Trigger For Sudden Cardiac Death Research Articles

The Role of the Electrocardiogram (ECG) In the Screening and Prevention of Sudden Cardiac Death in Sports

The Role of the Electrocardiogram (ECG) In the Screening and Prevention of Sudden Cardiac Death in Sports Abstract: Athletes carry a higher risk for sports-related sudden cardiac death compared to the general population. The majority of these athletes suffer from an undiagnosed heart disease. Since physical activity is an essential trigger for sudden cardiac death in individuals with undiagnosed, usually hereditary, heart disease, sports can lead to sudden cardiac death in these athletes. Different heart diseases lead to sudden cardiac death at different ages during sports. The electrocardiogram (ECG) is an important screening tool to identify individuals of all ages with heart disease that are associated with sports-related sudden cardiac death. These individuals can then be treated and lives can be saved.

Coronary Syndromes and High-Altitude Exposure—A Comprehensive Review

The aim of this review is to identify a preventive strategy in order to minimize the risk of adverse events in patients with coronary syndromes and acute exposure to high-altitude. For this purpose we searched the electronic database of PubMed, EMBASE, and Web of Science for studies published in the last 30 years in this field. The conclusions of this review are: patients with stable coronary artery disease on optimal treatment and in a good physical condition can tolerate traveling to high altitude up to 3500 m; on the other hand, patients with unstable angina or recent myocardial infarction no older than 6 months should take less interest in hiking or any activity involving high altitude. Air-traveling is contraindicated for patients with myocardial infarction within previous 2 weeks, angioplasty or intracoronary stent placement within previous 2 weeks, and unstable angina or coronary artery bypass grafting within previous 3 weeks. The main trigger for sudden cardiac death is the lack of gradual acclimatization to high-altitude and to the exercise activity, and the most important risk factor is prior myocardial infarction.

Abstract 15502: Exercise as a Risk Factor for Arrhythmic Mitral Valve Prolapse

Background: Mitral valve prolapse (MVP) is a common valvular abnormality found in approximately 2.4% of the population. Whereas most cases are benign, an increasingly recognized sequela of MVP is sudden cardiac death (SCD), but risk factors for SCD are not well-defined. Exercise has not been explored as a potential risk factor for SCD in MVP. Hypothesis: We tested the hypothesis that patients with MVP and SCD would be more likely to exercise or be competitive athletes than MVP controls with the capacity to exercise. Methods - The study population was generated from the Duke Epic EHR and determined by ICD-10 codes for MVP and SCD. A comparison group of patients with MVP with exercise data was used. Patients were included if they had guideline-based diagnosis of MVP on echocardiogram or cardiac magnetic resonance imaging. Exercise <1 hour per week was defined as being sedentary and time >1 hour per week or status as a competitive athletes were defined as habitual exercisers. Results: Of the 27 patients with MVP and SCD 18 had documentation of exercise time per week. There were 42 in the control group. Patients with SCD were younger [(54.8 +/-15.1) vs. (63.9 +/- 14.1) p= 0.03], and more likely to have bileaflet prolapse [13/18 (72%) vs. 15/42 (36%), p=0.01]. Patients with SCD were more likely to be habitual exercisers vs. sedentary [16/18 (89%) vs. 17/42 (40.5%), p = .025]. 20 patients with MVP and SCD had documentation of activity level at the time of event. 10 were exercising (50%), 5 (25%) working or doing housework, 4 (20%) resting and 1 (5%) sleeping. Conclusion: Exercise time >1 hour per week is associated with sudden cardiac death in Mitral Valve Prolapse. Exercise may be a trigger of SCD; however, more data is needed to better characterize exercise as a risk factor for SCD in this population.

Molecular autopsy and clinical family screening in a case of sudden cardiac death reveals ACTN2 mutation related to hypertrophic/dilated cardiomyopathy and a novel LZTR1 variant associated with Noonan syndrome

BackgroundGenetic cardiac diseases are the main trigger of sudden cardiac death (SCD) in young adults. Hypertrophic cardiomyopathy (HCM) is the most prevalent cardiomyopathy and accounts for 0.5 to 1% of SCD cases per year.MethodsHerein, we report a family with a marked history of SCD focusing on one SCD young adult case and one pediatric case with HCM.ResultsFor the deceased young adult, postmortem whole‐exome sequencing (WES) revealed a missense variant in the ACTN2 gene: c.355G > A; p.(Ala119Thr) confirming the mixed hypertrophic/dilated cardiomyopathy phenotype detected in the autopsy. For the pediatric case, WES allowed us the identification of a novel frameshift variant in the LZTR1 gene: c.1745delT; p.(Val582Glyfs*10) which confirms a clinical suspicion of HCM related to Noonan syndrome.ConclusionThe present study adds further evidence on the pathogenicity of ACTN2: p. Ala119Thr variant in SCD and expands the mutational spectrum of the LZTR1 gene related to Noonan syndrome.

