58 research outputs found

    Reference values for aerobic capacity estimated by cardiopulmonary exercise test on a cycle ergometer in a healthy Greek population

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    Objective: Aerobic capacity (AC) is inversely associated with a high risk of cardiovascular morbidity and mortality as well as all-cause mortality. Cardiopulmonary exercise testing (CPET) represents the gold standard for assessing exercise capacity based on maximum oxygen uptake (VO2max). The purpose of our study was to provide for the first time CPET-derived normative reference values in a Greek cohort of apparently healthy men and women on a cycle ergometer to evaluate their AC, and to compare our results with similar studies from other countries. Methods: A cohort of 194 apparently healthy subjects (118 males and 76 females, age range, 15-69 years) was submitted to CPET using a cycle ergometer. Mean ± SD values for several exercise parameters, VO2max included, were determined. We compared our results with existing data derived from USA and North Europe cohorts. Results: Male subjects achieved significantly higher levels of relative and absolute VO2max (p < 0.001) across all ages compared to female subjects. A decline in relative and absolute VO2max among older participants was observed in both sexes. Greek subjects had lower AC than the North Europe cohort and almost similar to the USA cohort. Conclusion: We provide the first reference data for AC in apparently healthy Greek subjects based on CPET using cycle ergometer. Our findings will allow for more accurate interpretation of CPET in several groups of healthy subjects or patients with CV diseases. The differences found between our reference values and those reported from the USA and northern European countries, underscore the need for individual countries to develop their own AC reference values

    Angiotensin II induces soluble fms-Like tyrosine kinase-1 release via calcineurin signaling pathway in pregnancy

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    Maternal endothelial dysfunction in preeclampsia is associated with increased soluble fms-like tyrosine kinase-1 (sFlt-1), a circulating antagonist of vascular endothelial growth factor and placental growth factor. Angiotensin II (Ang II) is a potent vasoconstrictor that increases concomitant with sFlt-1 during pregnancy. Therefore, we speculated that Ang II may promote the expression of sFlt-1 in pregnancy. Here we report that infusion of Ang II significantly increases circulating levels of sFlt-1 in pregnant mice, thereby demonstrating that Ang II is a regulator of sFlt-1 secretion in vivo. Furthermore, Ang II stimulated sFlt-1 production in a dose- and time-dependent manner from human villous explants and cultured trophoblasts but not from endothelial cells, suggesting that trophoblasts are the primary source of sFlt-1 during pregnancy. As expected, Ang II-induced sFlt-1 secretion resulted in the inhibition of endothelial cell migration and in vitro tube formation. In vitro and in vivo studies with losartan, small interfering RNA specific for calcineurin and FK506 demonstrated that Ang II-mediated sFlt-1 release was via Ang II type 1 receptor activation and calcineurin signaling, respectively. These findings reveal a previously unrecognized regulatory role for Ang II on sFlt-1 expression in murine and human pregnancy and suggest that elevated sFlt-1 levels in preeclampsia may be caused by a dysregulation of the local renin/angiotensin system

    Dexamethasone as adjuvant therapy to moxifloxacin attenuates valve destruction in experimental aortic valve endocarditis due to Staphylococcus aureus

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    Although the beneficial effects of dexamethasone have frequently been investigated in various serious-infection settings, insufficient data on valve histology and cardiac function for infective endocarditis are available. The efficacy of moxifloxacin for the treatment of experimental aortic valve endocarditis due to methicillin-susceptible Staphylococcus aureus and the long-term effects of dexamethasone were evaluated in the current study. Sixty-eight rabbits were randomly assigned to four groups: A, B, C, and D. Group A consisted of 18 animals and functioned as a control group. Groups B and C consisted of 11 and 23 subjects, respectively, which received moxifloxacin for 5 days in a human-like pharmacokinetic simulation. Group D consisted of 16 animals that were administered moxiffoxacin plus dexamethasone (0.25 mg;1kg of body weight twice a day intravenously). The group B animals were sacrificed a day after the completion of treatment, and group C and D animals were sacrificed after 12 days in order to monitor any possible relapse and allow microbiological, histopathological, and echocardiographic evaluation of the longterm effects of glucocorticoids. No differences in survival, sterilization rates, or inflammatory infiltration and calcification of valve tissue were observed among the treated groups. However, the degrees of valve damage and collagenization were significantly worse, the fibroblast content was higher, and fractional shortening of the left ventricle fluctuated significantly in group C compared to group D (all groups, P &lt; 0.05). We concluded that dexamethasone treatment for experimental S. aureus endocarditis attenuates valve destruction and preserves overall cardiac function without impeding the efficacy of moxifloxacin

    Hypertension‐mediated organ damage regression associates with blood pressure variability improvement three years after successful treatment initiation in essential hypertension

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    Abstract Blood pressure variability (BPV) has been associated with the development, progression, and severity of cardiovascular (CV) organ damage and an increased risk of CV morbidity and mortality. We aimed to explore any association between short‐term BPV reduction and hypertension‐mediated organ damage (HMOD) regression in hypertensive patients 3‐year post‐treatment initiation regarding BP control. 24‐h ambulatory blood pressure monitoring (24 h ABPM) was performed at baseline in 180 newly diagnosed and never‐treated hypertensive patients. We measured 24 h average systolic (24 h SBP) and diastolic BP (24 h DBP) as well as 24 h systolic (sBPV) and diastolic BPV (dBPV). Patients were initially evaluated and 3 years later regarding arterial stiffness (PWV), left ventricular hypertrophy (LVMI), carotid intima‐media thickness (cIMT), 24 h microalbumin levels (MAU), and coronary flow reserve (CFR). Successful BP treatment was defined as 24 h SBP/DBP < 130/80 mm Hg based on 2nd ABPM and subsequently, patients were characterized as controlled (n = 119, age = 53 ± 11 years) or non‐controlled (n = 61, age = 47 ± 11 years) regarding their BP levels. In the whole population and the controlled group, 24 h SBP/DBP, sBPV/dBPV, LVMI, and IMT were decreased. Additionally, LVMI improvement was related with both sBPV (p < .001) and dBPV reduction (r = .18, p = .02 and r = .20, p = .03, respectively). In non‐controlled hypertensives, PWV was increased. In multiple linear regression analysis, sBPV and dBPV reduction predicted LVMI improvement in total population and controlled group independently of initial office SBP, mean BP, and 24 h‐SBP levels. In middle‐aged hypertensive patients, a 3‐year antihypertensive treatment within normal BP limits, confirmed by 24‐h ABPM, leads to CV risk reduction associated with sBPV and dBPV improvement

    Pharmacodynamic comparison of low-dose ticagrelor to low-dose prasugrel in patients with prior myocardial infarction: the ALTIC-2 study

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    Given that patients with prior myocardial infarction and features of high ischemic and low bleeding risk may benefit by extending dual antiplatelet therapy beyond 1 year, we aimed of assessing platelet reactivity provided by ticagrelor 60 mg bid versus prasugrel 5 mg od in 20 such patients participating in a randomized, crossover study. The primary end point of platelet reactivity at the end of the two treatment periods (by VerifyNow, in PRU) was significantly lower for ticagrelor (31.9 PRU [95% CI 12.3–51.4]) compared with prasugrel (132.1 PRU [111.9–152.3]) with a least squares mean difference of –100.2 PRU (72.1–128.3, P < .001). This dedicated pharmacodynamic study showed that in post-myocardial infarction patients with high atherothrombotic risk and receiving P2Y12 receptor antagonist beyond 1 year, low-dose ticagrelor results in a significantly lower platelet reactivity compared to low-dose prasugrel
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