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

Enas, Enas A.; Varkey, Basil; Dharmarajan, T. S.; Paré, Guillaume; Bahl, Vinay K.

doi:10.1016/j.ihj.2019.03.004

Cited by 71 publications

(59 citation statements)

References 202 publications

(404 reference statements)

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“…Lp(a) is an independent risk factor for CVD, and levels are primarily genetically determined, with a small influence of environmental factors. Approximately, 20-30% of the world's population have an elevated Lp(a), defined as > 50 mg/dL or > 125 nmol/L [17]. There are exceptions to generally stable levels, including a stressful environment such as sepsis, in which Lp(a) levels are acutely elevated [18,19].…”

Section: Lp(a) and Antifibrinolytic Effectsmentioning

confidence: 99%

Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis

Moriarty

Gorby

Stroes

et al. 2020

Curr Atheroscler Rep

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Purpose of Review The COVID-19 pandemic has infected over > 11 million as of today people worldwide and is associated with significant cardiovascular manifestations, particularly in subjects with preexisting comorbidities and cardiovascular risk factors. Recently, a predisposition for arterial and venous thromboses has been reported in COVID-19 infection. We hypothesize that besides conventional risk factors, subjects with elevated lipoprotein(a) (Lp(a)) may have a particularly high risk of developing cardiovascular complications. Recent Findings The Lp(a) molecule has the propensity for inhibiting endogenous fibrinolysis through its apolipoprotein(a) component and for enhancing proinflammatory effects such as through its content of oxidized phospholipids. The LPA gene contains an interleukin-6 (IL-6) response element that may induce an acute phase-type increase in Lp(a) levels following a cytokine storm from COVID-19. Summary Thus, subjects with either baseline elevated Lp(a) or those who have an increase following COVID-19 infection, or both, may be at very high risk of developing thromboses. Elevated Lp(a) may also lead to acute destabilization of preexisting but quiescent atherosclerotic plaques, which might induce acute myocardial infarction and stroke. Ongoing studies with IL-6 antagonists may be informative in understanding this relationship, and registries are being initiated to measure Lp(a) in subjects infected with COVID-19. If indeed an association is suggestive of being causal, consideration can be given to systematic testing of Lp(a) and prophylactic systemic anticoagulation in infected inpatients. Therapeutic lipid apheresis and pharmacotherapy for the reduction of Lp(a) levels may minimize thrombogenic potential and proinflammatory effects. We propose studies to test the hypothesis that Lp(a) may contribute to cardiovascular complications of COVID-19.

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Section: Lp(a) and Antifibrinolytic Effectsmentioning

confidence: 99%

Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis

Moriarty

Gorby

Stroes

et al. 2020

Curr Atheroscler Rep

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“…In the literature, lp(a) has been identified as an independent risk factor for vascular disease and subjects with lp(a) values above 30 mg/dL have an increased risk of developing early atherosclerotic disease [16]. While lp(a) levels are mainly under genetic control and are less affected than other lipoproteins by age, sex, weight, and diet, there are a few exogenous factors, such as physical exercise, estrogen therapy, and endstage renal failure, that affect lp(a) serum concentrations [17].…”

Section: Discussionmentioning

confidence: 99%

Do antiepileptic drugs cause premature atherosclerosis by disturbing lipid metabolism?

