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[Case Report]

Ascending Thoracic Aortic Aneurysm in an Elite Runner

Susan Mehnert-Kay, MD; Louis E. Mulkey, DO


In Brief: A 41-year-old ultramarathon runner presented to his physician after having exercise-related chest pain that radiated down his left arm and seemed typical for myocardial ischemia. The patient had only a single risk factor. Extensive testing revealed a large thoracic aortic aneurysm. This case illustrates how the standard workup could miss this and other potentially lethal conditions in an extremely well-conditioned athlete.

Even the most conditioned athlete can have cardiac disease. When evaluating athletes, physicians must be cognizant of the limitations of the testing tools and select evaluation techniques that will give the most accurate information. Stress testing may not reveal life-threatening conditions for athletes in peak physical condition. The key factor is to take symptoms seriously from the beginning and not be falsely reassured by a patient's excellent overall physical condition.


A 41-year-old ultramarathon runner in prime condition had an isolated episode of left-sided chest pain and pain that radiated down his left arm during an easy 8-mile run. The pain resolved with walking. He began running again, and the pain returned. Again he walked, and this time he belched two or three times, and the pain resolved. He completed his run without any additional pain. He reported no shortness of breath, diaphoresis, or nausea. The patient presented to his family practice physician 2 days later.

He had not run since the episode of chest pain. He reported that he had run hard for 28 miles on hilly trails approximately 1 week before without pain. His workouts in the weeks before his presentation averaged 80 miles/wk. He had set course records on two 50-km runs during two consecutive weekends just 2 months prior to his episode of chest pain. He had maintained an active lifestyle since high school.

His medical history was significant for hypertension treated for the previous 8 years. At the time of presentation, his only medication was 50 mg/day of losartan potassium. Random blood pressure checks found systolics of 130 to 140 and diastolics of 80 to 100. The patient is a physician who does not smoke or use illicit drugs and occasionally drinks alcohol.

The patient's father had a small abdominal aortic aneurysm at age 69 that was found incidentally by abdominal ultrasound. Other family history was negative for hypertension, thoracic aortic aneurysm (TAA), Marfan syndrome, and other connective tissue diseases.

Physical Exam

Physical exam revealed a thin, well-conditioned athlete. His blood pressure was 140/108 mm Hg, and his pulse was regular in the 60s. Cardiac exam revealed normal sinus rhythm without murmur, rub, or gallop. His lungs were clear to auscultation in all fields. The patient's abdomen was soft, flat, and without bruits, and his extremities were without edema. Resting electrocardiogram (ECG) revealed normal sinus rhythm with slightly elevated ST segments in leads II, III, aVL, V2, and V3, consistent with early repolarization (figure 1).

Imaging Decisions

The differential diagnosis included a possible aberrant coronary artery, coronary artery disease, or esophageal disorder. On consultation with the patient and a cardiologist, it was clear that a treadmill stress test would not be revealing. Furthermore, a thallium treadmill test, if negative, would also not be reassuring because the patient's conditioning may have given his heart superior compensation that would mask any ischemic changes. Based on this belief, the cardiologist proceeded with cardiac catheterization to fully evaluate the patient's chest pain.


Cardiac catheterization revealed that the left main coronary artery was normal; the circumflex branch of the left coronary artery was moderate-sized, nondominant, and normal; the left anterior descending artery was normal; and the right coronary artery was large, dominant, and normal. The calculated ejection fraction was 73%. An angiogram revealed a significantly dilated ascending aorta starting at the aortic valve annulus consistent with a TAA. The aneurysm extended to the arch just before the takeoff of the great vessels and measured between 5 and 6 cm. The aortic valve appeared mildly distorted.

Follow-up magnetic resonance arteriography (MRA) and reconstruction of the thoracic aorta revealed a dilated aortic root measuring 47 mm and an aneurysm of the ascending aorta that had a maximum diameter of 43 mm (figure 2). The patient also had a trileaflet aortic valve with mild aortic insufficiency. MRA was believed to provide a more accurate measurement for the TAA than the angiogram.


At this point, the patient had two options. He was advised that his condition could be followed with 6-month interval measurements and maximal blood pressure control, or he could undergo immediate elective repair. Because he wished to maintain an active lifestyle, the patient decided to undergo elective repair. He also believed that his young age and exceptional physical conditioning would improve his survival chances and speed his recovery.

