Incidence Of Sudden Cardiac Death Research Articles

Abstract 12725: Day of the Week Variation of Unexpected Sudden Cardiac Death

Introduction: Data on day of the week (septadian) variation of unexpected sudden cardiac death (SCD) are limited. Methods: We evaluated the incidence of unexpected SCD on different days of the week in a consecutive series of 5,869 SCD victims from Northern Finland [the Fingesture study (Finnish Genetic Study of Arrhythmic Events)]. A medico-legal autopsy was performed on all unexpected sudden death victims as it is mandatory in Finland. The autopsies were performed between the years 1998-2017. Results: The incidence of unexpected SCD in the region of Northern Finland with approximately 600,000 inhabitants on average was 55 per 100,000 inhabitants per year. The mean incidence of unexpected SCD was higher during the days form Friday to Sunday (peaking on Saturday) than during the days from Monday to Thursday (8.54±0.72 vs. 7.22±0.19 SCDs per day of the week per 100,000 inhabitants per year, p<0.001, respectively) (Figure 1). The number of unexpected SCD victims with alcohol in blood was higher during the days form Friday to Sunday (peaking on Saturday) than during the days from Monday to Thursday (Figure 2). Conclusion: The incidence of unexpected SCD was highest during the days form Friday to Sunday, peaking on Saturday. There was a similar distribution of the number of SCD victims with alcohol in blood during the days of the week, suggesting that alcohol drinking with its adverse influences contributes to the septadian variation of unexpected SCD.

Abstract 17673: Sudden Cardiac Death as the First Manifestation of Heart Disease

Background: Clinical risk stratification is most challenging in the subgroup of individuals who present with sudden cardiac death (SCD) as the first manifestation of heart disease (SCD-FM) and there is a lack of current era population-based data. Hypothesis: Occurrence of SCD-FM SCD differs by ethnicity and access to health care. Methods: Consecutive out-of-hospital cases of SCD attended by emergency medical services were ascertained prospectively from a large ongoing population-based study in the Southwest US (population ~ 850K, 2015-2022) using an established multi-source ascertainment and adjudication process. A detailed review was conducted of the lifetime clinical record and available autopsy data, for each individual. SCD-FM cases were defined as SCD with no prior heart disease diagnosis. We calculated annual age-standardized incidence of overall SCD and SCD-FM per 100,000 residents using US census data. Ethnicity-stratified incidence of SCD-FM was calculated. Occurrence of all health care visits prior to SCD was evaluated. Results: From a total of 2681 SCD cases (age 71 ± 16, female 35%) age adjusted incidence of SCD was 40[38-41] per 100,000 out of which SCD-FM was 15[14-16] per 100,000 (n=1019 (38%), age 67±18, female 33%). There was no difference in SCD-FM incidence between Hispanic and non-Hispanic residents (15 [13-17] vs 15 [14-17], p=0.84). Individuals younger than 65 yr were more likely to have SCD-FM compared to those older than 65 yr (50% vs 33%, p <0.001). We observed that 91% of SCD-FM had visited healthcare providers and 3% had cardiac evaluations performed. Conclusion: A significantly higher proportion of SCD-FM were age <65 but the proportion of SCD-FM did not differ by ethnicity. The vast majority of SCD-FM (91%) underwent health care visits prior to SCD but cardiac evaluations were rare (3%). These findings highlight the need to discover and develop user-friendly, cost-effective pre-screening methods to reduce SCD-FM in the general population.

Abstract 15856: Genetics, Pathologic Characteristics, and Burden of Lethal Hypertrophic Cardiomyopathy Among Countywide Sudden Deaths

