac magnetic resonance imaging.

Ventricular arrhythmia (VA) bursts following recanalisation in acute ST-elevation myocardial infarction (STEMI) are related to larger infarct size (IS). Inadequate microvascular reperfusion, as determined by microvascular obstruction (MVO) using cardiac magnetic resonance imaging (CMR), is also known to be associated with larger IS. This study aimed to test the hypothesis that VA bursts identify larger infarct size in spite of optimal microvascular reperfusion. All 65 STEMI patients from the Maastricht ST elevation (MAST) study with brisk epicardial flow (TIMI 3), complete ST recovery post-percutaneous coronary intervention and early CMR were included. Using 24-hour Holter registrations from the time of admission, VA bursts were identified against subject-specific Holter background VA rates using a statistical outlier method. MVO and final IS were determined using delayed enhancement CMR. MVO was present in 37/65 (57%) of patients. IS was significantly smaller in the group without MVO (median 9.4% vs. 20.5%; p < 0.001). IS in the group with MVO did not differ depending on VA burst ( n = 28/37; median 20.8% vs. 19.7%; p = 0.64). However, in the group without MVO, VA burst was associated with significantly larger IS ( n = 17/28; median 10.5% vs. 4.1%; p = 0.037). In multivariable analyses, VA burst as well as anterior infarct location remained independent predictors of larger infarct size. In the presence of suboptimal reperfusion with MVO by CMR, VA burst does not further define MI size. However, with optimal TIMI 3 reperfusion and optimal microvascular perfusion (i.e. no MVO), VA burst is associated with larger IS, indicating that VA burst is a marker of additional cell death.

Effects of Renal Artery Denervation on Ventricular Arrhythmias in a Postinfarct Model

The therapeutic potential of renal denervation (RDN) for arrhythmias has not been fully explored. Detailed mechanistic evaluation is in order. The objective of the present study was to determine the antiarrhythmic potential of RDN in a postinfarct animal model and to determine whether any benefits relate to RDN-induced reduction of sympathetic effectors on the myocardium. Pigs implanted with single-chamber implantable cardioverter defibrillators to record ventricular arrhythmias (VAs) were subjected to percutaneous coronary occlusion to induce myocardial infarction. Two weeks later, a sham or real RDN treatment was performed bilaterally using the St Jude EnligHTN basket catheter. Parameters of ventricular remodeling and modulation of cardio-renal sympathetic axis were monitored for 3 weeks after myocardial infarction. Histological analysis of renal arteries yielded a mean neurofilament score of healthy nerves that was significantly lower in the real RDN group than in sham controls; damaged nerves were found only in the real RDN group. There was a 100% reduction in the rate of spontaneous VAs after real RDN and a 75% increase in the rate of spontaneous VAs after sham RDN (P=0.03). In the infarcted myocardium, presence of sympathetic nerves and tissue abundance of neuropeptide-Y, an indicator of sympathetic nerve activities, were significantly lower in the RDN group. Peak and mean sinus tachycardia rates were significantly reduced after RDN. RDN in the infarcted pig model leads to reduction of postinfarction VAs and myocardial sympathetic effectors. This may form the basis for a potential therapeutic role of RDN in postinfarct VAs.

Effect of Ventricular Arrhythmia Ablation in Patients With Heart Mate II Left Ventricular Assist Devices: An Evaluation of Ablation Therapy.

