Serum Lipoprotein(a) Level and Clinical Coronary Stenosis Progression in Patients With Myocardial Infarction Re-Revascularization Rate is High in Patients With High-Lp(a)

Abstract

Lp(a) level, the patients were classified into either a highLp(a) (serum Lp(a) level ≥30 mg/dl) or a low-Lp(a) (serum Lp(a) level <30 mg/dl) group for evaluation of the clinical coronary stenosis progression (CCSP) between the 2 groups. Because a serum Lp(a) level of 31 mg/dl was the 75 th percentile of this study population, we defined patients with a serum Lp(a) level ≥30 mg/dl as the high-Lp(a) group. We also evaluated hypertension (systolic blood pressure >140 mmHg, diastolic blood pressure >90 mmHg or receiv- Background High serum lipoprotein(a) (Lp(a)) levels are associated with coronary artery disease. Methods and ResultsThe serum Lp(a) levels of 130 patients with acute myocardial infarction (AMI) who underwent direct percutaneous coronary intervention were investigated. On the basis of Lp(a) level at 1 month after the onset of AMI, the patients were classified into 2 groups (high-Lp(a) (≥30 mg/dl) and low-Lp(a) (<30 mg/dl)) for evaluation of the clinical coronary stenosis progression (CCSP) rate. CCSP is defined as either target lesion revascularization (TLR) or new lesion revascularization (NLR). The CCSP rate was significantly higher in the high-Lp(a) group than in the low-Lp(a) group (65.8% vs 29.3%, p<0.01). In patients who had coronary stents in the acute phase (n=79), the CCSP and NLR rates were significantly higher in the high-Lp(a) group than in the low-Lp(a) group (45.0% vs 20.3%, p<0.05; 35.0% vs 6.8%, p<0.01), but there was no significant difference in TLR rate between the 2 groups (10.0% vs 13.6%, p=0.858).Conclusions High serum Lp(a) level is a significant risk factor for CCSP, but does not influence restenosis after stenting. (Circ J 2006; 70: 156 -162)

Hyperlipoproteinaemia(a) is a common cause of autosomal dominant hypercholesterolaemia

“…An association of high Lp(a) levels and atherogenesis in the general population has been described in some studies (Ariyo et al 2003;Gaw et al 2005;Kronenberg et al 1999;Morita et al 2006 ), but not in others (Cantin et al 1998;Grebe et al 2007). A metaanalysis of prospective studies concluded that subjects in the top third of baseline Lp(a) levels are at increased risk for CHD compared with those in the bottom third (Danesh et al 2000).…”

Usefulness of Lipoprotein (a) for Predicting Progression of Non-Culprit Coronary Lesions After Acute Myocardial Infarction

“…Since the introduction of coronary stents, the initial results of primary PCI have dramatically improved, 8, 9 The main cause of TLR is the growth of smooth muscle cells and fibroatheroma, which is thought to be strongly inhibited by the metallic scaffold of the stent. 10 However, this mechanism of TLR is different from that of non-TLR, so Lp(a) level was not associated with TLR. In addition, the procedure of primary PCI affects TLR.…”

High Lipoprotein(a) Levels are Associated With Long-Term Adverse Outcomes in Acute Myocardial Infarction Patients in High Killip Classes

“…Hoffmann et al24) have demonstrated by serial intravascular ultrasound studies that in-stent restenosis results from neointimal tissue proliferation, which has been attributed to Lp(a) in vitro 25). However, Morita et al26) studied patients with high Lp(a) levels undergoing POBA as well as PCI and found that there was less difference of TLR rate in the PCI group. Although not completely understandable, it has been suggested that the metallic scaffolding in stents strongly inhibits recoil, which results in the suppression of in-stent restenosis in patients with high serum Lp(a) levels.…”