Specific Populations: Female Athletes

The true incidence of sudden cardiac death (SCD) in US athletes is unknown. Current estimates are based largely on case identification through public media reports and estimated participation rates. The purpose of this study was to more precisely estimate the incidence of SCD in National Collegiate Athletic Association (NCAA) student-athletes and assess the accuracy of traditional methods for collecting data on SCD. From January 2004 through December 2008, all cases of sudden death in NCAA student-athletes were identified by use of an NCAA database, weekly systematic search of public media reports, and catastrophic insurance claims. During the 5-year period, there were 273 deaths and a total of 1 969 663 athlete participant-years. Of these 273 deaths, 187 (68%) were due to nonmedical or traumatic causes, 80 (29%) to medical causes, and 6 (2%) to unknown causes. Cardiovascular-related sudden death was the leading cause of death in 45 (56%) of 80 medical cases, and represented 75% of sudden deaths during exertion. The incidence of SCD was 1:43 770 participants per year. Among NCAA Division I male basketball players, the rate of SCD was 1:3100 per year. Thirty-nine (87%) of the 45 cardiac cases were identified in the NCAA database, only 25 (56%) by use of public media reports, and 9 (20%) from catastrophic claims data. SCD is the leading medical cause of death and death during exercise in NCAA student-athletes. Current methods of data collection underestimate the risk of SCD. Accurate assessment of SCD incidence is necessary to shape appropriate health policy decisions and develop effective strategies for prevention.

Sudden cardiac death (SCD) is the leading cause of mortality in athletes during sport. A variety of mostly hereditary, structural, or electrical cardiac disorders are associated with SCD in young athletes, the majority of which can be identified or suggested by abnormalities on a resting 12-lead electrocardiogram (ECG). Whether used for diagnostic or screening purposes, physicians responsible for the cardiovascular care of athletes should be knowledgeable and competent in ECG interpretation in athletes. However, in most countries a shortage of physician expertise limits wider application of the ECG in the care of the athlete. A critical need exists for physician education in modern ECG interpretation that distinguishes normal physiological adaptations in athletes from distinctly abnormal findings suggestive of underlying pathology. Since the original 2010 European Society of Cardiology recommendations for ECG interpretation in athletes, ECG standards have evolved quickly over the last decade; pushed by a growing body of scientific data that both tests proposed criteria sets and establishes new evidence to guide refinements. On 26-27 February 2015, an international group of experts in sports cardiology, inherited cardiac disease, and sports medicine convened in Seattle, Washington, to update contemporary standards for ECG interpretation in athletes. The objective of the meeting was to define and revise ECG interpretation standards based on new and emerging research and to develop a clear guide to the proper evaluation of ECG abnormalities in athletes. This statement represents an international consensus for ECG interpretation in athletes and provides expert opinion-based recommendations linking specific ECG abnormalities and the secondary evaluation for conditions associated with SCD.

Our purpose was to test the null hypothesis that beginning regular, moderate-intensity exercise in early pregnancy has no effect on fetoplacental growth. Forty-six women who did not exercise regularly were randomly assigned at 8 weeks either to no exercise (n = 24) or to weight-bearing exercise (n = 22) 3 to 5 times a week for the remainder of pregnancy. Outcome variables included antenatal placental growth rate and neonatal and placental morphometric measurements. The offspring of the exercising women were significantly heavier (corrected birth weight: 3.75 +/- 0.08 kg vs 3.49 +/- 0.07 kg) and longer (51.8 +/- 0.3 cm vs 50.6 +/- 0.3 cm) than those born to control women. The difference in birth weight was the result of an increase in both lean body mass and fat mass. In addition, midtrimester placental growth rate was faster (26 +/- 2 cm(3)/wk vs 21 +/- 1 cm(3)/wk) and morphometric indexes of placental function were greater in the exercise group. There were no significant differences in neonatal percentage body fat, head circumference, ponderal index, or maternal weight gain. These data indicate that beginning a moderate regimen of weight-bearing exercise in early pregnancy enhances fetoplacental growth.