Cardiac Imaging and Stress Testing Asymptomatic Athletes to Identify Those at Risk of Sudden Cardiac Death

Aims The athletic preparticipation evaluation (PPE) protocol proposed by the European Society of Cardiology includes history, physical examination and resting electrocardiogram (ECG). The aim of this study was to assess the results of adding constant-load ECG stress testing (EST) to the protocol for the evaluation of ventricular arrhythmias (VA) inducibility. Methods We evaluated a consecutive cohort of young athletes with history, physical examination, resting ECG and EST. Athletes with VA induced by EST underwent 24-hour 12-lead Holter monitoring and echocardiography. Cardiac magnetic resonance (CMR) was reserved for those with frequent, repetitive or exercise-worsened VA, and for athletes with echocardiographic abnormalities. Results Of 10,985 athletes (median age 15 years, 66% males), 451 (4.1%) had an abnormal history, physical examination or resting ECG and 31 (0.28%) were diagnosed with a cardiac disease and were at risk of sudden cardiac death. Among the remaining 10,534 athletes, VA at EST occurred in 524 (5.0%) and a previously missed at-risk condition was identified in 23 (0.22%); the most common ( N = 10) was an echocardiographically silent non-ischaemic left-ventricular fibrosis evidenced by CMR. The addition of EST increased the diagnostic yield of PPE by 75% (from 0.28% to 0.49%) and decreased the positive predictive value by 20% (from 6.9% to 5.5%). During a 32 ± 21 months follow-up, no cardiac arrests occurred among either eligible athletes or non-eligible athletes with cardiovascular disease. Conclusions The addition of exercise testing for the evaluation of VA inducibility to history, physical examination and ECG resulted in an increase of the diagnostic yield of PPE at the expense of an increase in false-positive findings.

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Researchers examine the risk factors for sudden cardiac death and management of at-risk patients

PsycEXTRA Dataset ◽

10.1037/e556542006-002 ◽

2002 ◽

Keyword(s):

Risk Factors ◽

At Risk ◽

Sudden Cardiac Death ◽

Cardiac Death ◽

Risk Patients

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Comparison of variant detection rate in genes between two cohorts of Czech living patients versus victims of sudden cardiac death with clinical / post mortem diagnosis of non-ischemic cardiomyopathy

European Heart Journal ◽

10.1093/ehjci/ehaa946.0338 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

E Borisincova ◽

P Votypka ◽

K Rucklova ◽

A Pilin ◽

M Kulvajtova ◽

...

Keyword(s):

At Risk ◽

Czech Republic ◽

Primary Prevention ◽

Sudden Cardiac Death ◽

Genetic Counselling ◽

Cardiac Death ◽

Detection Rate ◽

Funding Source ◽

Post Mortem ◽

Custom Made

Abstract Introduction Hereditary cardiomyopathy is associated with an increased risk of ventricular arrhythmia and sudden cardiac death (SCD). Genetic stratification substantiates risk assessment and enables the primary prevention of SCD in relatives at risk. We have analyzed the genetic aetiology of SCD in a representative Czech cohort with post mortem diagnosis of various forms of cardiomyopathy and compared it to living cases with these cardiac disorders. Patients and methods Between 2018 and 2019, altogether 47 victims of SCD with post mortem diagnosis of hypertrophic- (HCM; 18/47), arrhythmogenic- (ACM; 19/47) and dilated cardiomyopathy (DCM; 10/47) were identified. Concurrently, genetic testing was performed in 114 living patients (HCM 54/114, ACM 22/114, DCM 38/114). Genetic counselling and cardiologic examination had been carried out in first-degree relatives in all patients/SCD victims. Massively parallel sequencing (MiSeq platform; Illumina.com) was utilized for a custom-made panel comprising 100 candidate genes (Sophia Genetics, Switzerland). The presence of pathogenic variants was validated by Sanger DNA sequencing and through family segregation analyses. Results The causative detection rate (according to ACMG.net classes 4 or 5) in SCD victims with DCM was 60% (6/10) and in living patients with DCM 47.4% (18/38). Variants in TTN, RBM20, DES and FLNC (mainly truncating variants) prevailed in both groups. The detection rate in ACM was 5% (1/19 in SCN5A gene) in SCD victims and 31.8% (7/22) in living patients. Interestingly, the most prevalent mutated gene PKP2 in living patients was not detected in SCD victims. The detection rate in SCD victims with post mortem diagnosis of HCM was 16% (3/18) and in living patients 35% (19/54). The most prevalent gene was MYBPC3 in both groups, while PRKAG2 was detected in one SCD victim and in one living case who survived cardiac arrest. Conclusion Post-mortem genetic analysis in DCM yields a high detection rate and allows potentially effective primary prevention of SCD in relatives at risk. In contrast, the molecular autopsy of HCM and ACM renders a much lower yield which is below the mutation detection rate in living phenotype positive individuals. The results help to improve the genetic counselling in affected families in Czech Republic. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Ministry of Health of the Czech Republic

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How does amiodarone compare with other antiarrhythmic drugs for the secondary prevention of sudden cardiac death in at-risk adults?

