موردی کمیاب کوکائین القا شده آنوریسم آئورت: یک رویداد تشریحی / Rare Case of Cocaine-Induced Aortic Aneurysm: A Near Dissection Event

موردی کمیاب کوکائین القا شده آنوریسم آئورت: یک رویداد تشریحی Rare Case of Cocaine-Induced Aortic Aneurysm: A Near Dissection Event

  • نوع فایل : کتاب
  • زبان : انگلیسی
  • ناشر : Hindawi
  • چاپ و سال / کشور: 2018

توضیحات

رشته های مرتبط پزشکی
گرایش های مرتبط قلب و عروق
مجله گزارشات موردی در قلب و عروق – Case Reports in Cardiology
دانشگاه Department of Internal Medicine – MacNeal Hospital – USA

منتشر شده در نشریه هینداوی

Description

1. Introduction *oracic aortic aneurysm occurs due to increased aortic wall stress from hypertension and less commonly due to genetic and in4ammatory condition or prior cardiac surgery [1]. *e most feared complication is dissection [1, 2]. In the general population, aortic dissection occurs in 2.6–3.5 per 100,000 patient years [3]. In a study, 921 cases of acute aortic dissection presenting to IRAD (International Registry for Aortic Dissection) centers from 1996 through 2000 were studied, and only 5 (0.5%) cases were associated with cocaine use (p value 0.068). Cocaine seemed to have played a signi1cant role in precipitating aortic dissection among young cohort (age 44.4 ± 3.9 years, p value < 0.001) [4]. *is IRAD study suggested that cocaine is not likely to be responsible for >1% of aortic dissections. 2. Case Presentation 2.1.History. A 41-year-old white male with no signi1cant past medical history presented in the emergency department (ED) with chest pain. *e patient was having chest discomfort for one day. On the day of presentation, he had severe 10/10 intensity, central chest pain, aggravated with lying down and relieved with sitting up. He had associated dyspnea but denied fever, cough, presyncope, syncope, or palpitations. He denied any similar history in the past. *ere were no known heart murmurs. *ere was no history of sudden cardiac death or heart disease in family. He snorted cocaine every two weeks for several years, and the last use was a night before his symptoms started. He admitted to drinking alcohol in weekends but denied tobacco smoking. 2.2. Physical Exam. His vital signs in the ED was signi1cant for tachycardia, heart rate 110 beats/minute. Initial BP (blood pressure) in ED was 136/83 mmHg. On exam, he had blowing, decrescendo, grade II/VI diastolic murmur heard best in the third left intercostal space, and grade III/VI holosystolic murmur on the left sternal border. He had crackles at lung base but no pedal edema or jugular venous distension on exam. 2.3. Investigation and Management. EKG showed ST elevation suggestive of anterior and inferior infarct (Figure 1). Serial troponins three times were normal. Urine drug screen was positive for cocaine. Chest X-ray showed mild cardiomegaly. *e patient was admitted to the telemetry unit with presumptive diagnosis of pericarditis versus cocaineinduced coronary vasospasm. Transthoracic echocardiography (TTE) was performed for the concern of diastolic murmur and pericarditis. TTE showed 6.2 cm aortic root dilatation and severe AR (aortic regurgitation) with possible aortic dissection, EF 50%, and minimal MR (mitral regurgitation) and TR (tricuspid regurgitation).
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