Spontaneous Dissection of Coronary Artery Treated by Primary Stenting as the First Presentation of Systemic Lupus Erythematosus

Non-atherosclerotic causes of myocardial infarction should be considered in patients with no coronary artery disease risk factors. These causes include arterial emboli, severe prolonged coronary artery spasm, traumatic or spontaneous dissection of the coronary vessels, congenital anomalies, muscle bridge conditions, intimal proliferation, external compression, radiation-induced coronary artery disease, in situ thrombosis, cocaine abuse and vasculitis.2–23 We report the case of a 39-year-old woman with acute anterior myocardial infarction who was treated with thrombolytics and referred for elective coronary angiography based on her age. Case Report. A 39-year-old housewife with no history of oral contraceptive use and no risk factors was admitted to the Intensive Care Unit with the diagnosis of anterior myocardial infarction and treated with streptokinase 1.5 million IU without any complications. Laboratory studies revealed the following abnormal findings: hemoglobin, 10.7 gm/dl; red blood cell count, 4.16 x 1012/L; white blood cell count, 3.7 x 109/L (78% neutrophils and 21% lymphocytes); platelets, 105,000/Ul; erythrocyte sedimentation rate (ESR), 42 mm/hour; C-reactive protein, 1+ positive; and repeat ESR after one week, 60 mm/hour. On discharge, the patient was scheduled for elective coronary angiography, which was indicated by the occurrence of myocardial infarction in a 39-year-old with no risk factors. Six weeks later, a coronary angiogram was performed. The blood picture was similar to the initial one. The ESR at this time was 35 mm/hour. The coronary angiography report indicated a long, complex lesion in the proximal left anterior descending (LAD) coronary artery with the most significant stenosis noted distal and proximal to the first diagonal branch. The patient was referred for angioplasty. At angioplasty three months later, the Interventionalist observed the shape of the suspected atherosclerotic lesion, noted no apparent stenosis, and revised the diagnosis to that of a long spiral dissection in the LAD (Figures 1 and 2). The lesion appearance was unchanged compared to the examination three months prior. Treatment for a spontaneous dissection of the LAD commenced with the implantation of a 3 x 30 mm Palmaz Schatz stent, with a good result. Differential diagnostic considerations arose regarding the possible idiopathic or secondary nature of the lesion. It was noted that a consistently elevated ESR and mild but persistent pancytopenia had been evident in blood studies at all three admissions. Urinalysis revealed 1+ proteinuria. Further questioning revealed a history of transient skeletal pains, photosensitivity and a malar rash 6 months prior. She did not seek medical advice at that time. She was referred to the Departments of Nephrology and Rheumatology, where she was diagnosed with collagen vascular disease. The diagnosis of systemic lupus erythematosus was made according to the following clinical and laboratory findings: renal ultrasound indicated increased parenchymal echodensity and increased corticomedullary differentiation; renal biopsy showed lupus nephritis; 24-hour urine showed 1,450 mg protein; LE cell + ve; antinuclear antibodies (ANA) Discussion. In cases of myocardial infarction in young women with no risk factors, non-atherosclerotic causes should be considered. These causes include arterial emboli, severe prolonged coronary artery spasm, traumatic or spontaneous dissection of the coronary vessels, congenital anomalies, muscle bridge conditions, intimal proliferation, external compression, radiation-induced coronary artery disease, in situ thrombosis, cocaine abuse and vasculitis.2–23 Urgent coronary angiography is indicated in cases such as the one discussed above. The causes of coronary artery dissection can be either idiopathic or secondary to vasculitis. Secondary causes of vasculitis include periarteritis nodosa, hypersensitivity and granulomatosis angiitis (Wegner and Churg Strauss), SLE, rheumatoid arthritis, ankylosing spondylitis, infections (e.g., tuberculosis, leprosy, syphilis, anthrax, typhoid), Takayasu’s arteritis, Kawasaki’s disease, giant cell arteritis, Burger’s disease and Marfan’s syndrome. Unfortunately, despite the persistently raised ESR and pancytopenia, collagen diseases such as SLE were not considered. The lesion was initially misdiagnosed as an atherosclerotic lesion. The diagnosis of spontaneous dissection was missed. The high prevalence of atherosclerosis seen in daily practice can inadvertently blind practitioners to non-atherosclerotic and systemic causes of myocardial infarction. It is known that 25% of SLE patients have cardiac involvement. SLE can produce Libman Saches verruca and thickened dysfunctional valves in 9% and 8% of cases, respectively. Pericardial involvement, left ventricular systolic and diastolic dysfunction, pulmonary artery hypertension, and neonatal lupus syndrome are well known presentations in SLE.3–15 Coronary artery involvement in SLE can be due to atherosclerosis or vasculitis.16 Corticosteroid usage in cases such as SLE and heart transplants is a well known cause of premature coronary artery disease.8–19 Some research indicates that if SLE continues for more than two to three years, death will most likely be due to myocardial infarction rather than to SLE itself. There has been speculation that coronary artery disease was not described before the advent of glucocorticoid therapy.20 The role of the antiphospholipid antibody and its effect on platelet aggregation and clotting tendencies has been shown.23 Myocardial infarction in an 8-year-old girl with SLE21 and myocardial infarction due to coronary artery aneurysm22 were previously reported. In the literature, we found five reported cases of primary stenting for spontaneous dissection and no cases of spontaneous coronary artery dissection in SLE.24,25 In this case report, we presented a patient with spontaneous coronary artery dissection leading to myocardial infarction as the first presentation of SLE. The patient was successfully treated with primary stenting.

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