Cochrane Clinical Answers ◽

10.1002/cca.1276 ◽

2016 ◽

Author(s):

Jane Burch ◽

Dane Gruenebaum

Keyword(s):

At Risk ◽

Sudden Cardiac Death ◽

Secondary Prevention ◽

Cardiac Death ◽

Antiarrhythmic Drugs

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Brugada Syndrome: Fatal Consequences of a Must-Not-Miss Diagnosis

Critical Care Nurse ◽

10.4037/ccn2021499 ◽

2021 ◽

Vol 41 (5) ◽

pp. 15-22

Author(s):

L. Douglas Smith ◽

Sarah Gast ◽

Danielle F. Guy

Keyword(s):

At Risk ◽

Critical Care ◽

Sudden Cardiac Death ◽

Ventricular Arrhythmia ◽

Brugada Syndrome ◽

Cardiac Death ◽

Lifestyle Modification ◽

Genetic Disorder ◽

Cardiac Conduction ◽

St Segment Elevation

Background Brugada syndrome is a genetic disorder of cardiac conduction that predisposes patients to spontaneous ventricular arrhythmia and sudden cardiac death. Although Brugada syndrome is one of the most common causes of sudden cardiac death, patients presenting with the syndrome often go misdiagnosed. This error has potentially fatal consequences for patients, who are at risk for sudden cardiac death without appropriate management. Objective To increase the critical care professional’s knowledge of Brugada syndrome through detailed description of the characteristic electrocardiographic findings, an algorithmic approach to electrocardiogram evaluation, and a case report of a patient with a previously missed diagnosis of Brugada syndrome. The essential concepts of epidemiology, pathophysiology, clinical presentation, risk stratification, and management are reviewed for critical care professionals who may encounter patients with the syndrome. Diagnosis Patients typically present with syncope or cardiac arrest and an abnormal electrocardiographic finding of ST-segment elevation in the precordial leads. The diagnosis of Brugada syndrome centers on identification of its electrocardiographic characteristics by critical care professionals who routinely evaluate electrocardiograms. Critical care professionals, especially nurses and advanced practice nurses, should be proficient in recognizing the electrocardiographic appearance of Brugada syndrome and initiating appropriate management. Interventions Management strategies include prevention of sudden cardiac death through lifestyle modification and placement of an implantable cardioverter-defibrillator. Critical care professionals should be aware of commonly used medications that may exacerbate ventricular arrhythmia and place patients at risk for sudden cardiac death. Conclusion Increased awareness of Brugada syndrome among critical care professionals can decrease patient morbidity and mortality.

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Abstract 15714: Prediction of Sudden Cardiac Death With Automated High-Throughput Analysis of T-Wave Heterogeneity in Standard 12-Lead Electrocardiogram

Circulation ◽

10.1161/circ.130.suppl_2.15714 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Tuomas Kenttä ◽

Bruce D Nearing ◽

Kimmo Porthan ◽

Jani T Tikkanen ◽

Matti Viitasalo ◽

...

Keyword(s):

At Risk ◽

Relative Risk ◽

Sudden Cardiac Death ◽

General Population ◽

Cardiac Death ◽

Left Ventricular ◽

Adjusted Relative Risk ◽

T Wave ◽

Increased Risk ◽

Patients At Risk

Introduction: Noninvasive identification of patients at risk for sudden cardiac death (SCD) remains a major clinical challenge. Abnormal ventricular repolarization is associated with increased risk of lethal ventricular arrhythmias and SCD. Hypothesis: We investigated the hypothesis that spatial repolarization heterogeneity can identify patients at risk for SCD in general population. Methods: Spatial R-, J- and T-wave heterogeneities (RWH, JWH and TWH, respectively) were automatically analyzed with second central moment technique from standard digital 12-lead ECGs in 5618 adults (46% men; age 50.9±12.5 yrs.) who took part in Health 2000 Study, an epidemiological survey representative of the entire Finnish adult population. During average follow-up of 7.7±1.4 years, a total of 72 SCDs occurred. Thresholds of RWH, JWH and TWH were based on optimal cutoff points from ROC curves. Results: Increased RWH, JWH and TWH (Fig.1) in left precordial leads (V4-V6) were univariately associated with SCD (P<0.001, each). When adjusted with clinical risk markers (age, gender, BMI, systolic blood pressure, cholesterol, heart rate, left ventricular hypertrophy, QRS duration, arterial hypertension, diabetes, coronary heart disease and previous myocardial infarction) JWH and TWH remained as independent predictors of SCD. Increased TWH (≥102μV) was associated with a 1.9-fold adjusted relative risk (95% confidence interval [CI]: 1.2 - 3.1; P=0.011) and increased JWH (≥123μV) with a 2.0-fold adjusted relative risk for SCD (95% CI: 1.2 - 3.3; P=0.004). When both TWH and JWH were above threshold, the adjusted relative risk for SCD was 3.2-fold (95% CI: 1.7 - 6.2; P<0.001). When all heterogeneity measures (RWH, JWH and TWH) were above threshold, the risk for SCD was 3.7-fold (95% CI: 1.6 - 8.6; P=0.003). Conclusions: Automated measurement of spatial J- and T-wave heterogeneity enables analysis of high patient volumes and is able to stratify SCD risk in general population.

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