2022

Ann Clin Anal Med

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Aim: The aim of this study was to evaluate susceptibility to atherosclerosis in epileptic patients on carbamazepine and valproic acid monotherapy with lipid profile, lipoprotein (a) (lp(a)), oxidized low-density lipoprotein (LDL), adiponectin, and carotid artery intima-media thickness measurements. Material and Methods: Of the 108 patients with epilepsy included in the study, 64 (36 female, 28 male) were receiving valproic acid monotherapy and 44 (25 female, 19 male) were receiving carbamazepine monotherapy. The control group comprised 48 (30 female, 18 male) healthy participants. Liver and kidney function tests, cholesterol, triglycerides, LDL, high-density lipoprotein (HDL), lp(a), oxidized LDL, adiponectin, and common carotid (CCA) and internal carotid artery (ICA) intima-media thickness (IMT) were investigated in both the patient and control groups. Results: Mean age was 32.34±12.41 years in the valproic acid group, 32.70±11.64 years in the carbamazepine group, and 35.81± 11.76 years in the control group. Liver and kidney function test results were normal in all groups. Cholesterol levels were lower in the valproic acid group than the other groups. HDL levels were higher in the carbamazepine group than other groups. Adiponectin levels were lower in the valproic acid group. In all groups, cholesterol and LDL levels were higher in individuals older than 50 years old. When the patients were evaluated according to the duration of drug use, cholesterol and LDL levels were higher in patients who had used drugs for more than 5 years in the valproic acid group. There were no differences between the groups for triglyceride, oxidized LDL, or lp(a) levels or CCA and ICA IMT. Discussion: There are conflicting results in the literature regarding epilepsy and atherosclerosis associated with antiepileptic drug usage. In this study, no evidence was found of an increasing risk of arteriosclerosis associated with antiepileptic drugs by measuring lipids, lipoprotein, oxidized LDL, adiponectin levels, and CCA and ICA IMT. However, it is important to monitor lipid levels in the follow-up of patients with epilepsy, especially for patients requiring longterm antiepileptic therapy and also older patients.

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“…Moreover, the three methods all suggested that there was no signi cant correlation between Lp(a) variation rate and NLR in diabetic population. Previous studies have shown that the level of Lp(a) is affected by genetic factors and is relatively stable within an individual with a small variation rate [29]. Therefore, in this study, it was also shown that the variation rate of lp(a) is relatively small, and the diabetic subgroup itself has long-term chronic low-grade in ammation, which makes the variation of lp(a) in this subgroup relatively The in uence of the level of in ammation is interfered by the in ammatory factors of diabetes, which weakens the correlation between the two.…”

Section: Discussionmentioning

confidence: 99%

Variability In Non-HDL-C and Lp(a) Affect The Neutrophil To Lymphocyte Ratio In Patients Undergoing Elective Percutaneous Coronary Intervention

Zhang¹,

Xie³

et al. 2021

Preprint

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Objective: To evaluate the influence of the variability of Lipoprotein a (Lp(a)) and Non-high-density lipoprotein cholesterol (non-HDL-C) on the neutrophil to lymphocyte ratio (NLR) during the follow-up period in patients with coronary heart disease (CHD) after elective coronary intervention.Methods: A total of 3320 consecutive patients with CHD after percutaneous coronary intervention (PCI) in a multi-center from January 2010 to January 2019 were enrolled. The baseline demographic data were Analyzed, and the NLR levels in tertile groups according to the baseline Lp(a) and non-HDL-C levels were compared. Linear regression is used to analyze the association of the variation rate of Lp(a) and non-HDL-C with NLR; and subgroup analysis of the relevant factors were found. All verifications are verified by SD, CV, and VIM triple methods.Results: The NLR is significantly different among tertile Lp(a) variation groups in SD, CV and VIM methods, which is consistent in non-HDL-C variation rate except SD method. Multiple linear regression indicated that Lp(a) variability, age, gender, BMI, hypertension, eGFR were related to NLR, which was verified in age, gender, hypertension and non-diabetic subgroups. Non-HDL-C variability, age, gender, BMI, eGFR, statins, follow-up HDL-C and non-HDL-C were also related to NLR, and established in the above subgroups.Conclusion: The variation rate of Lp(a) and non-HDL-C are independent positive predictors of NLR after elective PCI.

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

Cited by 71 publications

References 202 publications

Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis

Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis

Do antiepileptic drugs cause premature atherosclerosis by disturbing lipid metabolism?

Variability In Non-HDL-C and Lp(a) Affect The Neutrophil To Lymphocyte Ratio In Patients Undergoing Elective Percutaneous Coronary Intervention

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