assessing myocardial perfusion after myocardial infarction评估心肌梗死后心肌灌注.pdf

Learning Forum Assessing Myocardial Perfusion after Myocardial Infarction Houman Ashrafi an, Girish Dwivedi, Roxy Senior* D E S C R I P T I O N o f C A S E 63-year-old man presented to our accident and emergency department with a 2-hour history of Acrushing central chest pain, excessive sweating, and diffi culty in breathing. Past history included non-insulin- dependent diabetes mellitus controlled by oral hypoglycaemic agents. On examination, he appeared unwell, with pulse of 94 beats per minute, blood pressure of 124/68 mm Hg, and respiratory rate of 20 breaths per minute. Jugular venous pressure was not elevated, but chest auscultation revealed bilateral basal crackles. Cardiovascular system examination was unremarkable. His electrocardiogram on admission showed 2 mm ST segment elevation in chest leads V1–V4 (Figure 1A). What Was the Clinical Diagnosis and Treatment? The combination of typical chest pain and electrocardiographic changes were characteristic of acute anteroseptal myocardial infarction. A presumptive diagnosis of probable left anterior descending (LAD) coronary artery occlusion was made. Our patient was promptly thrombolysed with recombinant plasminogen activator and managed as per our hospital’s acute myocardial infarction (AMI) protocol. This involved administration of diamorphine, aspirin, intravenous nitrates, heparin, a beta-blocker, an angiotensin DOI: 10.1371/journal.pmed.0030131.g001 converting enzyme inhibitor, and a statin. Figure 1. Electrocardiogram on Admission and after Thrombolytic Within 30 minutes of thrombolytic therapy, there was Therapy complete cessation of pain and subsidence of elevated ST (A) Electrocardiogram on admission showing 2 mm ST elevation in segments (Figure 1B). His peak CK and CK-MB were elev