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.

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.

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.

Commotio cordis: Another cardiac arrest "sine materia". The 1707 early report and interpretation by G.M. Lancisi.

Sudden death by commotio cordis is rare. It is the consequence of a blunt trauma of the chest overlying the heart. The mechanism is a cardiac arrest by ventricular fibrillation in the absence of grossly or microscopically apparent myocardial injury. It has been reproduced in animals. The first historical case was reported by Giovanni Maria Lancisi in his book "De Subitaneis Mortibus'' published in 1707. Sudden death occurred in a man receiving a powerful blow under the xiphoid cartilage. Lancisi advanced the hypothesis of acute heart failure by a diastolic stand still ("death in diastole'').

Clinical characteristics of electrical storm in patients with early repolarization syndrome.

BACKGROUND: Early repolarization syndrome (ERS) is an idiopathic ventricular fibrillation (VF) associated with inferolateral J waves. While electrical storm (ES) in ERS is not rare, their characteristics and risk factors are not fully understood. OBJECTIVE: This study aimed to clarify the significance of ES in ERS. METHODS: We evaluated 44 patients with ERS who experienced VF/sudden cardiac death or arrhythmic syncope. We assessed clinical characteristics to identify the risk factors for ES. RESULTS: In total, 13 patients (30%) experienced ES (ES group). Of these, 11 patients (85%) experienced ES during the acute phase of initial VF episodes and 2 patients (2%) experienced ES during follow-up. VF associated with ES occurred during therapeutic hypothermia in 6 of 13 patients (46%). The J-wave voltage during therapeutic hypothermia was higher in the ES group than that in the patients without ES. Isoproterenol was used in 5 patients (38%), which decreased J-wave voltage and relieved ES. Among the clinical markers, shorter QT and QTp intervals (the interval from QRS onset to the peak of T wave), pilsicainide-induced ST elevation, and high scores on the Shanghai Score System were associated with ES. Although pilsicainide induced ST elevation in 6 of 34 patients (18%), spontaneous Brugada electrocardiographic patterns did not appear to be associated with VF. Therapeutic hypothermia was also a risk factor for acute phase ES. CONCLUSION: Patients with ERS in the ES group frequently had short QT and QTp intervals, pilsicainide-induced ST elevations, and high Shanghai Score System scores. Therapeutic hypothermia was also associated with acute phase ES.

LDIAED: A lightweight deep learning algorithm implementable on automated external defibrillators.

Differentiating between shockable and non-shockable Electrocardiogram (ECG) signals would increase the success of resuscitation by the Automated External Defibrillators (AED). In this study, a Deep Neural Network (DNN) algorithm is used to distinguish 1.4-second segment shockable signals from non-shockable signals promptly. The proposed technique is frequency-independent and is trained with signals from diverse patients extracted from MIT-BIH, MIT-BIH Malignant Ventricular Ectopy Database (VFDB), and a database for ventricular tachyarrhythmia signals from Creighton University (CUDB) resulting, in an accuracy of 99.1%. Finally, the raspberry pi minicomputer is used to load the optimized version of the model on it. Testing the implemented model on the processor by unseen ECG signals resulted in an average latency of 0.845 seconds meeting the IEC 60601-2-4 requirements. According to the evaluated results, the proposed technique could be used by AED's.

Relation of Early Monomorphic Ventricular Tachycardia to Long-Term Mortality in ST-Elevation Myocardial Infarction.

Early ventricular tachycardia (VT) and ventricular fibrillation (VF) are associated with increased in-hospital mortality but do not influence the long-term prognosis in ST-elevation myocardial infarction (STEMI). Recent data advocate a differential approach to the type of arrhythmia and indicate long-term mortality hazard associated with monomorphic VT. We aimed to evaluate the prognostic value of early monomorphic VT compared to nonmonomorphic VT/VF in a nonselected cohort of STEMI patients. Consecutive STEMI patients admitted for primary percutaneous coronary intervention from 2007 to 2010 were included. Clinical characteristics were obtained from the Swedish national SWEDEHEART registry. The occurrence and type of early VT/VF were verified in medical records. All-cause mortality 8 years after STEMI was assessed using the Swedish Cause of Death Register. A total of 2,277 STEMI patients were included (age 66 ± 12 years, 70% male), among them 35 (1.5%) with early monomorphic VT and 115 (5.1%) with nonmonomorphic VT/VF. Patients with monomorphic VT had similar clinical characteristics compared to those with nonmonomorphic VT/VF. In total, 22 patients (63%) with monomorphic VT and 43 (37%) with nonmonomorphic VT/VF died by 8 years of follow-up (p = 0.011). Monomorphic VT was associated with a higher risk of all-cause mortality compared to nonmonomorphic VT/VF in univariate analysis (HR 2.03, 95% CI 1.21 to 3.39, p = 0.007) and after adjustment for age and history of myocardial infarction (MI) (HR 1.74, 95% CI 1.02 to 2.97, p = 0.041). Early monomorphic VT in STEMI is associated with a higher risk of all-cause mortality compared to nonmonomorphic VT/VF and deserves further studies to refine risk stratification strategies.

