Serum lipoprotein(a) level is related to thrombin generation and spontaneous intermittent coronary occlusion in patients with acute myocardial infarction.
BACKGROUND
Thrombotic occlusion of the infarct-related coronary artery is often intermittent in the early, evolving phase of acute myocardial infarction. To assess their relationship to this pattern of coronary occlusion, serum or plasma concentrations of cholesterol, triglyceride, lipoprotein(a), and coagulation and fibrinolytic factors were measured in venous blood before the initiation of thrombolytic therapy.


RESULTS
Thirty-two patients (23 men, 9 women: age, 30 to 70 years) with acute myocardial infarction received intravenous recombinant tissue plasminogen activator (20 to 60 megaunits) within 6 hours of the onset of symptoms. Continuous ECG ST-segment recording demonstrated intermittent occlusion of the infarct-related coronary artery in 12 patients (group 1) before the start of thrombolytic treatment and persistent occlusion in 20 patients (group 2). Groups 1 and 2 were similar in age, sex, race, duration of symptoms, blood sample collection time, location of the infarct-related coronary artery, and extent of coronary artery disease. The serum level (median [interquartile range]) of lipoprotein(a) was 34 (13 to 47) mg/dL versus 11.5 (5 to 27) mg/dL (P = .02), and the plasma level (median [interquartile range]) of thrombin-antithrombin III complex was 10.85 (6.4 to 21.5) versus 6.8 (4.2 to 8.7) micrograms/L-1 (P < .04) in groups 1 and 2, respectively. The levels of the other factors were similar in both groups.


CONCLUSIONS
The phenomenon of spontaneous intermittent closure and reopening of coronary arteries early during acute myocardial infarction in humans is associated with a higher level of lipoprotein(a) and of a marker of thrombin generation, suggesting that lipoprotein(a) and thrombin are closely related to coronary patency in these patients.
Haider
A W
AW
Division of Clinical Cardiology, Royal Postgraduate Medical School, Hammersmith Hospital, London, England. AGHA@FRAM.NHLBI.NIH.GOV
Andreotti
F
F
Thompson
G R
GR
Kluft
C
C
Maseri
A
A
Davies
G J
GJ
D000208:Acute Disease; D000328:Adult; D000368:Aged; D015415:Biomarkers; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood* / Q000150:complications; D004562:Electrocardiography; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005341:Fibrinolysin / Q000378:metabolism; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D008055:Lipids / Q000097:blood; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology; D010960:Plasminogen Activators / Q000008:administration & dosage; D013917:Thrombin / Q000096:biosynthesis*; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage; D014280:Triglycerides / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
D015415:Biomarkers; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008055:Lipids; D017270:Lipoprotein(a); D014280:Triglycerides; D014841:von Willebrand Factor; D005340:Fibrinogen; D010960:Plasminogen Activators; D013917:Thrombin; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin