Dimitris A Arfanakis

University Hospital of Heraklion, Irákleio, Attica, Greece

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Publications (14)81.57 Total impact

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    ABSTRACT: Monocyte chemoattractant protein-1 (MCP-1) and peroxisome proliferator-activated receptor-γ (PPAR-γ) play a significant role in monocyte activation, vascular inflammation, and atherogenesis. Angiotensin receptor blockers and calcium channel blockers are antihypertensive drugs with established efficacy and a favorable safety profile. We investigated the effect of telmisartan--an angiotensin receptor blocker with PPAR-γ agonist activity--and amlodipine on the activation state of peripheral blood monocytes with respect to MCP-1 and PPAR-γ gene expression in hypertensives. We recruited 31 previously untreated patients with essential hypertension who were randomly assigned to receive treatment with telmisartan (n = 16) or amlodipine (n = 15). Blood samples were taken before and 3 months after therapy initiation. Mononuclear cells were isolated and mRNAs of MCP-1 and PPAR-γ were estimated by real-time quantitative reverse transcription-polymerase chain reaction each time. The 2 treatments decreased all blood pressure components significantly (p <0.001). In contrast, in the amlodipine group, MCP-1 gene expression was significantly downregulated after treatment with telmisartan (from 21.4 ± 20.5 to 8.1 ± 6.5, p = 0.009), whereas the amlodipine group did not show any significant change (12.5 ± 8.5 vs 17.6 ± 16.4, p = NS). In addition, PPAR-γ mRNA levels showed a significant increase in telmisartan-treated patients (from 20 ± 18.5 to 42.6 ± 36, p = 0.006) and no significant alterations in the amlodipine group (from 29.6 ± 42.5 to 24.2 ± 27.7, p = NS). In conclusion, treatment with telmisartan results in a significant attenuation of MCP-1 gene expression and an increase of PPAR-γ gene expression in peripheral monocytes in patients with essential hypertension. Our findings may provide new insights into the cardiovascular protection of telmisartan in hypertensives.
    The American journal of cardiology 01/2011; 107(1):59-63. DOI:10.1016/j.amjcard.2010.08.048 · 3.58 Impact Factor
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    ABSTRACT: Abstract Monocyte chemoattractant protein-1 (MCP-1) and peroxisome proliferator-activated receptor-γ (PPAR-γ) play a significant role in monocyte activation, vascular inflammation, and atherogenesis. Angiotensin receptor blockers and calcium channel blockers are antihypertensive drugs with established efficacy and a favorable safety profile. We investigated the effect of telmisartan--an angiotensin receptor blocker with PPAR-γ agonist activity--and amlodipine on the activation state of peripheral blood monocytes with respect to MCP-1 and PPAR-γ gene expression in hypertensives. We recruited 31 previously untreated patients with essential hypertension who were randomly assigned to receive treatment with telmisartan (n = 16) or amlodipine (n = 15). Blood samples were taken before and 3 months after therapy initiation. Mononuclear cells were isolated and mRNAs of MCP-1 and PPAR-γ were estimated by real-time quantitative reverse transcription-polymerase chain reaction each time. The 2 treatments decreased all blood pressure components significantly (p <0.001). In contrast, in the amlodipine group, MCP-1 gene expression was significantly downregulated after treatment with telmisartan (from 21.4 ± 20.5 to 8.1 ± 6.5, p = 0.009), whereas the amlodipine group did not show any significant change (12.5 ± 8.5 vs 17.6 ± 16.4, p = NS). In addition, PPAR-γ mRNA levels showed a significant increase in telmisartan-treated patients (from 20 ± 18.5 to 42.6 ± 36, p = 0.006) and no significant alterations in the amlodipine group (from 29.6 ± 42.5 to 24.2 ± 27.7, p = NS). In conclusion, treatment with telmisartan results in a significant attenuation of MCP-1 gene expression and an increase of PPAR-γ gene expression in peripheral monocytes in patients with essential hypertension. Our findings may provide new insights into the cardiovascular protection of telmisartan in hypertensives.
