Sudden Cardiac Death in Athletes: What Sport-Rehabilitation Specialists Need to Know

2003 ◽  
Vol 12 (3) ◽  
pp. 259-271 ◽  
Author(s):  
Christian C. Evans ◽  
Sandra L. Cassady

Objective:To describe the underlying conditions that predispose athletes to sudden cardiac death (SCD) and review signs and symptoms that indicate an athlete is at risk.Data Sources:MEDLINE, theLos Angeles TimesandTriathlon Timesarchives, and other sources identified in the references of articles initially located therein. A total of 43 references were included.Conclusions:Most cases of SCD in younger athletes (≤35 years) are attributable to multiple hereditary conditions, with familial hyper-trophic cardiomyopathy being the primary cause, whereas the major cause of SCD in older athletes (>35 years) is coronary artery disease. Health-care professionals evaluating athletes should pay particular attention to past medical and family history. Items in an athlete’s screening that suggest increased risk include a history of chest pain, syncope, excessive shortness of breath, irregular heart rate or murmur, or a history of SCD in an immediate family member.

2021 ◽  
Vol 19 ◽  
Author(s):  
Jean-Jacques Monsuez ◽  
Marilucy Lopez-Sublet

: Persons living with HIV infection (PLWH) have been recognized to have an increased risk of sudden cardiac death (SCD). Prevention of this risk should theoretically be included in their long-term management. However, only a few approaches have been proposed to optimize such interventions. Targeting detection of the commonly associated conditions such as coronary artery disease, left ventricular dysfunction, heart failure, QT interval prolongation and ventricular arrhythmias is the first step of this prevention. However, although detection of the risk of SCD is a suitable challenge in PLWH, it remains uncertain whether optimized treatment of the identified risks would unequivocally translate into a decrease in SCD rates.


Author(s):  
Leila Emrahi ◽  
Shirin Shahbazi ◽  
Mehrnoush Toufan Tabrizi ◽  
Mohammad Mahdi Mortazavipour ◽  
Mir Ali Seyyedi

Background: Hypertrophic cardiomyopathy is a common genetic cardiovascular disease with autosomal dominant inheritance and MYBPC3 gene has been frequently linked to its pathogenesis. Since, carriers of the 25 nucleotides deletion located on intron 32 of the MYBPC3 are at increased risk of heart disease we aimed to investigate this variant in hypertrophic cardiomyopathy patients and healthy population. Methods: DNA was extracted from 350 Blood samples including 42 hypertrophic cardiomyopathies and 308 healthy subjects and the region containing the deletion was amplified by PCR method. PCR products were analyzed on agarose gel and genotyping results were recorded. Results: Genetic counseling results revealed that 26.2% of patients were sporadic cases vs 59.5% with positive family history and there was a history of sudden cardiac death in the first degree relatives of 42.3% of the patients. Genotyping results showed that all samples had a single band of 198 bp, indicating no MYBPC3Δ25bp variant in HCM patients as well as 308 controls. Bioinformatics assessments revealed that MYBPC3Δ25bp had a frequency of 0.00438 on Iranome database with the highest incidence reported in the Baloch population. Conclusion: Since hypertrophic cardiomyopathy is related to sudden cardiac death, population studies in terms of predisposing factors are of particular importance. Our study results showed that MYBPC3Δ25bpshould not be considered as risk factor in the patients of northwest of Iran. However, according to the bioinformatics findings and reports of neighboring countries, it is suggested that MYBPC3Δ25bp to be studied in the eastern and southern Iranian hypertrophic cardiomyopathy patients.


2021 ◽  
pp. jrheum.210139
Author(s):  
Lisandro D. Colantonio ◽  
Richard J. Reynolds ◽  
Tony R. Merriman ◽  
Angelo Gaffo ◽  
Jasvinder A. Singh ◽  
...  

Objective Determine the association of serum urate levels with sudden cardiac death and incident coronary heart disease (CHD), separately, among adults without a history of CHD. Methods We conducted a case-cohort analysis of Black and White participants ≥45 years of age enrolled in the REason for Geographic And Racial Differences in Stroke (REGARDS) study without a history of CHD at baseline between 2003 and 2007. Participants were followed for sudden cardiac death or incident CHD (i.e., myocardial infarction or death from CHD excluding sudden cardiac death) through December 31, 2013. Baseline serum urate was measured in a random sample of participants (n=840) and among participants who experienced sudden cardiac death (n=235) or incident CHD (n=851) during follow-up. Results Participants with higher serum urate levels were older and more likely to be male or Black. The crude hazard ratio (95%CI) per 1 mg/dL higher serum urate level was 1.26 (1.14-1.40) for sudden cardiac death and 1.17 (1.09-1.26) for incident CHD. After adjustment for age, gender, race, and cardiovascular risk factors, the hazard ratio (95%CI) per 1 mg/dL higher serum urate level was 1.19 (1.03-1.37) for sudden cardiac death and 1.05 (0.96-1.15) for incident CHD. Hazard ratios for sudden cardiac death were numerically higher among participants 45-64 versus ≥65 years of age, without versus with diabetes, and among those of White versus Black race, although p-values for effect modification were all ≥0.05. Conclusion Higher serum urate levels were associated with an increased risk for sudden cardiac death but not with incident CHD.


