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Spontaneous Coronary Artery Dissection Causing Acute Myocardial Infarction in a Post-Menopausal Woman (Full title below)
Spontaneous Coronary Artery Dissection Causing Acute Myocardial Infarction in a Post-Menopausal Woman with Rheumatological Disorder (Polymyositis): Treatment Dilemma
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From the *Department of Internal Medicine, Division of Rheumatology, and the §Department of Internal Medicine, Division of Cardiology, UTMB-Galveston, Galveston, Texas. The authors report no conflicts of interest regarding the content herein. Manuscript submitted December 30, 2008, provisional acceptance given February 24, 2009, and final version accepted March 9, 2009. Address for correspondence: Praveen Jajoria, MBBS, MPH, Department of Internal Medicine, UTMB-Galveston, 301 University Blvd., Galveston, TX 77555. E-mail: drpraveenjajoria@gmail.com
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J INVASIVE CARDIOL 2009;21:E132-E133 Spontaneous coronary artery dissection (SCAD) is a rare cause of acute myocardial infarction (AMI). It is most commonly seen in women with a mean age of 39 years with no known risk factors for coronary atherosclerosis. In the absence of coronary angiography, the condition remains undiagnosed and may lead to a lethal course. The spectrum of presentation is wide and varies from stable angina, unstable angina, acute myocardial infarction, cardiogenic shock and sudden cardiac death. The etiology of SCAD is still unclear. Similarly, there is no consensus regarding the treatment of this condition. We report a case of SCAD in an adult female who redeveloped symptoms 2 weeks after the initial diagnosis and the medical management of the disease in this patient. Later, the patient’s condition was successfully managed with percutaneous coronary intervention (PCI) and stent placement. Case Report. A 53-year-old Caucasian female presented to our hospital’s emergency room with mild diffuse chest discomfort of 9 hours’ duration associated with radiation to the left arm. The patient tried aspirin and nitroglycerin from her husband’s medication supply at home, with no pain relief. An electrocardiogram (ECG) revealed 1 mm ST-elevation in leads V3 and V4, along with ST depression in leads V5–V6, I, II and aVF. The patient had experienced a similar episode of chest discomfort 2 weeks prior to this admission when she was admitted to an outside hospital and underwent cardiac catheterization, which showed a plaque rupture with 90% stenosis, thrombolysis in myocardial infarction (TIMI) I flow and dissection in the left anterior descending artery (LAD). The patient was managed medically and discharged chest pain-free. This time, the patient had similar chest pain and later presented to our hospital. She had no history of coronary artery disease (CAD), hyperlipidemia, hypertension or any family history of sudden cardiac death. She was a non-smoker with no recent history of chest trauma. The patient was not on oral contraceptive pills or hormone replacement therapy, but was taking prednisolone for more than past 20 years for her rheumatological disorder (polymyositis). Physical examination of the patient was unremarkable, with no Marfanoid-like features. At the time of presentation, her blood pressure was 85/44 mmHg and her heart rate was 82 beats/minute, which responded well to intravenous fluids. Laboratory investigation showed no cardiac enzyme elevation at that time. She was considered for cardiac catheterization secondary to significant history and ECG findings. Coronary angiography showed a LAD dissection from the mid-to-distal part with 95% stenosis. The mid-LAD lesion was eccentric and flow through the vessel was reduced (thrombolysis in myocardial infarction [TIMI] 2). The rest of the coronary vessels were normal. Percutaneous coronary intervention (PCI) was performed with a 2.5 x 9 mm balloon over a Luge™ hydrophilic wire (Boston Scientific Corp., Natick, Massachusetts), which was carefully placed in the true lumen of the vessel identified by the wire entering into the side branches. After ballooning, 1 Taxus® Express™ II stent (Boston Scientific) was placed. The artery was too tortuous and the first stent straightened the vessel, creating a hinge point at the proximal edge, necessitating a second stent. Eventually, the patient received 2 Taxus Express II stents (2.5 x 12 mm and 2.5 x 16 mm) in the LAD. Post intervention, there was 0% residual stenosis. Since the mid and distal LAD was very tortuous and small-caliber, intravascular ultrasound (IVUS) was not performed. The patient was observed in-hospital for 3 days. Her hospital course was uneventful except for one episode of