title: Usefulness of changes in left ventricular wall thickness to predict full or partial pressure reperfusion in ST-elevation acute myocardial infarction.
abstract: Experimental studies have shown that if an acute transmural myocardial infarction is reperfused at full pressure there is an immediate and persisting increase in end-diastolic wall thickness (EDWT) due to massive intramural edema, with the amount of edema inversely related to the residual stenosis in the infarct-related artery. This study investigated if these findings are paralleled in the clinical setting and whether the resultant myocardial substrate differs after percutaneous coronary intervention (PCI) versus thrombolysis (the latter having a higher incidence of residual flow limiting stenosis in the culprit vessel). Eighty-eight consecutive patients with ST-elevation myocardial infarction were enrolled. Twenty-seven patients underwent primary PCI, 23 had rescue PCI, and 38 had thrombolysis. Standard M-mode and 2-dimensional echocardiographies were performed within 12 hours. Regional EDWT was measured in 904 infarct-related segments after the different reperfusion strategies and compared with 504 remote noninfarcted segments. EDWT of infarct-related segments after primary PCI was significantly increased compared with normal segments. At follow-up, after 6 months, EDWT of these segments was significantly decreased, indicating transmural infarction. EDWT of infarct-related segments after thrombolysis did not differ from that of normal segments. After rescue PCI, EDWT of infarct-related segments was significantly decreased compared with that of normal segments. In conclusion, full-pressure restoration of epicardial blood flow after transmural myocardial infarction causes an immediate increase in EDWT, easily detected by echocardiography. In contrast, pressure-limiting reperfusion (typical for thrombolysis) resultsin normal EDWT. This confirms experimental data that PCI and thrombolysis can differ in their resultant myocardial substrate.
authors.affiliation: Department of Cardiology, St. George's Hospital, London, United Kingdom.
authors.forename: Elisa
authors.initials: E
authors.lastname: Merli
authors.forename: George R
authors.initials: GR
authors.lastname: Sutherland
authors.forename: Bart
authors.initials: B
authors.lastname: Bijnens
authors.forename: Andreas
authors.initials: A
authors.lastname: Fischer
authors.forename: Marinela
authors.initials: M
authors.lastname: Chaparro
authors.forename: Tiia
authors.initials: T
authors.lastname: Karu
authors.forename: Stephen
authors.initials: S
authors.lastname: Sutcliffe
authors.forename: Anna
authors.initials: A
authors.lastname: Marciniak
authors.forename: Aigul
authors.initials: A
authors.lastname: Baltabaeva
authors.forename: Nicholas
authors.initials: N
authors.lastname: Bunce
authors.forename: Stephen
authors.initials: S
authors.lastname: Brecker
mesh_terms: D001026:Coronary Artery Bypass; D004452:Echocardiography; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000628:therapy; D015425:Myocardial Reperfusion; D010496:Pericardium; D015912:Thrombolytic Therapy