Post-mortem toxicology analysis in a young sudden cardiac death cohort

Risk of sudden cardiac death (SCD) increases with age, and several studies have examined the impact of different drugs on cardiovascular function. However, few studies have integrated epidemiological drug consumption data and genetic background in the context of cardiac death. We performed a retrospective population-based study in forensic sudden death cases from a 9-year period in Catalonia. The young cohort included 924 cases 18–50 years old, 566 of which had a cardiac cause of death. Complete autopsy, toxicological, and histopathological studies were performed. Molecular autopsy using next-generation sequencing was performed in nearly 400 cardiac cases. Cases related with fatal acute intoxication were excluded. Drug consumption prevalence was similar between forensic cases of cardiac and non-cardiac origin (62.5% versus 69.5%), with the exception of alcohol, which was more prevalent in the cardiac group than in the non-cardiac group (23.3% versus 17.1%). Individuals in the toxicology-positive group were carriers of more rare genetic variants and were significantly younger than the toxicology-negative group. Psychopharmacological drugs were identified in 22.3% of cardiac cases, and molecular autopsy identified an association between antiepileptic drugs or caffeine and pathogenic or likely pathogenic variants in arrhythmogenic genes. Specific substances could therefore play an essential role as triggers of SCD in genetically predisposed young people.

A Case Series of Concomitant Cardiac Electrical Disease among Takotsubo Syndrome Patients and Literature Review.

The pathophysiology of Takotsubo Syndrome (TTS) is not completely understood and the trigger of sudden cardiac death (SCD) in TTS is not clear either. We therefore sought to find an association between TTS and primary electrical diseases. A total of 148 TTS patients were analyzed between 2003 and 2017 in a bi-centric manner. Additionally, a literature review was performed. The patients were included in an ongoing retrospective cohort database. The coexistence of TTS and primary electrical diseases was confirmed in five cases as the following: catecholaminergic polymorphic ventricular tachycardia (CPVT, 18-year-old female) (n = 1), LQTS 1 (72-year-old female and 65-year-old female) (n = 2), LQTS 2 (17-year-old female) (n = 1), and LQTS in the absence of mutations (22-year-old female). Four patients suffered from malignant tachyarrhythmia and recurrent syncope after TTS. Except for the CPVT patient and one LQTS 1 patient, all other cases underwent subcutaneous ICD implantation. An event recorder of the CPVT patient after starting beta-blocker did not detect arrhythmias. The diagnosis of primary electrical disease was in 80% of cases unmasked on a TTS event. This diagnosis triggered a family clinical and genetic screening confirming the diagnosis of primary electrical disease. A subsequent literature review identified five cases as the following: a congenital atrioventricular block (n = 1), a Jervell and Lange-Nielsen Syndrome (n = 1), and a family LQTS in the absence of a mutation (n = 2), LQTS 2 (n = 1). A primary electrical disease should be suspected in young and old TTS patients with a family history of sudden cardiac death. In suspected cases, e.g., ongoing QT interval prolongation, despite recovery of left ventricular ejection fraction a family screening is recommended.

Sudden cardiac death during mountain sports activities

Sudden cardiac death (SCD) is an unanticipated and dramatic event resulting from cardiac causes. First reports on SCDs during mountain sports activities date back to the 1970s and 1980s of the last century. Relatively large datasets have been collected in Austria from 1985 onwards initiating systematic recordings and analyses of risk factors and triggers of SCDs during mountain sports activities. The results presented in this publication are derived from a literature search on reported SCDs that occurred during selected mountaineering activities with particular regard to study findings based on data collected in Austria. We found a relatively low SCD risk during mountaineering activities, amounting to about 1 SCD per 1 million activity days when hiking, trekking or ski touring, which is even lower during downhill skiing but higher in competitive cross-country skiing. The risk is much higher in men than in women and increases sharply above the age of 34. Main risk factors include prior myocardial infarction, coronary artery disease, arterial hypertension, hypercholesterolaemia and diabetes mellitus type 2, but regular and sport-specific activities turned out to be important protective factors. Unaccustomed physical exertion, in particular on the first days in the mountains (altitude), prolonged activities without rest and insufficient energy and fluid intake represent important SCD triggers. Besides considering these potential triggers during mountaineering activities, sports medical examination, appropriate pharmacological therapy of risk factors and physical preparation represent preventive key elements. Key Words: Exercise, Mountains, Cardiovascular, Risk, Triggers, Prevention

