Spontaneous Coronary Artery Dissection Accompanied with Antiphospholipid Syndrome and Leukemia

Abstract

SummaryWe report a rare spontaneous coronary artery dissection (SCAD) case accompanied by antiphospholipid syndrome (APS) and leukemia which was treated successfully with drug-eluted stents (DES) implantation. This young SCAD patient was initially diagnosed of acute myocardial infarction (AMI); however, except for 6 packyears of smoking, there were no risk factors or family history of coronary artery disease. Subsequently, we screened other clinical status like autoimmune diseases and finally found APS. In general, APS was associated with thromboembolism events, not coronary artery dissection. Our case indicated that SCAD could be a rare manifestation of APS which should draw our attention. In addition, our bail-out therapy acquired the expected effect.(Int Heart J Advance Publication) Key words: Percutaneous coronary intervention, Intravascular ultrasound, Antithrombins S CAD is defined as spontaneous coronary artery layers separation producing true and false lumen without human intervention, triggered primarily by intimal-luminal interface disruption or vasa vasorum rupture.1) It remains an infrequent clinical entity, predominantly affecting young women. Interestingly, our SCAD case was a very young man with APS and a 19 year history of diagnosed leukemia. To our knowledge, this is the first time a SCAD case accompanied by APS and leukemia has been reported. Case ReportA 29-year old man who had no risk factors for coronary artery disease, except for 6 pack-years of smoking and a past medical history of diagnosed leukemia 19 years ago, presented to our cardiology department with severe chest pain for 13 days. The severe chest pain occurred 13 days ago while he was at rest, radiating to the left upper limb with profuse sweating. The symptom did not relieve until he received morphine and nitrates in the local hospital. The troponin I test was positive and ECG showed ST segment elevation in the anterior and lateral leads ( Figure 1), which led to a diagnosis of AMI. Accordingly, primary percutaneous coronary intervention was suggested, but it was refused by the patient. Standard drug therapy with low molecular heparin, double antiplatelet, statin, and other secondary prevention medicines was applied at the local hospital. Then, based on his wish, the patient was transferred 13 days later with a stable condition to our hospital (regional heart center). Cardiac catheterization was performed, which showed type-D dissection from ostium to the mid segment of the left anterior descending artery (LAD) with contrast retention and TIMI flow grade 2; the other coronary arteries were smooth without any stenosis. The cholesterol level was within normal range. The LDL-c level was 57.28 mg/dL. Echocardiogram showed severe hypokinesis of the anterior wall and the apical segment of left ventricle. The left ventricular ejection fraction value was 48%. Considering the low risk factors or family history of heart diseases, we screened further for other clinical status like autoimmune diseases. The ENA test was negative, while the an...

Arterial Dissection in Antiphospholipid Syndrome Patients: Two Case Reports and a Literature Review

“…The following positive antiphospholipid antibodies were detected: aCL in 14 patients (73.68%), LAC in 9 patients (47.3%), A-B2GLP in 6 patients (31.5%) and aPE in 1 patient (5.2%). The different vessels involved included the internal carotid artery, aorta and coronary arteries in four patients each (21.05%), the vertebral artery and cerebral arteries in three patients (15.7%), and the superficial femoral artery in one patient (5.2%) [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] .…”

Acute Myocardial Infarction Caused by Coronary Spasm and Dissection Treated with Medical Therapy

“…), hormone therapy, coronary spasm, and idiopathic factors. [11][12][13][14][15][16] Triggering stresses include excessive exercise, intense mental stress, labor, Valsalva-type activity, drugs, and hormonal intensification. 12,[17][18][19] In the present case, tests for rheumatoid factor, antinuclear antibody, C-ANCA, and MPO-ANCA were all negative, as was the involvement of collagen disease.…”

“…Examination findings on admission were as follows: 16.37 ng/ mL; prothrombin time, > 100%; prothrombin timeinternational normalized ratio, 1.00; activated partial thromboplastin time, 35.7 seconds; brain natriuretic peptide, 37.2 pg/mL; thyroid-stimulating hormone, 0.79 μ IU/ mL; free triiodothyronine, 2.47 pg/mL; and free thyroxine, 0.97 ng/dL. All of the examined autoantibodies (rheumatoid factor, < 3 IU/mL; antinuclear antibody, < 40×; cytoplasmic antineutrophil cytoplasmic antibodies (C-ANCA), 0.6 IU/mL; and myeloperoxidase-anti-neutrophil cytoplasmic antibody (MPO-ANCA), 0.5 IU/mL) were negative.…”