chest pain. She was discharged in stable condition and free of chest pain. At 2-week follow up, the patient had no complaints and continued on medical treatment. Discussion. SCAD is a rare cause of angina pectoris and acute myocardial infarction,1–3 and was described by Pretty for the first time in 1931.4 Spontaneous dissection occurs commonly in the outer third of the media, with subsequent occlusion of the lumen due to inward expansion of the inner media.1 SCAD usually occurs in females during the peripartum period.2,5 It is also being reported in patients with atherosclerosis, the Ehler-Danlos syndrome, hypereosinophilic syndrome, sarcoidosis, mitral stenosis, Kawasaki’s disease, systemic lupus erythematosis (SLE), fibromuscular dysplasia, inflammatory bowel disease, during vigorous exercise and with oral contraceptive estrogen/progesterone therapy.1 In some patients, SCAAD can be completely asymptomatic, while in others, it can present as an acute coronary syndrome. SCAD is predominantly a single-vessel disease, with the LAD being being the most commonly involved vessel.6 Zampieri et al defined dissection as the detection at coronary angiography of a radiolucent area within the lumen of the vessel, with or without contrast persistence within the dissection after wash-out of contrast from the remaining portion of the vessel. The lumen of the vessel would be enlarged at the site of dissection, a pattern which is caused by the presence of dye inside the coronary wall and which is important in the differential diagnosis with intracoronary thrombus.7 The etiology of SCAD is still unclear after 75 years of the first reported case. SCAD seems to be caused by multiple factors. In peripartum females, it is attributed to progesterone, which is known to cause weakening of the vessels.8 Another suggested cause of SCAD is the eosinophilic infiltration of adventitia as inflammatory infiltrates with eosinophilic granulocytes, predominantly in the adventitia, which was found in 8 women at necropsy.2,6 Since SCAD can also affect men and post-menopausal women, and eosinophilic infiltration is not seen in every case,1,9 it is difficult to explain the etiology on the basis of the above-mentioned mechanism only. Our case was different than other cases reported thus far, since our patient was a post-menopausal woman with no risk factors for CAD, as has been seen in previous cases. She had none of the other risk factors that have been seen in association with SCAD in the literature. Although SCAD has been reported in patients with systemic lupus erythematosis (SLE), a connective tissue disorder, our patient presented with polymiositis, for which she had been on prednisolone 10 mg once daily for a long time. In Cushing’s disease, primary or secondary to high doses of steroids, patients have increased fragility of skin and vessel and increasing risk of CAD due to visceral obesity, systemic arterial hypertension, impairment of glucose tolerance, hyperlipidemia and thrombotic secondary to the side effects of high cortisol in body,10–12 but this was not the case with our patient. Also, our patient had no physical signs of Cushing’s disease. The treatment of SCAD is not standardized and there is no optimal therapy for SCAD universally accepted by physicians. It is clinician’s judgment and available resources that decide how to treat SCAD. In a literature review by Leone et al. it is shown that 46.7% cases were treated with CABG, 40% with PTCA and 23.3% with medical treatment.9 In this case report we treated our patient with multiple stents. This patient’s clinical course was complicated by failure to medical management as she was initially started on medical treatment but redeveloped symptoms within two weeks of treatment for which percutaneous cardiac intervention was performed and two drug eluting stents were placed. This supports the idea of aggressive invasive management of SCAD wherever treatment options are available. Due to the wide availability and frequent use of cardiac angiography, the incidence of SCAD has increased. It is time to standardize and make recommendations for the management of SCAD. From the *Department of Internal Medicine, Division of Rheumatology, and the §Department of Internal Medicine, Division of Cardiology, UTMB-Galveston, Galveston, Texas. The authors report no conflicts of interest regarding the content herein. Manuscript submitted December 30, 2008, provisional acceptance given February 24, 2009, and final version accepted March 9, 2009. Address for correspondence: Praveen Jajoria, MBBS, MPH, Department of Internal Medicine, UTMB-Galveston, 301 University Blvd., Galveston, TX 77555. E-mail: drpraveenjajoria@gmail.com
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