Background: Annual incidence of sudden cardiac death (SCD) is reported at 1% in cohorts with known hypertrophic cardiomyopathy (HCM), but these estimates presume arrhythmic cause and miss occult cases dying before diagnosis. Hypothesis: Prospective surveillance and postmortem investigation of community sudden deaths will uncover the true burden of presumed SCD (pSCD) and arrhythmic death (SAD) attributable to HCM. Objectives: Determine characteristics and precise contribution of HCM to population pSCD and SAD. Methods: POST SCD (POstmortem SysTematic Investigation of Sudden Cardiac Death) is a prospective cohort study using autopsy, clinical records, and toxicology to adjudicate arrhythmic (potentially rescuable with implantable defibrillator) or non-arrhythmic (e.g., tamponade, overdose) causes among pSCDs 0-90 years in San Francisco County. We included all incident cases from 2/1/11-3/1/14 (n=525) and approximately every 3rd day from 3/1/14-9/1/22 (n=497). We identified HCM victims via 3 parallel approaches: 1) pathology criteria; 2) echocardiogram (TTE) review; 3) genetic analysis. Results: Of 1022 pSCDs in the 11-year study period, we identified 13 cases with HCM, yielding a 2% contribution to arrhythmic death burden: 10 met pathology criteria; 2 via review of 203 TTEs (missed on initial report); 1 with pathogenic ALPK3 mutation. Only 2 of 13 (15%) pSCDs with HCM had premortem diagnosis. A greater proportion of pSCDs with HCM had autopsy-confirmed arrhythmic cause than pSCDs without HCM (11/13 [85%] vs. 547/1009 [54%], p=0.03). HCM contribution to pSCD burden decreased with age (p=0.003), highest among victims <35 years, accounting for 7.1% (6/84) of pSCDs and 9.4% (3/32) of SADs. Genetic testing of 317 consented pSCDs (5/12 meeting pathologic or TTE HCM criteria) yielded pathogenic mutations in 40% (2/5), and identified 1 additional case without clinical phenotype. Conclusions: In this 11-year countywide postmortem study, HCM meeting pathologic, clinical, or genetic criteria was associated with autopsy-confirmed arrhythmic cause of sudden death, accounting for 2% of SADs, highest in cases <35 years. As 85% of cases were undiagnosed before pSCD, the true burden of HCM-related sudden death may be substantially underestimated.

Plaque histological characteristics in individuals with sudden coronary death

Coronary artery disease (CAD) remains the leading cause of death in the Western world in individuals >20 years of age. CAD is the most common substrate underlying sudden cardiac death (SCD) in the Western world, being responsible for 50–75% of SCDs. In individuals dying suddenly with coronary thrombosis, plaque rupture occurs in 65%, plaque erosion in 30% and calcified nodule in 5%. We evaluated the extent of calcification in radiographs of hearts from patients dying of SCD and showed that calcification is absent in nearly 50% of erosion cases whereas only 10% of plaque rupture show no calcification. Conversely, stable plaques with >75% cross-sectional area luminal narrowing show the severest calcification (moderate to severe) in nearly 50% of cases. Identifying individuals who are susceptible to atherosclerosis may help reduce the incidence of SCD. The identification of coronary calcifications by noninvasive tools, however, only captures a fraction of complicating coronary lesions.

Extreme Risk of Sudden Cardiac Death within Three Months after Revascularization in Patients with Ischemic Left Ventricular Systolic Dysfunction.

The risk of sudden cardiac death (SCD) after coronary revascularization in patients with left ventricular (LV) systolic dysfunction has not been characterized completely. This study aims to evaluate the incidence and time course of SCD after revascularization in such patients. The determinants of SCD within 3 months after revascularization were also assessed. A cohort study of patients with reduced ejection fraction (EF 40%), who underwent revascularization was performed. The incidence of SCD was estimated to account for the competing risk of deaths due to other causes. 2317 patients were enrolled. With a median follow-up of 3.5 years, 162 (32.1%) of the 504 deaths were due to SCD. The risk of SCD was highest in the first 3 months after revascularization, with an incidence rate of 0.37%/month. The event rate decreased to 0.12%/month, 0.08%/month, 0.09%/month, 0.14%/month, and 0.19%/month at 3-6 months, 6-12 months, 1-3 years, 3-5 years, and 5-10 years, respectively. A history of ventricular tachycardia/ventricular fibrillation (hazard ratio [HR], 5.55; 95% confidence interval [CI], 1.33-23.19; p = 0.019) and triple vessel disease (HR, 3.90; 95% CI, 1.38-11.05; p = 0.010) were associated with the risk of SCD within 3 months. However, preoperative EF (in 5% increments) was not predictive (HR per 5% increase, 0.98; 95% CI, 0.62-1.55; p = 0.935). For patients with LV dysfunction, the risk of SCD was the highest during the first 3 months after revascularization. Further risk classification and treatment strategy are warranted. The name of the registry: Coronary Revascularization in Patients with Ischemic Heart Failure and Prevention of Sudden Cardiac Death. Registration number: ChiCTR2100044378.

Evaluation of Incidence and Risk Factors of Sudden Cardiac Death in Patients with Chronic Coronary Syndrome Attending Physical Training.