The Hidden Fragility in the Heart of the Athletes: A Review of Genetic Biomarkers.

Sudden cardiac death (SCD) is a devastating event which can also affect people in apparent good health, such as young athletes. It is known that intense and continuous exercise along with a genetic background that predisposes a person to the risk of fatal arrhythmias is a trigger for SCD. Therefore, knowledge of the athlete’s genetic conditions underlying the onset of SCD must be extended, in order to develop new effective prevention and/or therapeutic strategies. Arrhythmic features occur across a broad spectrum of cardiac diseases, sometimes presenting with overlapping phenotypes. The genetic basis of arrhythmogenic disorders has been greatly highlighted in the last 30 years, and has shown marked heterogeneity. The advent of next-generation sequencing has constantly updated our understanding of the genetic basis of arrhythmogenic diseases and is laying the foundation for precision medicine. With the exception of a few clinical cases involving a single athlete showing a highly suspected phenotype for the presence of a heart disease, there are few studies to date that analysed the applicability of genetic testing on cohorts of athletes. This evidence shows that genetic testing can contribute to the diagnosis of up to 13% of athletes; however, the presence of clinical markers is essential. This review aims to provide a reference collection on current knowledge of the genetic basis of sudden cardiac death in athletes and to review updated evidence on the effectiveness of genetic testing in early identification of athletes at risk for SCD.

Sudden cardiac death associated to substances of abuse and psychotropic drugs consumed by young people: A population study based on forensic autopsies

BackgroundToxic substances are one of the main risk factors for sudden cardiac death (SCD) in young people. However, there is limited information about this matter based on clinical research. The aim of this study was to analyze the use of substances of abuse (legal and illicit) and prescribed psychotropic drugs in young people who died by SCD. MethodsA population-based study performed in 15–35-year-olds who died by SCD in Biscay (Basque-Country) between 1991 and 2016. Cases were analyzed prospectively by a complete autopsy, toxicological and histopathological studies. A case was considered positive for exposure to cardiotoxic substances if smoking status was diagnosed or if toxicological analysis detected any drug associated with increased risk of SCD. ResultsThere were 204 SCD; 98 (48%) were exposed to a cardiotoxic substance, including smoking status (n = 72) and/or positive toxicology (n = 58). Illicit drugs (n = 29, mainly cannabis and cocaine), ethanol (n = 25), and prescribed psychotropic drugs (n = 11) were detected. Positive cases were more frequent in males than in females (54% vs. 19%). They were also more common in subjects who died by acute (86%) and chronic (71%) ischemic heart disease than in myocardial diseases (33%) and sudden arrhythmic death syndrome (36%). All positive cases of illicit drugs were males. Smoking status was very high in deaths due to acute ischemic heart disease. ConclusionsThe proportion of users of substances of abuse was unexpectedly high, even more prevalent than other cardiovascular risk factors. Toxic substances could play an important role as triggers of SCD in young people.

Cardiovascular screening of young athletes with electrocardiography in the UK: at what cost?

The promotion of exercise as a positive and powerful health intervention has never been more important, when consideration is given to the global epidemic of disease states related to a sedentary lifestyle. However, intensive exercise may be a trigger for sudden cardiac death in individuals harbouring quiescent cardiovascular diseases. Indeed, hereditary and congenital abnormalities of the heart are the most common cause of non-traumatic death during sport in young athletes.

Commode Cardia-Death by Valsalva Maneuver: A Case Series.