    The American Journal of Cardiology 01/2011; 107(1):59. · 3.43 Impact Factor
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    ABSTRACT: Angiopoietins (Angs) are important angiogenic and endothelial cell growth factors with many functions, including influence on the vascular wall. Pulse-wave velocity (pwv) is an independent marker of cardiovascular adverse outcome in hypertensives, although all the pathophysiological mechanisms that affect it have not yet been determined. We investigated the relationship between arterial stiffness and Ang-1 and Ang-2 gene expression in the peripheral blood monocytes of hypertensive patients. We studied 53 patients who had untreated grade-1 or grade-2 essential hypertension and no indications of other organic heart disease. Carotid-femoral (c-f) and carotid-radial (c-r) artery waveforms were measured and pwv was determined. The monocytes were isolated using anti-CD14(+) antibodies and mRNAs were estimated by real-time quantitative reverse transcription-PCR. Ang-1 gene expression was strongly correlated with both c-f-pwv (r=0.952, P<0.001) and c-r-pwv (r=0.898, P<0.001). Similarly, Ang-2 gene expression was significantly correlated with both c-f-pwv (r=0.471, P=0.002) and c-r-pwv (r=0.437, P=0.003). Our data provide important evidence that Ang-1 and Ang-2 gene expression levels in peripheral monocytes are closely related with pwv in patients with essential hypertension. This positive correlation may suggest a link between angiogenesis and arterial stiffness in those patients.
    Journal of human hypertension 05/2010; 24(5):306-11. DOI:10.1038/jhh.2009.95 · 2.80 Impact Factor
  • Journal of Hypertension 01/2010; 28. DOI:10.1097/01.hjh.0000379762.00012.7d · 4.22 Impact Factor
  • Journal of Hypertension 01/2010; 28. DOI:10.1097/01.hjh.0000378807.83550.24 · 4.22 Impact Factor
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    ABSTRACT: Although oxidative stress plays an important role in the pathophysiology of restenosis, its role following the implantation of sirolimus-eluting stents (SES) is unknown. We examined the relation between total peroxides (TP), a marker of oxidative stress, and in-stent late luminal loss over a 6-month follow-up in patients with stable coronary artery disease and compared the results from SES with those from bare metal stents (BMS). We enrolled 75 consecutive patients, who underwent successful PCI and were randomly allocated to SES (n=37) or BMS (n=38). Blood samples were taken 24 h before, at 24 h, 48 h and 1 month after angioplasty; levels of TP were determined on each occasion. Follow-up coronary angiography was performed 6-8 months later. TP levels in the BMS group were significantly higher at 24 h and 48 h compared to baseline (p=0.006 for both). At one month there was a significant decline from the 48 h levels (p=0.029) to levels slightly, but not significantly higher than baseline. In contrast, in SES TP levels showed no significant changes during the first 48 h, while they declined to levels somewhat lower than baseline at 30 days. A significant correlation was found between TP changes and in-stent late luminal loss at 6 months in both groups. Our study showed that patients with stable coronary artery disease who received SES have a different behavior of oxidative stress after stenting compared with BMS, and this could contribute to the difference in restenosis rate between these 2 types of stents.
    International journal of cardiology 02/2009; 142(1):33-7. DOI:10.1016/j.ijcard.2008.12.105 · 6.18 Impact Factor
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    ABSTRACT: The purpose of the present study was to determine the relationship between anemia and parameters derived from 24-hour ambulatory blood pressure monitoring. We found that patients with anemia had significantly elevated nocturnal systolic and mean blood pressure and a trend for increased diastolic blood pressure. In addition, anemic patients had significantly lower dipping status compared to patients with normal hemoglobin levels.