Regular physical activity is recommended topatients with chronic coronary syndrome (CCS). However, vigorous physical exercise occurs as a risk factor of sudden cardiac death (SCD). The effect of short-term and irregular exercise is controversial. The aim of this research is to assess the role of regular training in the incidence of SCD and to identify risk factors among patientswith CCS participating in a long-term training program. Data of risk factors, therapy, and participation were collected retrospectively for a 10-year period, assessing the length and regularity of participation. The incidence of SCD and related mortality was registered. ANOVA, χ2 test, and multinominal logistic regression and stepwise analysis were performed. The Incidence of chronic kidney disease (CKD) was higher (p < 0.01) and taking beta-blockers (BBs) was lower (p = 0.04) in the SCD group. Irregular training, lack of BBs, smoking, and CKD increased the risk of SCD, while female sex, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers (ACEI/ARBs), and BBs decreased the risk of SCD. Taking ACEI/ARBs and BBs proved to be a protective factor, emphasizing the use of optimal medical therapy. Assessment of cardiac risk factors and control of comorbidities also proved to be important. The occurrence of SCD was connected to irregular physical activity, probably relating to the adverse effects of ad hoc exercising.

Left cardiac sympathetic denervation in children with Jervell Lange-Nielsen syndrome and drug refractory torsades - A case series.

Long QT syndrome is an inherited malignant channelopathy which leads to life-threatening arrhythmia, with multiple genotypes. Jervell and Lange-Nielsen syndrome (JLNS) is an autosomal recessive subtype of this disease, characterized by congenital sensorineural deafness and a high incidence of sudden cardiac death (SCD). We prospectively followed up six children who underwent left cardiac sympathetic denervation (LCSD) for JLNS in view of high-risk features despite being on maximally tolerated doses of oral propranolol. Mean age at diagnosis was 2.75±0.39 years, with a significant delay between onset of symptoms and diagnosis (mean 7.2±3.5 months). All had sensorineural hearing loss, conforming to the JLNS phenotype. Mean QTc interval was 603±93ms, with T wave alternans (TWA) seen in all cases. All were started on propranolol and subsequently subjected to LCSD, and 3 underwent AAI permanent pacemaker implantation. Over a mean follow-up of 20 months, there was a significant reduction in QTc (603±93ms to 501±33ms, p=.04), which was persistent on follow-up (525±41ms) and only two out of six had persistent T wave alternans on ECG (p<.01). None of these children had presyncope, syncope, seizures, torsades de pointes, cardiac arrest or death on follow up following LCSD. Jervell Lange-Nielsen syndrome is a subtype of LQTS with high-risk features. LCSD, an effective therapeutic option for those having symptoms despite being on propranolol, results in significant reduction of QTc interval and amelioration of symptoms.

Cardiac Death After Transcatheter Aortic Valve Replacement With Contemporary Devices

BackgroundThe burden of cardiac death after transcatheter aortic valve replacement (TAVR), particularly from advanced heart failure (HF) and sudden cardiac death (SCD), remains largely unknown. ObjectivesThis study sought to evaluate the incidence and predictors of SCD and HF-related death in TAVR recipients treated with newer-generation devices. MethodsThis study included a total of 5,421 consecutive patients who underwent TAVR with newer-generation devices using balloon (75.7%) or self-expandable (24.3%) valves. ResultsAfter a median follow-up of 2 (IQR: 1-3) years, 976 (18.0%) patients had died, 50.8% from cardiovascular causes. Advanced HF and SCD accounted for 11.6% and 7.5% of deaths, respectively. Independent predictors of HF-related death were atrial fibrillation (HR: 2.17; 95% CI: 1.47-3.22; P < 0.001), prior pacemaker (HR: 1.79; 95% CI: 1.10-2.92; P = 0.01), reduced left ventricular ejection fraction (HR: 1.08 per 5% decrease; 95% CI: 1.01-1.14; P = 0.02), transthoracic approach (HR: 2.50; 95% CI: 1.37-4.55; P = 0.003), and new-onset persistent left bundle branch block (HR: 1.85; 95% CI: 1.14-3.02; P = 0.01). Two baseline characteristics (diabetes, HR: 1.81; 95% CI: 1.13-2.89; P = 0.01; and chronic kidney disease, HR: 1.72; 95% CI: 1.02-2.90; P = 0.04) and 3 procedural findings (valve in valve, HR: 2.17; 95% CI: 1.01-4.64; P = 0.04; transarterial nontransfemoral approach, HR: 2.23; 95% CI: 1.23-4.48; P = 0.01; and periprocedural ventricular arrhythmia, HR: 7.19; 95% CI: 2.61-19.76; P < 0.001) were associated with an increased risk of SCD after TAVR. ConclusionsAdvanced HF and SCD accounted for a fifth of deaths after TAVR in contemporary practice. Potentially treatable factors leading to increased risk of HF deaths and SCD were identified, such as arrhythmia/dyssynchrony factors for HF and valve-in-valve TAVR or periprocedural ventricular arrhythmias for SCD.

