Ventricular Arrhythmias After Primary Percutaneous Coronary Intervention for STEMI.

Importance: Currently, mortality risk for patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) with an uncomplicated postprocedure course is low. Less is known regarding the risk of in-hospital ventricular tachycardia (VT) and ventricular fibrillation (VF). Objective: To evaluate the risk of late VT and VF after primary PCI for STEMI. Design, Setting, and Participants: This cohort study included adults aged 18 years or older with STEMI treated with primary PCI between January 1, 2015, and December 31, 2018, identified in the US National Cardiovascular Data Registry Chest Pain-MI Registry. Data were analyzed from April to December 2020. Main Outcomes and Measures: Multivariable logistic regression was used to evaluate the risk of late VT (≥7 beat run of VT during STEMI hospitalization ≥1 day after PCI) or VF (any episode of VF≥1 day after PCI) associated with cardiac arrest and associations between late VT or VF and in-hospital mortality in the overall cohort and a cohort with uncomplicated STEMI without prior myocardial infarction or heart failure, systolic blood pressure less than 90 mm Hg, cardiogenic shock, cardiac arrest, reinfarction, or left ventricular ejection fraction (LVEF) less than 40%. Results: A total of 174 126 eligible patients with STEMI were treated with primary PCI at 814 sites in the study; 15 460 (8.9%) had VT or VF after primary PCI, and 4156 (2.4%) had late VT or VF. Among the eligible patients, 99 905 (57.4%) at 807 sites had uncomplicated STEMI. The median age for patients with late VT or VF overall was 63 years (IQR, 55-73 years), and 75.5% were men; the median age for patients with late VT or VF with uncomplicated STEMI was 60 years (IQR, 53-69 years), and 77.7% were men. The median length of stay was 3 days (IQR, 2-7 days) for the overall cohort with late VT or VF and 3 days (IQR, 2-4 days) for the cohort with uncomplicated STEMI with late VT or VF. The risk of late VT or VF was 2.4% (overall) and 1.7% (uncomplicated STEMI). Late VT or VF with cardiac arrest occurred in 674 patients overall (0.4%) and in 117 with uncomplicated STEMI (0.1%). LVEF was the most significant factor associated with late VT or VF with cardiac arrest (adjusted odds ratio [AOR] for every 5-unit decrease ≤40%: 1.67; 95% CI, 1.54-1.85). Late VT or VF events were associated with increased odds of in-hospital mortality in the overall cohort (AOR, 6.40; 95% CI, 5.63-7.29) and the cohort with uncomplicated STEMI (AOR, 8.74; 95% CI, 6.53-11.70). Conclusions and Relevance: In this study, a small proportion of patients with STEMI treated with primary PCI had late VT or VF. However, late VT or VF with cardiac arrest was rare, particularly in the cohort with uncomplicated STEMI. This information may be useful when determining the optimal timing for hospital discharge after STEMI.

Bleeding and Thrombosis in Patients With Out-of-Hospital Ventricular Tachycardia/Ventricular Fibrillation Arrest Treated With Extracorporeal Cardiopulmonary Resuscitation.

BACKGROUND: Extracorporeal cardiopulmonary resuscitation improves outcomes after out-of-hospital cardiac arrest. However, bleeding and thrombosis are common complications. We aimed to describe the incidence and predictors of bleeding and thrombosis and their association with in-hospital mortality. METHODS AND RESULTS: Consecutive patients presenting with refractory ventricular tachycardia/ventricular fibrillation out-of-hospital cardiac arrest between December 2015 and March 2022 who met the criteria for extracorporeal cardiopulmonary resuscitation initiation at our center were included. Major bleeding was defined by the Extracorporeal Life Support Organization's criteria. Adjusted analyses were done to seek out risk factors for bleeding and thrombosis and evaluate their association with mortality. Major bleeding occurred in 135 of 200 patients (67.5%), with traumatic bleeding from cardiopulmonary resuscitation in 73 (36.5%). Baseline demographics and arrest characteristics were similar between groups. In multivariable analysis, decreasing levels of fibrinogen were independently associated with bleeding (adjusted hazard ratio [aHR], 0.98 per every 10 mg/dL rise [95% CI, 0.96-0.99]). Patients who died had a higher rate of bleeds per day (0.21 versus 0.03, P<0.001) though bleeding was not significantly associated with in-hospital death (aHR, 0.81 [95% CI. 0.55-1.19]). A thrombotic event occurred in 23.5% (47/200) of patients. Venous thromboembolism occurred in 11% (22/200) and arterial thrombi in 15.5% (31/200). Clinical characteristics were comparable between groups. In adjusted analyses, no risk factors for thrombosis were identified. Thrombosis was not associated with in-hospital death (aHR, 0.65 [95% CI, 0.42-1.03]). CONCLUSIONS: Bleeding is a frequent complication of extracorporeal cardiopulmonary resuscitation that is associated with decreased fibrinogen levels on admission whereas thrombosis is less common. Neither bleeding nor thrombosis was significantly associated with in-hospital mortality.

