Positive tilt tests vary between 26% and 76% in these patients. In a series of 24 athletes with recurrent exercise-induced syncope, 19/24 were initially positive on tilt testing; after therapy only 2/24 remained positive.11 However, some may have been patients with underlying vasodepressor syncope exacerbated by exercise and may not have truly had “exercise-induced” syncope. It is not possible to define the exact sensitivity and specificity of tilt tests for these patients because of small sample sizes. We feel that a tilt test should be ordered, as it may suggest a diagnosis in some cases.
Invasive tests are not usually needed
Invasive electrophysiology testing has little role in athletes with syncope. Most well-conditioned athletes have a relative bradycardia due to high vagal tone, but it is extremely rare that they require a permanent pacemaker.12 Although some of these patients may have abnormal sinus node function when assessed by electrophysiology testing, to adequately test sinus node function in these patients you should perform autonomic blockade using atropine and propranolol; then an intrinsic heart rate (without the effects of autonomic tone) can be measured.
In most cases, you need to see the rhythm during an episode for accurate diagnosis. This requires a 12-lead ECG, and possibly a Holter monitor or event recorder. Remember that abnormal findings during a tilt table or electrophysiology test may be unrelated to the cause of syncope.
Anomalous take-off of coronary arteries should be excluded. In the past this required cardiac catheterization, but can now be assessed noninvasively with magnetic resonance angiography or CT.
What testing revealed about our patient
Our patient’s ECG showed nonspecific ST-T wave abnormality with no evidence of Wolff-Parkinson-White abnormality or conduction system disease. An echocardiogram showed a left ventricular end diastolic dimension of 50 mm (normal range, 40-62 mm) and a left ventricular ejection fraction of 55% (normal is 55%-60%). We saw no valvular abnormality and no evidence of left ventricular hypertrophy to suggest hypertrophic cardiomyopathy.
A stress test was performed using the Bruce protocol, during which the patient exercised for 13 minutes and achieved a heart rate of 184 bpm. She did not have any symptoms of loss of consciousness, and we saw no abnormal ST-T segment changes.
A tilt test was performed with and without isoproterenol, during which time her heart rate reached 125 bpm. There was no syncope or loss of consciousness.
A cardiac CT test was performed, which excluded coronary anomalies. The exercise test was repeated using a modified protocol with a pace set to simulate her level of exercise. The treadmill was set at a speed of 9.6 mph (a 6.25-minute mile) with no incline. Sixteen minutes into the test she had a sudden loss of consciousness and fell. She was diaphoretic with a weak, thready, rapid pulse and cool extremities.
Shortly after her fall, we recorded her blood pressure using a cuff sphygmomanometer—it was 169/95 mm Hg with a heart rate of 140 bpm. However, the patient had recovered consciousness by the time the blood pressure was recorded. The duration of loss of consciousness was less than 15 seconds. No hypotension or arrhythmias were recorded.
The exercise test with new protocol was repeated, but with placement of an intra-arterial blood pressure monitor and continuous electroencephalographic monitoring. Sixteen minutes into the test the patient requested that we stop, due to fatigue and leg pain. Just prior to this, at peak exercise, her blood pressure was 220/30 mm Hg and heart rate was 185 bpm. Immediately after stopping the tread-mill, we measured a precipitous drop in intra-arterial blood pressure—down 45/4 mm Hg—and her heart rate slowed to 178 bpm. This was associated with reproduction of clinical symptoms. She lay down, and her blood pressure recovered to >120 mm systolic within seconds.
Electroencephalographic monitoring did not show any epileptiform activity. Serum blood glucose recorded during the spell was 86 mg/dL. Our interpretation was that she had a brief precipitous vasodepressor syncope triggered by exercise.
Management: Changing habits, medication
You can advise patients with exercise-induced syncope to avoid strenuous exercise, but this is not acceptable for many athletes. If the patient is on certain drugs, such as vasodilators for the treatment of hypertension, these must be discontinued and another category of drug substituted, such as angiotensin-converting enzyme inhibitors.
The athlete should also increase his or her fluid and salt intake. This can be achieved with increased use of sports drinks or salt tablets (strength of recommendation [SOR]: B). Of course this must be done in moderation and titrated to each individual athlete’s needs.