The Valsalva maneuver is used in clinical medicine for the diagnosis and/or treatment of various cardiovascular conditions. It can also be used in activities of daily living, such as defecation. Due to the cardiovascular effects produced during the Valsalva maneuver, it may be contraindicated in certain medical conditions and could be a trigger of sudden cardiac death. The incidence and prevalence of death following Valsalva maneuver in the presence of underlying cardiovascular disease, or "commode cardia," has not been examined. In 2012, the Wayne County Medical Examiner's Office (Detroit, MI) investigated 21 deaths that occurred on the toilet, fourteen of which were due to cardiovascular disease. In another 31 deaths in the bathroom due to cardiovascular disease, the possibility that the decedent defecated immediately prior to death could not be excluded. Hence, the incidence of commode cardia in this population ranges from 2.3 to 7.4% of all cardiovascular-related deaths.

Abstract 12142: Electrolyte Abnormalities and Risk of Sudden Death in the General Population

Introduction: Electrolyte abnormalities are a substrate for arrhythmogenesis and could be the trigger for sudden cardiac death (SCD). We sought to determine the potential role of electrolyte abnormalities, irrespective of kidney function, in the occurrence of sudden death in the community. Hypothesis: Electrolyte abnormalities increases the risk for SCD in the community regardless of kidney function. Methods: SCD cases and controls from a large population based study in Northwest US (approx 1 million population, 2002-2014) were included if age ≥18 yrs with creatinine clearance (CrCl) and serum electrolytes available for analysis. For cases, CrCl and electrolytes were required to be measured within 90 days of the SCD event. Demographics and lab results were analyzed using student t-tests and chi-square tests. Multiple logistic regression was used to estimate independent association of risk factors with SCD. Results: We evaluated 483 SCD cases (65.8% male) and 886 controls (66.4% male). Cases were more likely to be older (68.8±14.3 vs 67.2±11.3, p=0.03), of black race (9.8 vs 3.2%, p<0.0001) and with worse CrCl (53.4±31.3 vs. 64.0±24.9 ml/min, p<0.0001). Overall, cases had lower levels of mean Na (137.3±4.2 vs 138.3±3.4 mEq/L, p<0.0001), Ca (9.0±0.7 vs 9.2±0.5 mg/dl, p<0.0001) and Mg (2.0±0.5 vs 2.1±0.4 mg/dl, p=0.007); and higher mean K (4.2±0.6 vs 4.1 ±0.5mEq/L, p=0.0008). Prevalence of hyponatremia (<136mEq/L), hyperkalemia (>5.2mEq/L), hypocalcemia (<8.5 mg/dl) and hypomagnesemia (<1.7 mg/dl) were also higher in cases (27.0 vs 16.2%, p<0.0001; 6.1 vs 1.4%, p<0.0001; 19.7 vs 7.9%, p<0.0001 and 20.4 vs 8.3%, p<0.0001, respectively). Adjusting for age, race and kidney function only hyperkalemia [OR 4.65 (95% CI 1.37-15.81), p=0.01], hypocalcemia [2.94 (1.68-5.13), p=0.0001] and hypomagnesemia [2.52 (1.36-4.66), p=0.003] remained significant, conferring a more than two to five-fold increase in SCD risk. Conclusions: Electrolyte abnormalities remain independently associated with increased risk of SCD in the community, even after adjusting for renal function.

Dialysate and Serum Potassium in Hemodialysis

Most patients with end-stage renal disease depend on intermittent hemodialysis to maintain levels of serum potassium and other electrolytes within a normal range. However, one of the challenges has been the safety of using a low-potassium dialysate to achieve that goal, given the concern about the effects that rapid and/or large changes in serum potassium concentrations may have on cardiac electrophysiology and arrhythmia. Additionally, in this patient population, there is a high prevalence of structural cardiac changes and ischemic heart disease, making them even more susceptible to acute arrhythmogenic triggers. This concern is highlighted by the knowledge that about two-thirds of all cardiac deaths in dialysis are due to sudden cardiac death and that sudden cardiac death accounts for 25% of the overall death for end-stage renal disease. Developing new approaches and practice standards for potassium removal during dialysis, as well as understanding other modifiable triggers of sudden cardiac death, such as other electrolyte components of the dialysate (magnesium and calcium), rapid ultrafiltration rates, and safety of a number of medications (ie, drugs that prolong the QT interval or use of digoxin), are critical in order to decrease the unacceptably high cardiac mortality experienced by hemodialysis-dependent patients.

