Onassis Cardiac Surgery Center Athens

Athens, Greece

Onassis Cardiac Surgery Center Athens

Athens, Greece
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Kolovou V.,Onassis Cardiac Surgery Center Athens | Marvaki A.,Onassis Cardiac Surgery Center Athens | Karakosta A.,Thriassio General Hospital | Vasilopoulos G.,Technological Educational Institute of Athens | And 6 more authors.
Lipids in Health and Disease | Year: 2012

Objective: One of the important proteins involved in lipid metabolism is the ATP-binding cassette transporter A1 (ABCA1) encoding by ABCA1 gene. In this study we evaluated the single nucleotide polymorphisms (SNPs) of ABCA1 gene. We analyzed SNPs in chromosome 9 such as rs2230806 (R219K) in the position 107620867, rs2230808 (R1587K) in the position 106602625 and rs4149313 (I883M) in the position 106626574 according to gender and lipid profile of Greek nurses. Methods: The study population consisted of 447 (87 men) unrelated nurses who were genotyped for ABCA1 gene polymorphisms. Additionally, lipid profile [total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol (LDL-C) and apolipoprotein A1] was evaluated. Results: The distribution of all three studied ABCA1 gene polymorphisms did not differ according to gender. However, only R219K genotype distribution bared borderline statistical significance (p = 0.08) between the two studied groups. Moreover, allele frequencies of R219K, R1587K and I88M polymorphisms did not differ according to gender. In general, blood lipid levels did not seem to vary according to ABCA1 gene polymorphisms, when testing all subjects or when testing only men or only women. However, a significant difference of LDL-C distribution was detected in all subjects according to R1587K genotype, indicating lower LDL-C levels with KK polymorphism (p = 0.0025). The above difference was solely detected on female population (p = 0.0053). Conclusions: The ABCA1 gene polymorphisms frequency, distribution and lipid profile did not differ according to gender. However, in the female population the KK genotype of R1587K gene indicated lower LDL-C levels. Further studies, involving a higher number of individuals, are required to clarify genes and gender contribution. © 2012 BioMed Central Ltd.

Vasiliadis I.,Onassis Cardiac Surgery Center Athens | Kolovou G.,Onassis Cardiac Surgery Center Athens | Kolovou V.,Onassis Cardiac Surgery Center Athens | Kolovou V.,Onassis Cardiac Surgery Center | And 9 more authors.
Endocrine | Year: 2014

We evaluated nuclear factor kappa B {NFkB, rs28362491 [-94ins/delATTG (W/D)]} and angiotensin converting enzyme {ACE; rs1799752 [Ins(I)/Del(D)]} gene polymorphisms and their correlation with thyroid function in patients with heart failure (HF). Peak oxygen uptake (VO2) was evaluated (by Weber classification) during a symptom-limited cardiopulmonary exercise test in 194 patients. Thyroid-stimulating hormone, triiodothyronine (T3), thyroxine (T4), and free (F) T3 and FT4 were also measured. According to their cardiovascular (CV) capacity, patients were subdivided into four groups: group A included patients with peak VO2 >20 ml/kg/min, group B 16-20 ml/kg/min, group C 10-16 ml/kg/min, and group D 6-10 ml/kg/min. Patients were also genotyped for NFkB and ACE genetic variants. T3 was increased and FT3 was decreased for every raise in Weber's classification (p = 0.007 and p = 0.012, respectively). Del carriers had elevated FT3 levels compared with Ins carriers (p = 0.021). Patients with II genotype had elevated T4 levels compared with ID genotype (p = 0.044). Both T4 and FT4 were decreased in D allele carriers (p = 0.007 and p = 0.045, respectively). Thyroid hormones correlated with CV capacity. Associations between the NFkB and ACE gene polymorphisms and thyroid hormones levels were also observed. Further larger studies are required to clarify genes contribution in HF. © 2013 Springer Science+Business Media New York.

Kolovou G.,Onassis Cardiac Surgery Center | Kolovou V.,Onassis Cardiac Surgery Center | Kolovou V.,Onassis Cardiac Surgery Center Athens | Vasiliadis I.,Onassis Cardiac Surgery Center | And 11 more authors.
Angiology | Year: 2014

Single nucleotide polymorphisms of angiotensin-converting enzyme (ACE) such as rs1799752, nuclear factor kappa B (NFkB) such as rs28362491 and cholesteryl ester transport protein (CETP) such as rs708272 (TaqB1) and rs5882 (I405V) were evaluated in nonagenarians, centenarians, and average life span individuals (controls). The study population (n = 307; 190 nonagenarians, 12 centenarians and 105 middle-aged controls) was genotyped for ACE, NFkB, and CETP genetic variants. The age of nonagenarian and centenarian group ranged between 90 and 111 years; centenarians and controls age ranged from 99 to 111, and from 18 to 80 years, respectively. The I carriers of ACE I/D gene were fewer in nonagenarians compared to centenarians (37.6% vs 62.5%, P =.016). The I carriers of ACE gene were more frequent in centenarians compared to controls (62% vs 41%, P =.045). No differences in frequency of common NFkB and CETP genotypes between patients with exceptional longevity and middle-aged patients were observed. © The Author(s) 2013.

