Dimitrios I Hatseras

Democritus University of Thrace, Komotina, East Macedonia and Thrace, Greece

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Publications (41)89.97 Total impact

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    ABSTRACT: Numerous inflammatory mediators such as C-reactive protein (CRP), fibrinogen, interleukin-18 (IL-18), and inter-cellular adhesion molecule-1 (ICAM-1) have been proposed for risk stratification in acute coronary syndrome (ACS) patients. However, interactions between these markers have made it difficult to assess their true role in risk prediction. Factor analysis is a multivariable statistical technique that reduces a large number of intercorrelated variables to a smaller set of independent clusters, underlining physiological relationships. The aim of this study was to investigate, using factor analysis, a clustering of pro-inflammatory markers, anti-inflammatory cytokines such as interleukin-10 (IL-10) and HDL cholesterol, and to determine their role in prediction of risk of recurrent coronary events in ACS patients. We assessed 320 consecutive patients (236 men; 67 years; IQ 58-74 years) admitted with ACS. The composite of cardiac death and re-hospitalization with non-fatal myocardial infarction, or unstable angina, was the pre-specified study end-point. Serum CRP, fibrinogen, HDL cholesterol, IL-10, IL-18 and ICAM-1 levels were measured at study entry. We assessed independent predictors of the combined end-point during a 1-year follow-up using multiple logistic regression analysis. Factor analysis identified three clusters which were arbitrarily interpreted as (1) a "systemic inflammation" cluster with positive loadings of CRP and fibrinogen, (2) a "local inflammation-endothelial dysfunction" cluster with positive loadings of IL-18 and ICAM-1 and (3) an "anti-inflammation" cluster comprising IL-10 and HDL cholesterol. Only the "anti-inflammation" cluster was a significant predictor (OR 0.66, 95% CI: 0.49-0.89) of adverse cardiac events during a 1-year follow-up and remained significant (OR 0.65, 95% CI: 0.48-0.88) in a multivariate model that included all three factors. Although inflammatory markers such as CRP predict future cardiovascular events in ACS patients, when all inflammatory mediators are taken into account in a prospective analysis of risk, markers reflecting anti-inflammatory mechanisms are better prognostic markers.
    Atherosclerosis 08/2007; 193(1):196-203. · 3.71 Impact Factor
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    ABSTRACT: The pro-inflammatory cytokine IL-18 has been suggested to play a role in atherogenesis and atheromatous plaque rupture leading to the acute coronary syndrome (ACS). Conversely, the anti-inflammatory cytokine IL-10 seems to have an atheroprotective role. Patients with unstable coronary artery disease show an imbalance between serum levels of pro- and anti-inflammatory cytokines, and studies have shown that IL-18/IL-10 ratio is an independent predictor of adverse in-hospital events in patients with ACS. We assessed the long-term prognostic significance of admission interleukin-18 (IL-18)/interleukin-10 (IL-10) ratio for recurrent coronary events during a 1-year follow-up in patients presenting with an ACS. We assessed independent predictors of the combined end-point using multiple logistic regression analysis, in 186 patients (138 men, 65+/-12 years) with ACS (75 STEMI, 65 NSTEMI and 46 unstable angina). The composite of cardiac death and re-hospitalization with non-fatal myocardial infarction, or unstable angina, was the pre-specified study end-point. Serum IL-10 and IL-18 levels were measured at study entry using commercially available ELISAs. During the 1-year follow-up, 48 (26%) patients had recurrent cardiac events and 138 (74%) were event-free. IL-18/IL-10 ratio predicted the occurrence of adverse cardiac events (OR 1.91, 95% CI 1.37-2.65, p<0.001), and was found to be an independent predictor among other established biochemical and clinical risk markers (OR 2.31, 95% CI 1.55-3.42, p<0.001). Serum IL-18/IL-10 ratio is an independent predictor of recurrent coronary events during long-term follow-up in patients presenting with ACS. Our study further supports the hypothesis that the balance between pro-inflammatory and anti-inflammatory cytokines may be an important determinant of patient outcome, suggesting a pathogenic role in plaque progression and instability.
