Protective effects of simvastatin on coronary artery function in swine with acute infection

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Protective effects of simvastatin on coronary artery function in swine with acute infection. / Liuba, Petru; Pesonen, Erkki; Forslid, Anders; Paakkari, Ilari; Hansen, Axel Kornerup; Kovanen, Petri; Pentikainen, Markku; Persson, Kenneth; Østergård, Grete.

In: Atherosclerosis, Vol. 186, No. 2, 2006, p. 331-336.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Liuba, P, Pesonen, E, Forslid, A, Paakkari, I, Hansen, AK, Kovanen, P, Pentikainen, M, Persson, K & Østergård, G 2006, 'Protective effects of simvastatin on coronary artery function in swine with acute infection', Atherosclerosis, vol. 186, no. 2, pp. 331-336. https://doi.org/10.1016/j.atherosclerosis.2005.08.017

APA

Liuba, P., Pesonen, E., Forslid, A., Paakkari, I., Hansen, A. K., Kovanen, P., ... Østergård, G. (2006). Protective effects of simvastatin on coronary artery function in swine with acute infection. Atherosclerosis, 186(2), 331-336. https://doi.org/10.1016/j.atherosclerosis.2005.08.017

Vancouver

Liuba P, Pesonen E, Forslid A, Paakkari I, Hansen AK, Kovanen P et al. Protective effects of simvastatin on coronary artery function in swine with acute infection. Atherosclerosis. 2006;186(2):331-336. https://doi.org/10.1016/j.atherosclerosis.2005.08.017

Author

Liuba, Petru ; Pesonen, Erkki ; Forslid, Anders ; Paakkari, Ilari ; Hansen, Axel Kornerup ; Kovanen, Petri ; Pentikainen, Markku ; Persson, Kenneth ; Østergård, Grete. / Protective effects of simvastatin on coronary artery function in swine with acute infection. In: Atherosclerosis. 2006 ; Vol. 186, No. 2. pp. 331-336.

Bibtex

@article{01530140a1c111ddb6ae000ea68e967b,
title = "Protective effects of simvastatin on coronary artery function in swine with acute infection",
abstract = "BACKGROUND:: The risk for coronary events may rise during acute infection. Perturbation in coronary endothelial function emerges as one important link. We investigated whether simvastatin could protect the coronary arterial function from the adverse effects of acute infection in swine. METHODS:: Coronary endothelium-dependent and -independent vasomotor responses were assessed by Doppler velocimetry in 12 Chlamydia pneumoniae-infected and 6 sham-infected swine 2 weeks after intratracheal inoculation. Half of animals from the infection group were pre-treated with simvastatin (80mg daily), while the remaining animals received placebo. The treatment was started 2 weeks prior to inoculation and continued until the end of the study. ANOVA was used for statistical calculations. Data are mean+/-S.D. RESULTS:: All animals inoculated with C. pneumoniae developed IgM antibodies against this organism. As compared to noninfected animals, peak-to-baseline coronary flow velocity (CFV) ratio after bradykinin was significantly decreased in infected animals regardless of statin treatment (p=0.01). Intracoronary 10(-6)M acetylcholine caused slight dilatory responses in both noninfected and infected-treated animals (CFV ratio: 1.6+/-0.2 and 1.4+/-0.2, respectively; p>0.1), while a velocity drop (CFV ratio: 0.7+/-0.1; p<0.01versus noninfected-infected and treated), indicating constriction, was observed in infected-nontreated animals; 10(-5)M acetylcholine caused vasoconstriction in all animals, with a significantly more prolonged response in the infected-nontreated group (p<0.01). Intracoronary adenosine and SNP induced similar dilatory responses in all groups (p>0.5). There were no differences in markers of systemic inflammation (fibrinogen, amyloid, and CRP) and lipid profile (HDL, LDL and total cholesterol) between the groups (p>0.2). CONCLUSION:: Acute infection is associated with impairment of the muscarinic and kinin-related reactivity of coronary circulation. These functional abnormalities are in part prevented by simvastatin through mechanisms unrelated to lipid lowering",
keywords = "LIFE, Chlamydia pneumoniae, endothelial dysfunction, atherosclerosis, inflammation, hypercholesterolaemia, vasoconstriction",
author = "Petru Liuba and Erkki Pesonen and Anders Forslid and Ilari Paakkari and Hansen, {Axel Kornerup} and Petri Kovanen and Markku Pentikainen and Kenneth Persson and Grete {\O}sterg{\aa}rd",
year = "2006",
doi = "10.1016/j.atherosclerosis.2005.08.017",
language = "English",
volume = "186",
pages = "331--336",
journal = "Atherosclerosis",
issn = "0021-9150",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