PubMed | Molecular Immunology Laboratory, General Hospital, Onassis Cardiac Surgery Center Athens, Aristotle University of Thessaloniki and Evangelismos Hospital
Type: | Journal: The open cardiovascular medicine journal | Year: 2014

This study is in line with two previous ones from our group. They evaluated the influence of ATP-binding cassette transporter A1 (ABCA1) gene polymorphisms [such as rs2230806 (R219K), rs2230808 (R1587K) and rs4149313 (I883M)] on the human lipid profile (defined as Optimal and Non-Optimal).The present study included 447 unrelated young women and men self-reported as being healthy and that attended the University of Nursing of Technological and Educational Institution. All subjects were genotyped and the ABCA1 polymorphisms (R219K, R1587K and I883M) were recorded. According to lipid profile [total cholesterol, triglyceride, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol (LDL-C)] the subjects were separated into those with optimal lipid profile (Optimal Group, n=209) and Non-Optimal Group (n=238).No statistical differences were observed in the distribution of R219K, R1587K and I883M polymorphisms according to the lipid profile (p>0.05 in all cases). No statistical differences were observed in the distribution of R219K, R1587K and I883M polymorphisms according to sex (p>0.05 in all cases). However, Logistic Regression revealed that subjects with RK (R1587K polymorphism) genotype had 69% increased risk on average of having LDL-C above normal limits as compared with those with RR genotype. Similarly, subjects with K allele (R1587K polymorphism) had 59% increased risk on average of having LDL-C above normal limits compared with those with R allele.These findings suggest that R1587K polymorphism of ABCA1 gene may influence the lipid profile. However, this needs to be confirmed by larger studies.

Bousoula E.,Onassis Cardiac Surgery Center Athens | Kolovou V.,Onassis Cardiac Surgery Center Athens | Perrea D.,National and Kapodistrian University of Athens | Kolovou G.,Onassis Cardiac Surgery Center Athens
Current Vascular Pharmacology | Year: 2015

Pharmacogenetics investigates heritable genetic polymorphisms that can effect responses to drug therapy. The main application of pharmacogenetics is genotype-guided dosing of medications and genotype-selection of treatment with the highest efficacy and lowest risk of adverse effects. Cardiovascular disease (CVD) is the leading cause of mortality and morbidity globally. Dyslipidemia is one of the classical risk factors for developing CVD. 3-hydroxy-3-methylglutaryl-coenzyme (HMG-CoA) reductase inhibitors called statins are the cornerstones in dyslipidemia treatment. However, there is a broad variation in individual responses to statin treatment. This variation may not only be due to environmental factors such as adherence to treatment, diet and exercise but also due to genetic factors. Many studies have focused on various genetic polymorphisms of genes that are involved in cholesterol metabolism, trying to define their contribution to a potential genotype-guided treatment against dyslipidemia. © 2015 Bentham Science Publishers.

Kolovou G.,Onassis Cardiac Surgery Center Athens | Ragia G.,Democritus University of Thrace | Kolovou V.,Onassis Cardiac Surgery Center Athens | Mihas C.,General Hospital of Kimi | And 6 more authors.
Open Cardiovascular Medicine Journal | Year: 2014

Background: One of the promises of human genetics is individualized therapy. Therefore, we evaluated the impact of CYP3A5 gene polymorphism on the effectiveness of simvastatin (a HMG-CoA reductase inhibitor). Methods: Patients (n = 191) with hypercholesterolemia were treated with simvastatin for at least 6 months and were genotyped for the CYP3A5 polymorphism. Results: The frequency of CYP3A5 polymorphism was 0.5% for WT (wild-type), 15.6% for HT (heterozygous, expressors) and 83.9% for HM (homozygous, non-expressors). Differences in lipid profile before and after dose-response of simvastatin treatment were described as % difference {[(variable after-variable before)/variable before]* 100}. There was a trend towards the decrease of low density lipoprotein cholesterol (LDL-C) in HT individuals who had a -35.2% reduction with a dose of 20 mg simvastatin and HM individuals who had a slightly higher decrease (-37.5%) despite the lower dose of simvastatin (10 mg, p = 0.07). Furthermore, HT genotype individuals had significantly higher than expected (6-8%) LDL-C % difference between 20 and 40 mg of simvastatin (-35.2 vs -49.2%, p = 0.037). In individuals with HM genotype a significant LDL-C % difference was found between 10 and 40 mg of simvastatin (-37.5 vs - 48.4%, p = 0.023). Conclusion: The individuals with HM polymorphism display a trend towards higher LDL-C reductions compared with HT polymorphism. Within the same genotype, differences between doses were also observed. These findings need to be confirmed in larger studies. © Kolovou et al.