    International journal of cardiology 05/2007; 117(3):333-9. · 6.18 Impact Factor
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    ABSTRACT: The aim of this study was to evaluate the sensitivity and specificity of aortic arch calcification for detection of severe coronary atherosclerosis in patients suffering from coronary artery disease (CAD), with or without type 2 diabetes. This study included 107 type 2 diabetic patients (68 men) with a mean age of 62.4 +/- 10.7 years and a mean diabetes duration of 14.2 +/- 5.9 years and 104 patients (63 men) with a mean age of 64.5 +/- 9.3 years who did not have diabetes. All patients had CAD, documented by coronary arteriography. Severe CAD was defined as atherosclerosis of the left main branch or atherosclerosis of three coronary arteries or atherosclerosis of the proximal part of the left anterior descending artery. Aortic arch calcification was assessed by means of posteroanterior chest X-rays, studied by a radiologist kept blind to the result of coronary arteriography. In type 2 diabetic patients, diagnosis of aortic arch calcification had 65.6% sensitivity and 86.9% specificity for detection of severe CAD. In patients without diabetes, diagnosis of aortic arch calcification had 47.7% sensitivity and 96.7% specificity for detection of severe CAD. Aortic arch calcification has a high specificity for detection of severe coronary atherosclerosis in patients with CAD. Sensitivity is higher in patients with type 2 diabetes, while specificity is slightly higher in non-diabetic patients.
    Acta clinica Belgica 01/2007; 62(1):52-5. · 0.59 Impact Factor
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    ABSTRACT: This study was designed to assess the relation between apolipoprotein E (apoE) genotype and serum interleukin (IL)-10 levels in patients with acute coronary syndrome (ACS) and chronic stable angina (CSA). Genetic variations in the apoE gene affect the risk for coronary artery disease (i.e., carriers of the e4 allele have an increased risk). Increased levels of C-reactive protein (CRP), an inflammatory marker, correlate with an increased risk of acute coronary events, whereas increased IL-10 concentrations have an atheroprotective role. Studies have reported a negative association between the apoE e4 allele and CRP levels. Apolipoprotein E genotypes were assessed in 166 consecutive ACS patients (119 men, mean age 68 years, interquartile range [IQR] 60 to 74 years) and 70 CSA patients (54 men, mean age 65 years, IQR 62 to 68 years). Serum IL-10 and CRP were assessed at study entry. Analysis of covariance showed that genetic variation in the apoE gene locus significantly influences serum IL-10 levels in both ACS (p = 0.009) and CSA patients (p = 0.013). Among ACS patients, IL-10 levels were lower in E3/E4 carriers compared with E3/E3 carriers (p = 0.01) and marginally lower compared with E2/E3 carriers (p = 0.065). Among CSA patients, IL-10 levels were lower in E3/E4 carriers compared with E2/E3 carriers (p = 0.004) and marginally lower compared with E3/E3 carriers (p = 0.086). The IL-10 concentrations differ in ACS and in CSA patients with different apoE genotypes. The e4 allele was associated with a trend toward lower IL-10 serum levels. Our results may provide an explanation of findings in previous studies that cardiovascular risk is higher in e4 carriers despite the presence of low CRP levels.
    Journal of the American College of Cardiology 01/2007; 48(12):2471-81. · 14.09 Impact Factor
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    ABSTRACT: We hypothesized that cholesterol content is increased in the circulating erythrocytes of patients with acute coronary syndrome (ACS) and may be a marker of clinical instability. We therefore sought to investigate whether cholesterol content differs in erythrocyte membranes of patients presenting with ACS compared to patients with chronic stable angina (CSA). Plaque rupture in ACS depends at least partly on the volume of the necrotic lipid core. Histopathologic studies have suggested that cholesterol transported by erythrocytes and deposited into the necrotic core of atheromatous plaques contributes to lipid core growth. Consecutive angina patients were prospectively assessed; 120 had CSA (83 men, age 64 +/- 11 years) and 92 ACS (67 men, 66 +/- 11 years). Total cholesterol content in erythrocyte membranes (CEM) was measured using an enzymatic assay, and protein content was assessed by the Bradford method. The CEM (median and interquartile range) was higher (p < 0.001) in ACS patients (184 microg/mg; range 130.4 to 260.4 microg/mg) compared with CSA patients (81.1 microg/mg; range 53.9 to 109.1 microg/mg) (analysis of covariance). Total plasma cholesterol concentrations did not correlate with CEM levels (r = -0.046, p = 0.628). This study shows, for the first time, that CEM is significantly higher in patients with ACS compared with CSA patients. These findings suggest a potential role of CEM as a marker of atheromatous plaque growth and vulnerability. Large ad hoc studies are required to establish the clinical importance and pathogenic significance of CEM measurement.
