Identified by Berg in 1963, lipoprotein(a) represents a key contemporary residual risk pathway in atherosclerotic cardiovascular disease (ASCVD) secondary prevention. Indeed, epidemiological and genetic studies have undoubtedly demonstrated that lipoprotein(a) is one of the strongest causal risk factors of ASCVD. Although a risk threshold has been set between 30 and 50 mg/dL, depending on the ethnicity, a linear risk gradient across the distribution has been demonstrated. In the context of the atherosclerotic process, hyperlipoproteinaemia(a) contributes to the atherosclerotic plaque formation by deposition of cholesterol in the same manner as low-density lipoprotein (LDL) cholesterol, due to the LDL particle component of lipoprotein(a). Lipoprotein(a) accumulates in human coronary and carotid atherosclerotic lesions. High concentrations of lipoprotein(a) are associated with accelerated progression of the necrotic core, but not with coronary calcium score (CAC), although in the latter case, the evaluation of lipoprotein(a) can overcome the potential limitation of CAC to capture the totality of ASCVD risk in asymptomatic individuals. Finally, in the absence of a pharmacological approach to lower lipoprotein(a) to the extent required to achieve a cardiovascular benefit, implementation strategies that increase awareness among the population, patients, and healthcare providers on the importance of lipoprotein(a) in the development of ASCVD are eagerly needed.
Role of lipoprotein(a) in plaque progressionIn: EUROPEAN HEART JOURNAL SUPPLEMENTS. - ISSN 1520-765X. - 24:suppl. 1(2022), pp. I72-I75. [10.1093/eurheartjsupp/suac071]
Role of lipoprotein(a) in plaque progression
M. RuscicaPrimo
Writing – Review & Editing
;A.S. RizzutoSecondo
Methodology
;A. CorsiniUltimo
Writing – Review & Editing
2022
Abstract
Identified by Berg in 1963, lipoprotein(a) represents a key contemporary residual risk pathway in atherosclerotic cardiovascular disease (ASCVD) secondary prevention. Indeed, epidemiological and genetic studies have undoubtedly demonstrated that lipoprotein(a) is one of the strongest causal risk factors of ASCVD. Although a risk threshold has been set between 30 and 50 mg/dL, depending on the ethnicity, a linear risk gradient across the distribution has been demonstrated. In the context of the atherosclerotic process, hyperlipoproteinaemia(a) contributes to the atherosclerotic plaque formation by deposition of cholesterol in the same manner as low-density lipoprotein (LDL) cholesterol, due to the LDL particle component of lipoprotein(a). Lipoprotein(a) accumulates in human coronary and carotid atherosclerotic lesions. High concentrations of lipoprotein(a) are associated with accelerated progression of the necrotic core, but not with coronary calcium score (CAC), although in the latter case, the evaluation of lipoprotein(a) can overcome the potential limitation of CAC to capture the totality of ASCVD risk in asymptomatic individuals. Finally, in the absence of a pharmacological approach to lower lipoprotein(a) to the extent required to achieve a cardiovascular benefit, implementation strategies that increase awareness among the population, patients, and healthcare providers on the importance of lipoprotein(a) in the development of ASCVD are eagerly needed.File | Dimensione | Formato | |
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