Long-term follow-up of patients with Brugada syndrome: Foremost risk factors associated with overall arrhythmic events.

Brugada syndrome (BS) is characterized by ST segment elevation in right precordial leads (V1-V3), ventricular tachycardia (VT), ventricular fibrillation (VF), and sudden cardiac death (SCD) in individuals without structural heart disease. The aim of this study is to contribute to the controversial issue of finding the most valuable marker that can predict poor prognosis during follow-up in patients with a diagnosis of BS. A total of 68 patients diagnosed with BS or had Brugada-type ECG change between January 1997 and July 2012 at the Department of Cardiology of Baskent University Faculty of Medicine, Ankara, Turkey, were included in this cohort study. Patients were screened every 6 months for arrhythmia-related syncope, SCD, appropriate and inappropriate defibrillation (shock), AF development and death; collectively defined as "arrhythmic events" and were the primary endpoints. Patients with and without arrhythmic events were compared. The mean age was 34.9 ±â€…12.2 years (9-71 years), and 52 (76.5%) patients were male. Mean follow-up was 49.6 ±â€…37.6 months (4-188 months). Univariate analysis showed that male sex (P = .004), type 1 electrocardiographic pattern (P = .008), SCD (P = .036), VT/VF history (P = .046), requirement for electrophysiological studies (P = .034), implantable cardioverter-defibrillator placement (P = .014) were found to demonstrate significant differences in patients with and without arrhythmic events. In multivariable analyzes, spontaneous type 1 ECG presence (HR = 8.54, 95% CI: 0.38-26.37; P = .003) and VT/VF history (HR = 9.21, 95% CI: 0.004-1.88; P = .002) were found to be independently associated with arrhythmic events. We found the presence of spontaneous type 1 ECG and a history of VT/VF to be associated with increased likelihood of overall arrhythmic events in BS. Given the higher risk of poor prognosis, we recommend additional measures in patients with BS who have these features.

Association between survival and number of shocks for pulseless ventricular arrhythmias during pediatric in-hospital cardiac arrest in a national registry.

BACKGROUND: Annually 15,200 children suffer an in-hospital cardiac arrest (IHCA) in the US. Ventricular fibrillation or pulseless ventricular tachycardia (VF/pVT) is the initial rhythm in 10-15% of these arrests. We sought to evaluate the association of number of shocks and early dose escalation with survival for initial VF/pVT in pediatric IHCA. METHODS: Using 2000-2020 data from the American Heart Association's (AHA) Get with the Guidelines®-Resuscitation (GWTG-R) registry, we identified children >48 hours of life and ≤18 years who had an IHCA from initial VF/pVT and received defibrillation. RESULTS: There were 251 subjects (37.7%) who received a single shock and 415 subjects (62.3%) who received multiple shocks. Baseline and cardiac arrest characteristics did not differ between those who received a single shock versus multiple shocks except for duration of arrest and calendar year. The median first shock dose was consistent with AHA dosing recommendations and not different between those who received a single shock versus multiple shocks. Survival was improved for those who received a single shock compared to multiple shocks. However, no difference in survival was noted between those who received 2, 3, or ≥4 shocks. Of those receiving multiple shocks, no difference was observed with early dose escalation. CONCLUSIONS: In pediatric IHCA, most patients with initial VF/pVT require more than one shock. No distinctions in patient or pre-arrest characteristics were identified between those who received a single shock versus multiple shocks. Subjects who received a single shock were more likely to survive to hospital discharge even after adjusting for duration of resuscitation.

