American Journal of Emergency Medicine (2012) 30, 1306–1309
www.elsevier.com/locate/ajem
Correspondence
Sudden death in competitive athletes: does a circadian variation in occurrence exist?☆ To the Editor, Sudden death (SD) is an unexpected death, occurring within 1 hour from onset of symptoms, in ordinary conditions of life, and in presence of witnesses [1]. Most SDs are sudden cardiac deaths (SCDs) because coronary heart disease (CHD) is the most frequent cause, but pulmonary embolism, rupture of aortic aneurysms, and stroke are also included [2]. According to recent data, CHD causes approximately 1 of every 6 deaths in the United States, with approximately 1 myocardial infarction (MI) every 34 seconds [3]. The percentage of CHD deaths occurring out of the hospital is 70%, and 50% of men and 64% of women who died suddenly of CHD have no previous symptoms [3]. Many studies have shown that the occurrence of acute cardiovascular events, including SCD [4-11], is not evenly distributed in time but respects circadian (approximately 24 hours) patterns [12]. Sudden death of competitive athletes represents a shocking event for all people, is often highly publicized, heightens public awareness and concern, and has devastating impact on athletes, coaches, sports organizations, communities, and families [13]. In the lack of available data, we aimed to investigate whether a circadian pattern of SD in athletes exists, searching across multiple public, nonspecialized Web databases, cases of SD that occurred in competitive athletes during their competition, from the year 2000. Different databases were independently cross-searched from 2 authors with specific different competence: a medical doctor (ADG) and a journalist (FA) with sport competence (active athlete). The collected cases were included in 2 groups for analysis: group A, cases with precise (± 30 minutes) time of SD, and group B, cases with probable (within a 6-hour interval: night, 00:0005:59 AM; morning, 06:00-11:59 AM; afternoon, 12:00-
☆ Funding support: Supported, in part, by a scientific grant “FAR— Fondo di Ateneo per la Ricerca scientifica,” University of Ferrara, Italy.
0735-6757/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
05:59 PM; and evening, 06:00-11:59 PM). Group A was analyzed applying partial Fourier series, by means of a chronobiologic software that selects the harmonic(s) best explaining the variance of the data [14]. The percentage of rhythm (PR: percentage of the overall variability of data about the arithmetic mean) and the F test statistic are used to test the hypothesis of zero amplitude null hypothesis (absence of periodicity). The software also calculates the acrophase (peak) of each single harmonic and the peak and trough times of the overall best fitted curve. Significance was assumed for P b .05. Group B was analyzed by means of χ2 test goodness of fit [15]. Thirty-seven athletes with SD were included in group A (Table), and a total of 63 were included in group B (age, 18-37 years; mean, 26.6 ± 4.8 years). As for group A, chronobiologic analysis yielded a significant circadian variation, characterized by a bimodal frequency peak. The main circadian peak (periodicity, 24 hours; PR, 52.5%; P b .001) was registered at 04:58 PM (95% confidence limits [CL], 15:32-18:24 PM), and a smaller accessory peak (periodicity, 12 hours; PR, 14.7%; P = .029) was found at 08:29 AM/PM (96% CL, 06:34-09:18). Overall, the circadian rhythm (peak at 07:00 PM, trough at 2:56 AM) was highly significant (PR, 67.3%; P b .001) (Fig. 1). For group B, χ2 test showed a statistically significant difference (χ2, 10.0; P = .024), with highest frequency of cases in the evening (n = 25, 39.7%) and lowest during night time (n = 7, 11.1%) (Fig. 2). This preliminary study shows that also in athletes, SD exhibits a circadian pattern of onset, characterized by 2 frequency peaks. Muller et al [6] first revealed a prominent circadian morning incidence of SCD, with low nocturnal incidence [6], remarkably similar to that reported for nonfatal MI [4]. After adjustment for individual wake time, the onset of events was higher during the first 3 hours after awakening [16]. A same pattern was confirmed also for cardiac arrests [17-19], and further studies revealed the existence of a second peak in the afternoon-evening hours, maybe attributable to arrhythmias. Arrhythmic events exhibit circadian rhythm, also in apparently healthy subjects [20]. Arntz et al [21] reported a marked circadian variation in the occurrence of SD with a primary morning peak and a secondary afternoon peak. The subgroup of patients with ventricular
