Exercise induced neurally mediated syncope in an elite rower: a treatment dilemma.

CASE REPORT In March 2002, a 25 year old white woman presented to the British Olympic Medical Centre after bouts of syncope and pre-syncope. The athlete was an international rower, competing in the single sculls event, and was training an average of 10 sessions/week. Training sessions included rowing and weight training, with training across the full range of intensities. The presenting symptoms included two episodes of syncope after 2000 m maximal tests on a rowing ergometer, together with episodes of pre-syncope on water that had not resulted in syncope. All episodes of pre-syncope/ syncope occurred immediately after exercise in a seated position. The duration of syncope was not formally documented but was described as lasting one or two minutes, with periods of malaise lasting for considerable periods (more than one hour) after syncope. There had been no previous examination of heart rate and/or blood pressure response during these episodes. Separately the patient noted a tendency for pre-syncope and syncope during medical procedures. There was no family history of heart disease including sudden ‘‘unexplained’’ death. On examination, the athlete was in sinus rhythm with bradycardia (about 40 beats/min) and sinus arrhythmia. All other measures, including PR and QT interval, were within normal limits. Resting blood pressure was 110/70 mm Hg. Echocardiography showed normal intracardiac dimensions (maximum left ventricular wall thickness; 10 mm) with normal systolic function of both left and right ventricles. Origins of left and right coronary arteries were normal. Mild pulmonary valve regurgitation was noted (inaudible clinically). During integrated cardiopulmonary exercise stress testing, the athlete completed level 5 of a BRUCE protocol stopping because of maximal exercise capacity. It is recognised that the BRUCE protocol is not specific to rowing; however, it allows optimal interrogation of electrocardiogram and blood pressure during exercise. Further, the use of an ambulatory mode of exercise may better facilitate the specific symptoms reported in this case. In general, however, every effort should be made to replicate the mode of exercise associated with symptoms. The athlete achieved maximum oxygen consumption of 60.6 ml/kg/min (185% of age and sex predicted) and a maximum heart rate of 186 beats/min. Blood pressure and heart rate response during exercise was normal. There were no inducible electrocardiogram changes or arrhythmias. On cessation of exercise, however, there was an immediate fall in heart rate (186 to 100 beats/min). Blood pressure measured at maximum exercise and within one minute after exercise showed a precipitate fall (200/90 to 110/60 mm Hg respectively). The athlete reported symptoms of pre-syncope similar to those experienced during previous episodes. A tilt test was not used because of the non-specific nature of such a test in elite athletes. The athlete was diagnosed with mild exercise induced vasovagal syndrome. This condition may be considered benign; however, the rower in this case study was an international calibre single scull rower, thus the potential for a syncopal episode on water and subsequent immersion and drowning left us with a treatment dilemma.