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

Ikenaga, Hiroki; Ishihara, Masaharu; Inoue, Ichiro; Kawagoe, Takuji; Sakai, Yuji; Miura, Fumiharu; Nakama, Yasuharu; Dai, Kazuoki; Otani, Takayuki; Ejiri, Kentaro; Oda, Nozomu; Nakamura, Masayuki; Miki, Takashi

doi:10.1253/circj.cj-11-0365

Cited by 28 publications

(33 citation statements)

References 25 publications

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“…Ikenaga et al (36) measured Lp(a) levels 1 week after AMI and divided the patients into two groups based on high Lp(a) (>40 mg/dL) and low Lp(a) (≤40 mg/dL) levels. The incidence of MACE during 5 years was significantly higher in the high Lp(a) group than in the low Lp(a) group (Fig.…”

Section: Introductionmentioning

confidence: 99%

“…5). This difference was primarily driven by a higher incidence of new lesions that required revascularization in the high Lp(a) group (36). Cho et al (37) measured serum Lp(a) levels in 832 consecutive AMI patients on admission and divided them into tertiles according to serum Lp(a) levels: Lp(a) levels of <13.8, 13.8–30.6, and >30.6 mg/dL.…”

Section: Introductionmentioning

confidence: 99%

“…(b) Revascularization for new lesions in patients with high or low Lp(a) levels. Reprinted from Ikenaga et al (36) after permission from J-Stage …”

Section: Introductionmentioning

confidence: 99%

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Potential of lipoproteins as biomarkers in acute myocardial infarction

Khan

Ekhzaimy²,

Khan³

et al. 2017

Anatol J Cardiol

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Acute myocardial infarction (AMI), commonly known as heart attack, is a medical emergency that is potentially fatal if not promptly and pro- perly managed. The early diagnosis of AMI is critically important for the timely institution of pharmacotherapy to prevent myocardial damage and preserve cardiac function. Ischemic insults during AMI cause myocardial tissue damage, releasing the cardiac muscle protein troponin T into the blood stream. Therefore, serum troponin T levels are used as a sensitive and specific indicator of myocardial injury for diagnosing AMI. However, there remains a requirement for developing technologies for more accurate biomarkers or signatures for AMI diagnosis or prognosis. Previous studies have implicated impaired lipid metabolism as a causative factor in AMI development. Lipoproteins are important constituents of lipid metabolism; their levels in the blood stream are a convenient biomarker tool for monitoring lipid metabolism. This review summarizes recent findings (data of studies from 2001 to 2016) regarding the biomarker potentials of various lipoproteins, including low-density lipoprotein, oxidized low-density lipoprotein, high-density lipoprotein, lipoprotein-a, and remnant lipoprotein, for the risk stratification of AMI.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Potential of lipoproteins as biomarkers in acute myocardial infarction

Khan

Ekhzaimy²,

Khan³

et al. 2017

Anatol J Cardiol

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“…With regard to the high homology with Plg, one might expect that apo (a) affects angiogenesis in a similar way that Plg does. Furthermore, Lp (a) plasma concentrations are mainly controlled by the rate of apo (a) de novo biosynthesis, whereas Lp (a) catabolism might have only small effects (Lawn et al 1996;Ikenaga et al, 2011). Iwabayashi et al (2012) documented the effect of Lp (a) on EPCs, showing the presence of LP (a) could significantly diminish the angiogenic function of EPCs via acceleration of senescence, reactive oxygen species production, and functional impairment of the endothelial cell lineage.…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein (a) Impairs Endothelial Progenitor Cell-Mediated Angiogenesis

Ren

Zhang

et al. 2013

DNA and Cell Biology

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Improvement of blood flow and promotion of angiogenesis are important therapeutic measures for the treatment of ischemic peripheral vascular diseases. Since apolipoprotein (a) (apo (a)) is a glycoprotein with repetitive kringle domains exhibiting 75% to 98% structural homology with plasminogen (Plg), apo (a) may also have a negative effect on endothelial progenitor cell (EPC)-induced angiogenesis through Plg-like inhibitory effects on EPC proliferation, adhesion, migration, and angiogenesis. To evaluate the effect of apo (a) on EPCs-induced angiogenesis, EPCs were isolated from the bone marrow of apo (a) transgenic mice, wild-type litter mates, and normal mice. These cells were cultured without or with apo (a) before transplantation. Hindlimb ischemia models were surgically induced in mice, which then received an intravenous injection of 3 · 10 5 EPCs. At 3, 7, and 14 days post EPC transplantation, the adhesion, migration abilities, and capillary density in calf muscles were assessed. Results indicate that apo (a) significantly reduced the adhesion and migration abilities of EPCs. Furthermore, the tubule-like formation of EPCs on Matrigel gels was damaged. In vivo experiments showed the homing of EPCs to ischemic peripheral vascular, and the number of capillary vessels decreased significantly in apo(a) transgenic mice. This study demonstrated that apo (a) could attenuate the adhesion, migration, and homing abilities of EPCs and could impair the angiogenesis ability of EPCs.

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“…13, 14 Hcy is an intermediate metabolite of methionine that contributes to arterial disease through several mechanisms, such as endothelial dysfunction, increased permeability of lipid and inflammatory cells, lipoprotein oxidation, vascular inflammation, smooth muscle proliferation, platelet activation, and abnormalities in the clotting cascade. [15][16][17] The Hcy concentration may be influenced by environmental and genetic factors, whereas changes in the plasma concentration of Lp(a) are more than 90% under genetic control.…”

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confidence: 99%