Christos Papamichael

National and Kapodistrian University of Athens, Athínai, Attica, Greece

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Publications (163)701.79 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: TNF-like cytokine 1A (TL1A)-mediated interactions are involved in atheromatic plaque formation. In stable coronary artery disease (CAD) we examined whether circulating TL1A levels correlate with coronary and/or peripheral atherosclerosis extent and predict future cardiovascular events. In this cross-sectional study, peripheral vascular studies and TL1A serum measurements were performed in 122 consecutive patients with angiographically confirmed CAD who were followed for a median of 41.9months. TL1A levels were compared against controls (n=63) and 20 patients with acute coronary syndrome (ACS). TL1A was higher in ACS than the 2 other groups (p<0.001). In stable CAD, after adjustment for traditional risk factors independent positive correlations between TL1A serum levels and reflected waves (p=0.049), and carotid atheromatic plaque score (p=0.049) were evident. In stable patients with a history of ACS, TL1A levels correlated with worse endothelial function (p=0.006), extent of CAD assessed by Gensini score (p=0.042), and cardiac mortality (p=0.051). This pilot study suggests that serum TL1A measurements are of clinical value in CAD. Studies on the pathogenetic role of TL1A in atherosclerosis and its sequelae are warranted. Copyright © 2014 Elsevier Ltd. All rights reserved.
    Cytokine 01/2015; 72(1). DOI:10.1016/j.cyto.2014.12.016 · 2.87 Impact Factor
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    ABSTRACT: The aim of this study was to evaluate the effect of hormone therapy (HT) in the endothelial function of 46,XY disorders of sexual development (DSD) patients with female phenotype. Biochemical and ultrasound measurements were performed in 20 patients at initiation of oral 2 mg 17β-estradiol/1 mg norethisterone acetate, and after 6 months of therapy. Lipid profile, including total cholesterol (TC), LDL, HDL, triglycerides (TG) and Atherogenic Index of Plasma (AIP), as well as levels of VE-Cadherin, E-Selectin, Thrombomodulin and vWf were determined. Ultrasonographic examinations included evaluation of flow-mediated dilatation (FMD) and measurement of Carotid and Femoral Intima Media Thickness (IMT). HT raised HDL (35.4 mg/dl versus 40.1 mg/dl, p = 0.019) while lowering TG (166 mg/dl versus 109 mg/dl, p = 0.026) and AIP (0.24 versus 0.04, p = 0.007). No changes were noted in TC and LDL (215.7 mg/dl versus 192.25 mg/dl and 87.46 mg/dl versus 76.35 mg/dl, respectively). There was significant reduction of VE-Cadherin (4.05 ng/ml versus 2.20 ng/ml, p = 0.002) and E-selectin (73.98 ng/ml versus 56.73 ng/ml, p = 0.004). No change was observed in Thrombomodulin and vWf (11.76 ng/ml versus 13.90 ng/ml and 80.75% versus 79.55%, respectively). FMD improved significantly (5.4% versus 8.15%, p = 0.003), while only carotid bulb IMT decreased significantly (0.65 mm versus 0.60 mm, p = 0.018). Overall, HT was found to improve biochemical and ultrasound markers of endothelial function in 46,XY DSD patients with female phenotype.
    Gynecological Endocrinology 06/2014; DOI:10.3109/09513590.2014.925868 · 1.14 Impact Factor
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    ABSTRACT: Context. Recent evidence suggests that primary hyperparathyroidism (pHPT) is linked with hypertension and subclinical atherosclerosis. These associations have not been examined in postmenopausal women, in whom cardiovascular risk steeply rises after menopausal transition. Objective. To assess whether pHPT is associated with hemodynamic markers and subclinical atherosclerosis in postmenopausal women under a cross-sectional case-control design. Methods. One hundred and two postmenopausal women with pHPT and 102 women matched 1:1 for age and menopausal status, were consecutively recruited. In all patients, flow-mediated dilatation, carotid-femoral pulse wave velocity, reflected waves, aortic blood pressures (BP), intima-media thickness and the presence of plaques in the carotid and common femoral arteries were measured. Results. Women with pHPT had higher aortic and peripheral BP (p<0.05 for all) but no correlation was observed with subclinical atherosclerosis. After adjusting for possible confounders, pHPT was an independent determinant of peripheral and aortic diastolic BP (p<0.05 for all). The association with systolic BP was lost after adjusting for CRP. Further adjustment for PTH and D3 levels, revealed that PTH but not D3 was an independent determinant of all BP parameters. Both peripheral and aortic BP increased across PTH tertiles as compared to the control group but this association lost significance after adjustment for CRP. Conclusions. These results suggest that pHPT may increase peripheral and aortic BP through PTH and inflammatory-mediated mechanisms. A direct impact of the disease on the arterial wall cannot be implicated despite the large number of markers of subclinical atherosclerosis measured in this study.
    Journal of Clinical Endocrinology &amp Metabolism 05/2014; 99(8):jc20134273. DOI:10.1210/jc.2013-4273 · 6.31 Impact Factor
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    ABSTRACT: Meal patterns and their relationship with cardiovascular disease are insufficiently examined with important clinical implications. Our aim was to investigate associations between eating frequency (EF) and early markers of atherosclerosis.
    Clinical nutrition (Edinburgh, Scotland) 05/2014; 34(2). DOI:10.1016/j.clnu.2014.04.022 · 3.94 Impact Factor
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    ABSTRACT: Context: Although adrenal incidentalomas (AI) are associated with high prevalence of cardiovascular risk (CVR) factors, it is not clear if patients with non-functioning AI (NFAI) have increased CVR. Objective: To investigate CVR in patients with NFAI. Design: Case-control study. Setting: The study was performed in a tertiary general hospital. Patients: Sixty normotensive, euglycemic patients with AI and 32 healthy controls (C) with normal adrenal imaging. Main Outcome Measures: All participants underwent adrenal imaging, biochemical and hormonal evaluation and the following investigations: (i) Measurement of Carotid intima-media thickness (IMT) and Flow-mediated dilatation (FMD) (ii) 2-h 75g oral glucose tolerance test and calculation of insulin resistance indices (HOMA,QUICKI,MATSUDA) (iii) Intravenous ACTH stimulation test (iv) Low-dose dexamethasone suppression test (LDDST) (v) NaCl (0.9%) post-dexamethasone saline infusion test. Results: Based on cut-offs obtained from controls autonomous cortisol secretion was documented in 26 patients (group CSAI) whereas 34 exhibited adequate cortisol and aldosterone suppression (group NFAI). IMT measurements were higher and FMD lower in CSAI-group compared to both NFAI and C, and in NFAI-group compared to C. HOMA index was higher and QUICKI and Matsuda indices were lower in CSAI- and NFAI-groups compared to C as well as in CSAI- compared to NFAI-group. The area under the curve for cortisol after ACTH stimulation (AUC-C) was higher in CSAI-group compared to NFAI-group and C, and in NFAI-group compared to C. In CSAI-group, IMT correlated with cortisol, UFC and cortisol after LDDST, whereas in NFAI-group IMT correlated with AUC-C and UFC. Conclusions: Patients with CSAI without hypertension, diabetes and/or dyslipidemia exhibit adverse metabolic and CVR factors. In addition, apparently NFAIs are associated with increased insulin resistance and endothelial dysfunction that correlate with subtle but not autonomous cortisol excess.