    Journal of the American College of Cardiology 01/2007; 49(21):2081-2089. · 14.09 Impact Factor
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    ABSTRACT: Sustained monomorphic ventricular tachycardia (SMVT) in the course of a prime acute myocardial infarction is not a common arrhythmia and its prognostic significance has not been specifically elucidated. The aim of the study was to estimate the prognostic implications of the occurrence of sustained monomorphic ventricular tachycardia in the early phase (<72 h) of a prime acute myocardial infarction. We studied 690 consecutive patients admitted to the coronary care unit with a diagnosis of a prime myocardial infarction. SMVT was observed in 18 (2.6%) patients and we followed these patients for establishing the prognostic value of the arrhythmia according to the clinical characteristics. Patients with SMVT had a more extensive myocardial infarction based on the peak of the CK-MB isoenzyme activity (480+/-290 IU/L, vs 270+/-190 IU/L, P < .01), and higher mortality rate (40% vs 9%, P < .001). The independent predictors of SMVT were CK-MB (odds ratio [OR] 12.4), presence of complex ventricular arrhythmias (OR = 5.7), a wide QRS complex > or =130 milliseconds (OR = 4.8) and Killip class (OR = 4.8). The SMVT was itself an independent predictor of mortality (OR = 5.0). Compared with patients with ventricular fibrillation or polymorphic ventricular tachycardia, those with SMVT had a higher CK-MB activity, higher rate of wide QRS > or =130 milliseconds (33% vs 8%, P < .002), had a worse hemodynamic condition (Killip class >I:58% vs 23%, P < .04) and higher recurrence rate of ischemic events (68% vs 16%, P < .05). During the one year follow-up period, 4 patients (36.3%) of the 11 survivors from those with SMVT died of cardiac related causes. SMVT during the first 72 h of a prime myocardial infarction is an index of a larger healing myocardium with acute very complexed electrophysiological changes and it is an independent predictor of in-hospital mortality and a prognostic factor of a poor one year outcome.
    Journal of electrocardiology 01/2007; 40(1):72-7. · 1.08 Impact Factor
  • Atherosclerosis Supplements - ATHEROSCLER SUPPL. 01/2007; 8(1):118-118.
  • Atherosclerosis Supplements - ATHEROSCLER SUPPL. 01/2007; 8(1):102-102.
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    ABSTRACT: The aim of this study was to investigate whether frequency of concomitant peripheral arterial disease (PAD) is associated with angiographic severity of coronary artery disease (CAD), as well as to ascertain if diabetic patients differ from those without diabetes in the association between these two manifestations of atherosclerosis. This study included 302 patients (229 men, mean age 62.2 +/- 11.5 years) with documented CAD, divided into groups I-III, according to the angiographic severity of coronary atherosclerosis. Group I comprised 140 patients (104 men) with severe CAD, group II comprised 63 patients (48 men) with moderate CAD and group III comprised 99 patients (77 men) with mild CAD. Each of the groups I-III was further divided into the subgroups of diabetic and non-diabetic patients. Included were also 88 patients (42 men, mean age 61.7 +/- 9.5 years) without CAD and a control group of 60 healthy volunteers (30 men), aged 18-40 years. PAD was diagnosed by means of a Doppler apparatus. Frequency of PAD was associated with angiographic severity of CAD (p = 0.0001). This association was shown both in diabetic (p = 0.012) and in non-diabetic patients (p = 0.0041). Significantly (p < or = 0.01) higher frequency of PAD among diabetic patients was found in each of the groups I-III. Among patients with CAD, frequency of concomitant PAD is associated with angiographic severity of coronary atherosclerosis. This association is demonstrated both in diabetic and in non-diabetic patients. Finally, PAD is significantly more frequent in diabetic patients, irrespective of the angiographic severity of CAD.
