Mr. J.L., a 64-year-old man with an essentially unremarkable past medical history, was referred for a stress test because of symptoms of exertional chest tightness lasting more than a year and a recent one-minute syncope, when returning uphill to work after lunch. He denied feelings of palpitations or dizziness, and history or symptoms suggestive of a seizure disorder. He also denied associated symptoms of headache, nausea or vomiting, visual problems or focal weakness. He admitted to occasional heartburn. He’d been fairly active in the past.
He had no history of hypertension, diabetes or cardiac disease. His cholesterol level was normal. He’d quit cigarettes over 30 years ago, after smoking for 10-15 years. There was no family history of premature coronary heart disease. He drinks socially when entertaining and works at a grocery store.
After the syncope, he saw his family physician and had a normal physical exam with blood pressure (BP) of 140/90 mm Hg and regular rhythm. He was diagnosed with angina and started on metoprolol 25 mg twice a day, a coated aspirin a day and nitrospray as required. He had a 24-hr Holter monitor and a carotid duplex scan; both studies were unremarkable. There were no reported pathologic pauses or runs. He was referred for a stress test to further stratify his cardiovascular risk.
The history was confirmed before considering the stress test. Specifically, he had no history of headaches or seizure disorder. He felt occasional exertional chest tightness that resolved with rest. These symptoms had lasted for over a year and were stable in nature. They didn’t bother him at rest. He denied sensations of palpitations or dizziness before exercise and claimed he felt no symptoms of orthopnea, paroxysmal nocturnal dyspnea or ankle edema.
Physical examination revealed a man of stated age and average build, with a BP of 130/88 mm Hg and a regular but feeble pulse. Head and neck exam revealed a normal jugular venous pressure, moderate delay in carotid upstroke, and transmitted systolic murmur in the carotids. Heart sounds revealed single S2 with a grade 2/6 late peaking systolic murmur in aortic area with radiation to carotids and 1/6 systolic murmur at apex with radiation to axilla. Lungs were clear. There were no abdominal bruits, nor any pedal edema or focal weakness.
After examining Mr. J.L., the stress test was deemed to be high-risk and was cancelled, and another study requested. What’s your diagnosis?
Because of the clinically high likelihood of severe aortic stenosis that probably caused the recent syncopal episode, an urgent echocardiogram was performed. It showed severe calcification of aortic valve with severe to critical aortic stenosis.
Mr. J.L. was transferred to a regional cardiac care centre where a detailed echocardiogram showed peak gradient of 175 mm Hg and a calculated aortic valve area of just 0.6 cm sq. He underwent urgent aortic valve replacement and has been doing well since. Apparently this patient hadn’t been fully assessed before he was referred for a stress test. This case further highlights the importance of physical examination.
Asymptomatic aortic stenosis has an excellent prognosis but it worsens once symptoms of angina, syncope or congestive heart failure develop, unless surgical correction is performed. About half of these patients will be dead within 2, 3 and 5 years after onset of congestive heart failure, syncope and angina, respectively.
It’s essential to assure that a patient doesn’t have significant aortic stenosis before exercise testing. Important clues to the severity of disease include weak pulse, low pulse volume, delayed carotid upstroke and soft but late peaking systolic murmur, presence of S4 and evidence of LVH, especially in someone who’s already experienced syncope. Vasodilators should be avoided in such patients, as they reduce total peripheral resistance without delivering the expected increase in cardiac output because of fixed outflow obstruction. Similarly, stress testing is contraindicated in severe aortic stenosis.
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