    The Journal of Clinical Endocrinology and Metabolism 04/2014; 99(8):jc20134064. DOI:10.1210/jc.2013-4064 · 6.31 Impact Factor
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    ABSTRACT: Background and Aims Meal patterns and their relationship with cardiovascular disease are insufficiently examined with important clinical implications. Our aim was to investigate associations between eating frequency (EF) and early markers of atherosclerosis. Methods In this cross - sectional study, we consecutively recruited 164 healthy subjects (46.8±9.3years, 62 men). EF among other dietary parameters and markers of subclinical atherosclerosis, including flow mediated dilatation (FMD), pulse wave velocity (PWV), intima-media thickness (IMT) and the presence of plaques in the carotid arteries were evaluated in all volunteers. Results EF was positively associated with total energy intake (EI) and a favorable profile in terms of adiposity, glucose tolerance and blood lipids. Subjects with an increased EF (> median), had significantly lower IMT (p=0.024) and prevalence of plaques (5.3% vs. 21.3%, p=0.003), as compared to those below median. IMT and the prevalence of plaques were also significantly lower in those with increased EF compared with subjects with low EF belonging to the same group of energy intake (EI) by EI median. By multivariate regression analysis, carotid plaques remained significantly associated with EF (OR: 0.71, 95%CI 0.56 to 0.89), while IMT also remained significantly associated with EF after adjustment for age and dietary factors (beta:-0.010, 95%CI: -0.020 to -0.0002), but not after adding obesity-related risk factors. Conclusion Increased EF is associated with lower prevalence of subclinical atherosclerosis in the carotid arteries in apparently healthy individuals. Whether consumption of the same amount of energy in more eating episodes favorably affects cardiovascular risk should be further investigated.
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    ABSTRACT: The metabolic dysfunction accompanying the polycystic ovary syndrome (PCOS) may increase the risk of hypertension and cardiovascular disease (CVD). Although menopause per se may be an additional risk factor of CVD, the association between PCOS in postmenopausal women and cardiovascular risk has not been adequately investigated. We aimed to evaluate the effect of PCOS on markers of subclinical atherosclerosis in nondiabetic postmenopausal women. This cross-sectional study included 286 postmenopausal women with intact ovaries. PCOS phenotype was defined if three of the following were present: insulin resistance, current hyperandrogenism or history of clinical androgen excess, history of infertility, central obesity and history of irregular menses. Traditional CVD risk factors, as well as indices of arterial structure (intima-media thickness, atheromatous plaques presence) and function [flow-mediated dilation, pulse wave velocity (PWV), augmentation index] were compared between women with a PCOS phenotype and the rest of the sample, who served as controls. Women with the PCOS phenotype (N = 43) had higher SBP and triglycerides and lower high-density lipoprotein (HDL)-cholesterol than controls. Mean values of PWV differed significantly between PCOS cases and controls (9.46 ± 1.74 vs. 8.60 ± 1.51 m/s, P = 0.001, univariate). Multivariate regression analysis showed that the PCOS phenotype, age and SBP were the only independent predictors of PWV. Arterial stiffness is increased in asymptomatic, nondiabetic women with a putative PCOS phenotype, independently of age, BMI or blood pressure. This might present one mechanism through which PCOS increases the risk of CVD and hypertension later in life.
    Journal of Hypertension 10/2013; 31(10):1998-2004. DOI:10.1097/HJH.0b013e3283630362 · 4.22 Impact Factor
  • European Neuropsychopharmacology 10/2013; 23:S345-S346. DOI:10.1016/S0924-977X(13)70544-3 · 5.40 Impact Factor
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    ABSTRACT: Interactions between TNF-like Cytokine 1A (TL1A) and its receptors, death receptor-3 (DR3) and decoy receptor-3 (DcR3) may be important in atherogenesis. We hypothesized that dysregulation of this system predicts formation of new atheromatic plaques in rheumatoid arthritis (RA). Forty-five patients were prospectively followed up for 40.5±3.6months. Serum concentrations of TL1A and DcR3 were measured at baseline and carotid and femoral arteries examined by ultrasound at baseline and at the end of follow-up. Individual serum levels of TL1A correlated with the progression of carotid atheromatic plaque height (Spearman rho=0.550, p=0.003). Patients with low TL1A and undetectable DcR3 serum levels at baseline showed significantly fewer newly formed carotid plaques during the next 3.5years than the remaining patients (P=0.016). Univariate analysis showed that a "low TL1A/DcR3" immunophenotype predicted a preserved atherosclerosis profile in carotid (P=0.026), or carotid and/or femoral arteries (P=0.022). Dysregulated TL1A-induced signaling may be associated with risk for accelerated atherosclerosis in RA.