Patients with advanced heart failure (HF) are predisposed to ventricular arrhythmias (VAs), particularly following implantation of a left ventricular assist device (LVAD). There is minimal evidence for appropriate management strategies. This study aimed to compare the burden of VA and response to ablation performed either before or following LVAD implantation. We created a retrospective cohort of patients who underwent both VA ablation and Heart Mate II (Thoratec, Pleasanton, CA, USA) LVAD implantation at Mayo Clinic (Rochester, MN, USA). Patients were stratified based on whether they underwent VA ablation before (pre-LVAD) or after LVAD (post-LVAD) implantation. Descriptive analyses assessed 6-month arrhythmia burden in relation to LVAD implantation and VA ablation. A total of 9 patients underwent both LVAD implantation and VA ablation. There were 3 and 6 patients, respectively, in the pre-LVAD and post-LVAD cohorts. Among patients in the pre-LVAD cohort, the median number of VAs tended to increase after ablation (9 vs. 72) and decreased after LVAD implantation (72 vs. 63). Similarly among patients in the post-LVAD cohort, the median burden of VAs increased after LVAD implantation (1 vs. 22) and the median burden decreased after ablation (22 vs. 13). Two of 6 patients had substrate related to the LVAD inflow cannula site, while other substrate was not related directly to the cannula. In patients with progressive HF and LVAD implantation, ablation is associated with reduced VA rates. In LVAD patients, most VAs arise from substrate unrelated to the inflow cannula site.

Ventricular arrhythmia burst is an independent indicator of larger infarct size even in optimal reperfusion in STEMI

ObjectiveWe hypothesized that ventricular arrhythmia (VA) bursts during reperfusion phase are a marker of larger infarct size despite optimal epicardial and microvascular perfusion. Methods126 STEMI patients were studied with 24h continuous, 12-lead Holter monitoring. Myocardial blush grade (MBG) was determined and VA bursts were identified against subject-specific background VA rates in core laboratories. Delayed-enhancement cardiovascular magnetic resonance imaging was used to determine infarct size. ResultsIn the group with MBG 3 no significant differences were found for baseline characteristics between burst versus no burst (102 vs. 24). In those with optimal epicardial and microvascular reperfusion (TIMI 3, stable ST-recovery, and MBG 3), VA burst was associated with larger infarct size (N=102/126; median 11.0 vs. 5.1%; p=0.004). ConclusionIn the event of MBG 3, VA bursts were associated with significantly larger infarct size even if optimal epicardial and microvascular reperfusion was present.

Impact of revascularization in patients with sustained ventricular arrhythmias, prior myocardial infarction, and preserved left ventricular ejection fraction

The impact of revascularization on recurrent ventricular arrhythmias (VAs) in patients with coronary artery disease and relatively preserved left ventricular ejection fraction (LVEF) is unknown. The purpose of this study was to determine the impact of revascularization on recurrent VAs or death. A cohort study was conducted on consecutive patients with prior myocardial infarction and LVEF ≥40% presenting with a first clinical sustained VA in the absence of an acute coronary syndrome. The impact of revascularization on recurrent VAs and all-cause mortality was assessed. A total of 274 patients (mean age 66.1 ± 9.7 years, 85.4% male, mean LVEF 48.3% ± 7.2%) were included in the study. Eight-eight patients (32.1%) underwent coronary revascularization. During mean follow-up of 6.2 ± 5.1 years, 140 (51.1%) died or had recurrent sustained VAs or appropriate implantable-cardioverter defibrillator therapy. Revascularization was not associated with a significantly lower rate of recurrent VAs or death (multivariable hazard ratio [HR] 0.86, 95% confidence interval [CI] 0.60-1.24, P = .43) regardless of whether it was complete or incomplete (HR 0.65, 95% CI 0.25-1.69, P = .37) or was performed by percutaneous or surgical means (HR 1.02, 95% CI 0.53-1.94, P = .96). An implantable-cardioverter defibrillator was associated with a significant reduction in mortality (HR 0.23, 95% CI 0.09-0.55, P = .001). Patients with prior myocardial infarction and LVEF ≥40% who present with sustained VAs in the absence of an acute coronary syndrome remain at high risk for recurrent VAs and all-cause death. Coronary revascularization does not systemically mitigate this risk.

