Management of a Spontaneous Supra-aortic Arterial Dissection

A Case Report

Omar M. Sharaf; Tomas D. Martin; Eric I. Jeng


J Med Case Reports. 2021;15(283) 

In This Article

Case Presentation

A 50-year-old morbidly obese (body mass index 44.16 kg/m2) Caucasian gentleman with uncontrolled hypertension presented to a nearby emergency department with shortness of breath and sudden-onset, intermittent, substernal chest pain radiating to both sides of his jaw and to his right arm. He had an intact neurological examination and was without focal or motor deficits. Past medical history is negative for prior cardiovascular interventions, and his family medical history was negative for cardiovascular and/or aneurysmal disease. He denies cocaine and/or illicit drug use, and was a 20-pack-year smoker who quit 7 years prior. On examination, the patient was malignantly hypertensive at 261/142 mmHg and with sinus tachycardia at a heart rate of 121 beats per minute. His work-up consisted of an electrocardiogram which showed sinus tachycardia with no ST changes, a troponin level of 0.019 ng/mL within normal limits, and computed tomographic angiography (CTA) revealing an innominate artery dissection with extension distally through the right subclavian artery into the opening of the axillary artery (Figure 1). He was transferred to the University of Florida Health—Aortic Disease Center where the patient was treated with continuous intravenous infusions of clevidipine and esmolol for anti-impulse therapy (titrated to goal systolic blood pressure of less than 120 mmHg, heart rate less than 80 beats per minute) to prevent worsening dissection, and aspirin[3] to minimize risk of thromboembolic sequelae. At 24 hours from presentation a repeat CTA of the chest and neck was performed, confirming an unchanged dissection of the innominate artery without propagation into the ascending aorta or aortic arch. Transthoracic echocardiography showed normal right and left ventricular systolic and diastolic function with no hemodynamically significant valvular dysfunction. The patient was subsequently discharged 72 hours after admission without pain or symptoms, on an oral medication regimen of amlodipine (5 mg daily), labetalol (600 mg three times a day), and aspirin (81 mg daily). He presented to his 3-month, 6-month, and 1-year follow-up clinic appointments with adequate blood pressure control equal bilaterally at 122/80 mmHg, no evidence of upper extremity muscle atrophy, and no neurologic deficits. Interval CTA showed aneurysmal enlargement of the innominate artery from 2.65 to 3.41 cm (Figure 2). The decision was made to continue interval medical management with amlodipine, labetalol, and aspirin, with close follow-up and a plan for surgical intervention if aneurysmal growth persists and/or debilitating symptoms present.

Figure 1.

Computed tomographic angiography chest results at initial admission. Innominate artery demonstrates distinct widening on coronal oblique view (a) after takeoff from the aortic arch. This (red arrow, a) represents the origin of dissection, which separates the true lumen (below red arrow, a) from the false lumen (above red arrow, a). Extension distally into the subclavian artery is observed (pink arrow, a). Axial imaging (b) shows true and false lumens in both the subclavian artery (red arrow, b) and the axillary artery (pink arrow, b), evidencing distal extension of dissection. Aortic involvement is absent—no true and false lumens are identified.

Figure 2.

Sagittal computed tomographic angiography of the chest and neck at initial presentation (a) and at 3-month follow-up (b). Imaging reveals slightly increased diameter of the innominate artery after takeoff from the aortic arch compared to diameter at initial presentation. True and false lumens are separated by intimal flap (red arrows, a and b).