    Clinical Immunology 03/2013; 147(2):144-150. DOI:10.1016/j.clim.2013.03.002 · 3.99 Impact Factor
  • 03/2013; DOI:10.1530/endoabs.32.P207
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    ABSTRACT: J Clin Hypertens (Greenwich). 2012; 14:630-636. © 2012 Wiley Periodicals, Inc. The possible effects of sesame oil on hemodynamics are unknown. The aim of the study was to investigate the acute and long-term effects of sesame oil on hemodynamic responses in hypertensive men. The authors enrolled 30 hypertensive men in a two-phase study. In the first phase, patients consumed 35 g of either sesame oil or control oil. Central and peripheral blood pressure, pulse wave velocity, augmentation index (AI), C-reactive protein, tumor necrosis factor α, malonydealdehyde, and total antioxidant capacity (TAC) were assessed at fast and 2 hours postprandially. In the second phase, patients consumed 35 g of either sesame oil or control oil daily for 2 months. The above-mentioned parameters were assessed before and following 15, 30, and 60 days of oil consumption. Sesame oil decreased central and peripheral diastolic pressures 1 hour postprandially (P=.006). Fifteen days of sesame oil intake decreased peripheral systolic blood pressure (P=.016) and heart rate-corrected AI75 (P=.017) and increased TAC (P=.007). This is the first study to demonstrate a favorable acute and long-term effect of sesame oil on hemodynamics in hypertensive men. Further research is warranted to establish the potential protective role of sesame oil.
    Journal of Clinical Hypertension 09/2012; 14(9):630-6. DOI:10.1111/j.1751-7176.2012.00649.x · 2.96 Impact Factor
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    ABSTRACT: We tested the hypotheses that monthly fluctuations in markers of arterial stiffness and blood pressure hemodynamics differ between women with and without premenstrual syndrome. We also assessed hypertension prevalence and arterial stiffening in postmenopausal women with or without history of premenstrual symptoms. Twenty one pre-menopausal women with premenstrual syndrome and 15 women without were prospectively examined in three distinct phases of their menstrual cycle (menses, late follicular and luteal phase). Pulse-wave velocity and analysis were used to assess arterial stiffness and wave reflection indices, respectively. Endothelial function was evaluated by flow-mediated vasodilation. In a cross-sectional substudy, 156 postmenopausal women were assessed for possible associations between retrospectively reported PMS symptoms and hypertension. In women with premenstrual syndrome, arterial stiffness significantly increased during the luteal and menses phase (late follicular: 6.48 ± 1.07, luteal: 7.1 ± 1.26, menstruation: 7.12 ± 1.19 m/s, p = 0.003), while blood pressure peaked at the menses phase. Significant interactions between PMS and changes in arterial stiffness and blood pressure but not endothelial function, were observed. Changes in PWV were significantly associated with concomitant changes in blood pressure, C-reactive protein and the severity of PMS symptoms. The prevalence of hypertension (20.9% vs. 40.9%, p = 0.041) and pulse-wave velocity values (8.64 ± 1.52 vs. 9.37 ± 1.1, p = 0.046) were higher in postmenopausal women with 7 or more reported PMS symptoms. Arterial stiffness differences remained significant after adjustment for confounding factors. These results imply that PMS may affect arterial stiffness and BP monthly variability. Whether PMS is associated with new onset hypertension later in life needs further evaluation.