Stereotactic arrhythmia radioablation and its implications for modern cardiac electrophysiology: results of an EHRA survey.

Stereotactic arrhythmia radioablation (STAR) is a treatment option for recurrent ventricular tachycardia/fibrillation (VT/VF) in patients with structural heart disease (SHD). The current and future role of STAR as viewed by cardiologists is unknown. The study aimed to assess the current role, barriers to application, and expected future role of STAR. An online survey consisting of 20 questions on baseline demographics, awareness/access, current use, and the future role of STAR was conducted. A total of 129 international participants completed the survey [mean age 43 ± 11 years, 25 (16.4%) female]. Ninety-one (59.9%) participants were electrophysiologists. Nine participants (7%) were unaware of STAR as a therapeutic option. Sixty-four (49.6%) had access to STAR, while 62 (48.1%) had treated/referred a patient for treatment. Common primary indications for STAR were recurrent VT/VF in SHD (45%), recurrent VT/VF without SHD (7.8%), or premature ventricular contraction (3.9%). Reported main advantages of STAR were efficacy in the treatment of arrhythmias not amenable to conventional treatment (49%) and non-invasive treatment approach with overall low expected acute and short-term procedural risk (23%). Most respondents have foreseen a future clinical role of STAR in the treatment of VT/VF with or without underlying SHD (72% and 75%, respectively), although only a minority expected a first-line indication for it (7% and 5%, respectively). Stereotactic arrhythmia radioablation as a novel treatment option of recurrent VT appears to gain acceptance within the cardiology community. Further trials are critical to further define efficacy, patient populations, as well as the appropriate clinical use for the treatment of VT.

Biomarker Periodic Repolarization Dynamics Indicates Enhanced Risk for Arrhythmias and Sudden Cardiac Death in Myocardial Infarction in Pigs.

BACKGROUND: Periodic repolarization dynamics (PRD) is an electrocardiographic biomarker that captures repolarization instability in the low frequency spectrum and is believed to estimate the sympathetic effect on the ventricular myocardium. High PRD indicates an increased risk for postischemic sudden cardiac death (SCD). However, a direct link between PRD and proarrhythmogenic autonomic remodeling has not yet been shown. METHODS AND RESULTS: We investigated autonomic remodeling in pigs with myocardial infarction (MI)-related ischemic heart failure induced by balloon occlusion of the left anterior descending artery (n=17) compared with pigs without MI (n=11). Thirty days after MI, pigs demonstrated enhanced sympathetic innervation in the infarct area, border zone, and remote left ventricle paralleled by altered expression of autonomic marker genes/proteins. PRD was enhanced 30 days after MI compared with baseline (pre-MI versus post-MI: 1.75±0.30 deg2 versus 3.29±0.79 deg2, P<0.05) reflecting pronounced autonomic alterations on the level of the ventricular myocardium. Pigs with MI-related ventricular fibrillation and SCD had significantly higher pre-MI PRD than pigs without tachyarrhythmias, suggesting a potential role for PRD as a predictive biomarker for ischemia-related arrhythmias (no ventricular fibrillation versus ventricular fibrillation: 1.50±0.39 deg2 versus 3.18±0.53 deg2 [P<0.05]; no SCD versus SCD: 1.67±0.32 deg2 versus 3.91±0.63 deg2 [P<0.01]). CONCLUSIONS: We demonstrate that ischemic heart failure leads to significant proarrhythmogenic autonomic remodeling. The concomitant elevation of PRD levels in pigs with ischemic heart failure and pigs with MI-related ventricular fibrillation/SCD suggests PRD as a biomarker for autonomic remodeling and as a potential predictive biomarker for ventricular arrhythmias/survival in the context of MI.

A case report of ventricular fibrillation following Shockwave intravascular lithotripsy during percutaneous coronary intervention.

BACKGROUND: Shockwave intravascular lithotripsy (S-IVL) is widely used during percutaneous coronary intervention (PCI) of calcified coronary arteries. Ventricular capture beats during S-IVL are common but arrhythmias are rare. CASE PRESENTATION: A 75-year-old woman was scheduled for PCI to a short, heavily calcified chronic total occlusion of the right coronary artery. After wiring of the occlusion, S-IVL was used to predilated the calcified stenosis. During S-IVL, the patient developed ventricular fibrillation twice. CONCLUSION: To our knowledge, this is only the second reported case of VF during S-IVL. Although very rare, it is important to be aware of this potential and serious complication.