Author(s):  
Pattara Rattanawong ◽  
Jakrin Kewcharoen ◽  
Chanavuth Kanitsoraphan ◽  
Timothy Barry ◽  
Anusha Shanbhag ◽  
...  

Background Brugada syndrome is an inherited cardiac channelopathy associated with major arrhythmic events (MAEs). The presence of a positive family history of sudden cardiac death (SCD) as a risk predictor of MAE remains controversial. We aimed to examine the association between family history of SCD and MAEs stratified by age of SCD with a systematic review and meta‐analysis. Methods and Results We searched the databases of MEDLINE and EMBASE from January 1992 to January 2020. Data from each study were combined using the random‐effects model. Fitted metaregression was performed to evaluate the association between the age of SCD in families and the risk of MAE. Twenty‐two studies from 2004 to 2019 were included in this meta‐analysis involving 3386 patients with Brugada syndrome. The overall family history of SCD was not associated with increased risk of MAE in Brugada syndrome (pooled odds ratio [OR], 1.11; 95% CI, 0.82–1.51; P =0.489, I 2 =45.0%). However, a history of SCD in family members of age younger than 40 years of age did increase the risk of MAE by ≈2‐fold (pooled OR, 2.03; 95% CI, 1.11–3.73; P =0.022, I 2 =0.0%). When stratified by the age of cut point at 50, 45, 40, and 35 years old, a history of SCD in younger family member was significantly associated with a higher risk of MAE (pooled OR, 0.49, 1.30, 1.51, and 2.97, respectively; P =0.046). Conclusions A history of SCD among family members of age younger than 40 years was associated with a higher risk of MAE.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Lisandro D Colantonio ◽  
Richard Reynolds ◽  
Tony Merriman ◽  
Angelo Gaffo ◽  
Jasvinder A Singh ◽  
...  

Background: Higher serum urate (SU) levels were shown to causally increase the risk for sudden cardiac death (SCD) in a Mendelian randomization analysis of white adults, most of whom had coronary heart disease (CHD). It is unclear if these results are generalizable to more racially diverse adults without CHD. Objective: To assess the risk for SCD and incident CHD associated with SU levels in adults without a history of CHD using data from a large, population-based cohort of US black and white men and women ≥45 years of age, the REason for Geographic And Racial Differences in Stroke (REGARDS) study. Methods: We conducted a case-cohort analysis of REGARDS study participants without a history of CHD at baseline between 2003 and 2007. Participants were followed for SCD or incident CHD (i.e., myocardial infarction or CHD death excluding SCD) from baseline through December 31, 2013. Baseline SU levels were measured in a random sample of participants (n=840) and among 235 participants with SCD and 851 participants with incident CHD. Results: Participants with higher SU levels were older and more likely to be black and male. The crude hazard ratio (95%CI) per 1 mg/dL higher SU level was 1.26 (1.14, 1.40) for SCD and 1.17 (1.09, 1.26) for incident CHD. Analyses modeling SU levels using splines supported that these associations were linear. After multivariable adjustment, higher SU levels remained associated with an increased risk for SCD, but not for incident CHD ( Table ). There was no effect modification in the association of SU levels with SCD or incident CHD by either age, gender, race or chronic kidney disease. However, the increased risk for SCD associated with higher SU levels was present in whites but not among blacks. Limitations: The study has limited statistical power for subgroup comparisons. Race differences in the association between SU levels and SCD require further investigation. Conclusions: In adults without a history of CHD, higher SU levels appear to be an independent risk factor for SCD, but no association was detected with incident CHD.


2009 ◽  
Vol 76 (6) ◽  
pp. 652-658 ◽  
Author(s):  
Patrick H. Pun ◽  
Thomas R. Smarz ◽  
Emily F. Honeycutt ◽  
Linda K. Shaw ◽  
Sana M. Al-Khatib ◽  
...  