He underwent repair with a synthetic graft that was placed along with a 27-mm St Jude valve conduit (St Jude Medical, St Paul). The ascending aorta was also found to be massively dilated. The sinuses of Valsalva were also grossly enlarged, and the aortic valve was insufficient. Unfortunately, the pathologic specimen was never received by the laboratory, so exact measurements are not available.

His recovery was uneventful. He returned to work 6 weeks postoperatively and resumed running 4 months after surgery. Nine months later, he continues to run only slightly slower than previously. His only hindrance is the effect of a beta-blocker, which he will continue indefinitely to protect his graft from increased shear forces and his left ventricle from hypertrophy. He is also taking a calcium-channel blocker for blood pressure control.


Aortic aneurysms remain the 13th most common cause of death in the United States, with an estimated incidence of 5.9 cases per 100,000 person-years (1). Mean age at diagnosis ranges from 59 to 69. TAA affects predominately men (2:1 to 4:1) (1). A phenomenon known as familial nonsyndromic TAA exists in 19% of patients who have TAA. These patients are younger at the time of diagnosis (mean age, 56.8 years) than patients with sporadic TAA (mean age, 64.3 years) (2). Preexisting hypertension has been found in 73% of familial nonsyndromic cases and 75% of sporadic cases (2).

Our case is unique in three primary respects. First is the age of the patient—far below the average age of 56 to 64 years. Second is the presenting symptom of chest pressure with radiation down the left arm relieved by relative rest. Obviously this is more typical for myocardial ischemia, and after his workup and surgery, no explanation for his pain was ever found. There was no evidence of dissection in this case.

Third, the choice of evaluation methods in this patient was critical to his ultimate survival. Given his age, medical history, family history, and overall level of conditioning, it would have been easy to stop the evaluation after a relatively normal ECG and normal physical exam. Treadmill testing, either standard or thallium, would have given false reassurance. The decision to proceed with the cardiac catheterization for a definitive diagnosis most likely saved his life.

The obvious danger of TAA is dissection or rupture. The assessment for risk of rupture is related to the site, cause, size, and expansion rate of the aneurysm (3). According to Coady et al (3), the median size of ascending or arch aneurysms at rupture or dissection is 5.9 cm. The literature supports elective prophylactic surgical repair of TAA because elective surgery has a mortality rate of 9% compared with 21.7% for emergency surgery (4,5). The recommended size of TAA to be considered for elective resection is 5.5 cm (5,6).

Closing Remarks

The superior physical condition of athletes may mask serious problems. Pain that occurs during exercise but then subsides may not be taken seriously. Lack of risk factors and negative results on standard tests should not lead to a false sense of security. Additional testing may uncover life-threatening conditions.


  1. Coady MA, Rizzo JA, Goldstein LJ, et al: Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections. Cardiol Clin 1999;17(4):615-635
  2. Coady MA, Davies RR, Roberts M, et al: Familial patterns of thoracic aortic aneurysms. Arch Surg 1999;134(4):361-367
  3. Pitt MP, Bonser RS: The natural history of thoracic aortic aneurysm disease: an overview. J Card Surg 1997;12(2 suppl):270-278
  4. Coady MA, Rizzo JA, Hammond GL, et al: Surgical intervention criteria for thoracic aortic aneurysms: a study of growth rates and complications. Ann Thorac Surg 1999;67(6):1922-1926
  5. Coady MA, Rizzo JA, Hammond GL, et al: What is the appropriate size criterion for resection of thoracic aortic aneurysms? J Thorac Cardiovasc Surg 1997;113(3):476-491
  6. Coady MA, Rizzo JA, Elefteriades JA: Developing surgical intervention criteria for thoracic aortic aneurysms. Cardiol Clin 1999;17(4):827-839

Dr Mehnert-Kay is a clinical assistant professor and Dr Mulkey is an assistant professor in the Department of Family Medicine at the University of Oklahoma College of Medicine in Tulsa. Address correspondence to Susan Mehnert-Kay, MD, University of Oklahoma College of Medicine, Dept of Family Medicine, 9920 E 21st St, Tulsa, OK 74129; e-mail to [email protected].


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