    VASA.: Zeitschrift für Gefässkrankheiten. Journal for vascular diseases 11/2006; 35(4):227-31. · 1.01 Impact Factor
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    ABSTRACT: To investigate the potential effect of gliclazide on serum ICAM-1 (intercellular adhesion molecule-1) and VCAM-1 (vascular cell adhesion molecule-1) levels in poorly controlled type 2 diabetic patients. The study included 104 patients, randomly divided into two groups. Group A comprised 53 patients (26 men) treated with gliclazide with a mean age of 67.5+/-9.9 years, a mean diabetes duration of 13.4+/-5.4 years and a mean HbA1c of 8.6+/-1.1%. Group B comprised 51 patients (25 men) treated with glibenclamide with a mean age of 66.4+/-10.9 years, a mean diabetes duration of 13.2+/-6.1 years and a mean HbA1c of 8.4+/-1.3%. A third group of 30 healthy controls (15 men) with a mean age of 63.3+/-10.4 years was also included. Serum levels of ICAM-1 and VCAM-1 were measured at the beginning of the study and after six months of treatment. Pretreatment serum ICAM-1 and VCAM-1 levels did not differ between groups A and B, while they were significantly higher (P=0.0001) than in healthy controls. No significant difference in HbA1c, body mass index, blood pressure control and lipid profile between the two groups was observed after the sixth month of treatment. In group A, serum ICAM-1 levels after six months of treatment were significantly reduced from 623.12+/-61.17 ng/ml to 370.14+/-49.92 ng/ml (P=0,01), while no reduction was found in VCAM-1 levels. In group B, no reduction was found in serum ICAM-1 and VCAM-1 levels after the end of the study. Our results suggest that gliclazide treatment reduces serum ICAM-1 levels in poorly controlled type 2 diabetic patients. This reduction is independent of the hypoglycaemic action of gliclazide.
    Diabetes & Metabolism 10/2006; 32(4):344-9. · 2.39 Impact Factor
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    ABSTRACT: The presence of systemic inflammation determined by elevations in high-sensitivity C-reactive protein (hs-CRP) has been associated with persistence of atrial fibrillation (AF). The influence of inflammation markers, such as hs-CRP, on the recurrences of lone AF, however, has not been clarified. We tested the hypothesis of whether, in patients with a first paroxysmal episode of lone AF, the hs-CRP levels were elevated, and whether elevated hs-CRP could predict the recurrence rate of lone AF in patients without antiarrhythmic drugs. Using a case-control study design, the hs-CRP levels in 125 patients with a documented symptomatic first paroxysmal episode of lone AF was compared with the hs-CRP levels in 65 control patients. hs-CRP levels are presented as median values with the interquartile range (25th to 75th percentiles). The hazard ratio compared the 75th percentile of hs-CRP with the 25th percentile. In the arrhythmia group, hs-CRP was higher than in the control patients (median 0.23 mg/dl, interquartile range 0.12 to 0.49, vs 0.087 mg/dl, interquartile range 0.058 to 0.098, p <0.001). After adjusting for baseline characteristics, including, age, gender, and baseline blood pressure, hs-CRP remained a significant predictor of recurrent AF (hazard ratio 1.15, 95% confidence interval 1.04 to 1.24, p = 0.002) at 2 years of follow-up. In conclusion, this study is the first to document that the first paroxysmal episode of lone AF is associated with elevated hs-CRP levels, suggesting that hs-CRP may be a marker for inflammatory states that may promote the initiation of lone AF. These pathways may represent a novel mechanism by which structural changes resulting from inflammation could induce lone AF. The elevated hs-CRP levels could also predict the recurrence rate of lone AF in patients without antiarrhythmic drugs.
    The American Journal of Cardiology 03/2006; 97(5):659-61. · 3.21 Impact Factor
  • European Journal of Cardiovascular Prevention & Rehabilitation - EUR J CARDIOVASC PREV REHABIL. 01/2006; 13.
  • Eleni Hatzinikolaou-Kotsakou, Dimitrios I Hatseras
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    ABSTRACT: Fibrin D-dimers levels have been advocated as a useful clinical marker of thrombogenesis. It is accepted that patients with atrial fibrillation (AF) are characterized by increased levels of plasmatic d-dimers. AF is a high risk factor for hypercoagulability, with a substantial risk of thromboembolism. The most effective way of minimizing the increased thromboembolic risk and treating patients' symptoms is to return the heart rhythm to sinus rhythm by electrical or chemical cardioversion. However, cardioversion of AF itself leads to a further increased risk of thromboembolism. A marker of coagulation activation would be useful to identify patients at the highest thromboembolic risk after cardioversion in AF patients. Indicators of hypercoagulability, such as d-dimers, appear to be a useful parameter for assessing the degree of hypercoagulability of AF patients after cardioversion. Mean changes in plasma d-dimers levels could be used as a useful clinical marker of the clotting state after the return of atrial systole.
    Future Cardiology 01/2006; 2(1):55-61.
