A 28-year-old, moderately obese man with dyslipidemia (low-density lipoprotein 163 mg/dL, high-density lipoprotein 33 mg/dL), hypertension, active tobacco use (1 pack per day), and a family history for premature coronary artery disease (CAD) initially presented with burning, nonexertional chest discomfort exacerbated by deep inspiration. His initial electrocardiogram (ECG; Fig. 1A) was interpreted as pericarditis because of the diffuse mild ST-segment elevation and PR-segment depression. An echocardiogram demonstrated normal left ventricular systolic function and a trivial pericardial effusion. He was treated with nonsteroidal antiinflammatories and his symptoms resolved. Follow-up ECG performed the next morning (Fig. 1B) demonstrated sinus rhythm, persistent mild ST elevation, and biphasic T waves in leads V3-V4 as well as in leads III and aVF. Four months later, the patient returned with similar symptoms of chest discomfort and was admitted with the diagnosis of unstable angina. The admission ECG was unremarkable showing no persistent PR or ST-T abnormalities. He was ruled out for myocardial infarction by serial enzymes. An exercise myocardial perfusion imaging study was obtained. The patient exercised for 7 minutes 33 seconds on a standard Bruce protocol, obtained 9.4 METs, and reached 69% of maximum predicted heart rate. His exercise ECG revealed up to 2.5 mm of ST-segment elevation in leads V3-V5 accompanied by chest discomfort. The patient's chest pain resolved with cessation of exercise and 1 sublingual nitroglycerin. The ECG returned to baseline within 3 minutes of recovery. He was referred for coronary angiography and was found to have a proximal left anterior descending (LAD) stenosis and underwent percutaneous coronary intervention with stenting. He was discharged home on postprocedure day 3.
Numerous procedures have been proposed for the correction of symptomatic subclavian artery occlusive disease, none of which have been uniformly accepted by vascular surgeons. During the past 21 months we have successfully treated six patients with symptomatic subclavian artery occlusive disease by the construction of an axillary-axillary artery bypass. There were three complications in this small series, a wound hematoma, a case of median nerve parasthesias, and a late graft thrombosis, possibly caused by external pressure on the graft. These complications have not caused any serious morbidity. All patients have been followed to the present time, all have experienced symptomatic improvement and none has developed any symptoms of donor arm ischemia. Axillary-axillary artery bypass is currently our procedure of choice for the correction of symptomatic subclavian artery occlusive disease because of its effectiveness, absence of serious morbidity and ease of performance.
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