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Lipoprotein(a) and Risk of Myocardial Infarction and Coronary Artery Diseases
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Lipoprotein(a) and Risk of Myocardial Infarction and Coronary Artery Diseases
Lipoprotein(a) and Risk of Myocardial Infarction and Coronary Artery Diseases
Journal Article

Lipoprotein(a) and Risk of Myocardial Infarction and Coronary Artery Diseases

2024
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Overview
Higher levels of lipoprotein(a) {Lp(a)} are genetically regulated, which is a causal risk factor for cardiovascular disease (CVD) [1-3]. The variability in Lp(a) levels between subjects and population groups is difficult to fully explain by genetic factors, which indicates that 1t might be due to other environmental factors such as diet and nutrients and physical activity [1]. Randomized controlled clinical trials have demonstrated that diets lower in saturated fats may influence Lp(a) concentrations, which is usually in higher direction to the concentrations of low density lipoprotein (LDL) cholesterol [1, 4]. Interestingly, physical activity or exercise has not been found to have consistent effects, because it ranged from no to minimal or moderate effects upon Lp(a) levels, modulated by age and the type, duration and intensity of exercise modality [1]. Replacement of hormones in postmenopausal women lowers Lp(a) levels, which depends on the type of hormones, dose of estrogen and addition of progestogen. It seems that the current evidence supports a role for diet, hormones and related conditions, and liver and kidney diseases in modifying Lp(a) levels [1-5], although there are gaps in knowledge about the value of Lp(a) in AMI [6-12].

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