Angiographic features at ischemia- or infarct-related sites in patients with acute coronary syndrome: morphology changing in a relatively short time.
OBJECTIVE
Coronary cineangiography was reviewed in patients with acute coronary syndrome to investigate whether angiographic features at identifiable ischemia- or infarct-related lesions can change in terms of luminal diameter and morphology in a short period after development, and whether the amount of thrombus with/without underlying ruptured plaque is the major determinant.


METHODS
The present study included 72 patients with unstable angina, 118 with acute myocardial infarction (< 1 month after onset) and 137 with old myocardial infarction (> or = 1 month after onset). The coronary angiographic findings were compared with those from patients with stable effort angina. The groups of patients were subdivided into two groups based on whether antiplatelet and/or anticoagulant therapy, or fibrinolytic therapy with subsequent anticoagulant agents (antiplatelet and/or anticoagulant, or fibrinolytic therapy) were administered. The morphologies of the ischemia- or infarct-related lesions were classified as totally occlusive, simple (Type I lesion) or complex. Complex lesions were further subdivided into Type IIa lesions indicative of the presence of thrombus accumulation with/without an underlying ruptured atheromatous plaque, e.g., narrowing with irregular, poorly defined or hazy borders, sharp leading or trailing edges that overhang or are perpendicular to vessel walls, and globular endoluminal negative images, Type IIb lesions with two or more serial, closely spaced narrowings together with multiple irregularities, and Type IIc lesions indicative of the presence of some parts of ruptured plaque with a smaller amount of thrombus, e.g., luminal narrowing with extraluminal contrast pooling, single or paired short thin linear radiolucencies with/without a variable degree of outpouching, and narrowing with definite outpouching with/without radiolucency, and Type IId lesions showing narrowing with morphology not included in Type IIa-IIc lesions. The coronary angiographic findings were related to the elapsed time before the coronary angiographic study, and whether each patient underwent antiplatelet and/or anticoagulant, or fibrinolytic therapy.


RESULTS
Ischemia- or infarct-related lesions were totally occlusive in 9.7% of patients with unstable angina, 40.7% of those with acute myocardial infarction and 21.9% of those with old myocardial infarction. Total occlusion was significantly more prevalent in patients with acute myocardial infarction than in those with stable effort angina (23.9%, p < 0.05), and total occlusion was more frequent in patients without antiplatelet and/or anticoagulant, or fibrinolytic drugs (50.6% vs 17.1%, p < 0.01). The presence of total occlusion decreased with time after development, and the decrease was more significant with the use of antiplatelet and/or anticoagulant, or fibrinolytic drugs. Type IIa morphology was significantly prevalent immediately after the initial episode, and Type IIa and IIc morphologies increased in the late period, and were more frequent with the use of antiplatelet and/or anticoagulant, or fibrinolytic drugs.


CONCLUSIONS
The severity of the luminal diameter at ischemia- or infarct-related lesions sites can progress or even regress in a relatively short period in patients with acute coronary syndrome, and the amount of accumulated thrombus with/without underlying ruptured plaque is a major determinant of luminal diameter narrowing and angiographic morphology.
Koiwaya
Y
Y
First Department of Internal Medicine, Miyazaki Medical College, Kihara 5200, Kiyotake, Miyazaki 889-1692.
Nagoshi
T
T
Doi
H
H
Eto
T
T
D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000000981:diagnostic imaging*; D000925:Anticoagulants / Q000627:therapeutic use; D002932:Cineangiography; D017023:Coronary Angiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging* / Q000188:drug therapy; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D015912:Thrombolytic Therapy; D013997:Time Factors
D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors