Acute inferior wall myocardial infarction induced by aortic dissection in a young adult with Marfan syndrome: A case report

paythelady.612 shared this article with you from Inoreader Acute inferior wall myocardial infarction induced by aortic dissection in a young adult with Marfan syndrome: A case report Μέσω pubmed: "world j clin cases"... World J Clin Cases. 2021 Feb 6;9(4):970-975. doi: 10.12998/wjcc.v9.i4.970. ABSTRACT BACKGROUND: Aortic dissection (AD) is an emergent and life-threatening disorder, and its in-hospital mortality was reported to be as high as 24.4%-27.4%. AD can mimic other more common disorders, especially acute myocardial infarction (AMI), in terms of both symptoms and electrocardiogram changes. Reperfusion for patients with AD may result in catastrophic outcomes. Increased awareness of AD can be helpful for early diagnosis, especially among younger patients. CASE SUMMARY: We report a 28-year-old man with acute left side chest pain without cardiovascular risk factors. He was diagnosed with acute inferior ST-segment elevation myocardial infarction (STEMI), which, based on illness history, physical examination, and intraoperative findings, was eventually determined to be type A AD caused by Marfan syndrome. Emergent coronary angiography revealed t he anomalous origin of the right coronary artery as well as eccentric stenosis of the proximal segment. Subsequently, computed tomography angiography (CTA) showed intramural thrombosis of the ascending aorta. Finally, the patient was transferred to the cardiovascular surgery department for a Bentall operation. He was discharged 13 d after the operation, and aortic CTA proved a full recovery at the 2-year follow-up. CONCLUSION: It is essential and challenging to differentiate AD from AMI. Type A AD should be the primary consideration in younger STEMI patients without cardiovascular risk factors but with outstanding features of Marfan syndrome. PMID:33585646 | PMC:PMC7852626 | DOI:10.12998/wjcc.v9.i4.970 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.