A governing equation for rotor and wavelet number in human clinical ventricular fibrillation: Implications for sudden cardiac death.

BACKGROUND: Ventricular fibrillation (VF) is characterized by multiple wavelets and rotors. No equation to predict the number of rotors and wavelets observed during fibrillation has been validated in human VF. OBJECTIVE: The purpose of this study was to test the hypothesis that a single equation derived from a Markov M/M/∞ birth-death process could predict the number of rotors and wavelets occurring in human clinical VF. METHODS: Epicardial induced VF (256-electrode) recordings obtained from patients undergoing cardiac surgery were studied (12 patients; 62 epochs). Rate constants for phase singularity (PS) (which occur at the pivot points of rotors) and wavefront (WF) formation and destruction were derived by fitting distributions to PS and WF interformation and lifetimes. These rate constants were combined in an M/M/∞ governing equation to predict the number of PS and WF in VF episodes. Observed distributions were compared to those predicted by the M/M/∞ equation. RESULTS: The M/M/∞ equation accurately predicted average PS and WF number and population distribution, demonstrated in all epochs. Self-terminating episodes of VF were distinguished from VF episodes requiring termination by a trend toward slower PS destruction, slower rates of PS formation, and a slower mixing rate of the VF process, indicated by larger values of the second largest eigenvalue modulus of the M/M/∞ birth-death matrix. The longest-lasting PS (associated with rotors) had shorter interactivation time intervals compared to shorter-lasting PS lasting <150 ms (∼1 PS rotation in human VF). CONCLUSION: The M/M/∞ equation explains the number of wavelets and rotors observed, supporting a paradigm of VF based on statistical fibrillatory dynamics.

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

[Figure: see text].

Excess ischemic tachyarrhythmias trigger protection against myocardial infarction in hypertensive rats.

Increased level of C-reactive protein (CRP) is a risk factor for cardiovascular diseases, including myocardial infarction and hypertension. Here, we analyzed the effects of CRP overexpression on cardiac susceptibility to ischemia/reperfusion (I/R) injury in adult spontaneously hypertensive rats (SHR) expressing human CRP transgene (SHR-CRP). Using an in vivo model of coronary artery occlusion, we found that transgenic expression of CRP predisposed SHR-CRP to repeated and prolonged ventricular tachyarrhythmias. Excessive ischemic arrhythmias in SHR-CRP led to a significant reduction in infarct size (IS) compared with SHR. The proarrhythmic phenotype in SHR-CRP was associated with altered heart and plasma eicosanoids, myocardial composition of fatty acids (FAs) in phospholipids, and autonomic nervous system imbalance before ischemia. To explain unexpected IS-limiting effect in SHR-CRP, we performed metabolomic analysis of plasma before and after ischemia. We also determined cardiac ischemic tolerance in hearts subjected to remote ischemic perconditioning (RIPer) and in hearts ex vivo. Acute ischemia in SHR-CRP markedly increased plasma levels of multiple potent cardioprotective molecules that could reduce IS at reperfusion. RIPer provided IS-limiting effect in SHR that was comparable with myocardial infarction observed in naïve SHR-CRP. In hearts ex vivo, IS did not differ between the strains, suggesting that extra-cardiac factors play a crucial role in protection. Our study shows that transgenic expression of human CRP predisposes SHR-CRP to excess ischemic ventricular tachyarrhythmias associated with a drop of pump function that triggers myocardial salvage against lethal I/R injury likely mediated by protective substances released to blood from hypoxic organs and tissue at reperfusion.

Comparison of Circadian Variation for In-Hospital Versus Out-of-Hospital Sudden Cardiac Arrest Survivors.

Several studies have reported circadian periodicity of sudden cardiac arrest (SCA). It remains unclear to what extent this circadian rhythm is influenced by variation in patients' activities. One way to elucidate this is to compare patients with out-of-hospital cardiac arrests (OHCAs) with those with in-hospital cardiac arrests (IHCAs). We therefore examined the presence of a circadian pattern of SCA in a large cohort of OHCA and IHCA survivors. A total of 1,433 consecutive survivors of SCA in the Pittsburgh area from 2002 to 2012 were included. Patient demographics, including clinical histories and details of SCA, were collected. The distribution of SCA throughout the day was tested for differences using the chi-square test. Of the 1,224 patients analyzed, 706 had IHCA and 518 OHCA. We observed a nadir of SCA in the nighttime hours between 12 a.m. and 6 a.m. in both IHCA and OHCA groups (p <0.001), although this pattern was more blunted in the IHCA group. Patients who had an SCA in the nighttime window had more co-morbidities (p = 0.01). The circadian pattern was noted to be absent in patients with higher co-morbidity burden in IHCA only. In conclusion, the typical pattern of nighttime nadir in SCA is observed in patients with both OHCA and IHCA but is blunted in the hospital and especially in sicker patients. This suggests a common mechanistic pathway of SCA transcending differences in physical activities of patients and a difference in how co-morbidities interact with the timing of SCA in the inpatient setting.