RIS

TY - JOUR

T1 - Protective effects of simvastatin on coronary artery function in swine with acute infection

AU - Liuba, Petru

AU - Pesonen, Erkki

AU - Forslid, Anders

AU - Paakkari, Ilari

AU - Hansen, Axel Kornerup

AU - Kovanen, Petri

AU - Pentikainen, Markku

AU - Persson, Kenneth

AU - Østergård, Grete

PY - 2006

Y1 - 2006

N2 - BACKGROUND:: The risk for coronary events may rise during acute infection. Perturbation in coronary endothelial function emerges as one important link. We investigated whether simvastatin could protect the coronary arterial function from the adverse effects of acute infection in swine. METHODS:: Coronary endothelium-dependent and -independent vasomotor responses were assessed by Doppler velocimetry in 12 Chlamydia pneumoniae-infected and 6 sham-infected swine 2 weeks after intratracheal inoculation. Half of animals from the infection group were pre-treated with simvastatin (80mg daily), while the remaining animals received placebo. The treatment was started 2 weeks prior to inoculation and continued until the end of the study. ANOVA was used for statistical calculations. Data are mean+/-S.D. RESULTS:: All animals inoculated with C. pneumoniae developed IgM antibodies against this organism. As compared to noninfected animals, peak-to-baseline coronary flow velocity (CFV) ratio after bradykinin was significantly decreased in infected animals regardless of statin treatment (p=0.01). Intracoronary 10(-6)M acetylcholine caused slight dilatory responses in both noninfected and infected-treated animals (CFV ratio: 1.6+/-0.2 and 1.4+/-0.2, respectively; p>0.1), while a velocity drop (CFV ratio: 0.7+/-0.1; p<0.01versus noninfected-infected and treated), indicating constriction, was observed in infected-nontreated animals; 10(-5)M acetylcholine caused vasoconstriction in all animals, with a significantly more prolonged response in the infected-nontreated group (p<0.01). Intracoronary adenosine and SNP induced similar dilatory responses in all groups (p>0.5). There were no differences in markers of systemic inflammation (fibrinogen, amyloid, and CRP) and lipid profile (HDL, LDL and total cholesterol) between the groups (p>0.2). CONCLUSION:: Acute infection is associated with impairment of the muscarinic and kinin-related reactivity of coronary circulation. These functional abnormalities are in part prevented by simvastatin through mechanisms unrelated to lipid lowering

AB - BACKGROUND:: The risk for coronary events may rise during acute infection. Perturbation in coronary endothelial function emerges as one important link. We investigated whether simvastatin could protect the coronary arterial function from the adverse effects of acute infection in swine. METHODS:: Coronary endothelium-dependent and -independent vasomotor responses were assessed by Doppler velocimetry in 12 Chlamydia pneumoniae-infected and 6 sham-infected swine 2 weeks after intratracheal inoculation. Half of animals from the infection group were pre-treated with simvastatin (80mg daily), while the remaining animals received placebo. The treatment was started 2 weeks prior to inoculation and continued until the end of the study. ANOVA was used for statistical calculations. Data are mean+/-S.D. RESULTS:: All animals inoculated with C. pneumoniae developed IgM antibodies against this organism. As compared to noninfected animals, peak-to-baseline coronary flow velocity (CFV) ratio after bradykinin was significantly decreased in infected animals regardless of statin treatment (p=0.01). Intracoronary 10(-6)M acetylcholine caused slight dilatory responses in both noninfected and infected-treated animals (CFV ratio: 1.6+/-0.2 and 1.4+/-0.2, respectively; p>0.1), while a velocity drop (CFV ratio: 0.7+/-0.1; p<0.01versus noninfected-infected and treated), indicating constriction, was observed in infected-nontreated animals; 10(-5)M acetylcholine caused vasoconstriction in all animals, with a significantly more prolonged response in the infected-nontreated group (p<0.01). Intracoronary adenosine and SNP induced similar dilatory responses in all groups (p>0.5). There were no differences in markers of systemic inflammation (fibrinogen, amyloid, and CRP) and lipid profile (HDL, LDL and total cholesterol) between the groups (p>0.2). CONCLUSION:: Acute infection is associated with impairment of the muscarinic and kinin-related reactivity of coronary circulation. These functional abnormalities are in part prevented by simvastatin through mechanisms unrelated to lipid lowering

KW - LIFE

KW - Chlamydia pneumoniae

KW - endothelial dysfunction

KW - atherosclerosis

KW - inflammation

KW - hypercholesterolaemia

KW - vasoconstriction

U2 - 10.1016/j.atherosclerosis.2005.08.017

DO - 10.1016/j.atherosclerosis.2005.08.017

M3 - Journal article

VL - 186

SP - 331

EP - 336

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

IS - 2

ER -

ID: 8030283