OBJECTIVES: To determine whether a long-term treatment with beta-blockers influences the inflammatory activity in carotid artery disease by reducing the carotid plaque levels of lipoprotein-associated phospholipase A2 (Lp-PLA2), its enzymatic products lysophosphatidylcholine (lysoPCs), and of soluble urokinase plasminogen activator receptor (suPAR). MATERIALS AND METHODS: One hundred and thirty-four patients with significant symptomatic or asymptomatic carotid stenosis undergoing surgery were prospectively included and divided into two groups (Group A or B) based on the absence or presence of an on-going long-term oral treatment with beta-blockers. The harvested carotid plaques were analyzed for the levels of lysoPCs using mass spectrometry and Lp-PLA2 and suPAR by Enzyme-linked immunosorbent assay (ELISA). RESULTS: Plaques of patients on long-term treatment with beta-blockers revealed lower levels of Lp-PLA2 (Group A 0.752 ± 0.393 ug/g vs. Group B 0.644 ± 0.445 ug/g, P=.049) as well as suPAR (Group A 0.044 ± 0.024 μg/g vs. Group B 0.036 ± 0.025 μg/g, P=.028). Levels of Lp-PLA2 and suPAR were positively correlated (r=.637, P<.0001). Lp-PLA2 and suPAR levels were also correlated (P<.0001) with the three lysoPC species tested (lysoPC 16:0, lysoPC 18:0. lysoPC 18:1). All the above-mentioned findings were confirmed after correction for age, gender, hypertension, coronary artery disease, and statin usage. CONCLUSIONS: The reduced levels of Lp-PLA2 and suPAR in human carotid plaques of subjects on long-term treatment with beta-blockers suggest their possible protective role in plaque inflammation. Our findings support an even more selective Lp-PLA2 and suPAR inhibition as a possible strategy for the prevention of cardiovascular disease.
OBJECTIVES: To determine whether a long-term treatment with beta-blockers influences the inflammatory activity in carotid artery disease by reducing the carotid plaque levels of lipoprotein-associated phospholipase A2 (Lp-PLA2), its enzymatic products lysophosphatidylcholine (lysoPCs), and of soluble urokinase plasminogen activator receptor (suPAR). MATERIALS AND METHODS: One hundred and thirty-four patients with significant symptomatic or asymptomatic carotid stenosis undergoing surgery were prospectively included and divided into two groups (Group A or B) based on the absence or presence of an on-going long-term oral treatment with beta-blockers. The harvested carotid plaques were analyzed for the levels of lysoPCs using mass spectrometry and Lp-PLA2 and suPAR by Enzyme-linked immunosorbent assay (ELISA). RESULTS: Plaques of patients on long-term treatment with beta-blockers revealed lower levels of Lp-PLA2 (Group A 0.752 ± 0.393 ug/g vs. Group B 0.644 ± 0.445 ug/g, P=.049) as well as suPAR (Group A 0.044 ± 0.024 μg/g vs. Group B 0.036 ± 0.025 μg/g, P=.028). Levels of Lp-PLA2 and suPAR were positively correlated (r=.637, P<.0001). Lp-PLA2 and suPAR levels were also correlated (P<.0001) with the three lysoPC species tested (lysoPC 16:0, lysoPC 18:0. lysoPC 18:1). All the above-mentioned findings were confirmed after correction for age, gender, hypertension, coronary artery disease, and statin usage. CONCLUSIONS: The reduced levels of Lp-PLA2 and suPAR in human carotid plaques of subjects on long-term treatment with beta-blockers suggest their possible protective role in plaque inflammation. Our findings support an even more selective Lp-PLA2 and suPAR inhibition as a possible strategy for the prevention of cardiovascular disease.
Authors: Danny J Eapen; Pankaj Manocha; Nima Ghasemzadeh; Riyaz S Patel; Hatem Al Kassem; Muhammad Hammadah; Emir Veledar; Ngoc-Anh Le; Tomasz Pielak; Christian W Thorball; Aristea Velegraki; Dimitrios T Kremastinos; Stamatios Lerakis; Laurence Sperling; Arshed A Quyyumi Journal: J Am Heart Assoc Date: 2014-10-23 Impact factor: 5.501
Authors: Iziah E Sama; Rebecca J Woolley; Jan F Nauta; Simon P R Romaine; Jasper Tromp; Jozine M Ter Maaten; Peter van der Meer; Carolyn S P Lam; Nilesh J Samani; Leong L Ng; Marco Metra; Kenneth Dickstein; Stefan D Anker; Faiez Zannad; Chim C Lang; John G F Cleland; Dirk J van Veldhuisen; Hans L Hillege; Adriaan A Voors Journal: Eur J Heart Fail Date: 2020-04-03 Impact factor: 15.534