Sports cardiology - a general practice oriented update

As a sub-speciality, Sports Cardiology focuses on sport and physical training interacting with cardiac issues. Particularly, Sports Cardiology deals with the so-called "Sports Paradox", which implicates the fact the on one side regular physical training leads to a multitude of relevant health benefits. But on the other hand, exercise can also be a trigger for sudden cardiac death, particularly in case of an underlying cardiac disease. However, health benefits by regular training outweigh potential risks by far, but only if an adequate cardiac screening and individual recommendations for sports participation have been provided. This review highlights various aspects of Sports Cardiology like strategies to prevent sudden cardiac death in sports and training recommendations in patients with an underlying cardiovascular disease.

Kcne2 Deletion Creates a Multisystem Syndrome Predisposing to Sudden Cardiac Death

Sudden cardiac death (SCD) is the leading global cause of mortality, exhibiting increased incidence in patients with diabetes mellitus. Ion channel gene perturbations provide a well-established ventricular arrhythmogenic substrate for SCD. However, most arrhythmia-susceptibility genes, including the KCNE2 K(+) channel β subunit, are expressed in multiple tissues, suggesting potential multiplex SCD substrates. Using whole-transcript transcriptomics, we uncovered cardiac angiotensinogen upregulation and remodeling of cardiac angiotensinogen interaction networks in P21 Kcne2(-/-) mouse pups and adrenal remodeling consistent with metabolic syndrome in adult Kcne2(-/-) mice. This led to the discovery that Kcne2 disruption causes multiple acknowledged SCD substrates of extracardiac origin: diabetes mellitus, hypercholesterolemia, hyperkalemia, anemia, and elevated angiotensin II. Kcne2 deletion was also a prerequisite for aging-dependent QT prolongation, ventricular fibrillation and SCD immediately after transient ischemia, and fasting-dependent hypoglycemia, myocardial ischemia, and AV block. Disruption of a single, widely expressed arrhythmia-susceptibility gene can generate a multisystem syndrome comprising manifold electric and systemic substrates and triggers of SCD. This paradigm is expected to apply to other arrhythmia-susceptibility genes, the majority of which encode ubiquitously expressed ion channel subunits or regulatory proteins.

The Importance of the Electrocardiogram (Ecg) in the Setting of Sports Pre-Participation Screening

The regular practice of physical and sporting activities is one of the most important measures in cardiovascular prevention. It is to be recommended at all ages as it improves fitness and significantly reduces cardiovascular morbidity and mortality. However, exercise can become a trigger of Sudden Cardiac Death (SD) in patients with often, underlying cardiovascular disease.

Arrhythmias and conduction disturbances in obstructive sleep apnoea: the heart of the problem?

Heart rhythm disorders temporally associated with obstructive apnoeic events have been highlighted for more than 30 years. An ECG from polysomnographic recordings enables both sleep medicine specialists and cardiologists to address occasional very impressive paroxysmal atrioventricular conduction blocks or sinus pauses (of up to 10 s during rapid eye movement (REM) sleep) [1]. The pathophysiology of these disorders induced by respiratory events is obviously complex and represents an exciting challenge in the context of integrative human physiology. The role of acute and chronic imbalances in the autonomic nervous system (ANS) associated with obstructive sleep apnoeas or hypopnoeas (OSA) has been clearly demonstrated in many cellular mechanisms of myocardial adaptation to such repeated stresses [2–4]. In addition, these autonomic disorders are now recognised as independent risk factors or triggers of sudden cardiac death not only in heart failure patients [5] but also in people with preserved systolic/diastolic left ventricular function [6, 7]. Although sleep is normally a time when the parasympathetic modulation of the heart predominates and myocardial electrical stability is enhanced, OSA disturbs this quiescence, creating an autonomic profile in which both profound vagal activity leading to bradycardia and sympathetic overactivity favouring ventricular ectopy are commonly observed [8]. The authors of a review paper published in the current issue of the European Respiratory Journal [9] must be congratulated for successfully detailing of the mechanisms present during apnoea/hypopnoea that can lead to heart rhythm disturbances. This paper is, for me, a remarkable teaching tool that I will use again in the future due to its clarity and its “updated” literature review. In a second part …

Dilated Cardiomyopathy: A Disease of the Myocardium

Cardiomyopathies are defined as cardiac diseases of the myocardium with associated cardiac dysfunction. They are cardiac diseases in which heart muscle disease and/or measurable deterioration of cardiac muscle function occurs due to various causes, such as genetic and sporadic mutations of muscle proteins, as well as external factors such as hypertension, ischemia, and inflammation. In 1995, the WHO/International Society and Federation of Cardiology (ISFC) classified primary cardiomyopathy caused by intrinsic factors into five groups according to the dominant pathophysiology: dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restricted cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and unclassified cardiomyopathy. Among these cardiomyopathies, DCM is the most prevalent and the most common reason for cardiac transplantation in adults and children. Many recent findings indicate that genetic and sporadic mutations of a number of muscle proteins, such as myofibrillar, structural, and Ca(2+) regulating proteins, can cause DCM. In such cases, certain mutations often induce DCM with cardiac arrhythmia that is recognized as a potential trigger of sudden cardiac death. Thus, effective prognostic determination and appropriate cardiac care depend on accurate molecular and genetic diagnoses.