    Atherosclerosis 07/2012; 224(1):170-6. DOI:10.1016/j.atherosclerosis.2012.05.037 · 3.97 Impact Factor
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    ABSTRACT: Rheumatoid arthritis (RA) is associated with increased cardiovascular morbidity and mortality attributed to both classical risk factors and chronic inflammation. We assessed longitudinally the factors associated with new carotid plaques in nondiabetic RA patients and apparently healthy individuals. In our present prospective observational study, carotid plaques were identified by ultrasonography at baseline and follow-up end, separated by an average of 3.6 ± 0.2 years, in 64 patients (mean age 59.2 ± 12.0 and disease duration at baseline 7.8 ± 6.2 years, 83% women, clinical and laboratory evaluation every 3 to 6 months). In a substudy, 35 of the patients were matched 1:1 for traditional cardiovascular risk factors with 'healthy' controls and were studied in parallel. New atherosclerotic plaques formed in 30% of patients (first plaque in 9%) who were significantly older than the remaining patients. Tobacco use, blood pressure, body mass index, average cumulative low-density lipoprotein, high-sensitivity C-reactive protein, erythrocyte sedimentation rate level, RA stage, functional class, disease duration and treatment modalities during follow-up did not differ significantly between subgroups after application of the Bonferroni correction. RA was in clinical remission, on average, for approximately 70% of the follow-up time and was not different between subgroups. Multivariate analysis including all the above parameters revealed that age (P = 0.006), smoking (P = 0.009) and duration of low-dose corticosteroid use (P = 0.016) associated independently with new plaque formation. RA patients displayed similar numbers of newly formed carotid plaques to the tightly matched for traditional cardiovascular risk factors 'healthy' controls, although more patients than controls had carotid plaques at baseline. Formation of new atherosclerotic plaques in this small cohort of patients with well-controlled RA depended mainly on traditional cardiovascular risk factors and corticosteroid use, whereas an adverse effect of residual systemic inflammation was not readily detectable.
    Arthritis research & therapy 03/2012; 14(2):R44. DOI:10.1186/ar3757 · 4.12 Impact Factor
  • Maturitas 03/2012; 71:S34. DOI:10.1016/S0378-5122(12)70138-X · 2.86 Impact Factor
  • Maturitas 03/2012; 71:S34. DOI:10.1016/S0378-5122(12)70139-1 · 2.86 Impact Factor
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    ABSTRACT: Background: The aim of the study was to investigate the effects of sesame oil on endothelial function and to detect the underlying mechanisms, both in the postprandial state and after long-term consumption.Design: We enrolled 30 hypertensive men in a two-phase study. In the first phase, 26 volunteers consumed 35 g of either sesame oil or control oil. Endothelial function, inflammatory activation and nitric oxide syntase (NOS) inhibition was assessed after a 12-hour fast and 2 hours after consumption of an oil-containing standardized meal. In the second phase, 30 volunteers consumed 35 g of sesame oil or control oil daily for 2 months and the above-mentioned parameters were assessed at baseline, 15, 30 and 60 days.Methods: Endothelial function was estimated by endothelium-dependent FMD (flow-mediated dilatation) of the brachial artery.Results: Flow-mediated dilatation (FMD) improved significantly both after acute (p = 0.001) and long-term sesame oil consumption (p = 0.015, p = 0.005 and p = 0.011 for 15, 30 and 60 days respectively). Intracellular adhesion molecule (ICAM) levels decreased significantly after only 60 days of daily sesame oil intake (p = 0.014). By contrast, no changes were observed in the control group in either phase of the study.Conclusions: This is the first study to show that sesame oil consumption exerts a beneficial effect on endothelial function and this effect is sustained with long-term daily use.
