پارگی خود به خودی عروق كرونری در بيمار مبتلا به ديسپلازي رشته ای-عضلانی
ترجمه نشده

پارگی خود به خودی عروق كرونری در بيمار مبتلا به ديسپلازي رشته ای-عضلانی

عنوان فارسی مقاله: گزارش موردی از یک حمله شدید قلبی در نتيجه پارگی خود به خودی عروق كرونری در بيمار مبتلا به ديسپلازي رشته ای-عضلانی
عنوان انگلیسی مقاله: Case Report of an Acute Myocardial Infarction as a Result of Spontaneous Coronary Artery Dissection in a Patient with Fibromuscular Dysplasia
مجله/کنفرانس: گزارشات موردی در قلب شناسی - Case Reports in Cardiology
رشته های تحصیلی مرتبط: پزشکی
گرایش های تحصیلی مرتبط: قلب و عروق
نوع نگارش مقاله: گزارش موردی (Case Report)
شناسه دیجیتال (DOI): https://doi.org/10.1155/2019/3051616
دانشگاه: Moscow State University of Medicine and Dentistry Named After A.I. Evdokimov, Clinical Hospital Named After I.V. Davidovsky, Moscow, Russia
صفحات مقاله انگلیسی: 5
ناشر: هینداوی - Hindawi
نوع ارائه مقاله: ژورنال
نوع مقاله: ISI
سال انتشار مقاله: 2019
فرمت مقاله انگلیسی: PDF
وضعیت ترجمه: ترجمه نشده است
قیمت مقاله انگلیسی: رایگان
آیا این مقاله بیس است: خیر
آیا این مقاله مدل مفهومی دارد: ندارد
آیا این مقاله پرسشنامه دارد: ندارد
آیا این مقاله متغیر دارد: ندارد
کد محصول: E13030
رفرنس: دارای رفرنس در داخل متن و انتهای مقاله
فهرست مطالب (انگلیسی)

1- Introduction

2- Case Report

3- Discussion

4- Conclusion

References

بخشی از مقاله (انگلیسی)

Introduction

Spontaneous coronary artery dissection (SCAD) is an underdiagnosed and rare cause of myocardial infarction (MI). SCAD is defined as the separation of the coronary artery wall by hemorrhage with or without intimal tear. SCAD causes acute coronary syndrome in 1.7% to 4% of cases [1]. We report a case of a patient with acute MI caused by SCAD with marked progression of dissection within 4 days and spontaneous healing in 2 months.

2- Case Report

A 47-year-old woman with a 4-day history of chest pain, which had begun directly after emotional stress (air travel), was transferred to our clinic from another hospital. The patient was normosthenic, had practiced gymnastics in youth, and had no signs of joint hypermobility syndrome or other connective tissue disorder. She had smoked for a long time and had arterial hypertension grade 2. She had never experienced chest pain before and was very active in her everyday life. An electrocardiogram upon admission to our clinic revealed a sinus rhythm with a 2 mm ST elevation in leads II, III, aVF, V3-V5, “-” and T V3-V5 (Figure 1). On echocardiography, an apex dyskinesis was found; the left ventricle ejection fraction was 56%. The level of cardiac troponin-I was 13.2 ng/mL, confirming the development of acute myocardial infarction. We analysed the first angiogram, which had been performed in another clinic. It revealed 70– 75% smooth extended narrowing in the middle segment of the left anterior descending artery, and no signs of atherosclerosis in the proximal segment of LAD or the remaining arteries were found. Side branches were absolutely normal as well (Figure 2). It looked like a subintimal hematoma. We repeated the coronary angiography upon admission on day 4; the extension of the culprit lesion to the distal segment of the LAD was observed (Figure 3). Because of the high risk of intima rupture, intravascular visualization was not performed. This finding on the second angiogram confirmed our initial suspicion and corresponded to SCAD type 2. Considering that the association of SCAD and FMD is a well-known fact, we performed angiography of the renal and carotid arteries [2].