ESC CardioMed ◽  
2018 ◽  
pp. 2305-2308
Author(s):  
Efstathios K. Iliodromitis ◽  
Dimitrios Farmakis

There are three main groups in the general population as far as sudden cardiac death (SCD) is concerned: individuals without a known history or predisposing factors for heart disease; individuals with known risk factors for heart disease or SCD; and patients with diagnosed ischaemic, structural, or electrical cardiac conditions, acquired or genetic, that are associated with an increased risk for SCD. Although SCD literature focuses mainly on patients with known heart disease, approximately 50% of SCD cases occur in individuals belonging to the first two groups. The annual incidence of SCD in the general population ranges between 0.6 and greater than 1.4 per 1000 individuals. SCD occurs more commonly in men than in women and with an incidence that increases with age due to the increase in coronary artery disease. The commonest aetiologies for SCD in the general population are coronary artery disease and cardiomyopathy, accounting for 80% and 10–15% of cases, respectively. A number of factors have been related to an increased risk for SCD in the general population including genetic predisposition, risk factors for atherosclerosis, strenuous physical activity and sports, electrocardiographic abnormalities, elevated levels of biomarkers, and abnormalities in imaging and other diagnostic techniques. However, large-scale prospective studies that confirm the feasibility, clinical efficacy, and cost-effectiveness of using these factors for broad mass screening for SCD are generally lacking and therefore risk stratification for SCD in the general population remains challenging.


2020 ◽  
Vol 3 (2) ◽  
pp. 70-73
Author(s):  
Juwairiya Syed Iqbaluddin ◽  
Fathima Murthuza ◽  
Sumaiya Iqbal

Brugada syndrome (BrS) is a rare, autosomal dominant genetic disorder with mutation in the SCN5A gene. It is associated with an increased risk of arrhythmias and sudden cardiac death. BrS can be diagnosed by characteristic electrocardiogram (ECG) findings and significant events, such as syncope, palpitations, nocturnal respiratory agonia, and family history of sudden cardiac death below the age of 45 years. Special investigations, such as electrophysiology study, ajmaline provocation test, and genetic testing, play an important role in its diagnosis. This case report describes a patient who presented with chest pain and dizziness along with a positive family history of sudden cardiac deaths below the age of 45 years. He was discovered to have type 2 Brugada pattern on ECG, and by ajmaline provocation test, the type 1 pattern was unmasked, which established a definitive diagnosis of BrS. The patient was then advised for an implantable cardioverter-defibrillator. This case highlights the need for physicians to be competent in identifying patients with BrS in order to provide the necessary management and prevent fatal outcomes.


PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e59905 ◽  
Author(s):  
Adriana Huertas-Vazquez ◽  
Christopher P. Nelson ◽  
Xiuqing Guo ◽  
Kyndaron Reinier ◽  
Audrey Uy-Evanado ◽  
...  

Author(s):  
Anat Milman ◽  
Elijah R. Behr ◽  
Belinda Gray ◽  
David C. Johnson ◽  
Antoine Andorin ◽  
...  

Background: Brugada syndrome (BrS) is associated with mutations in the cardiac sodium channel gene, SCN5A. However, genetic studies of patients with BrS with arrhythmic events have been limited. We sought to compare various clinical, ECG, and electrophysiological parameters according to SCN5A genotype in a large cohort of BrS probands with first arrhythmic event. Methods: Survey on Arrhythmic Events in Brugada Syndrome is a survey of 10 Western and 4 Asian countries, gathering 678 patients with BrS with first arrhythmic event. Only probands were included, and SCN5A genotype adjudicated. Patients without appropriate genetic data were excluded. Associations of genotype with clinical features were analyzed. Results: The study group comprised 392 probands: 92 (23.5%) SCN5A+ (44 pathogenic/likely pathogenic [P/LP] and 48 variants of unknown significance) and 300 (76.5%) SCN5A−. SCN5A missense variants and the patients hosting them were similar regardless of adjudication. A higher proportion of patients with P/LP were pediatric (<16 years) compared with SCN5A− (11.4% versus 3%, P =0.023). The proportion of females was higher among patients with P/LP compared with SCN5A − (18.2% versus 6.3%, P =0.013). P/LP probands were more likely to have a family history of sudden cardiac death compared with SCN5A − (41.9% versus 16.8%, P <0.001). A higher proportion of patients with P/LP were White compared with SCN5A− (87.5% versus 47%, P <0.001). Ethnicity (odds ratio, 5.41 [2.8–11.19], P <0.001) and family history of sudden cardiac death (odds ratio, 2.73 [1.28–5.82], P =0.009) were independent variables associated with P/LP genotype following logistic regression. Conclusions: The genetic basis of BrS has a complex relationship with gender, ethnicity, and age. Probands hosting a P/LP variant tended to experience their first arrhythmic event at a younger age and to have events triggered by fever compared with patients with SCN5A− . In addition, they were more likely to be White and to have family history of sudden cardiac death. Among females, a P/LP variant suggests an increased risk of being symptomatic. This association should be further studied on an ethnically specific basis in large prospectively collected international cohorts.


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