    01/2012; 20(2). DOI:10.1177/2047487312437625
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    ABSTRACT: To compare the prevalence of subclinical atherosclerosis between postmenopausal women and men of similar age early after the onset of menopause. In the first part of this cross-sectional study 186 non-diabetic young postmenopausal women (n = 101, menopausal age ≤ 10 years) and men (n = 85) aged 40-60 years without overt CVD were consecutively recruited from the outpatients clinics of an academic hospital. Subclinical carotid atherosclerosis was assessed by high-resolution ultrasonography. The presence of carotid atherosclerosis was defined as either increased carotid intima-media thickness (IMT>0.9 mm) and/or the presence of plaques. In the second part, 1:1 matching for age and traditional risk factors (hyperlipidemia, smoking, hypertension and BMI) was performed between men and women of this cohort resulting in a matched sub-sample of 76 subjects. By multivariate analysis, gender was not an independent determinant of any measure of carotid atherosclerosis. In the matched sub-sample, carotid IMT and the number of segments with atherosclerosis did not significantly differ between women and men (0.734 ± 0.119 mm and 1.47 ± 1.6 versus 0.717 ± 0.138 mm and 1.47 ± 1.5, p = 0.575 and p = 0.999, respectively). Also, the prevalence of increased IMT (60.5% in both genders), carotid plaques and subclinical atherosclerosis (31.6% and 63.2% versus 28.9% and 65.8%, p = 0.803 and p = 0.811, respectively) was similar between men and women. The prevalence and severity of carotid atherosclerosis was similar between men and young postmenopausal women matched for traditional risk factors. Whether these women may be better risk stratified irrespective of gender should be further assessed in prospective studies.
    Atherosclerosis 12/2011; 221(2):508-13. DOI:10.1016/j.atherosclerosis.2011.12.006 · 3.97 Impact Factor
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    ABSTRACT: Interleukin (IL)-6 is a pleiotropic proinflammatory cytokine involved in the pathogenesis of both atherosclerosis and rheumatoid arthritis. The role of the IL-6/IL-6 receptor pathway in the documented acceleration of atherosclerosis in rheumatoid arthritis has not been examined. In a non-randomized prospective pilot study we asked whether endothelial dysfunction, defined as impaired flow mediated dilatation (FMD), and aortic stiffness, assessed by pulse wave velocity (PWV) improve after 3 and 6 monthly therapeutic infusions of the anti-IL-6 receptor antibody tocilizumab for active rheumatoid arthritis. We found that FMD increased from 3.3 ± 0.8 to 4.4 ± 1.2 to 5.2 ± 1.9% (p = 0.003), whereas PWV decreased from 8.2 ± 1.2 to 7.7 ± 1.3 to 7.0 ± 1.0m/s (p < 0.001). Whether these beneficial arterial changes are direct effects of the IL-6/IL-6 receptor pathway inhibition, maintained over time and translate into better clinical outcome warrants further studies.
    Atherosclerosis 12/2011; 219(2):734-6. DOI:10.1016/j.atherosclerosis.2011.09.015 · 3.97 Impact Factor
  • Artery Research 12/2011; 5(4):152. DOI:10.1016/j.artres.2011.10.020
  • Artery Research 12/2011; 5(4):158–159. DOI:10.1016/j.artres.2011.10.044

Publication Stats

4k Citations
701.79 Total Impact Points


  • 2004–2014
    • National and Kapodistrian University of Athens
      • Division of Clinical Therapeutics
      Athínai, Attica, Greece
    • Universität Heidelberg
      • Department of Neurology
      Heidelburg, Baden-Württemberg, Germany
  • 1998–2014
    • Harokopion University of Athens
      Athínai, Attica, Greece
  • 1992–2013
    • Alexandra Regional General Hospital
      Athínai, Attica, Greece
  • 2012
    • University of Texas Medical Branch at Galveston
      • Department of Internal Medicine
      Galveston, TX, United States
  • 1998–2012
    • Κωνσταντοπούλειο νοσοκομείο Νέας Ιωνίας (Η Αγία Όλγα)
      Athínai, Attica, Greece
  • 2007
    • Alexandria University
      Al Iskandarīyah, Alexandria, Egypt
  • 2006
    • Eginition Hospital Athens
      Athínai, Attica, Greece
    • University of Mississippi
      • Department of Physiology and Biophysics
      Mississippi, United States
  • 2005
    • National Technical University of Athens
      • School of Mechanical Engineering
      Athínai, Attica, Greece
    • Aglaia Kyriakou Children's Hospital
      Athínai, Attica, Greece