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Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction.

ABSTRACT: Lipoprotein(a) [Lp(a)] is a circulating lipoprotein, and its level is largely determined by variation in the Lp(a) gene (LPA) locus encoding apo(a). Genetic variation in the LPA gene that increases Lp(a) level also increases coronary artery disease (CAD) risk, suggesting that Lp(a) is a causal factor for CAD risk. Lp(a) is the preferential lipoprotein carrier for oxidized phospholipids (OxPL), a proatherogenic and proinflammatory biomarker. Lp(a) adversely affects endothelial function, inflammation, oxidative stress, fibrinolysis, and plaque stability, leading to accelerated atherothrombosis and premature CAD. The INTER-HEART Study has established the usefulness of Lp(a) in assessing the risk of acute myocardial infarction in ethnically diverse populations with South Asians having the highest risk and population attributable risk. The 2018 Cholesterol Clinical Practice Guideline have recognized elevated Lp(a) as an atherosclerotic cardiovascular disease risk enhancer for initiating or intensifying statin therapy.

SUBMITTER: Enas EA

PROVIDER: S-EPMC6620428 | biostudies-literature | 2019 Mar - Apr

REPOSITORIES: biostudies-literature

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Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction.

Enas Enas A EA Varkey Basil B Dharmarajan T S TS Pare Guillaume G Bahl Vinay K VK

Indian heart journal 20190320 2

Lipoprotein(a) [Lp(a)] is a circulating lipoprotein, and its level is largely determined by variation in the Lp(a) gene (LPA) locus encoding apo(a). Genetic variation in the LPA gene that increases Lp(a) level also increases coronary artery disease (CAD) risk, suggesting that Lp(a) is a causal factor for CAD risk. Lp(a) is the preferential lipoprotein carrier for oxidized phospholipids (OxPL), a proatherogenic and proinflammatory biomarker. Lp(a) adversely affects endothelial function, inflammat ...[more]

PMID: 31280836

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Project description:Background:Risk stratification models with incorporation of biochemical markers have received attention recently. In acute myocardial infarction (AMI) one such marker is lipoprotein(a) (Lp(a)). Lp(a) has prothrombotic and proinflammatory properties. High levels of Lp(a) probably contribute to the additional adverse effects in AMI, as it enhances the damaging effect of acute thrombosis. This study aimed to evaluate serum Lp(a) as a predictor of major adverse cardiovascular events (MACE) in hospitalized-acute myocardial infarction patients. Methods:A prospective cohort study was conducted at Sanglah Hospital, Denpasar, during June-August 2018, among 66 people by consecutive sampling. Samples that met the inclusion and exclusion criteria were examined for serum Lp(a) at the time of admission and the occurrence of MACE during hospitalization was observed. Data regarding serum Lp(a), demography, smoking history, dyslipidemia, hypertension, diabetes mellitus, and MACE were collected. Log rank test and Cox proportional hazards regression were conducted with SPSS version 20 for Windows. Results:During observation, MACE occurred in 25 (38%) patients, including cardiogenic shock in 7 (10.6%) patients, heart failure in 20 (30.3%) patients, cardiovascular death in 5 (7, 6%) patients, malignant arrhythmias in 5 (7.6%) patients, and postinfarction angina in 5 (7.6%) patients. After the Log rank test, a significant difference in survival was observed (p = 0.001) between groups of high Lp(a) (survival rate of 60.6 hours; 95% CI 43.3-77.9) and low Lp(a) (average survival of 104.3 hours, 95% CI 91.4-117.2). The hazard ratio of high Lp(a) against MACE was 4.63 (p=0.002), and it increased to 4.69 in multivariate analysis with Cox proportional hazards regression test (p=0.003). Conclusion:The high level of Lp(a) in AMI patients was a risk factor for the occurrence of MACE during hospitalization. Patients with high Lp(a) also had worse survival compared to patients with low Lp(a).

Project description:Background Real-world data on low baseline low-density lipoprotein cholesterol (LDL-C) levels and long-term postdischarge cardiovascular outcomes in patients with acute coronary syndrome are limited. Methods and Results Of the 10 719 patients enrolled in the Korean registry of acute myocardial infarction between January 2004 and August 2014, we identified 5532 patients who were event free from death, recurrent myocardial infarction, or stroke during the in-hospital period after successful percutaneous coronary intervention. The co-primary outcomes were 3-point major adverse cardiovascular events (a composite of nonfatal stroke, nonfatal myocardial infarction, and cardiovascular death) and cardiovascular death at 5 years. Of 5532 patients with acute myocardial infarction (mean age, 62.1±12.8 years; 75.0% men), 446 cardiovascular deaths (8.1%) and 695 three-point major adverse cardiovascular events (12.6%) occurred at 5 years. In the continuous analysis of LDL-C, the risk of cardiovascular events increased steeply as LDL-C levels decreased from 100 mg/dL. For categorical analysis of LDL-C (<70, 70-99, and ≥100 mg/dL), as LDL-C levels decreased, clinical outcomes worsened (237/3759 [6.3%] in LDL-C ≥100 mg/dL versus 123/1291 [9.5%] in LDL-C 70-99 mg/dL versus 86/482 [17.8%] in LDL-C <70 mg/dL for cardiovascular death; P-trend<0.001; and 417/3759 [11.1%] in LDL-C ≥100 mg/dL versus 172/1291 [13.3%] in LDL-C 70-99 mg/dL versus 106/482 [22.2%] in LDL-C <70 mg/dL for 3-point major adverse cardiovascular event; P-trend<0.001). In a Cox time-to-event multivariable model with LDL-C levels ≥100 mg/dL as the reference, the baseline LDL-C level <70 mg/dL was independently associated with an increased incidence of cardiovascular death (adjusted hazard ratio, 1.68 [95% CI, 1.30-2.17]) and 3-point major adverse cardiovascular event (adjusted hazard ratio, 1.37 [95% CI, 1.10-1.71]). Conclusions In this Korean acute myocardial infarction registry, the baseline LDL-C level <70 mg/dL was significantly associated with an increased incidence of long-term cardiovascular events after discharge. (COREA [Cardiovascular Risk and Identification of Potential High-Risk Population]-Acute Myocardial Infarction Registry; NCT02806102). Registration URL: https://www.clinicaltrials.gov/; Unique identifier: NCT02806102.

Dataset Information

Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction.

Publications

Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction.

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