Genetics of sudden cardiac death in children and young athletes

Sudden cardiac death is a rare but socially devastating event. The most common causes of sudden cardiac death are congenital electrical disorders and structural heart diseases. The majority of these diseases have an incomplete penetrance and variable expression; therefore, patients may be unaware of their illness. In several cases, physical activity can be the trigger for sudden cardiac death as first symptom. Our purpose is to review the causes of sudden cardiac death in sportive children and young adults and its genetic background. Symptomatic individuals often receive an implantable cardioverter-defibrillator, the preventive treatment for sudden cardiac death in most of cases due to channelopathies, which can become a challenging option in young and active patients. The identification of one of these diseases in asymptomatic patients has similarly a great impact on their everyday life, especially on their ability to undertake competitive physical activities, and the requirement of prophylactic treatment. We review main causes of sudden cardiac death in relation to its genetics and diagnostic work-up

Screening for Sudden Cardiac Death in the Young

Sudden cardiac death (SCD) in the young (SCDY) has a devastating impact on families, care providers, and the community and attracts significant public and media attention. Sudden cardiac death is defined as an abrupt and unexpected death due to a cardiovascular cause, typically occurring 1 hour from the onset of symptoms. Depending on the source, “young” is variably defined as those less than 25, 30, 35, or 40 years of age. Estimates of the incidence of SCDY (not including infants) vary broadly from 0.6 to 6.2 per 100 000 persons. 1–3 Sudden infant death syndrome (SIDS) may be related to SCD in some infants. Sudden infant death syndrome is defined as the sudden death of an infant 1 year of age that cannot be explained after a thorough investigation is conducted, including an autopsy, death scene evaluation, and review of the clinical history. The incidence of SIDS ranges from 50 to 100 in 100 000,4 and emerging data suggest that as many as 10% to 15% of SIDS deaths are associated with functional cardiac ion channelopathy gene variants.5 The most common diagnoses that increase risk for SCDY include hypertrophic cardiomyopathy (HCM), coronary artery anomalies of wrong sinus origin, myocarditis, arrhythmogenic right ventricular cardiomyopathy, and ion channelopathies.6 The latter category includes hereditary diseases such as the congenital long-QT syndromes (LQTS), catecholaminergic polymorphic ventricular tachycardia, and Brugada syndrome, among other less common channelopathies. These diseases are typically undetected before the SCD event. Estimated prevalence rates of these conditions range from 1 per 500 persons for HCM to 1 per 2500 for the LQTS. SCD related to these diagnoses has been documented in infancy and during competitive athletics. In addition, prescription stimulant use for treatment of attention deficit hyperactivity disorder (ADHD) has been postulated to be a trigger for SCD.7,8 Sudden cardiac death in the young is a critical public health issue. A young life cut short represents a devastating event for families, and is associated with many lost productive years. There is significant dissonance among experts in the field about the best approach to prevent SCDY in the United States. Some experts support the implementation of largescale cardiovascular screening programs in infants, in athletes, or in all children to identify at-risk individuals in an effort to prevent SCDY. Cardiovascular screening for SCDY typically involves the addition of an ECG to the current standard of care of history and physical examination. Echocardiography and genetic testing represent alternative or additional screening modalities. Observational data from the Veneto region of Italy suggest that ECG screening can successfully identify at-risk cardiovascular diseases and dramatically reduce the incidence of SCD in competitive athletes.9,10 Proponents of ECG screening in the United States suggest that it can be effective, feasible, and cost-effective. 11 Critics of ECG screening cite a lack of evidence to support its effectiveness or feasibility in the United States; lack of clinical accuracy; cost implications; and the potential clinical, financial, and emotional consequences of falsepositive screening test results. 12 Cost estimates for a national ECG screening program in the United States for