Kolovou V.,Onassis Cardiac Surgery Center Athens | Lagou E.,Onassis Cardiac Surgery Center Athens | Mihas C.,General Hospital of Kimi | Vasiliki G.,Thriassio Hospital | And 6 more authors.
Open Cardiovascular Medicine Journal | Year: 2015

Background: Hypertension, one of the most important risk factors for premature cardiovascular disease, is a major worldwide public health problem. Angiotensin-1-converting enzyme (ACE) and angiotensinogen (AGT) gene polymorphisms are thought to be associated with primary hypertension. In the present study, we examined the frequency of these gene polymorphisms in an adult population with and without essential hypertension. Furthermore, we evaluated the effect of ACE and AGT gene polymorphisms on ramipril treatment efficacy in the hypertensive patients. Methods: A total of 166 adults (83 hypertensives and 83 normotensives) were involved in the study and genotyped for AGTM235T (rs699), AGTT174M (rs4762) and ACEI/D (rs1799752) gene polymorphisms. Results: The genotype and allele distribution of the AGTM235T variant significantly differed between hypertensives and normotensives [odds ratio (OR) = 1.57% (T vs M allele), 95% confidence intervals (CIs): 1.01 - 2.44; p=0.045 for hypertensives]. However, none of the 3 studied Simple Nucleotide Polymorphisms were associated with the blood pressure-lowering response to ramipril. Conclusion: These results suggest that AGTM235T gene polymorphism is associated with essential hypertension. However, none of the AGTM235T, AGTT174M and ACEI/D gene polymorphisms influenced ramipril effectiveness. © Kolovou et al.

Cokkinos D.V.,Academy of Athens | Cokkinos D.V.,Onassis Cardiac Surgery Center Athens | Chryssanthopoulos S.,Academy of Athens
Heart Failure Reviews | Year: 2016

Thyroid hormones have many cardioprotective actions expressed mainly through the action of T3 on thyroid receptors α1 and β1. They are procontractile anti-apoptotic, anti-inflammatory, and anti-fibrotic, promote angiogenesis and regeneration, and have beneficial effects on microRNA profiles. They have proven to be anti-remodeling in numerous animal studies, mostly in rodents; a specific action on the border zone has been described. Studies in humans with DIPTA have been in conclusion. Remodeling can be defined as an increase of ≥20 % of the end-diastolic or end-systolic volume, together with a return to the fetal phenotype. An overview of animal and clinical studies is given. © 2016, Springer Science+Business Media New York.

PubMed | Onassis Cardiac Surgery Center Athens
Type: Journal Article | Journal: Journal of atherosclerosis and thrombosis | Year: 2016

Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disorder, which leads to premature cardiovascular diseases. Microsomal triglyceride transport protein (MTP) inhibitors, such as lomitapide, offer a new therapeutic approach for treating these patients. We evaluated the lipid lowering (LL) efficacy of lomitapide according to several gene variants in MTP. Four clinically and/or molecularly defined HoFH patients were treated with lomitapide in addition to conventional high intensity LL therapy and regular lipoprotein apheresis. Two patients responded to the therapy, with a significant reduction of LDL cholesterol (LDL-C50%, hyper-responders). Sequencing of all exonic and intronic flanking regions of the MTP gene in all patients revealed 36 different variants. The hyper-responders to lomitapide shared six common variants: rs17533489, rs79194015, rs745075, rs41275715, rs1491246, and rs17533517, which were not seen in hypo-responders (reduction in LDL-C50%). We suggest that in HoFH variants in the MTP gene may impact on the therapeutic response to lomitapide, but this requires further investigation.

PubMed | Onassis Cardiac Surgery Center Athens and General Hospital of Elefsina Thriassio
Type: | Journal: Current medicinal chemistry | Year: 2017

The limited distribution of lipoprotein (a) (Lp(a)) to humans, Old World primates and to the European hedgehog, has raised considerable interest and speculation regarding its possible physiological role. Lp(a) has variable circulating concentrations (<0.1 - >100 mg/ml) which are highly genetically determined in humans. These characteristics gave rise to several theories concerning the origins and evolution of Lp(a). Lp(a) has a protective role after injury since Lp(a) particles bind to macrophages and platelets membrane receptors, leading to fibrin activation and injury healing. On the other hand, Lp(a) seems to be implicated in the formation of atheromatic plaques but also in cerebrovascular events and stenosis of the aortic valve. The main genetic factor determining plasma Lp(a) levels is the Lp(a) gene (LPA). Most Caucasian people have normal plasma Lp(a) concentrations, but there is important distribution variation according to race. Women seem to have increased Lp(a) levels compared with men, while diabetes mellitus type 2 favours lower plasma Lp(a) levels. Nutrition, hormones and several drugs may also influence circulating Lp(a) levels.

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