TY - JOUR
T1 - Relationship between Circulating PCSK9 and Markers of Subclinical Atherosclerosis-The IMPROVE Study
AU - IMPROVE Study Grp
AU - Coggi, Daniela
AU - Frigerio, Beatrice
AU - Bonomi, Alice
AU - Ruscica, Massimiliano
AU - Ferri, Nicola
AU - Sansaro, Daniela
AU - Ravani, Alessio
AU - Ferrante, Palma
AU - Damigella, Manuela
AU - Veglia, Fabrizio
AU - Capra, Nicolo
AU - Lupo, Maria Giovanna
AU - Macchi, Chiara
AU - Savonen, Kai
AU - Silveira, Angela
AU - Kurl, Sudhir
AU - Giral, Philippe
AU - Pirro, Matteo
AU - Strawbridge, Rona Juliette
AU - Gigante, Bruna
AU - Smit, Andries Jan
AU - Tremoli, Elena
AU - Amato, Mauro
AU - Baldassarre, Damiano
PY - 2021/7/19
Y1 - 2021/7/19
N2 - (1) Background and purpose: circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) is one of the key regulators of cholesterol metabolism. Despite this, its role as a player in atherosclerosis development is still matter of debate. Here, we investigated the relationships between this protein and several markers of subclinical atherosclerosis. (2) Methods: the IMPROVE study enrolled 3703 European subjects (54-79 years; 48% men; with >= 3 vascular risk factors), asymptomatic for cardiovascular diseases. PCSK9 levels were measured by ELISA. B-mode ultrasound was used to measure markers of carotid subclinical atherosclerosis. (3) Results: in the crude analysis, PCSK9 levels were associated with several baseline measures of carotid intima-media thickness (cIMT) (all p < 0.0001); with cIMT change over time (Fastest-IMTmax-progr) (p = 0.01); with inter-adventitia common carotid artery diameter (ICCAD) (p < 0.0001); and with the echolucency (Grey Scale Median; GSM) of both carotid plaque and plaque-free common carotid IMT (both p < 0.0001). However, after adjustment for age, sex, latitude, and pharmacological treatment, all the afore-mentioned correlations were no longer statistically significant. The lack of correlation was also observed after stratification for sex, latitude, and pharmacological treatments. (4) Conclusions: in subjects who are asymptomatic for cardiovascular diseases, PCSK9 plasma levels do not correlate with vascular damage and/or subclinical atherosclerosis of extracranial carotid arteries.
AB - (1) Background and purpose: circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) is one of the key regulators of cholesterol metabolism. Despite this, its role as a player in atherosclerosis development is still matter of debate. Here, we investigated the relationships between this protein and several markers of subclinical atherosclerosis. (2) Methods: the IMPROVE study enrolled 3703 European subjects (54-79 years; 48% men; with >= 3 vascular risk factors), asymptomatic for cardiovascular diseases. PCSK9 levels were measured by ELISA. B-mode ultrasound was used to measure markers of carotid subclinical atherosclerosis. (3) Results: in the crude analysis, PCSK9 levels were associated with several baseline measures of carotid intima-media thickness (cIMT) (all p < 0.0001); with cIMT change over time (Fastest-IMTmax-progr) (p = 0.01); with inter-adventitia common carotid artery diameter (ICCAD) (p < 0.0001); and with the echolucency (Grey Scale Median; GSM) of both carotid plaque and plaque-free common carotid IMT (both p < 0.0001). However, after adjustment for age, sex, latitude, and pharmacological treatment, all the afore-mentioned correlations were no longer statistically significant. The lack of correlation was also observed after stratification for sex, latitude, and pharmacological treatments. (4) Conclusions: in subjects who are asymptomatic for cardiovascular diseases, PCSK9 plasma levels do not correlate with vascular damage and/or subclinical atherosclerosis of extracranial carotid arteries.
KW - PCSK9
KW - subclinical atherosclerosis
KW - carotid artery
KW - intima-media thickness
KW - echolucency
KW - SUBTILISIN/KEXIN TYPE 9
KW - INTIMA-MEDIA THICKNESS
KW - CAROTID-ARTERY
KW - EUROPEAN POPULATION
KW - CARDIOVASCULAR RISK
KW - VASCULAR EVENTS
KW - ASSOCIATION
KW - PLAQUES
KW - PLASMA
KW - PREDICTORS
U2 - 10.3390/biomedicines9070841
DO - 10.3390/biomedicines9070841
M3 - Article
SN - 2227-9059
VL - 9
JO - Biomedicines
JF - Biomedicines
IS - 7
M1 - 841
ER -