Abstract 17176: Prognostic Importance of Defibrillator Appropriate Shocks and Anti Tachycardia Pacing in Mild Heart Failure Patients

Background: Previous studies had shown that patients with heart failure (HF) who receive implantable cardioverter-defibrillator (ICD) for primary prevention are at increased risk for mortality if they receive a shock. However, information about the prognostic importance of therapies [both shock and anti-tachycardia pacing (ATP)] delivered for a different ventricular arrhythmia (VA) rate is limited. Methods: We evaluated the risk for death among 1790 ICD implanted patients from the Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy using a time dependent analysis. Patients were categorized to mutually exclusive groups by either the rate of the treated VA (categorized at 200 bpm) or the type of the therapy and VA rate (ATP or shock both categorized at 200 bpm), the reference group was patients that had no device therapy. Results: During a median follow-up time of 4 years 423 patients had appropriate ICD therapy, with 163 receiving therapy for VA&lt; 200 bpm only, and 260 for VA≥200 bpm. ICD therapy for VA≥200 was associated with significant increased mortality (HR=2.27 CI 1.48-3.48, p&lt;.001), while therapy for VA&lt;200 was not different from the no therapy group (HR=1.45 CI=0.86-2.44, p=0.162). Accordingly, in a second model both shocks and ATPs for VA≥200 were associated with increased mortality (HR=2.96 CI 1.91-4.60 p&lt;.001 and HR=2.22 CI 0.96-5.14, p=0.063 respectively), while shocks and ATPs for VA&lt;200 did not differ from the no therapy group (HR=1.43 CI 0.52-3.92 p=0.489 and HR=1.43 CI 0.80-2.56, p=0.232 respectively). Conclusions: In mild HF patients, who receive ICD for primary prevention, mortality is associated with the rate of the arrhythmia rather than the device rendered therapy.

Prospective evaluation of where reperfusion ventricular arrhythmia “bursts” fit into optimal reperfusion in STEMI

BackgroundEarly reperfusion of ischemic myocytes is essential for optimal salvage in acute myocardial infarction. VA (ventricular arrhythmia) bursts after recanalization of the culprit vessel have been found to be related to larger infarct size (IS), using SPECT. ObjectiveThe hypothesis was tested that this finding could be confirmed in an independent cohort using a more accurate technique, i.e. delayed-enhancement cardiovascular magnetic resonance imaging (DE-CMR). MethodsAll 196 patients from the PREPARE and MAST studies who had 24-hour, continuous, 12-lead Holter, started before primary percutaneous coronary intervention resulting in brisk TIMI (thrombolysis in myocardial infarction) 3 flow and stable ST-recovery were included. VA bursts were identified against subject-specific background VA rates using a previously published statistical outlier method. IS was assessed using DE-CMR. Angiography, Holter and DE-CMR results were assessed in core laboratories, blinded to all other data. ResultsVA bursts were present in 154/196 (79%) of patients. Baseline characteristics between the groups with and without bursts were similar. VA burst was associated with significantly larger infarct size in the population as a whole (median 11.3% vs 5.3%; p=0.001) and also when divided in non-anterior (median 9.9% vs 4.9%; p=0.003) and anterior myocardial infarction (median 21.4% vs 12.0%; p=0.48), the latter not reaching statistical significance due to the small subset of patients. ConclusionBeyond the classical markers of “optimal” reperfusion such as TIMI 3 flow and stable ST-segment recovery, VA bursts occurring during the reperfusion phase are an early electrobiomarker of larger IS. Clinical trial registration: PREPARE: ISRCTN71104460 http://www.controlled-trials.com/ISRCTN71104460.

