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Stiffening of large arteries, clinically manifesting as increased aortic pulse wave velocity (PWV), is an inevitable outcome of aging. Among other mechanisms, impaired glucose metabolism plays an important role, leading to the deposition of advanced glycation end products (AGEs). This process is counterbalanced by the circulating soluble receptor for AGEs (sRAGE). We investigated the association between arterial stiffness on one side and multiple circulating biomarkers and the degree of skin deposition of AGEs on the other. In a cross-sectional design, 867 participants based on a general population sample (Czech post-MONICA studies) were examined. PWV was measured by SphygmoCor device (AtCor Medical Ltd.), while skin AGEs were measured using a dedicated autofluorescence method (AGE Reader mu ). To quantify the circulating status of AGEs, carboxymethyl lysine (CML) and sRAGE concentrations were assessed by ELISA, along with conventional glucose metabolism indicators. When analyzing the whole sample using multiple linear or logistic regression models and after adjustment for potential covariates, a significant association with PWV was found for fasting glycemia, HbA1c, sRAGE, skin AGEs, and the skin AGE-to-sRAGE ratio. Among these parameters, stepwise models identified the strongest association for the skin AGEs and AGE-to-sRAGE ratio, and this was also true when diabetic subjects were excluded. In contrast, neither CML nor its ratio relative to sRAGE showed any association with arterial stiffness. In conclusion, skin AGEs along with their ratio relative to sRAGE were closely associated with arterial stiffness and is a better indicator of the current status of deposited AGEs than other relevant factors.

Advanced glycation end products (AGEs) are involved in several pathophysiologic processes in vascular diseases, including progressive loss of elasticity of the vessel wall (arterial stiffness). Circulating soluble receptors for AGEs (sRAGE) act as a decoy and counterbalanced the harmful properties of AGEs as the natural protective factor. We compared the role of circulating or skin-deposed AGEs and sRAGE regarding the natural course of arterial stiffening. In a prospective cohort study, we longitudinally followed 536 general population-based subjects (subsample of Czech post-MONICA study). Aortic pulse-wave velocity (PWV) was measured twice (at baseline and after ~8 years of follow-up) using a SphygmoCor device (AtCor Medical Ltd), and the intraindividual change in PWV per year (∆PWV/year) was calculated. Concentrations of sRAGE and carboxymethyl lysine (circulating AGEs) were assessed at the follow-up visit by ELISA, while skin AGEs were measured using the autofluorescence-based device AGE Reader. Using multiple regressions, we found significant association between ∆PWV/year as a dependent variable, and both, sRAGE and skin AGEs as independent ones (each on its own model). However, the closest associations to ∆PWV/year were found for the ratio of these two factors (skin AGEs/sRAGE) [β coeff = 0.0747 (SE 0.0189), p < 0.0001]. In a categorized manner, subjects with skin AGEs/sRAGE ratio ≥ 3.3 showed about twofold higher risk having ΔPWV/year ≥ 0.2 m/s [adjusted odds ratio was 2.09 (95% CI: 1.35–3.22), p = 0.001]. In contrast, neither circulating AGEs nor circulating AGEs/sRAGE showed any significant relation to ΔPWV/year. In conclusion, skin AGEs/sRAGE ratio seems to be a more sensitive biomarker of vascular aging than these single factors themselves or circulation status of AGEs.

Circulating levels of soluble receptor for advanced glycation end-products (sRAGE) have been suggested to have a protective role in neutralizing advanced glycation end-products (AGEs) and their pathological effects on vessel walls. We aimed to investigate the association between the circulating concentration of sRAGE and the dynamics of arterial wall stiffening as a manifestation of vascular aging in the general population. In a prospective cohort study, we longitudinally followed 530 general-population-based subjects (subsample of Czech post-MONICA study). Aortic pulse wave velocity (PWV) was measured twice (at baseline and after ~8 years of follow-up) using a SphygmoCor device (AtCor Medical Ltd), and the intraindividual change in PWV per year (∆PWV/year) was calculated. Concentrations of sRAGE were assessed at baseline by ELISA (R&D Systems). The average ∆PWV/year significantly decreased across the sRAGE quintiles (p = 0.048), and a drop by one sRAGE quintile was associated with an ~21% increase in the relative risk of accelerated age-dependent stiffening (∆PWV/year ≥ 0.2 m/s). Subjects in the bottom quintile of sRAGE (<889.74 pg/mL) had a fully adjusted odds ratio of accelerated stiffening of 1.72 (95% CI: 1.06–2.79), p = 0.028, while those with high sRAGE concentrations (≥1695.2 pg/mL) showed the opposite effect [odds ratio 0.55 (95% CI: 0.33–0.90), p = 0.017]. In conclusion, the circulating status of sRAGE independently influenced the individual progression of arterial stiffness over time. This finding strongly supports the hypothesis that high sRAGE has a protective role against vascular aging.

