A careful measurement of the corrected QT interval (QTc) is essential. The normal value of the QTc interval is <0.43 seconds. Prolonged QT interval may be due to presence of genetic or acquired (ie, drug-related) long QT syndrome. Acquired long QT syndrome can occur when a patient is taking an anti-arrhythmics such as amiodarone, or, more rarely, an antipsychotic such as haloperidol and ziprasidone.
Echocardiogram. All patients should have an echocardiogram before exercise stress testing to look for abnormalities such as aortic stenosis, left ventricular hypertrophy, and hypertrophic cardiomyopathy. When assessing for left ventricular enlargement, keep in mind that the left ventricular mass may be larger than what is seen in nonathletes. This condition, known as “athlete’s heart,” is mainly due to an increase in the cardiac cavity size and some increases in the left ventricular thickness. These patients show a preserved left ventricular ejection fraction.2
Pulmonary hypertension can also be evaluated using echocardiography; however, this is a rare cause of exercise-induced syncope.
Stress testing. Stress testing can reveal several different abnormalities found among patients with exercise-induced syncope. It may reveal ischemic changes on the electrocardiogram that suggest atherosclerotic coronary artery disease or anomalous take-off of the coronary arteries. Stress testing may also provoke neurocardiogenic syncope.
EEG and CT. Electroencephalography can show changes that suggest epilepsy as a cause of syncope. Exercise-induced temporal lobe seizures are extremely rare, but are another possible cause of loss of consciousness.
Computerized tomography of the chest combined with coronary CT angiography can be very useful in evaluating patients for structural abnormalities such as aortic dissection, pulmonary embolism, and especially coronary anomalies.
The search for other mechanisms
After patients have undergone the standard round of testing as described above, any further investigation will need to be customized to the patient. If structural cardiac abnormalities and arrhythmias are excluded (as was the case with our patient), the potential diagnoses are narrowed to neurocardiogenic syncope and orthostatic hypotension—2 common causes of sudden-onset syncope with sudden recovery.
Neurocardiogenic syncope. A common final mechanism of any syncope is a drop in blood pressure and low cerebral perfusion. This may be triggered by stimulation of the carotid baroreceptor reflex via cardiac hypercontractility, inadequate cardiac filling, or volume depletion. Volume depletion is more likely in endurance athletes who are exposed to prolonged exertion, such as marathon runners. Some patients with vasovagal mechanism may experience an aura of nausea prior to the loss of consciousness.
Another important mechanism of exercise-induced syncope is sudden vasodilatation or lack of vasoconstriction.3 Syncope can occur at peak exercise or immediately after stopping exercise. Syncope occurring after stopping exercise may be due to overwhelming vagal input during sympathetic withdrawal.
Several of these physiologic changes are accentuated during exercise and contribute to syncope. A strong cardiac contraction associated with exercise can trigger an abnormal baroreceptor reflex by stimulating cardiac mechanoreceptors.
Orthostatic intolerance. Syncope in distance athletes is sometimes due to orthostatic intolerance. Orthostatic hypotension may occur due to volume depletion and the increased contractility of the athlete’s heart—this may subsequently induce a neurocardiogenic mechanism of syncope. This is evaluated by measuring upright blood pressure after prolonged exertion.
Echocardiograms performed in athletes during upright tilt testing have proven that strong cardiac contractions occur during orthostatic stress.4 It has also been shown that syncopal athletes have a stronger cardiac contraction than nonsyncopal athletes.5 Athletes have increased cardiac distensibility—ie, increased variations of internal cardiac diameter over a range of equivalent filling pressures. This causes the cardiac contraction to be on the steep part of the Starling pressure; volume curve, so that a sudden drop in filling pressure results in a sudden fall in cardiac output and low blood pressure.6 Other researchers have found evidence against this, however.7
Loss of blood pressure can be caused by either sudden sympathetic withdrawal or parasympathetic overload. In some patients, syncope cannot be blocked by the use of atropine.8 A short diastolic filling time resulting from a rapid rate during exercise may decrease the ventricular filling in athletes and also result in low cardiac output due to the mechanism described above.
Orthostatic intolerance has been reported in ultra-marathon runners due to volume depletion;9 however, in light of the relatively short time to onset in our patient, and the lack of orthostasis after recovery, we did not suspect that this mechanism was at work.
Tilt table testing can be helpful
Reports on exercise-induced syncope in athletes show that a significant percentage of patients have a positive tilt table test, suggesting either an associated or independent abnormality of autonomic regulation.10