A 58-year-old male gynecologist with well-treated hypertension and no symptoms wants to start exercising and asks his cardiologist to give him a stress test. He is a nonsmoker, has a normal BMI, and does not take aspirin. He has never had a coronary angiogram. The patient\u2019s cardiologist asks him to discontinue his acebutolol, which he takes for the hypertension, so that he can undergo an \u201cunmasked\u201d exercise stress test. The patient discontinues the medication on the morning of the test.<\/p>\n
The stress test results are normal, and the patient feels reassured. He recovers for a few minutes, showers, and is sent home with a green light to exercise. Before he even exits the hospital, however, he begins to experience chest heaviness, nausea, and sweating.<\/p>\n
He returns to the cardiology department, where he is found to have low blood pressure and a slow heart rate, initially thought to be a delayed vasovagal response to the stress test. However, an ECG shows an ST-segment-elevation MI in the inferior leads. Prompt catheterization reveals a huge thrombus in the right coronary artery.<\/p>\n
The patient undergoes immediate, successful primary PCI and stent placement, and he is admitted to the CCU. On day 3, he is discharged in good condition with prescriptions for aspirin, prasugrel, acebutolol, and atorvastatin.<\/p>\n
Questions:<\/b><\/p>\n Response:<\/strong><\/p>\n James Fang<\/a><\/p>\n November 3, 2014<\/p>\n 1. Could the exercise stress test have caused this patient\u2019s MI (by provoking a rupture in a plaque that is presumed to be stable but turns out not to be), or was the MI inevitable \u2014 and more likely to be fatal if it had happened outside the hospital?<\/em><\/p>\n MI is a known but rare complication of exercise stress testing (the risk is likely less than 1 in 1000, according to multiple large series). Possible mechanisms include increased shear stress at the point of modest plaques, increased thrombogenic milieu related to the increased adrenergic environment, and previously asymptomatic high-grade lesions leading to supply-and-demand mismatch. But it is at best speculative to suggest that the stress test \u201ccaused\u201d the MI. It is also difficult to say the MI was \u201cinevitable,\u201d but no doubt the patient was at risk given his CV risk factor(s). Having an MI in a medical environment can expedite diagnosis and therapy, although paradoxically hospitalized patients often have greater door-to-balloon times because the MI may not be recognized.<\/p>\n 2. Would it have made any difference if the patient had been on aspirin or hadn\u2019t stopped his beta-blocker?<\/em><\/p>\n Aspirin and beta-blockade may have had some effect, in the context of the pathophysiology of STEMI, but it appears that the patient had underlying CAD. Withholding the beta-blocker to improve the sensitivity of the test helps only to identify flow-limiting lesions and would not improve the accuracy of diagnosing less severe coronary atherosclerosis.<\/p>\n 3. Would the patient-requested stress test have been considered \u201cinappropriate\u201d in this case, even though it helped to prevent a potentially fatal event? (See the recent CardioExchange discussion on this topic<\/a>.)<\/em><\/p>\n I do not believe that this stress test was \u201cinappropriate\u201d because this scenario is a guideline-recognized indication \u2014 i.e., testing sedentary people before initiating a rigorous exercise program. Interestingly, concomitant imaging does not appear to have been ordered.<\/p>\n 4. Should people at high risk for ACS events take aspirin before exercising? What about healthy individuals and athletes (e.g., marathon runners) who are about to engage in intense activity?<\/em><\/p>\n I\u2019m not aware of any evidence that aspirin use before exercise in patients at high risk for ACS reduces that risk, but it is an interesting hypothesis. I suspect, however, that it would take a large study to show any benefit, given that event rates would probably be low.<\/p>\n \n Follow-Up:<\/b><\/p>\n\n