Early atherosclerosis and Chlamydia pneumoniae infection in the coronary arteries

Hortoványi, Eszter; Illyés, G.; Kádár, Anna

doi:10.1007/bf03033713

Cited by 4 publications

(4 citation statements)

References 14 publications

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“…The present study showed that the medial layer became thicker with intimal layer thickening in coronary arteries with only a mild increase in intimal area, in agreement with a previous histological study using human coronary arteries with early atherosclerosis (7). Medial hypertrophy in early atherosclerosis is attributable to hypertrophy or proliferation of medial smooth muscle cells and increased amount of extracellular matrix that were induced by growth factors and/or cytokines (3).…”

Section: Discussionsupporting

confidence: 92%

Relationship of a thinned medial layer to the attenuated contractile response in atherosclerotic coronary arteries

Nakamura

Horikoshi

Kugiyama

2020

American Journal of Physiology-Heart and Circulatory Physiology

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Coronary arteries with advanced atherosclerosis do not necessarily have greater contractile responses than those with early atherosclerosis. This study aimed to clarify the relationship between thickness of the medial layer and the contractile response to acetylcholine (ACh) in coronary artery using optical coherence tomography (OCT). The OCT and the vasomotor response to ACh in the left anterior descending coronary artery were assessed in 32 patients with previous myocardial infarction. The intimal and medial layer areas were measured by planimetric analysis of the OCT images. The coronary contractile response to ACh had a positive linear relationship with medial area ( r = 0.61, P < 0.001). In contrast, the relationship between the coronary contractile response to ACh and intimal area was described by an inverted U-shaped curve that was fitted to a quadratic regression model ( R2 = 0.35, P = 0.002, y-axis, contraction; x-axis, intimal area). The contractile response increased as the intimal layer thickened up to the inflection point; thereafter, the contractile response declined. The relationship between medial area and intimal area was also described by an inverted U-shaped curve that was fitted to a quadratic regression model ( R2 = 0.41, P < 0.01, y-axis, medial area; x-axis, intimal area). The medial area increased as the intimal area thickened up to the inflection point; thereafter, the medial area thinned. In conclusion, the thinned medial layer was associated with the attenuated contractile response in a coronary artery with greater atherosclerosis. NEW & NOTEWORTHY This is the first clinical study to show the relationship between the contractile response and the thickness of medial smooth muscle layer in coronary artery of patients with previous myocardial infarction using OCT. The contractile response to acetylcholine was attenuated, and medial layer area was thinned in coronary artery with greater atherosclerosis compared with those in coronary artery with mild or moderate atherosclerosis. The coronary contractile response was positively correlated with thickness of the medial layer in coronary arteries with either mild or greater atherosclerosis. Thus, coronary arteries with advanced atherosclerosis do not necessarily have greater contractile responses than those with early atherosclerosis, which could be related to the thinned medial layer.

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Section: Discussionsupporting

confidence: 92%

Relationship of a thinned medial layer to the attenuated contractile response in atherosclerotic coronary arteries

Nakamura

Horikoshi

Kugiyama

2020

American Journal of Physiology-Heart and Circulatory Physiology

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“…As for the association between C. pneumoniae and the extent of coronary atherosclerosis, several studies have demonstrated a significant association between C. pneumoniae and the severity of coronary atherosclerosis, while others have failed to demonstrate such an association (10,(20)(21). Additionally, our study established a statistically significant correlation between advanced atherosclerotic coronary arteries and the presence of C. pneumoniae DNA.…”