Vericiguat suppresses ventricular tachyarrhythmias inducibility in a rabbit myocardial infarction model.

BACKGROUND: The VICTORIA trial demonstrated a significant decrease in cardiovascular events through vericiguat therapy. This study aimed to assess the potential mechanisms responsible for the reduction of cardiovascular events with vericiguat therapy in a rabbit model of myocardial infarction (MI). METHODS: A chronic MI rabbit model was created through coronary artery ligation. Following 4 weeks, the hearts were harvested and Langendorff perfused. Subsequently, electrophysiological examinations and dual voltage-calcium optical mapping studies were conducted at baseline and after administration of vericiguat at a dose of 5 µmol/L. RESULTS: Acute vericiguat therapy demonstrated a significant reduction in premature ventricular beat burden and effectively suppressed ventricular arrhythmic inducibility. The electrophysiological influences of vericiguat therapy included an increased ventricular effective refractory period, prolonged action potential duration, and accelerated intracellular calcium (Cai) homeostasis, leading to the suppression of action potential and Cai alternans. The pacing-induced ventricular arrhythmias exhibited a reentrant pattern, attributed to fixed or functional conduction block in the peri-infarct zone. Vericiguat therapy effectively mitigated the formation of cardiac alternans as well as the development of reentrant impulses, providing additional anti-arrhythmic benefits. CONCLUSIONS: In the MI rabbit model, vericiguat therapy demonstrates anti-ventricular arrhythmia effects. The vericiguat therapy reduces ventricular ectopic beats, inhibiting the initiation of ventricular arrhythmias. Furthermore, the therapy successfully suppresses cardiac alternans, preventing conduction block and, consequently, the formation of reentry circuits.

The Pharmacologic Management of Cardiac Arrest.

The effectiveness of pharmacologic management of cardiac arrest patients is widely debated; however, several studies published in the past 5 years have begun to clarify some of these issues. This article covers the current state of evidence for the effectiveness of the vasopressor epinephrine and the combination of vasopressin-steroids-epinephrine and antiarrhythmic medications amiodarone and lidocaine and reviews the role of other medications such as calcium, sodium bicarbonate, magnesium, and atropine in cardiac arrest care. We additionally review the role of ß-blockers for refractory pulseless ventricular tachycardia/ventricular fibrillation and thrombolytics in undifferentiated cardiac arrest and suspected fatal pulmonary embolism.

Arrhythmia onsets triggered by acute myocardial ischemia are not mediated by lysophosphoglycerides accumulation in ventricular myocardium.

Lysophosphoglycerides (LPLs) have been reported to accumulate in myocardium and serve as a cause of arrhythmias in acute myocardial ischemia. However, in this study we found that LPLs level in the ventricular myocardium was decreased by the onset of acute myocardial ischemia in vivo in rats. Decreasing of LPLs level in left ventricular myocardium, but not right, was observed within 26 min of left myocardial ischemia, regardless of whether arrhythmias were triggered. Lower LPLs level in the ventricular myocardium was also observed in aconitine-simulated ventricular fibrillation (P < 0.0001) and ouabain-simulated III° atrioventricular block (P < 0.0001). Shot-lasting electric shock, e.g., ≤ 40 s, decreased LPLs level, while long-lasting, e.g., 5 min, increased it (fold change = 2.27, P = 0.0008). LPLs accumulation was observed in long-lasting myocardial ischemia, e.g., 4 h (fold change = 1.20, P = 0.0012), when caspase3 activity was elevated (P = 0.0012), indicating increased cell death, but not coincided with higher frequent arrhythmias. In postmortem human ventricular myocardium, differences of LPLs level in left ventricular myocardium was not observed among coronary artery disease- and other heart diseases-caused sudden death and non-heart disease caused death. LPLs level manifested a remarkable increasing from postmortem 12 h on in rats, thus abolishing the potential for serving as biomarkers of sudden cardiac death. Token together, in this study we found that LPLs in ventricular myocardium were initially decreased by the onset of ischemia, LPLs accumulation do not confer arrhythmogenesis during acute myocardial ischemia. It is necessary to reassess the roles of LPLs in myocardial infarction.