  • Atherosclerosis Supplements - ATHEROSCLER SUPPL. 01/2006; 7(3):87-87.
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    ABSTRACT: Matrix metalloproteinases (MMPs) are expressed in atherosclerotic plaques. Acute coronary syndromes may be precipitated by MMPs through degradation of the fibrous cap and subsequent plaque disruption. Serine proteases such as plasmin activate MMPs and may contribute to plaque events. Thrombolysis with recombinant tissue plasminogen activator (rtPA) is widely used for treatment of acute ST segment elevation myocardial infarction (STEMI). In the present study we assessed whether thrombolytic therapy with rtPA in patients with STEMI influences serum levels of MMP-2 and MMP-9. We recruited 108 patients (92 men, mean age 64 +/- 12 years) with STEMI, of whom 84 (78%) received thrombolytic treatment with rtPA and 24 (22%) did not. MMP-2 and MMP-9 levels were assessed at hospital admission (baseline), and at 24 and 72 h after admission, using a commercially available ELISA. Overall, MMP-9 levels were higher in the thrombolysis group compared to patients without thrombolysis (p < 0.001). Thrombolysis treatment significantly affected the change in MMP-9 levels during the 72-h study period (p < 0.001). The present study showed that thrombolysis could affect circulating levels of MMP-9 in STEMI patients. Whether this effect may lead to plaque instability deserves further investigation.
    Thrombosis Research 01/2006; 118(2):221-7. · 3.13 Impact Factor
  • Atherosclerosis Supplements - ATHEROSCLER SUPPL. 01/2006; 7(3):533-533.
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    ABSTRACT: Extracellular matrix metabolism (ECM) has an important role in left ventricular (LV) remodeling in chronic heart failure (CHF). Matrix metalloproteinases (MMPs) are involved in the regulation of extracellular matrix (ECM) metabolism. We investigated the effect of levosimendan, a novel calcium sensitizer, on serum levels of MMP-2. Our study population consisted of 60 consecutive patients with advanced heart failure who were admitted to hospital with an acute decompensation of their CHF. Patients were randomized to levosimendan (n = 30; 18 men, aged 65 +/- 3 years) or placebo (n = 30; 15 men, aged 67 +/- 4 years). Serum MMP-2 levels were assessed before and after treatment with levosimendan or placebo, using a commercially available ELISA. Serum levels of MMP-2 were reduced from 427 ng/ml 95%CI 372-484 to 371 ng/ml 95%CI 329-413 in the levosimendan treated group and from 433 ng/ml 95%CI 422-444 to 425 ng/ml 95%CI 414-436 in the placebo group. Repeated measurements ANOVA showed that treatment with levosimendan significantly affected levels of MMP-2 (p = 0.019). The present study showed that levosimendan may beneficially affect ECM remodeling in patients with acutely decompensated CHF. Whether these effects translate into added clinical benefits, as suggested by an improved ejection fraction in the levosimendan group, deserves further investigation.
    Cardiovascular Drugs and Therapy 01/2006; 19(6):399-402. · 2.67 Impact Factor
  • European Journal of Heart Failure Supplements 01/2006; 5(1):6-6.
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    European Journal of Heart Failure Supplements 01/2006; 5(1):3-3.
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    ABSTRACT: It has been reported that circulating matrix metalloproteinase (MMP) levels are upregulated in patients with chronic heart failure. However, experimental studies indicate that differences in the profiles of MMPs and tissue inhibitors of metalloproteinase (TIMPs) may exist in ischemic compared with nonischemic cardiomyopathy. This study examined whether circulating levels of MMPs and TIMP-1 are related to the pathogenesis of heart failure. Circulating levels of MMP-2, MMP-3, and TIMP-1 were assessed in 52 patients with compensated end-stage chronic heart failure, including 26 patients (mean 64 +/- 7 years; 10 men) with ischemic cardiomyopathy (IC) and 26 (mean age 66 +/- 6 years; 14 men) with idiopathic dilated cardiomyopathy (IDC). Serum MMP-2 (p <0.001) and MMP-3 (p <0.001) levels were higher in patients with IDC than in those with IC. Serum TIMP-1 levels were lower in patients with IDC (p = 0.011) than in those with IC. This study shows that in patients with compensated end-stage chronic heart failure, circulating levels of MMP-2, MMP-3, and TIMP-1 are associated with the pathogenesis of heart failure.
    The American Journal of Cardiology 11/2005; 96(10):1449-51. · 3.21 Impact Factor