The effects of early coronary patency on the evolution of myocardial infarction: a prospective arteriographic study.
The effects of early spontaneous coronary patency on the evolution of myocardial infarction were evaluated in 41 patients. They had coronary arteriography (mean (SEM)) 3.1 (0.2) hours after the onset of chest pain with repeat studies 90 minutes and three days later. In 12 (29%) patients the infarct related coronary artery was patent at the first arteriogram (group 1). A further 10 patients, nine of whom received thrombolytic treatment, showed early recanalisation of the infarct related coronary artery within 90 minutes of treatment (group 2). In the remainder the infarct related coronary artery was persistently occluded (group 3). Baseline values for infarct location, the sum of ST elevation in all leads, QRS scores, and serum creatine kinase activity did not permit discrimination between the groups. Nevertheless, patterns of ST segment change and enzyme release in group 1 were closely similar to those that occurred in response to thrombolysis in group 2. Thus compared with group 3, groups 1 and 2 showed earlier 50% reduction in the sum of peak ST elevation in all leads and earlier peaking of serum creatine kinase activity. Importantly, creatine kinase release was significantly attenuated in group 1, rising to a peak serum activity (mean (SEM)) of only 1242 (415) IU/1. Analysis of angiographic left ventricular ejection fractions at three days indicated limitation of infarct size in groups 1 and 2 compared with group 3. Mean (SEM) ejection fraction, however, was best preserved in group 1 (62(6)%) and in this group the frequency of non-Q wave infarction was higher than in groups 2 and 3. Thus in patients who present with a patent infarct related coronary artery early during infarction: (a) there is a reduction in the pattern of infarct size as reflected by attenuation of release of creatine kinase, preservation of left ventricular ejection fraction, and a relatively high frequency of non-Q wave infarction; (b) patterns of ST segment change and creatine kinase release resemble those that occur after successful thrombolytic treatment, suggesting that early coronary patency is the result of spontaneous recanalisation of a previously occluded artery.
Timmis
A D
AD
Department of Cardiology, Guy's Hospital, London.
Griffin
B
B
Crick
J C
JC
Nelson
D J
DJ
Sowton
E
E
D000328:Adult; D000368:Aged; D016255:Anistreplase; D017023:Coronary Angiography; D003327:Coronary Disease / Q000150:complications; D003331:Coronary Vessels / Q000473:pathology*; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D010958:Plasminogen / Q000627:therapeutic use; D011446:Prospective Studies; D013300:Streptokinase / Q000627:therapeutic use; D013997:Time Factors
D005343:Fibrinolytic Agents; D016255:Anistreplase; D010958:Plasminogen; D003402:Creatine Kinase; D013300:Streptokinase