|Home | About | Journals | Submit | Contact Us | Français|
Collapse after prolonged endurance exercise is common and usually benign. This case study reports a triathlete who suffered a vaso‐vagal associated collapsed after exercise. Misdiagnosis of myocardial injury in the presence of elevated cardiac troponins and ECG anomalies led to inappropriate management and highlights the difficulty in treating the collapsed athlete following arduous exercise.
In April 2006 a 43‐year‐old Caucasian male club level triathlete presented to the CRY Centre for Sports Cardiology for a follow‐up consultation. In March 2006, after completion of an Ironman triathlon (4.2 km swim, 180 km bike, 42 km run) in a personal best time, the athlete received a massage during which he experienced presyncopal symptoms. He received fluid resuscitation (500 ml, 1% saline) and recovered well. After a long period of standing in the heat the athlete reported presyncopal symptoms and collapsed, without syncope. Blood pressure was measured at 75/40 mm Hg, and after further fluid resuscitation (500 ml, 1% saline) he was referred to the cardiology department of the local hospital. The athlete was conscious and alert with normal core temperature, blood glucose and plasma sodium, and was otherwise asymptomatic.
On admission his ECG demonstrated minor ST‐segment elevation in anterior lateral and inferior leads (fig 11)) and his cardiac troponin‐I (cTnI) was mildly raised at 0.06 U/l. An ECG was normal with mild, concentric left ventricular hypertrophy. The athlete underwent diagnostic cardiac catheterisation, which demonstrated normal coronary arteries. Owing to the mildly raised cTnI and minor ST‐segment elevation, he was diagnosed with mild myopericarditis and advised to avoid exercise for 6 weeks.
On follow‐up, 2 weeks after being discharged from hospital, the resting 12‐lead ECG demonstrated similar findings of marginal ST‐segment elevation in anterior lateral and inferior leads (fig 22).). Echocardiography demonstrated mild concentric left ventricular hypertrophy (12 mm) in the presence of normal diastolic and systolic function. There was no evidence of myocarditis or pericarditis and the athlete was immediately cleared for training and competition.
Exercise‐associated collapse is common after prolonged endurance exercise1 and is usually benign, however in some circumstances can be severe and life threatening. Benign causes of collapse include exhaustion, postural hypotension, dehydration and leg cramps. Serious causes include hyponatraemia, heatstroke, hypoglycaemia, hypothermia, cardiac arrest and other medical conditions.2 In the presence of a conscious, alert athlete presenting with normal blood glucose and plasma sodium, and normal core temperature, as observed in the athlete in the present case study, the likely cause of collapse is a vaso‐vagal response leading to postural hypotension that may be exacerbated by dehydration.
Although the health benefits of regular, moderate‐intensity physical activity are well recognised, there is a growing body of evidence demonstrating an acute reduction in cardiac function and the presence of humoral markers of cardiac myocyte damage (cTnT and cTnI) that may be above acute myocardial infarction cut‐off levels after ultra‐endurance exercise.3 Among this work are a number of studies examining the Ironman triathlon.4,5 The prevalence of increases in cTnT or cTnI, or both, after exercise is not fully known. However, in a recent study, 78% of runners investigated after a marathon presented evidence of minor cardiomyocyte damage.6 Previous studies have suggested that these changes are likely to be physiological owing to their rapid (<24 h) return to baseline values and of no clinical significance. Indeed, the latest work from our own laboratory demonstrates a peak in cTnT at 3 h after exercise with a subsequent fall to baseline levels at 24 h after exercise (unpublished findings). These findings are in direct contrast to the kinetics of cardiac troponin release observed after myocardial infarction, where an initial release of unbound troponin is followed by a continued release of the structurally bound troponin as it degrades, resulting in a sustained rise in circulating troponin for many days after infarction.7
The level of cTnI seen in the athlete in the present study is similar to that previously described in athletes after ultra‐endurance exercise and probably represented a physiological response to prolonged arduous exercise. The use of single measures of cardiac troponins should be viewed with caution after prolonged exercise. Serial measures would help to eliminate myocardial infarction as a cause of the raised cardiac troponins.
A number of ECG changes are seen in athletes that are associated with physiological anomalies and of no clinical significance.8 The diffuse minor ST‐segment elevations seen in the athlete's ECG in this study represent a normal variant as shown by their presence at follow‐up examination. Furthermore, the absence of echocardiographic evidence of myocardial or pericardial injury supports the evidence for a physiological substrate underpinning the observed ECG changes. The use of ECG for screening athletes before ultra‐endurance competition may aid in the identification of disease after prolonged exercise and avoid misdiagnosis and mismanagement of the athlete.
We acknowledge the support of Cardiac Risk in the Young (CRY) in the support of this study.
Conflict of interest: None declared.