Effort syncope in patients with aortic stenosis (AS) has long been recognized in the medical literature. Recent guidelines regarding exercise testing by the American Heart Association and American College of Cardiology list moderate to severe AS as a contraindication for exercise testing. The following report illustrates the potential danger of exercising adult patients with AS. In addition, we review the mechanisms responsible for effort syncope in aortic stenosis and the value and limits of exercise testing in patients with AS, discuss how to monitor patients with AS during exercise testing, and define clinical situations in which exercise testing may be of value in AS.
A 68-year-old retired, physically active high school teacher was evaluated in an emergency room with the complaint of syncope. He had no history of chest pain, symptoms of congestive heart failure, palpitations, or myocardial infarction. A heart murmur had been present since childhood. He quit smoking in 1956, his cholesterol level was 268, and his hypertension had been treated intermittently for five years; there was no diabetes mellitus or family history of heart disease. He was receiving no medication, but had previously been on therapy with hydrochlorothiazide. He had no allergies. His surgical history included only an uncomplicated transurethreal resection of the prostate in 1984.
Despite the history of syncope and a systolic murmur, the patient was exercise tested by his private internist Standing prior to exercise, the heart rate was 82 and blood pressure 142/90 mm Hg. At one minute (stage 1A of the Bruce protocol) the patients heart rate was 134 and blood pressure 140/88 mm Hg. At three minutes, (1.7 mph/10 percent grade) the patients heart rate was 138 and blood pressure was 132/84 mm Hg. At the end of four minutes of exercise, the ST segments were depressed and at six minutes the patient became diaphoretic, dyspneic, and there were frequent PACs. The treadmill test was discontinued, and as the patient was getting off, he lost consciousness. Continuous rhythm strips revealed marked sinus bradycardia as low as 20-30 bpm followed by frequent PVCs and asystole for 12 s with ventricular escape beats. There was 3 mm of downsloping ST depression which flattened at maximal exercise, after chest compressions, adequate ventilation, and epinephrine, there was restoration to a slow junctional rhythm accelerating to sinus tachycardia. Blood pressure was restored and the patient regained consciousness. He was subsequently referred to cardiology where the following physical examination was performed.