It has been suggested that accumulation of advanced glycation end products (AGEs) is involved in several pathophysiological processes in the vessel wall. We hypothesized that low levels of the soluble receptor for AGEs (sRAGE) might be associated with increased arterial stiffness, a manifestation of vascular ageing in the general population. Using a cross-sectional design, we analyzed 1077 subjects from the Czech post-MONICA study. The aortic pulse wave velocity (aPWV) was measured using a Sphygmocor device. sRAGE concentrations were assessed in frozen samples using enzyme-linked immunosorbent assay methods (R&D Systems). aPWV significantly (P<0.0001) increased across the sRAGE quartiles. An aPWV of 1 m s(-1) was associated with a 37% increase in the risk of low sRAGE (<918 pg ml(-1), bottom quartile; P-value=0.018). In a categorized manner, subjects in the bottom sRAGE quartile had an odds ratio of an increased aPWV (⩾9.3 m s(-1)), adjusted for all potential confounders of 2.05 (95% confidence interval: 1.26-3.32; P=0.004), but this was only the case for non-diabetic hypertensive patients. In contrast, a low sRAGE was rejected as an independent predictor of an increased aPWV in normotensive or diabetic subjects using similar regression models. In conclusion, low circulating sRAGE was independently associated with increased arterial stiffness in a general population-based sample, but this was only observed in hypertensive non-diabetic patients.

Background Advanced glycation end products (AGEs) are involved into several pathophysiologic processes in vascular diseases, including progressive loss of elasticity of vessel wall (arterial stiffness). Circulating soluble receptor for AGEs (sRAGE) act as a decoy and counterbalanced the harmful properties of AGEs as the natural protective factor [ 1 , 2 ]. We compared the role of circulating or skin-deposed AGEs and sRAGE regarding natural course of arterial stiffening. Methods In a prospective cohort study, we longitudinally followed 536 general-population-based subjects (subsample of Czech post-MONICA study). Aortic pulse wave velocity (PWV) was measured twice (at baseline and after ~8 years of follow-up) using a SphygmoCor device (AtCor Medical Ltd.), and the intraindividual change in PWV per year (∆PWV/year) was calculated. Concentrations of sRAGE and carboxylmethyl lysine (circulating AGEs) were assessed at follow-up visit by ELISA, while skin AGEs were measured using autofluorescence-based device AGE Reader. Results Using multiple regressions, we found significant association between ∆PWV/year as dependent variable and both, sRAGE and skin AGEs as independent ones (each on its own model). However, the closest association to ∆PWV/year were found for ratio of these two factors (skin AGEs/sRAGE) [coeff = 0.0747 (SE 0.0189), p < 0.0001]. In categorized manner, subjects with skin AGEs/sRAGE ratio ≥3.3 showed about two-fold higher risk having PWV/year ≥0.2 m/sec [adjusted odds ratio was 2.09 (95% CI: 1.35–3.22), p = 0.001]. In contrast neither circulating AGEs nor circulating AGEs/sRAGE showed any significant relation to PWV/ year. Conclusions Skin AGEs/sRAGE ratio seems to be more sensitive biomarker of vascular ageing than these single factors themselves or circulation status of AGEs [ 3 ].

We aimed to establish the association between sclerostin (a glycoprotein involved in bone metabolism) and development of pulse wave velocity (PWV) in the general population. A prospective cohort study with a total of 522 subjects. Aortic PWV was measured twice (at baseline and after approximately 8 years of follow-up) and intraindividual change in PWV per year (ΔPWV/year) was calculated. ΔPWV/year increased across the sclerostin quintiles, but generally in a strong age-dependent manner. However, a significant independent positive association between sclerostin and ΔPWV/year was observed exclusively in C allele carriers of rs5186 polymorphism for the angiotensin II receptor 1 (n = 246). Sclerostin concentrations were associated with an accelerated natural course of arterial stiffening, but only in interaction with renin-angiotension system.