Inducibility of ventricular arrhythmias in early repolarization syndrome and Brugada syndrome: From the J-wave associated with prior cardiac event (J-PREVENT) registry

BackgroundAlthough electrophysiological study is often performed in Brugada syndrome (BrS) to assess inducibility of ventricular arrhythmias (VA), the utility of electrophysiological study in early repolarization syndrome (ERS) remains unknown. The aim of the present multi-center observational study was to compare inducibility of VA in ERS with BrS, and to investigate any association between inducibility and recurrence of arrhythmic events in these patients. MethodsThe J-PREVENT registry consists of patients with early repolarization or Brugada type 1 ECGs, a history of prior cardiac events, and no structural heart disease. Patients in the registry with implantable cardioverter-defibrillators (ICDs) and who underwent electrophysiological study were enrolled. VA inducibility was assessed by programmed electrical stimulation performed at two different sites in the right ventricle with up to three extrastimuli. The occurrence of VA during follow-up was determined by interrogation of the patients׳ ICDs. ResultsOf the 79 patients studied (72 males, mean age 44±13 years), 21 patients (27%) had ERS, and 58 had BrS, 20 of whom also had early repolarization in the inferolateral leads. VA was induced in 9 patients (43%) and 45 (78%) with ERS and BrS, respectively (p=0.006). During a median follow-up of 1453 days, occurrence rate of VA was similar between ERS and BrS (p=0.35). Inducibility was not associated with occurrence of VA in either syndrome. ConclusionsIn patients with ERS with prior history of cardiac events, VA was induced in 43% of patients during electrophysiological study, approximately half that of BrS. Inducibility was not associated with occurrence of VA during follow-up, although this was true of BrS patients as well. Electrophysiological study may play a limited role in risk stratification in ERS.

Reperfusion ventricular arrhythmia 'bursts' predict larger infarct size despite TIMI 3 flow restoration with primary angioplasty for anterior ST-elevation myocardial infarction

Aims Successful epicardial reperfusion with primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) can paradoxically evoke myocardial reperfusion injury, which may be signalled by temporally associated ventricular arrhythmias (VAs). We correlated reperfusion VA 'bursts' with final infarct size (IS) in patients with restored TIMI 3 flow following PCI for anterior STEMI. Methods and results All 128 anterior STEMI patients with final TIMI 3 flow had continuous 24 h digital 12-lead ECG with simultaneous Holter recording initiated prior to PCI, and Day 7/discharge SPECT imaging IS assessment. Angiography, SPECT imaging, continuous ST recovery, and quantitative rhythm analyses were performed. Reperfusion VA bursts were defined against patient-specific background VA rates and timed as concomitant with or following first angiographic TIMI 3 flow restoration associated with > or =50% stable ST recovery; they were then correlated with IS and global left ventricular ejection fraction (LVEF) at Day 7/discharge. Bursts occurred in 81/128 (63%) patients and were significantly correlated with larger IS and worse LVEF (median: 21.0 vs. 10.0%, P < 0.001; 35.5 vs. 46.5%, P < 0.001, respectively). In multivariable analyses that adjusted for known predictors of IS, the association of bursts with larger IS remained significant; similar results were seen for worse LVEF. Conclusion Reperfusion VA bursts predict larger IS despite TIMI 3 flow restoration with > or =50% stable ST recovery following PCI for anterior STEMI. Well-characterized reperfusion VAs may provide a novel biomarker of reperfusion injury.

Abstract 654: Ventricular Arrhythmia Following Alcohol Septal Ablation for Hypertrophic Obstructive Cardiomyopathy: Clinical Predictors of Events

Alcohol septal ablation (ASA) is a non-surgical alternative to septal myectomy for treatment of symptomatic, drug refractory hypertrophic obstructive cardiomyopathy (HOCM). The effect of ASA on the risk of ventricular arrhythmia (VA) is unknown. There is a theoretic concern for pro-arrhythmia at the site of myocardial injury. We examined the rates of sudden cardiac death (SCD) and VA (defined as VA requiring ICD therapy or documented VT/VF) among all 88 patients treated with ASA at Massachusetts General Hospital between 1998 and 2004. Of these patients, 37 had either an ICD or a permanent pacemaker in situ that enabled surveillance for VA events. Patients were classified as either high-risk (one of the following: VA or positive EP study, syncope due to suspected VA, family history of SCD, septal thickness ≥30mm by echocardiography, or failure to augment sBP &gt;20mmHg on stress testing), or low-risk (no high-risk features). There was no mortality attributable to sudden cardiac death (mean follow up 35±21mo). The event rate for VA in low-risk patients was 3.0% per year (2/18 patients), and 6.3% annually among high-risk patients (4/16 patients). Device data were not available on three patients. In a stepwise Cox proportional hazards multivariate analysis that included pre-ASA arrhythmia, peri-ASA arrhythmia, pre-ASA gradient, change in gradient after ASA, peak CK-MB, and post-ASA gradient, only post-ASA gradient predicted future VA (HR 1.06, 95% CI 1.03–1.10, p &lt;0.001). In this single center experience, ASA was not associated with SCD or with high rates of VA. The post-ASA gradient correlates with the risk of ventricular arrhythmia after ASA.

