Letters to the Editor

To the Editor: Recently, I have treated a number of patients with functioning dialysis fistulae or synthetic arteriovenous grafts referred for arm swelling developing after pacemaker insertion (Figure A). Invariably, a stenosis or occlusion develops at the subclavian vein puncture site. In some instances, restoration of antegrade flow through the obstruction using angioplasty and stenting is possible; however, in other cases, endovascular recanalization is impossible and the fistula or graft must be ligated. The recently established Dialysis Outcomes Quality Initiative1 has recommended that subclavian access should only be used when jugular options are not available in patients on hemodialysis. It is well known that trauma due to venipuncture and indwelling catheters incite venous stenosis and occlusion.2,3 In a dialysis patient, a subclavian stenosis can effectively render the ipsilateral extremity unfit for fistula or graft creation or worse require sacrifice of an existing mature access site. Since veins are a precious resource in patients requiring dialysis, any intervention that jeopardizes venous access sites is a disservice to this patient population and should be avoided. An internal jugular vein access is preferred and should be performed. Yours sincerely, Brian Funaki, MD University of Chicago Hospitals Chicago, Illinois Clinical Characteristics, Evaluation, Treatment and Prognosis of Spontaneous Coronary Dissection To the Editor: It is with interest that we read the recent papers from the November issue of the Journal of Invasive Cardiology dealing with spontaneous coronary artery dissection (SCAD).1–4 Presentation of acute myocardial infarction (AMI) in populations considered at low risk for coronary disease requires an extensive evaluation. SCAD is an infrequently considered but potentially lethal entity that predominantly affects women. The importance of hormonal changes is usually underscored. To further delineate characteristics associated with this entity, we realized a study of all patients admitted with AMI and SCAD. We found 7 cases over a 5-year period. Six (85%) were female, mean age was 39.4 years, six (85%) did not have traditional coronary risk factors, three (43%) were in the peripartum period, and 3 (43%) were using oral contraceptives (OC). All 7 (100%) presented typical angina. The mean time to treatment was 3.7 hours, ECG showed ST segment elevation in 6 (85%), clinical stage on admission was Killip I in 100%, mean CK peak elevation was 577 ± 127 IU/L, coronary angiography showed compromise of left anterior descendant in 4 (57%) (Figure 1), an intracoronary stent was implanted in the index hospitalization in 5 (71%), and the 6-month reintervention free rate was 85%. SCAD is an infrequently considered cause of AMI. Our series confirmed the predominance of the female gender, the relative young age, the low incidence of coronary risk factors, and the predilection for left anterior descendant artery. Changes in the hormonal milieu associated with peripartum period and the use of OC may cause a weakening of the vessel media in susceptible patients. SCAD is associated with a high early morbimortality.5,6 Both, fibrinolytic and surgical therapeutic alternatives may either cause further clinical deterioration or be hazardous.7–9 When anatomical and technical factors allow it, PTCA with stent implantation offers an excellent prognosis. We must consider a wider spectrum of clinical diagnosis when evaluating AMI in young patients (Table 1). It is possible that numerous patients in which coronary involvement was not considered might have suffered significant ischemia with loss of the therapeutic window for lack of clinical suspicion (e.g., presumed cases of peripartum cardiomyopathy, puerperal thromboembolism, viral cardiomyopathy or sudden cardiac death). A high index of suspicion for SCAD must be exercised when evaluating young women during the peripartum period or OC users. Table 1. Acute myocardial infarct in the young 1. Accelerated atherosclerosis acelerada: e.g., familial hypercholesterolemia, homocystinuria 2. Coronary spasm: e.g., cocaine, triptanes, 5-fluoruracil 3. Embolism/thrombosis: e.g., embolism from thrombus in the left ventricle, myxoma or endocarditis, paradoxical embolism, vasculitis 4. Anatomical abnormality: e.g., aberrant coronary origin, external compression, aneurysm: congenital, post Kawasaki or traumatic 5. Coronary artery dissection: e.g., spontaneous coronary artery dissection (primary), secondary coronary dissection

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