Association of coronary angiography with ST-elevation and no ST-elevation in patients with refractory ventricular fibrillation - A substudy of the DOuble SEquential External Defibrillation for Refractory Ventricular Fibrillation (DOSE-VF randomized control trial).

BACKGROUND: Refractory ventricular fibrillation or pulseless ventricular tachycardia (rVF/pVT) during out-of-hospital cardiac arrest (OHCA) is associated with poor survival. Double sequential defibrillation (DSED) and vector change (VC) improved survival for rVF/pVT in the DOSE-VF RCT. However, the role of angiography and percutaneous coronary intervention (angiography/PCI) during the trial is unknown. OBJECTIVES: To determine the incidence of ST-elevation (STE) and no ST-elevation (NO-STE) on post-arrest ECG and the use of angiography/PCI in patients with rVF/pVT during the DOSE-VF RCT. METHOD: Adults (≥18-years) with rVF/pVT OHCA randomized in the DOSE-VF RCT who survived to hospital admission were included. The primary analysis compared the proportion of angiography in STE and NO-STE. We performed regression modelling to examine association between STE, the interaction with defibrillation strategy, and survival to discharge controlling for known covariates. RESULTS: We included 151 patients, 74 (49%) with STE and 77 (51%) with NO-STE. The proportion of angiography was higher in the STE cohort than NO-STE (87.8% vs 44.2%, p < 0.001); similarly the proportion of PCI was also higher (75.7% vs 9.1%, p < 0.001). Survival to discharge was similar between STE and NO-STE (63.5% vs 51.9%, p = 0.15). Use of angiography/PCI did not differ between defibrillation strategies. Decreased age (OR 0.95, 95% CI 0.92-0.98; p = 0.001) and angiography (OR 9.33, 95% CI 3.60-26.94; p < 0.001) were predictors of survival; however, STE was not. CONCLUSION: We found high rates of angiography/PCI in patients with STE compared to NO-STE, however similar rates of survival. Angiography was an independent predictor of survival. Improved rates of survival employing DSED and VC were independent of angiography/PCI.

The impact of alternate defibrillation strategies on shock-refractory and recurrent ventricular fibrillation: A secondary analysis of the DOSE VF cluster randomized controlled trial.

BACKGROUND: The DOSE VF randomized controlled trial (RCT) employed a pragmatic definition of refractory ventricular fibrillation (VF after three successive shocks). However, it remains unclear whether the underlying rhythm during the first three shocks was shock-refractory or recurrent VF. OBJECTIVE: To explore the relationship between alternate defibrillation strategies employed during the DOSE VF RCT and the type of VF, either shock-refractory VF or recurrent VF, on patient outcomes. METHODS: We performed a secondary analysis of the DOSE VF RCT. We categorized cases as shock-refractory or recurrent VF based on pre-randomization shocks (shocks 1-3). We then analyzed all subsequent (post-randomization) shocks to assess the impact of standard, vector change (VC) or double sequential external defibrillation (DSED) shocks on clinical outcomes employing logistic regression adjusted for Utstein variables, antiarrhythmics, and epinephrine. RESULTS: We included 345 patients; 60 (17%) shock-refractory VF, and 285 (83%) recurrent VF. Patients in recurrent VF had greater survival than shock-refractory VF (OR: 2.76 95% CI [1.04, 7.27]). DSED was superior to standard defibrillation for survival overall, and for patients with shock-refractory VF (28.6% vs 0%, p = 0.041) but not for those in recurrent VF. DSED was superior to standard defibrillation for return of spontaneous circulation (ROSC) and neurologic survival for shock-refractory and recurrent VF. VC defibrillation was not superior for survival or ROSC overall, for shock-refractory, or recurrent VF groups, but was superior for VF termination across all groups. CONCLUSION: DSED appears to be the superior defibrillation strategy in the DOSE VF trial, irrespective of whether the preceding VF is shock-refractory or recurrent.

A Case of Ventricular Fibrillation in Masked Long-QT Syndrome Coexisting with Coronary Vasospasm.