Reperfusion ventricular arrhythmia 'bursts' in TIMI 3 flow restoration with primary angioplasty for anterior ST-elevation myocardial infarction: a more precise definition of reperfusion arrhythmias

We sought to define reperfusion-induced ventricular arrhythmias (VAs) more precisely through simultaneous angiography, continuous ST-segment recovery, and beat-to-beat Holter analyses in subjects with anterior ST-elevation myocardial infarction (STEMI) undergoing primary angioplasty [percutaneous coronary intervention (PCI)]. All 157 subjects with final TIMI 3 flow had continuous 12-lead electrocardiography with simultaneous Holter recording initiated prior to PCI for continuous ST-segment recovery and quantitative VA analyses. Ventricular arrhythmia bursts were detected against subject-specific background VA rates using a statistical outlier method. For temporal correlations, timing and quality of reperfusion were defined as first angiographic TIMI 3 flow with >or=50% stable ST-segment recovery. Almost all subjects had VAs [156/157 (99%)], whereas VA bursts during or subsequent to reperfusion occurred in 97/157 (62%). The majority of VA bursts (72%) arose within 20 min of reperfusion (95% CI: 26.7, 72), with onset at a median of 4 min post-reperfusion (IQR: 0-43) Bursts comprised a median of 1290 ventricular premature complexes (VPCs) (IQR: 415-4632) and persisted for a median of 105 min (IQR: 35-250). Most background VAs occurred as single VPCs; bursts typically comprised runs of three or more VPCs. Subjects with bursts had higher absolute peak ST segments and more frequent worsening of ST elevation immediately after reperfusion. Ventricular arrhythmia bursts temporally associated with TIMI 3 flow restoration and stable ST-segment recovery (reperfusion VA bursts) can be precisely defined in subjects with anterior STEMI and may constitute a unique electric biosignal of myocellular response to reperfusion.

The Clinical Analyses of Tombstoning ST Segment in Anterior wall Acute Myocardial Infarction

目的 探讨前壁急性心肌梗塞(AMI)ST段呈墓碑形抬高的临床意义.方法68例前壁AMI分为ST段呈墓碑形抬高组(A组,19例)和ST段呈常态形抬高组(B组,49例),比较两组患者的心电图(ECG)特点及临床资料.结果(1)A组出现对应导联ST段下移13例(68.42%),B组14例(28.57%)(P＜0.05);(2)A组QT间期离散度(QTd)(69.98±18.26ms)明显高于B组(60.11±16.94ms)(P＜0.01);(3)室性心律失常A组11例(57.89%),B组9例(18.36%)(P＜0.05);(4)A组血清磷酸肌酸激酶(CK)及其同工酶(CK-MB)峰值为(2317.1±657.4)u/L和(264.4±127.9)u/L,明显高于B组的(1892.2±548.9)u/L和(137.6±88.5)u/L(分别为P＜0.005和P＜0.01):(5)冠脉造影A组17例(89.47%)呈多支病变,B组30例(61.22%)(P＜0.01).结论AMI后ST段呈墓碑形抬高患者梗死面积大,室性心律失常发生率高,冠状动脉病变严重。