Relationship Between Lipoprotein(a) and Spontaneous Recanalization of Infarct-related Arteries in the Early Phase of Acute Myocardial Infarction
Address for correspondence: Hong Seog Seo Guro Hospital Cardiovascular Center Korea University 97 Gurodong-Gil Guro-gu Seoul, Republic of Korea, 152-703 Korea
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Jin Won Kim, Hong Seog Seo, Soon Yong Suh, Cheol Ung Choi, Eung Ju Kim, Seung-Woon Rha, Chang Gyu Park, Dong Joo Oh Cardiovascular Center, Korea University Guro Hospital, Seoul, Republic of Korea
Background: Lipoprotein(a) (Lp[a]) is known to inhibit the fibrinolysis system and promote thrombus formation. Hypothesis: We retrospectively investigated the influences of Lp(a) on infarct-related artery patency in the early phase of acute myocardial infarction (AMI). Methods: In 144 patients with ST-segment elevation, myocardial, coronary angiography (CAG) was performed within 12 h of the onset of symptoms. Subjects were divided into 2 groups according to the thrombolysis in myocardial infaction (TIMI) grade, Group I (TIMI 0–1, n = 94) versus Group II (TIMI 2–3, n = 50). The Gensini score and 0- to 3-vessel disease score estimated the severity and extent of coronary artery disease (CAD), respectively. Lp(a), lipid profile and c-reactive protein (CRP) were measured before any medications including thrombolytics were given. Results: The Lp(a) level was higher in Group I than in Group II. There was a weak correlation between Lp(a) level and Gensini score. By multivariate logistic regression analysis, a Lp(a) level was a predictor of infarct-related artery patency in the early phase of AMI. There were no significant differences in the location of the infarct-related arteries, extent of CAD, time from pain to CAG, number of risk factors, and hs-CRP values between the 2 groups. Conclusion: The Lp(a) level was significantly higher in patients with persistent occlusion compared with those with spontaneous recanalization of infarct-related arteries in the early phase of AMI. Key words: Lipoprotein(a), acute myocardial infarction, recanalization, thrombolysis in myocardial infarction flow Introduction It is well known that Lipoprotein(a) (Lp[a]) is preferentially retained in the arterial wall by binding to several extracellular matrix components.1,2 Because of the structural homology of apo(a) and plasminogen, Lp(a) might compete with and inhibit the thrombolytic activity of tissue plasminogen.3,4 Although increased Lp(a) concentrations have been observed in patients with several thrombotic occlusive disorders,5 – 7 the prothrombotic activity of Lp(a) in vivo is not well established. Acute myocardial infarction (AMI) is caused by occlusive thrombosis superimposed on the ruptured plaque of a coronary artery. Considering its antithrombolytic properties, Lp(a) could prevent spontaneous reperfusion during the acute stage of myocardial infarction (MI). Therefore, in the present study, we investigate the influence of Lp(a) on spontaneous recanalization of infarct-related arteries in the early phase of acute myocardial infarction.
diagnosed as ST-segment elevation myocardial infarction (STEMI) were eligible for this study. The diagnosis of AMI required characteristic chest pain lasting for more than 30 min, typical electrocardiographic changes and an increase in serum CK-MB to at least 3 times the upper normal limit or Troponin T was >0.10 ng/mL. The infarctrelated arteries were identified using a combination of electrocardiogaphic findings, left ventricular wall motion abnormalities on echocardiography, scintigraphic findings and angiographic findings. All subjects had to be aged 70% luminal diameter narrowing occurred, and the patients were defined as having 0-, 1-, 2-, or 3-vessel disease according to the number of involved vessels. Multiple lesions in the same artery were regarded as 1-vessel disease. Antegrade flow in the infarct-related artery was graded according to the thrombolysis in myocardial infarction (TIMI) scoring system by two cardiologists prior to PCI; grade 0: arteries with no perfusion; grade 1: penetration of contrast material without perfusion; grade 2: partial perfusion; grade 3: complete perfusion. The infarctrelated artery was classified as patent if the TIMI perfusion grade was 2 or 3, or otherwise occluded.
on the patency of infarct-related arteries were analyzed using a multivariate logistic regression model. Statistical significance was accepted at p