Sudden cardiac death and thymic hyperplasia in adults: myth or reality? A case report

BackgroundSudden cardiac death is a major public health concern. The incidence of sudden cardiac death in young adults remains unclear and is generally underestimated.Case presentationThis is a case report of a 24-year-old man with a silent pathological history, who suddenly collapsed in a restaurant during dinner with his workmates. Autopsy and ancillary examination revealed focal atrioventricular node fibrosis and thymic hyperplasia.ConclusionsThymic hyperplasia has been considered a cause of sudden death in the past century. The mode of death was explained through nosographic entities such as status lymphaticus or thymic asthma, which are currently consigned to history books. Nevertheless, recent studies have sought to determine the relationship between thymic hyperplasia and sudden unexpected deaths in adults. Moreover, isolated fibrosis of the atrioventricular node is a rare condition that can remain undiagnosed even after a full autopsy. This report aims to provide a concise review of the existing literature concerning sudden cardiac death and discuss the so-called “thymic death” theory, which is now considered a myth. Was the finding of thymic hyperplasia and atrioventricular node fibrosis a coincidence? Should the myth surrounding “thymic death” be re-examined?

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#3173 INCIDENCE AND RISK FACTORS OF SUDDEN CARDIAC DEATH IN END STAGE RENAL DISEASE PATIENTS UNDERGOING HAEMODIALYSIS: A RETROSPECTIVE STUDY

Abstract Background &amp; aims: End Stage Renal Disease (ESRD) patients undergoing haemodialysis are prone to suffer from Sudden Cardiac Death (SCD). The present study was sought to evaluate the incidence and risk factors of SCD in ESRD patients on haemodialysis in Pakistani population. Methods The study recruited 202 eligible ESRD patients undergoing haemodialysis. Baseline characteristics of the study participants with and without Sudden Cardiac Arrest (SCA) were recorded using self-reported questionnaires. SCA and SCD events were identified by reviewing medical records and death certificates. Results Out of 202 patients, 37 (18.3%) suffered from the episode of SCA, 18 (48.6%) of which succumbed to death. ESRD patients who endured SCA were statistically older in comparison with their non-SCA counterparts (58.2 ± 11.4 vs. 52.3 ± 9.3 years, P&amp;lt;0.001). The HTN (67.6% versus 64.8%, P = 0.001), DM (62.2% versus 59.4%, P = 0.004), CAD (45.9% versus 41.8%, P = 0.001) and Congestive Heart Failure (CHF) (35.1% versus 34.5%, P = 0.002) were significantly prevalent in ESRD cohort with SCA in contrast to non-SCA. We also found LVH (62.2% versus 48.5%, P&amp;lt;0.001), ventricular tachycardia (51.4% versus 30.9%, P&amp;lt;0.001) and ventricular fibrillation/flutter (56.8% versus 25.5%, P&amp;lt;0.001) to be statistically higher in ESRD patients on haemodialysis with SCA event. Through multivariate logistic regression analysis, we evidenced hypokalemia (OR = 1.247, CI 1.214 – 1.278, P&amp;lt;0.001); CAD (OR 1.886, CI 1.469 – 2.342, P&amp;lt;0.001); LVH (OR 1.861, CI 1.392 – 1.953, P&amp;lt;0.001); ventricular tachycardia (OR = 1.253, CI 1.012 – 1.386, P&amp;lt;0.001); and ventricular fibrillation/flutter (OR = 0.547, CI 0.518 – 0.773, P&amp;lt;0.001) to be significantly and independently associated with SCD in ESRD patients on haemodialysis. Conclusion The prevalence of SCD among ESRD patients on haemodialysis with SCA episode is very high. CAD and ventricular tachyarrhythmias were statistically significant among ESRD patients on haemodialysis with SCA in comparison with non-SCA and were independently associated with the prevalence of in-patient SCD among ESRD patients with SCA on haemodialysis.

Has COVID-19 changed the spectrum of arrhythmias and the incidence of sudden cardiac death?

Arrhythmic manifestations of COVID-19 include atrial arrhythmias such as atrial fibrillation or atrial flutter, sinus node dysfunction, atrioventricular conduction abnormalities, ventricular tachyarrhythmias, sudden cardiac arrest, and cardiovascular dysautonomias including the so-called long COVID syndrome. Various pathophysiological mechanisms have been implicated, such as direct viral invasion, hypoxemia, local and systemic inflammation, changes in ion channel physiology, immune activation, and autonomic dysregulation. The development of atrial or ventricular arrhythmias in hospitalized COVID-19patients has been shown to portend ahigher risk of in-hospital death. Management of these arrhythmias should be based on published evidence-based guidelines, with special consideration of the acuity of COVID-19 infection, concomitant use of antimicrobial and anti-inflammatory drugs, and the transient nature of some rhythm disorders. In view of new SARS-CoV‑2 variants that may evolve, the development and use of newer antiviral and immunomodulator drugs, and the increasing adoption of vaccination, clinicians must remain vigilant for other arrhythmic manifestations that may occur in association with this novel but potentially deadly disease.

Prophylactic rivaroxaban in the early post-discharge period reduces the rates of hospitalization for atrial fibrillation and incidence of sudden cardiac death during long-term follow-up in hospitalized COVID-19 survivors.

Introduction: While acute Coronavirus disease 2019 (COVID-19) affects the cardiovascular (CV) system according to recent data, an increased CV risk has been reported also during long-term follow-up (FU). In addition to other CV pathologies in COVID-19 survivors, an enhanced risk for arrhythmic events and sudden cardiac death (SCD) has been observed. While recommendations on post-discharge thromboprophylaxis are conflicting in this population, prophylactic short-term rivaroxaban therapy after hospital discharge showed promising results. However, the impact of this regimen on the incidence of cardiac arrhythmias has not been evaluated to date. Methods: To investigate the efficacy of this therapy, we conducted a single center, retrospective analysis of 1804 consecutive, hospitalized COVID-19 survivors between April and December 2020. Patients received either a 30-day post-discharge thromboprophylaxis treatment regimen using rivaroxaban 10mg every day (QD) (Rivaroxaban group (Riva); n = 996) or no thromboprophylaxis (Control group (Ctrl); n = 808). Hospitalization for new atrial fibrillation (AF), new higher-degree Atrioventricular-block (AVB) as well as incidence of SCD were investigated in 12-month FU [FU: 347 (310/449) days]. Results: No differences in baseline characteristics (Ctrl vs Riva: age: 59.0 (48.9/66.8) vs 57 (46.5/64.9) years, p = n.s.; male: 41.5% vs 43.7%, p = n.s.) and in the history of relevant CV-disease were observed between the two groups. While hospitalizations for AVB were not reported in either group, relevant rates of hospitalizations for new AF (0.99%, n = 8/808) as well as a high rate of SCD events (2.35%, n = 19/808) were seen in the Ctrl. These cardiac events were attenuated by early post-discharge prophylactic rivaroxaban therapy (AF: n = 2/996, 0.20%, p = 0.026 and SCD: n = 3/996, 0.30%, p < 0.001) which was also observed after applying a logistic regression model for propensity score matching (AF: χ 2-statistics = 6.45, p = 0.013 and SCD: χ 2-statistics = 9.33, p = 0.002). Of note, no major bleeding complications were observed in either group. Conclusion: Atrial arrhythmic and SCD events are present during the first 12months after hospitalization for COVID-19. Extended prophylactic Rivaroxaban therapy after hospital discharge could reduce new onset of AF and SCD in hospitalized COVID-19 survivors.

Clinical and genetic characteristics and course of congenital long QT syndrome: A ten-year single center experience

Abstract Funding Acknowledgements Type of funding sources: None. Background Long QT syndrome (LQTS) is an inherited primary arrhythmia syndrome associated with life-threatening ventricular arrhythmia. Objective To report the clinical and genetic characteristics and outcome of LQTS patients in single center inherited arrhythmia clinic. Methods Retrospective review of patients diagnosed LQTS and evaluated by ECG, 12 lead holter, exercise test and genetic testing in inherited arrhythmia clinic from January 212 to January 2022. Results 101 patients (32 families) were included, mean age 24.3± 17 years. Thirteen patients (12.8%) were diagnosed after previous cardiac arrest and six patients (6%) had syncope. Seventy (69.3%) were identified as having LQTS during family screening. 97 patients (97%) were confirmed to have a pathogenic mutation for LQTS genes. Beta blockers were recommended to 74 patients (73%), flecainide to 20 (19.8%). Nine patients (8.9%) received an ICD for secondary prevention and one patient (1%) for primary prevention. During 5.8 ± 2.7 years, dose of beta-blockers increased from propranolol 70 ±42 mg to 105 ±60.3 mg (p= 0.0004), QTC shortening (479 ± 36.9 to 466 ±30.1 msec, p=0.01) in ECG and maximal QTC measured in 12 lead holter (521± 43.9 to 505± 37.8 msec, p=0.01). Maximal heart rates measured in 12 lead holter and exercise test were reduced ( 130± 24.5 to 116 ± 20.2 beats/min p=0.0001 and 152.6±22 to 145± 20.58 beats/min, p=0.043). Seven patients (6.9%) experienced ventricular arrhythmia, five received appropriate ICD shock and two patients that declined beta blockers experienced syncope due to polymorphic ventricular tachycardia and cardiac arrest. The one patient that had the ICD for primary prevention, experienced polymorphic ventricular tachycardia that was successfully treated by the ICD. Conclusions Intensive clinical follow up and an optimal medical therapy in a specialized arrhythmia clinic is associated with a relatively low incidence of sudden cardiac death and a low rate of ICD utilization in LQTS patients.

Ventricular pre-excitation in young patients: long term follow-up and natural history in a contemporary cohort

Abstract Funding Acknowledgements Type of funding sources: None. Background Ventricular preexcitation (VPE) due to atrio-ventricular accessory pathways (AP) has been associated to a higher incidence of sudden cardiac death (1,2). The incidence of major arrhythmic events (MAE) may be higher in children (1,3), but most of the past studies recruited a high proportion of patients with congenital heart disease (CHD), treated with outdated pharmacological therapy (1). Transcatheter ablation (TCA) of the AP is a safe and effective therapy and it is nowadays the standard of care (1,2). However, it may be less effective and more dangerous in smaller and younger children (1,3). It is described that patients may spontaneously lose VPE during childhood (1), but the natural history of VPE is not well understood yet. Purpose To study the natural history of VPE. We focused especially on the likelihood of spontaneous resolution of VPE during growth, the possible associated factors, and the incidence of MAE during a long follow up in a contemporary paediatric cohort. Methods We retrospectively recruited patients diagnosed with VPE at age 0 to 12, referred from 1993 to 2021 to two tertiary care hospitals. Significant CHD and double AP were excluded. The primary outcome was the spontaneous resolution of VPE, defined by the loss of short PR and delta wave seen in at least two consecutive ECG and/or on 24-hour Holter monitoring. The follow up stopped when the patients reached 16 years of age, met the primary outcome or effective TCA was performed. Given the time-to-event dependency of the condition, the survival analysis of VPE considered the left truncation resulted from the recruitment of patients after the first days of life. Results We recruited 153 patients with a median age of diagnosis of 4.9 (0.2 – 8.4). The median follow-up time was 4.9 (1.6 – 8) years. During follow-up, 42 (28%) patients spontaneously loss VPE. The left truncated Kaplan-Meier survival curve of VPE is shown in Picture 1. It estimates that VPE would persist in 53% (40.1-70.2) and 33.8% (23.7-48.4) of patients at the age of 1 and 16, respectively. Symptoms and intermittent preexcitation were the only variables significantly associated with lower (OR 0.2) and higher probability (OR 3.45) of SR of VPE. The vast majority of patients with symptoms was treated with drug therapy before the age of 8, and TCA was safely delayed thereafter. None of the patients experienced a MAE during follow up. Conclusion According to our data, a large proportion of paediatric patients are likely to spontaneously lose VPE within the first year of life, and a spontaneous resolution may occur later during childhood in a non-negligible number of cases. The absence of symptoms and/or intermittent preexcitation are significant predictors of loss of VPE. The results of our study are of the utmost clinical relevance, since they support a wait-and-see strategy, especially in very young children with VPE.

Predictive value of scar burden assessed by cardiac MRI on sudden cardiac death in cardiac resynchronization therapy patients: a systematic review and meta-analysis

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Ministry of Innovation and the National Research, project no. RRF-2.3.1-21-2022-00003 and Project no. RRF-2.3.1-21-2022-00004 (MILAB) has been implemented with the support provided by the European Union. Background Myocardial fibrosis (MF) is associated with a higher prevalence of ventricular arrhythmias (VA) and sudden cardiac death (SCD). Late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR) can accurately evaluate the extent of MF. Clinical evidence suggests that scar assessment may help the decision of adding an implantable cardioverter defibrillator (ICD) to cardiac resynchronization therapy (CRT) to reduce the risk of VA and SCD. Purpose In this systematic review and meta-analysis, we collected and analyzed evidence pertaining to the association between scar burden and the risk of VA and SCD, and we evaluated the impact of appropriate device choice for CRT. Methods We performed a systematic literature search on MEDLINE using the PubMed, Embase, Scopus and CENTRAL databases. The target population were adults with heart failure with reduced ejection fraction who underwent CRT. The primary outcome was the association between the incidence of VA and/or SCD and scar burden assessment. Meta-analyses were performed using the META and DMETAR packages in R, using a random-effects model. The risk of bias was assessed using RoB2and the quality of evidence was evaluated using the GRADE assessment. Results 6 eligible articles have been included in our study, with a total of 1548 patients, of whom 465, 696, and 387 have been implanted with an ICD, CRT-D, CRT-P respectively. Altogether 62,68 % of the total population were LGE-CMR positive. The proportion of appropriate ICD shock reached 15,65 % in the total population during the median follow-up time of 51,59 months. The risk of developing appropriate ICD shocks in the LGE positive population was almost 70% higher (Hazard ratio 1,69, 95% Confidence interval: 1,29- 2,21; p&amp;lt;0,001) compared to LGE negative patients. Conclusion In our meta-analysis, LGE-CMR was significantly associated with appropriate device therapy and can identify a subgroup of patients with an increased risk of life-threatening VA. Based on our results performing an MRI before device implantation might be important to select the high-risk patients for SCD in the elderly with ischaemic etiology and older age.

Sudden cardiac death after heart transplantation: a population-based study.

The epidemiology of sudden cardiac death (SCD) after heart transplantation (HTx) remains imprecisely described. We aimed to assess the incidence and determinants of SCD in a large cohort of HTx recipients, compared with the general population. Consecutive HTx recipients (n = 1246, 2 centres) transplanted between 2004 and 2016 were included. We prospectively assessed clinical, biological, pathologic, and functional parameters. SCD was centrally adjudicated. We compared the SCD incidence beyond the first year post-transplant in this cohort with that observed in the general population of the same geographic area (registry carried out by the same group of investigators; n = 19 706 SCD). We performed a competing risk multivariate Cox model to identify variables associated with SCD. The annual incidence of SCD was 12.5 per 1,000 person-years [95% confidence interval (CI), 9.7-15.9] in the HTx recipients cohort compared with 0.54 per 1,000 person-years (95% CI, 0.53-0.55) in the general population (P < 0.001). The risk of SCD was markedly elevated among the youngest HTx recipients with standardized mortality ratios for SCD up to 837 for recipients ≤30 years. Beyond the first year, SCD was the leading cause of death. Five variables were independently associated with SCD: older donor age (P = 0.003), younger recipient age (P = 0.001) and ethnicity (P = 0.034), pre-existing donor-specific antibodies (P = 0.009), and last left ventricular ejection fraction (P = 0.048). HTx recipients, particularly the youngest, were at very high risk of SCD compared with the general population. The consideration of specific risk factors may help identify high-risk subgroups.

Arrhythmic Risk Stratification among Patients with Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a cardiac muscle disorder characterized by generally asymmetric abnormal hypertrophy of the left ventricle without abnormal loading conditions (such as hypertension or valvular heart disease) accounting for the left ventricular wall thickness or mass. The incidence of sudden cardiac death (SCD) in HCM patients is about 1% yearly in adults, but it is far higher in adolescence. HCM is the most frequent cause of death in athletes in the Unites States of America. HCM is an autosomal-dominant genetic cardiomyopathy, and mutations in the genes encoding sarcomeric proteins are identified in 30-60% of cases. The presence of this genetic mutation carries more than 2-fold increased risk for all outcomes, including ventricular arrhythmias. Genetic and myocardial substrate, including fibrosis and intraventricular dispersion of conduction, ventricular hypertrophy and microvascular ischemia, increased myofilament calcium sensitivity and abnormal calcium handling, all play a role as arrhythmogenic determinants. Cardiac imaging studies provide important information for risk stratification. Transthoracic echocardiography can be helpful to evaluate left ventricular (LV) wall thickness, LV outflow-tract gradient and left atrial size. Additionally, cardiac magnetic resonance can evaluate the prevalence of late gadolinium enhancement, which when higher than 15% of LV mass is a prognostic maker of SCD. Age, family history of SCD, syncope and non-sustained ventricular tachycardia at Holter ECG have also been validated as independent prognostic markers of SCD. Arrhythmic risk stratification in HCM requires careful evaluation of several clinical aspects. Symptoms combined with electrocardiogram, cardiac imaging tools and genetic counselling are the modern cornerstone for proper risk stratification.