    International journal of cardiology 01/2009; 142(1):95-6. DOI:10.1016/j.ijcard.2008.11.096 · 6.18 Impact Factor
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    ABSTRACT: We investigated whether the serum markers of collagen turnover differed in various forms of atrial fibrillation (AF) and in sinus rhythm (SR) in humans. Structural alterations and fibrosis have been implicated in the generation and perpetuation of AF. Serum C-terminal propeptide of collagen type-I (CICP), C-terminal telopeptide of collagen type-I (CITP), matrix metalloproteinase-1, and tissue inhibitor of matrix metalloproteinases-1 were measured as markers of collagen synthesis and degradation in 70 patients with AF and 20 healthy control subjects in SR. C-terminal propeptide of collagen type-I and CITP were significantly higher in AF patients than in control subjects (91 +/- 27 ng/ml vs. 67 +/- 11 ng/ml, p < 0.001 and 0.38 +/- 0.20 ng/ml vs. 0.25 +/- 0.08 ng/ml, p < 0.001, respectively). Persistent AF patients had higher levels of CICP (105 +/- 28 ng/ml vs. 80 +/- 21 ng/ml, p < 0.001), but not CITP, compared with those with paroxysmal AF. Patients with persistent AF had lower levels of matrix metalloproteinase-1 but increased levels of tissue inhibitor of matrix metalloproteinases-1 compared with patients with paroxysmal AF (11.90 +/- 4.79 ng/ml vs. 14.98 +/- 6.28 ng/ml, p = 0.03 and 155 +/- 45 ng/ml vs. 130 +/- 38 ng/ml, p < 0.001, respectively). Tissue inhibitor of matrix metalloproteinases-1 levels were significantly lower in control subjects compared with those in both paroxysmal and persistent AF patients (102 +/- 15 ng/ml vs. 130 +/- 38 ng/ml vs. 155 +/- 45 ng/ml, respectively, p < 0.001). Serum markers of collagen type-I turnover differed significantly between patients with AF and SR. Furthermore, these markers also differed significantly between paroxysmal and persistent AF patients, suggesting that the intensity of the extracellular synthesis and degradation of collagen type-I may be related to the burden or type of AF.
    Journal of the American College of Cardiology 07/2008; 52(3):211-5. DOI:10.1016/j.jacc.2008.03.045 · 15.34 Impact Factor
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    ABSTRACT: Diabetes mellitus (DM) may cause an increase in the inflammatory status and oxidative stress as well as sympathetic nervous system overactivity, even in the absence of any other organic heart disease. We investigated the effect of perindopril, an angiotensin-converting enzyme inhibitor (ACE-i), on indexes of systemic inflammation and oxidative stress in normotensive patients with type 2 DM. We also examined the effect of the drug on the disturbances of left ventricular myocardial adrenergic innervation that may be seen in these patients. We studied 62 normotensive patients with type 2 DM, who were randomized to receive perindopril (n=32) or placebo (n=30). At the start of the study and after 6 months' therapy blood samples were taken to evaluate total peroxides (TP), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha), and the patients underwent a (123)I-metaiodobenzylguanidine myocardial scintigraphy study. ACE-i caused a significant reduction in levels of cytokines and TP (P<0.001 for IL-6 and TNF-alpha, P=0.001 for TP). There was also a reduction in total defect score (P<0.001) and the heart to mediastinum ratio at 10 min and 4 h was improved (P<0.001 for both). No significant alterations were observed in the placebo group. Our data indicate that the addition of ACE-i to the medication of normotensive diabetic type 2 patients may improve the disturbed myocardial adrenergic innervation, the systemic inflammatory status and oxidative stress. Our findings indicate the cardioprotective action of ACE-i and suggest that earlier treatment might be appropriate in those patients.
    Journal of Human Hypertension 04/2008; 22(3):191-6. DOI:10.1038/sj.jhh.1002310 · 2.69 Impact Factor
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    ABSTRACT: Although previous studies have indicated that vascular endothelial growth factor (VEGF) plays an important role in the vascular-healing process after stent implantation, its effect on in-stent restenosis is unclear. We assessed VEGF serum protein levels and gene expression in peripheral monocytes in relation to in-stent restenosis after implantation of sirolimus-eluting (SES) and bare metal stents (BMS) in a non-blinded, randomized study. Forty-two patients (28 men, age 62 +/- 11 years) with stable angina, who underwent elective single-vessel percutaneous coronary intervention, were randomized to SES (n = 21) or BMS (n = 21) implantation. VEGF protein levels in the BMS group showed an increasing trend (P = 0.083), whereas in the SES group they decreased significantly (P = 0.002). BMS induced up-regulation of VEGF mRNA levels, whereas for SES down-regulation was observed. There was no correlation between serum levels and late luminal loss. A significant correlation was found between VEGF gene expression and late luminal loss in both groups (BMS: r = 0.98, P < 0.001; SES: r = 0.65, P = 0.002). SES, in comparison with BMS, results in lower VEGF protein levels and gene expression in peripheral monocytes. The latter shows a positive relationship with in-stent late-luminal loss, suggesting an essential role in the reduced in-stent restenosis seen in SES.