Although long-QT syndrome (LQTS) with a normal range QT interval at rest leads to fatal ventricular arrhythmias, it is difficult to diagnose. In this article, we present a rare case of a patient who suffered a cardiac arrest and was recently diagnosed with LQTS and coronary vasospasm. A 62-year-old man with no syncopal episodes had a cardiopulmonary arrest while running. During coronary angiography, vasospasm was induced and we prescribed coronary vasodilators, including calcium channel blockers. An exercise stress test was performed to evaluate the effect of medications and accidentally unveiled exercise-induced QT prolongation. He was diagnosed with LQTS based on diagnostic criteria. Pharmacotherapy and an implantable cardioverter defibrillator were used for his medical management. It is extremely rare for LQTS and coronary vasospasm to coexist. In cases of exercise-induced arrhythmic events, the exercise stress test might be helpful to diagnose underlying disease.

Enhancing the accuracy of shock advisory algorithms in automated external defibrillators during ongoing cardiopulmonary resuscitation using a cascade of CNNEDs.

Delivery of continuous cardiopulmonary resuscitation (CPR) plays an important role in the out-of-hospital cardiac arrest (OHCA) survival rate. However, to prevent CPR artifacts being superimposed on ECG morphology data, currently available automated external defibrillators (AEDs) require pauses in CPR for accurate analysis heart rhythms. In this study, we propose a novel Convolutional Neural Network-based Encoder-Decoder (CNNED) structure with a shock advisory algorithm to improve the accuracy and reliability of shock versus non-shock decision-making without CPR pause in OHCA scenarios. Our approach employs a cascade of CNNEDs in conjunction with an AED shock advisory algorithm to process the ECG data for shock decisions. Initially, a CNNED trained on an equal number of shockable and non-shockable rhythms is used to filter the CPR-contaminated data. The resulting filtered signal is then fed into a second CNNED, which is trained on imbalanced data more tilted toward the specific rhythm being analyzed. A reliable shock versus non-shock decision is made when both classifiers from the cascade structure agree, while segments with conflicting classifications are labeled as indeterminate, indicating the need for additional segments to analyze. To evaluate our approach, we generated CPR-contaminated ECG data by combining clean ECG data with 52 CPR samples. We used clean ECG data from the CUDB, AFDB, SDDB, and VFDB databases, to which 52 CPR artifact cases were added, while a separate test set provided by the AED manufacturer Defibtech LLC was used for performance evaluation. The test set comprised 20,384 non-shockable CPR-contaminated segments from 392 subjects, as well as 3744 shockable CPR-contaminated samples from 41 subjects with coarse ventricular fibrillation (VF) and 31 subjects with rapid ventricular tachycardia (rapid VT). We observed improvements in rhythm analysis using our proposed cascading CNNED structure when compared to using a single CNNED structure. Specifically, the specificity of the proposed cascade of CNNED structure increased from 99.14% to 99.35% for normal sinus rhythm and from 96.45% to 97.22% for other non-shockable rhythms. Moreover, the sensitivity for shockable rhythm detection increased from 90.90% to 95.41% for ventricular fibrillation and from 82.26% to 87.66% for rapid ventricular tachycardia. These results meet the performance thresholds set by the American Heart Association and demonstrate the reliable and accurate analysis of heart rhythms during CPR using only ECG data without the need for CPR interruptions or a reference signal.

Analysis of the Association between Copy Number Variation and Ventricular Fibrillation in ST-Elevation Acute Myocardial Infarction.

Sudden cardiac death due to ventricular fibrillation (VF) during ST-elevation acute myocardial infarction (STEAMI) significantly contributes to cardiovascular-related deaths. Although VF has been linked to genetic factors, variations in copy number variation (CNV), a significant source of genetic variation, have remained largely unexplored in this context. To address this knowledge gap, this study performed whole exome sequencing analysis on a cohort of 39 patients with STEAMI who experienced VF, aiming to elucidate the role of CNVs in this pathology. The analysis revealed CNVs in the form of duplications in the PARP2 and TTC5 genes as well as CNVs in the form of deletions in the MUC15 and PPP6R1 genes, which could potentially serve as risk indicators for VF during STEAMI. The analysis also underscores notable CNVs with an average gene copy number equal to or greater than four in DEFB134, FCGR2C, GREM1, PARM1, SCG5, and UNC79 genes. These findings provide further insight into the role of CNVs in VF in the context of STEAMI.