Aortic disease can present as an acute chest pain syndrome. Although aortic dissection is the most common etiology, other processes such as intramural hematoma (IMH) and penetrating atherosclerotic ulcers are being increasingly recognized. They can all be accurately identi ed by computed tomography (CT) imaging or transesophageal echocardiography. The overlap between these processes regarding de nition and mechanism is controversial. Treatment for all three conditions has thus far been dictated by location, wherein ascending or arch involvement (Stanford type A) necessitates surgery and descending disease (type B) is treated medically. Small studies suggest that subgroups of type A IMH may be treated medically with good outcomes.Key words: acute aortic syndrome; aortic intramural hematoma; penetrating atherosclerotic ulcer
Case presentationA 75-year-old woman presented with acute aortic syndrome.Twenty-four hours after arriving on a ight from London, England to San Francisco, California, our patient experienced the sudden onset of severe pleuritic chest and upper abdominal pain which radiated to her left arm and back. The pain was not affected by exertion, but decreased upon leaning forward. After 36 hours of pain, she developed severe dyspnea and presented to the emergency room. Nitroglycerin relieved her pain. She received one injection of low molecular weight heparin.The patient reported a recent low-grade temperature and non-productive cough. Her cardiovascular risk factors included hypertension and post-menopausal status. There was no history of diabetes mellitus, hypercholesterolemia, smoking, angina, myocardial infarction, congestive heart failure, deep venous thrombosis, anemia, hepatitis or tuberculosis. She had irritable bowel syndrome, managed with omeprazole, anti-spasmodics, and pancreatic enzyme supplements. Other medications were aspirin and nifedipine.On physical examination, the patient was a thin, anxious, Indian woman in moderate distress. The blood pressure was 116/75 mmHg in both upper extremities. The pulse was 98 and regular. The oxygen saturation level was 94% on 2 l of oxygen.Jugular venous pulsation was seen at 6 cm. There were no carotid bruits. The cardiac exam had a normal S1 and S2 without rubs, gallops, or murmurs. The lungs were clear bilaterally. The abdomen was soft and non-tender, without organomegaly, masses, or bruits. The extremities were normal with palpable pulses and without edema, tenderness, or cyanosis. Admission laboratory evaluation was signi cant for a CPK of 90 mg/dl with an MB relative index of 3.1 (normal ,3). The cardiac troponin T was slightly elevated at 0.07 ng/ml (normal ,0.01), WBC 13 000, Hct 33%, sodium 125 mmol/l, BUN 12 mg/dl (4.3 mmol/l), Cr 0.9 mg/dl (80 mmol/l), glucose 233 mg/dl (12.9 mmol/l), AST 146 IU/l, ALT 100 IU/l, total bilirubin 1.5 mg/dl (26 mmol/l) and alkaline phosphatase 74 IU/l. The initial electrocardiogram showed sinus rhythm with mild diffuse ST elevation and PR depression (Figure 1) and the chest X-ray revealed a tortuous ...