Section: Discussionsupporting

confidence: 68%

Detection of Chlamydia Pneumoniae in Atherosclerotic Coronary Arteries

Sessa

Pietro²,

Schiavoni³

et al. 2004

Int J Immunopathol Pharmacol

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Chlamydia pneumoniae has recently been associated with the development of coronary heart diseases by sero-epidemiological studies and by direct detection of the organism in atherosclerotic tissues. The aim of our study was to employ a semi-nested PCR approach to investigate the presence of C. pneumoniae in both normal and atherosclerotic coronary arteries of humans obtained at autopsy. Moreover, we have evaluated the role of infection with C. pneumoniae in relation to the extent of coronary atherosclerosis. One hundred and eighty coronary artery specimens were collected at autopsy from 60 consecutive subjects (three arterial segments from each subject). Atherosclerosis in each arterial segment was graded histologically by the Stary classification. Thirty normal coronary arteries were also taken at autopsy as control. PCR results evidenced the presence of C. pneumoniae DNA in atherosclerotic coronary arteries in 19 (31.7 %) of 60 subjects examined, while none of the 30 subjects with non-atherosclerotic tissues was positive (p=O.OOI). Moreover, of the 180 atherosclerotic specimens examined, C. pneumoniae DNA was detected in 3.4 % (2/59) of mild atherosclerotic lesions, and in 14.0% (17/121) of advanced atherosclerotic lesions (p=0.05). Our results demonstrate that the presence of C. pneumoniae DNA may be associated with the severity of coronary atherosclerosis.

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“…Clinical results have demonstrated that there is detectable C. pneumoniae in hypertropic human coronaries using immunohistochemistry, which may affect the lesion progression [16]. The seropositivity of C. pneumoniae was associated with a higher plasma level of ICAM-1 and VCAM-1 [11].…”

Section: Discussionmentioning

confidence: 99%

GroEL1, from Chlamydia pneumoniae, Induces Vascular Adhesion Molecule 1 Expression by p37AUF1 in Endothelial Cells and Hypercholesterolemic Rabbit

et al. 2012

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The expression of vascular adhesion molecule-1 (VCAM-1) by endothelial cells may play a major role in atherogenesis. The actual mechanisms of chlamydia pneumoniae (C. pneumoniae) relate to atherogenesis are unclear. We investigate the influence of VCAM-1 expression in the GroEL1 from C. pneumoniae-administered human coronary artery endothelial cells (HCAECs) and hypercholesterolemic rabbits. In this study, we constructed the recombinant GroEL1 from C. pneumoniae. The HCAECs/THP-1 adhesion assay, tube formation assay, western blotting, enzyme-linked immunosorbent assay, actinomycin D chase experiment, luciferase reporter assay, and immunohistochemical stainings were performed. The results show that GroEL1 increased both VCAM-1expression and THP-1 cell adhesives, and impaired tube-formation capacity in the HCAECs. GroEL1 significantly increased the VCAM-1 mRNA stability and cytosolic AU-binding factor 1 (AUF1) level. Overexpression of the p37AUF1 significantly increased VCAM-1 gene expression in GroEL1-induced bovine aortic endothelial cells (BAECs). GroEL1 prolonged the stability of VCAM-1 mRNA by increasing both p37AUF1 and the regulation of the 5′ untranslated region (UTR) of the VCAM-1 mRNA in BAECs. In hypercholesterolemic rabbits, GroEL1 administration enhanced fatty-streak and macrophage infiltration in atherosclerotic lesions, which may be mediated by elevated VCAM-1 expression. In conclusion, GroEL1 induces VCAM-1 expression by p37AUF1 in endothelial cells and enhances atherogenesis in hypercholesterolemic rabbits.

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Early atherosclerosis and Chlamydia pneumoniae infection in the coronary arteries

Cited by 4 publications

References 14 publications

Relationship of a thinned medial layer to the attenuated contractile response in atherosclerotic coronary arteries

Relationship of a thinned medial layer to the attenuated contractile response in atherosclerotic coronary arteries

Detection of Chlamydia Pneumoniae in Atherosclerotic Coronary Arteries

GroEL1, from Chlamydia pneumoniae, Induces Vascular Adhesion Molecule 1 Expression by p37AUF1 in Endothelial Cells and Hypercholesterolemic Rabbit

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