Correspondence Cases of sudden death of competitive athletes with precise time of death
Athlete
Age
Hour
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37
24 24 33 28 24 30 24 28 37 25 22 28 35 27 24 33 19 21 36 26 19 24 25 31 26 26 25 32 26 31 23 34 30 27 23 20 37
5:45 11:50 2:37 7:41 10:30 10:14 9:00 3:30 4:15 9:15 8:30 8:46 5:18 0:00 11:51 9:00 5:03 5:30 9:30 10:30 11:30 5:10 12:13 3:30 7:20 8:21 8:53 6:05 7:00 1:15 10:45 1:06 4:10 2:43 7:11 3:50 10:00
PM AM PM PM PM PM AM PM PM PM PM AM PM AM AM PM PM PM AM AM PM PM PM AM PM AM PM PM PM PM PM PM PM PM PM PM PM
fibrillation as initially documented arrhythmia showed a similar circadian variation, whereas patients with asystole or pulseless bradyarrhythmias were more evenly distributed during the daytime. Moreover, patients older than 65 years had a monophasic distribution, whereas younger patients had morning and afternoon peaks. Two peaks, approximately of the same size (8-11 AM, 4-7 PM) were confirmed in a large cohort, out-of-hospital cardiac arrests [22]. The evening peak was attributed primarily to the patients found in ventricular fibrillation, whereas arrests with other arrhythmias exhibited mainly a morning peak. Because previous studies could be exposed to the selection bias of excluding nocturnal unwitnessed deaths, Tofler et al [23] studied patients with implanted cardioverter/defibrillator and confirmed that a higher proportion of ventricular tachyarrhythmias began in the late morning. Again, Behrens
Sport discipline
Date
Country
Soccer Boxing Baseball Soccer Soccer Soccer Soccer Soccer Cycling Boxing Soccer Marathon Soccer Cycling Soccer Soccer Hockey Cycling Marathon Marathon Soccer Basketball Soccer Soccer Hockey Football Soccer Soccer Soccer Soccer Football Soccer Soccer Soccer Soccer Soccer Volleyball
05/10/2000 25/10/2000 02/06/2002 26/06/2003 25/01/2004 27/10/2004 28/11/2004 12/04/2005 15/06/2005 01/04/2007 25/08/2007 03/11/2007 29/12/2007 11/03/2008 03/04/2008 07/07/2008 13/10/2008 05/02/2009 20/08/2009 20/08/2009 22/10/2009 26/10/2009 15/11/2009 16/11/2009 08/12/2009 17/01/2010 06/03/2010 06/05/2010 08/05/2010 27/10/2010 27/04/2011 04/08/2011 13/11/2011 15/03/2012 17/03/2012 18/03/2012 24/03/2012
Romania USA USA Cameroon Hungary Brasil Argentina UK Italy Philippines Spain USA UK Portugal Croatia Romania Russia Belgium USA USA Italy Portugal Italy Mexico Sweden USA Nigeria Croatia Brasil Spain USA Japan Belgium India UK Italy Italy
5 4 3
N
Table
1307
2 1 0 TIME (hours)
Fig. 1 Circadian distribution of cases of sudden death in competitive athletes during competition with precise (±30 minutes) time of death (n = 37). Superimposed is the best fitting curve.
1308
Correspondence
20
Anna Maria Malagoni MD, PhD Fabio Manfredini, MD Vascular Diseases Center University of Ferrara Italy E-mail addresses:
[email protected] [email protected]
18 16 14
N
12 10 8 6
Roberto Manfredini MD Clinica Medica University of Ferrara Italy E-mail address:
[email protected]
4 2 0 NIGHT
MORNING
AFTERNOON
EVENING
Fig. 2 Circadian distribution of cases of sudden death in competitive athletes during competition with both precise and probable (within 6-hour period) time of death (n = 63).
doi:10.1016/j.ajem.2012.04.027
References et al [24] found that shock episodes terminating potentially life-threatening ventricular tachyarrythmias exhibited a primary morning peak and a secondary one, much smaller, between 4 and 8 PM. Regular exercise reduces the incidence of CHD and MI [25], but vigorous activity may enhance the risk of MI and SD among patients with occult or overt CHD [26,27]. Although with the limitations of small sample size and the possible conditioning effect of competition time schedule, it is interesting that the circadian pattern of SD onset in athletes resembles that of common people, with evening and morning peaks. It is possible that, in addition to vigorous exercise during competition, temporally related physiologic changes determining electrical myocardial vulnerability may also play a triggering role. Further studies on larger databases will test these preliminary data and provide useful insights for prevention. Alfredo De Giorgi MD Clinica Medica University of Ferrara Italy E-mail address:
[email protected] Federica Achilli La Nuova Ferrara Ferrara, Italy E-mail address:
[email protected] Fabio Fabbian MD Marco Pala MD Alessandra Mallozzi Menegatti Clinica Medica University of Ferrara Italy E-mail addresses:
[email protected] [email protected] [email protected]
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