    European Heart Journal 04/2008; 29(6):733-40. DOI:10.1093/eurheartj/ehn060 · 14.72 Impact Factor
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    ABSTRACT: Stent implantation causes significant injury to the vascular wall, resulting in inflammatory activation. Although sirolimus-eluting stents (SES) have anti-inflammatory properties, their effect on periprocedural systemic inflammatory response has not been sufficiently investigated. Eighty-one patients with stable coronary artery disease involving severe stenosis of one major epicardial coronary artery underwent coronary angioplasty with stent implantation and randomly received either SES or bare metal stents (BMS). Blood samples were taken 24h before, at 24h, 48 h and 1 month after the angioplasty and levels of high sensitive C-reactive protein (hsCRP), interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta), and monocyte chemoattractant protein-1 (MCP-1) were determined. HsCRP after BMS implantation increased over 24h (p<0.001) and then remained steady, as did IL-6 and IL-1 beta similarly. In contrast, their levels in SES patients decreased to below baseline by the end of the month. MCP-1 levels increased by the end of 1 month (p<0.001) in the BMS group, whereas in SES they steadily decreased, becoming significantly lower than baseline from 48 h (p=0.015). In conclusion, patients with SES exhibit an attenuation of the postprocedural systemic inflammatory activation during a 1-month follow-up after stent implantation. This might partially explain the reduced restenosis rate associated with SES.
    Atherosclerosis 11/2007; 194(2):433-8. DOI:10.1016/j.atherosclerosis.2006.08.029 · 3.71 Impact Factor
  • European Journal of Cardiovascular Prevention and Rehabilitation 01/2006; 13. DOI:10.1097/00149831-200605001-00248 · 3.69 Impact Factor
  • European Journal of Cardiovascular Prevention and Rehabilitation 01/2006; 13. DOI:10.1097/00149831-200605001-00104 · 3.69 Impact Factor
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    ABSTRACT: Even in high-risk population groups, not all patients have the same risk of sudden cardiac death (SCD). Given the emerging data about the amino-terminal fragment of the brain natriuretic peptide prohormone (NT-proBNP) value in heart failure, we planned to evaluate the importance of NT-proBNP levels in predicting the occurrence of malignant arrhythmias in patients with ischemic cardiomyopathy and implantable cardioverter-defibrillators (ICDs). Prospective study. Tertiary referral center. Thirty five ambulatory patients with previous myocardial infarction, left ventricular ejection fraction < 35%, and ICDs for primary prevention of SCD according to Multicenter Automatic Defibrillator Implantation Trial I criteria. Venous blood samples for plasma NT-proBNP measurement were obtained after 30 min of supine rest from all patients at the beginning of the study. Patients were evaluated every 2 months, or sooner in cases of device discharges, during a 1-year follow-up period. Data concerning arrhythmias and device therapy were stored at the time of device interrogation on each follow-up visit. During 1-year follow-up, 11 of 35 patients (31.4%) received 18 antiarrhythmic device therapies for ventricular tachyarrhythmia (VT). Patients who experienced such arrhythmias had NT-proBNP levels of 997.27 +/- 335.14 pmol/L (mean +/- SD), whereas those without VT had NT-proBNP levels of 654.87 +/- 237.87 pmol/L (p = 0.001). An NT-proBNP cutoff value of 880 pmol/L had a sensitivity of 73%, a specificity of 88%, a positive predictive value of 80%, and a negative predictive value of 88% for the prediction of occurrence-sustained VT events. To achieve the maximum benefit by ICD therapy, more precise risk stratification is required, even in high-risk, post-myocardial infarction patients. Plasma NT-proBNP levels comprise a promising method that could help in the better identification of a patient group with an even higher risk of sudden death.
    Chest 10/2005; 128(4):2604-10. DOI:10.1378/chest.128.4.2604 · 7.13 Impact Factor