PO-03-151 TEN-YEAR EFFECTS OF AMBIENT PM2.5 EXPOSURE SIGNIFICANTLY INCREASE SUDDEN CARDIAC DEATH, CARDIOVASCULAR AND ALL-CAUSE MORTALITIES: A NATIONWIDE COHORT STUDY.

Cardiovascular mortality and morbidity have been associated with the air pollution, but the chronic effects and its relation between pollutants and sudden cardiac death remain unclear. The study aimed to investigate the associations between sudden cardiac death, mortality, MACE and air pollutant in a 10-year follow-up nationwide cohort. This study used the National Health Insurance Research Database and comprised 16,778,374 participants over 20 years old staying in the same districts during 10-year follow-ups between 2008 to 2017 in Taiwan. Incidences of sudden cardiac death, all-cause and cardiovascular mortalities, heart failure, myocardial infarction and MACE were compared among air pollutant exposures (PM2.5, PM10, O3, NOx, NO, NO2, CO and SO2) to different quintiles. Mean 10-year exposures of all pollutants at different districts were obtained from Taiwan Environmental Protection Administration Database. The incidences of sudden cardiac death, all-cause and cardiovascular mortalities, myocardial infarction, stroke and MACE increased after mean PM2.5 exposure >23.8μg/m3 and were highest at the upper quantile (>33.0μg/m3) of PM 2.5 exposure, when compared to the other quantiles (p<0.001). All those incidences remained the same when mean PM2.5 exposure was below 23.7μg/m3(lowest & 2nd quantiles). These findings were not found in PM10, O3, NOx, NO, NO2, CO and SO2 pollutants among different quantiles, respectively. Details are show in Fig. A to H. Very long-term (10-year) exposure to ambient PM2.5 significantly increased the risk of sudden cardiac death cardiac and all-cause mortality. A positive correlated increase of those morbidities and mortalities happened after a mean PM2.5 cut-off value of 23.7μg/m3 .

PO-03-227 INCIDENCE AND AUTOPSY RATES OF SUDDEN CARDIAC DEATH IN NORTHERN FINLAND

Sudden cardiac death (SCD) is one of the most common modes of death in Western societies. The exact incidence and etiological background of SCD is somewhat unknown due to the low number of autopsies performed in sudden death victims. In prior autopsy studies approximately 40% of sudden death victims have other than cardiac cause for the event and in most countries autopsy rates are between 5-25%. Determine the incidence of SCD and autopsy rates for sudden death in Northern Finland. We performed a death certificate review of all out of hospital or hospice deaths in 2016 in Northern Finland. Death was determined to be sudden if it occurred within one hour of occurrence of symptoms or if the victim was found dead. Information on autopsy, cause of death, and demographical data were collected. From a total of 6620 deaths 1412 occurred out of hospital/hospice. Death was classified as sudden in 1067 (16.1%) victims. Mean age was 70.1 yrs (±16.5 yrs) and 66.9% were male. Autopsy rate for all sudden deaths was 73.7%. Among victims under 70yrs autopsy rate was 90.8% and in under 50 yrs 96.2%. In all 785 autopsied sudden deaths 421 (53.6%) were SCD i.e. cardiac cause for death. In a population of 740 000 out of hospital/hospice sudden death incidence in 2016 was 144/100 000 and SCD incidence on 2016 was 77/100 000. Autopsied sudden cardiac death (N=421) was caused by ischemic heart disease (310, 73.6%), hypertensive heart disease (48, 11.4%), cardiomyopathy (50, 11.9%) or other cardiac causes (13, 3.1%). Autopsy rates of sudden death in Northern Finland are high. The utilization of autopsies in sudden death provide the premises for accurate SCD incidence calculations. The results confirm the assumption that a large part of sudden deaths are non-cardiac and common cardiac diseases are the most frequent cause of SCD in unselected general population.