Sports-related sudden cardiac death in Spain. A multicenter, population-based, forensic study of 288 cases

Author(s):  
Benito Morentin ◽  
M. Paz Suárez-Mier ◽  
Ana Monzó ◽  
Javier Ballesteros ◽  
Pilar Molina ◽  
...  
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jari Laukkanen

α 2B -adrenoceptors mediate contraction of vascular smooth muscle and induce coronary vasoconstriction in humans. A variant of the human α 2B -adrenoceptor gene that encodes a D of three residues in an intracellular acidic motif has been shown to confer decreased receptor desensitization. This receptor variant could, therefore, be involved in cardiovascular diseases associated with enhanced vasoconstriction. Our aim was to study whether an insertion/deletion (I/D) polymorphism in the α 2B -adrenoceptor gene is associated with the risk for sudden cardiac death. This study was part of a prospective population-based study investigating risk factors for cardiovascular diseases in a cohort of middle-aged men from eastern Finland. The study is based on 1606 men 42 to 60 years of age followed for an average time of 17 years. In this study population, 338 men (21%) had the D/D genotype; 467 (29 %) had the I/I genotype, and 801 (50%) had a heterozygous genotype. There were 76 sudden cardiac deaths during follow-up. In a Cox model adjusting for other coronary risk factors (age, systolic blood pressure, smoking, diabetes, serum LDL and HDL cholesterol, body mass index and exercise-induced myocardial ischemia), men with the D/D or I/D genotype had 1.95 time (95% confidence interval, 1.07 to 3.55, P = 0.029) higher risk to experience sudden cardiac death (20 events for D/D genotype, 13 events for I/I genotype and 43 events for I/D genotype) compared with men carrying the I/I genotype. The α 2B -adrenoceptor genotype was associated with coronary heart disease death but not with hypertension. The D/D and I/D genotypes of the α 2B -adrenoceptor are novel genetic risk predictors for sudden cardiac death.


EP Europace ◽  
2017 ◽  
Vol 19 (suppl_3) ◽  
pp. iii236-iii236
Author(s):  
A. Ngantcha ◽  
S. Mbouh ◽  
K. Tibarzawa ◽  
C. Saka ◽  
J. Wa ◽  
...  

2017 ◽  
Vol 46 (4) ◽  
pp. 1230-1238 ◽  
Author(s):  
Aimé Bonny ◽  
Kemi Tibazarwa ◽  
Samuel Mbouh ◽  
Jonas Wa ◽  
Réné Fonga ◽  
...  

Author(s):  
Jari A. Laukkanen ◽  
Hassan Khan ◽  
Sudhir Kurl ◽  
Peter Willeit ◽  
Jouni Karppi ◽  
...  

2008 ◽  
Vol 9 (6) ◽  
pp. 595-600 ◽  
Author(s):  
Alessandro Filippi ◽  
Emiliano Sessa ◽  
Giampiero Mazzaglia ◽  
Serena Pecchioli ◽  
Rachele Capocchi ◽  
...  

2014 ◽  
Vol 66 ◽  
pp. S69 ◽  
Author(s):  
R. Narain ◽  
J. Mayers ◽  
H. Dhutia ◽  
A. Malhotra ◽  
A. Merghani ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Mirabel ◽  
J.S Hulot ◽  
A Lillo-Lelouet ◽  
X Jouven ◽  
E Marijon

Abstract Background Sudden cardiac death (SCD) in cancer patients regardless of their therapies has not been addressed. Methods Population-based registry (2011) via multiple sources to collect every case of SCD in Paris and its suburbs, covering a population of 6.6 million. Data of SCD patients (2011–2017) were analysed by identifying patients with known cancer or past medical history of cancer. Categorical variables were compared using chi-square test or Fisher's exact test; continuous variables using Student t-test or Wilcoxon rank sum test, as appropriate. Results Of 22,570 out of hospital cardiac arrests, 3,311 SCD patients (124 cancer patients and 3,187 non cancer patients) were admitted alive to the hospital and were included in the analysis. Characteristics of patients and cardiac arrest circumstances differed on univariate analysis (Table). The final aetiology of SCD varied: more respiratory causes to SCD (pulmonary embolism and hypoxia) among cancer patients and less acute coronary artery syndromes. Conclusions SCD in cancer patients differs significantly when compared to non-cancer patients. Coronary events are less prominent whereas respiratory causes are common aetiologies in cancer. Funding Acknowledgement Type of funding source: None


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