title: [Prevention of left ventricular aneurysm formation and left ventricular remodeling caused by percutaneous transluminal coronary angioplasty performed 24-48 hours after onset of acute myocardial infarction].
abstract: The prevention of left ventricular aneurysm formation and left ventricular remodeling by percutaneous transluminal coronary angioplasty (PTCA) performed 24 to 48 hours after onset of acute myocardial infarction was investigated. Left ventriculography and coronary angiography were performed in 25 patients within 24 hours of onset of acute myocardial infarction. The patients were divided into two groups; reperfusion group (n = 17) and successful PTCA group (n = 8). The reperfusion group and the PTCA group included patients whose infarct-related coronary arteries were successfully reperfused to 99%, Thrombolysis in Myocardial Infarction (TIMI) grade II or III, immediately after coronary thrombolysis. However, the reperfusion group did not include the patients with spontaneous reperfusion or reperfusion after PTCA. The PTCA group consisted of patients who underwent successful PTCA performed within 24 to 48 hours after onset of infarction (mean 28.4 +/- 6.0 hours). Non-reperfusion in the acute phase was defined as TIMI grade 0-I. The size of the ventricular aneurysm in the PTCA group was significantly reduced compared with the reperfusion group (PTCA group 4.2 +/- 8.7%, reperfusion group 27.2 +/- 6.6%; p < 0.01). The increase of left ventricular end-diastolic volume (delta LVEDVI) from the acute to chronic phases was calculated to estimate left ventricular remodeling. There was a significant difference between the two groups in delta LVEDVI (PTCA group 4 +/- 19 ml/m2, reperfusion group 19 +/- 17 ml/m2; p < 0.05). PTCA performed within 24 to 48 hours after onset in patients with acute myocardial infarction and infarct-related coronary arteries, resulting in reperfusion to 99% TIMI grade II or III immediately after coronary thrombolysis, prevents left ventricular aneurysm formation and remodeling.
authors.affiliation: First Department of Internal Medicine, Kinki University School of Medicine, Osaka.
authors.forename: K
authors.initials: K
authors.lastname: Kanamasa
authors.forename: I
authors.initials: I
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Koka
authors.forename: N
authors.initials: N
authors.lastname: Ishida
authors.forename: T
authors.initials: T
authors.lastname: Sasaki
authors.forename: T
authors.initials: T
authors.lastname: Nakabayashi
authors.forename: K
authors.initials: K
authors.lastname: Nakagawa
authors.forename: K
authors.initials: K
authors.lastname: Takada
authors.forename: H
authors.initials: H
authors.lastname: Kato
authors.forename: N
authors.initials: N
authors.lastname: Otani
authors.forename: K
authors.initials: K
authors.lastname: Ishikawa
authors.forename: R
authors.initials: R
authors.lastname: Katori
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D005260:Female; D006322:Heart Aneurysm / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000628:therapy*; D015425:Myocardial Reperfusion; D015912:Thrombolytic Therapy; D016277:Ventricular Function, Left