We analyzed to what extent measurement protocol influenced individual blood pressure (BP) and achievement of treatment target in patients with coronary heart disease. In a subsample of Czech EUROASPIRE III–V survey participants (n = 913), we compared the per-protocol BP measurement (by automated oscillometric device OMRON at the beginning of survey procedure) with control auscultatory measurement (by physician during interview). Per-protocol approach produced significantly (p < 0.0001) higher BP values (by 9/6 mmHg in median) than auscultatory measurements and led to markedly higher proportion of patients over target BP (less than 140/90 mmHg; 59.3 vs 34.9% [p < 0.0001], per-protocol vs auscultatory technique, respectively). Per-protocol oscillometric technique was not equivalent to conventional auscultatory measurement and seriously over-rated the real nonachievement of BP target in observational surveys.

Background Although invasively measured blood pressure (invBP) is regarded as a “gold standard” in critically ill cardiac patients, the non-invasive BP is still widely used, at least at the initiation of medical care. The erroneous interpretation of BP can lead to clinical errors. We therefore investigated the agreement of both methods with respect to some common clinical situation. Methods We included 85 patients hospitalized for cardiogenic shock. We measured BP every 6 h for the first 72 h of hospitalization, in all patients. Each set of BP measurements included two invasive (invBP), two auscultatory (auscBP), and two oscillometric (oscBP) BP measurements. InvBP was considered as a gold standard. Mean non-invasive arterial pressure (MAP) was calculated as ( diastolic pressure + (pulse pressure ÷ 3)) . We used Bland-Altman analysis and we calculated concordance correlation coefficients to assess agreement between different BP methods. Results We obtained 967 sets of BP measurements. AuscMAP and oscMAP were on average only 0.4 ± 8.2 and 1.8 ± 8.5 mmHg higher than invMAP, respectively. On the other hand, auscSBP and oscSBP were on average − 6.1 ± 11.4 and − 4.1 ± 9.8 mmHg lower than invSBP, respectively. However, the mean differences and variability for systolic and diastolic BP variability were large; the 2 standard deviation differences were ± 24 and 18 mmHg. In hypotension, non-invasive BP tended to be higher than invBP while the opposite was true for high BP values. Clinical conditions associated with hypotension generally worsened the accuracy of non-invasive MAP. Conclusions Mean arterial pressure measured non-invasively appears to be in good agreement with invasive MAP in patients admitted for cardiogenic shock. Several clinical associated with hypotension can affect accuracy of non-invasive measurement. Auscultatory and oscillometric measurements had similar accuracy even in patients with arrhythmia.

Background Accumulation of advanced glycation end-products (AGEs) is one of pathophysiological processes, responsible for progressive stiffening of vessel wall. In contrast, soluble isoform of receptor for AGEs (sRAGE) act as “decoy” and physiological defense against circulating AGEs. We hypothesized that low levels of sRAGE might be associated with accelerated age-dependent arterial stiffening. Methods We followed 429 population-based subjects (mean age 50.8 (±11.7) years, 41.5% males) in prospective study. Aortic pulse wave velocity (aPWV) was measured using a Sphygmocor device. sRAGE concentrations were assessed in frozen samples by ELISA methods (R&D Systems). Baseline examination was done in 2008/9, while follow-up visit in 2016/17 (median time of follow-up was 7.6 years) Results Mean intra-individual increase of aPWV during follow-up was 1.37 (±1.88) m/sec and was inversely associated with baseline sRAGE concentration — the aPWVV difference [follow-up minus baseline] across its quintiles was 2.08((±1.89), 1.51(±2.16), 1.20(±2.10), 0.99(±1.70), 1.13(±1.21) in 1st–5th quintiles of sRAGE, resp.; p = 0.003 (adjusted for age, gender and baseline mean arterial pressure) Baseline concentration of sRAGE <917 pg/mL (1st quintile) was associated with about two-fold higher risk, that aPWV increased by more than 0.8 m/sec (expectable “secular” age-dependent increase) even if adjusted for baseline risk profile and pharmacotherapy [fully adjusted odds ratio was 1.95 (95%CI: 1.12–3.39, p = 0.018]. Conclusions Low concentration of circulating sRAGE was in our sample of generally healthy subjects associated with markedly accelerated age-dependent arterial stiffening, probably as a consequence of higher deposition of AGEs in vessel wall ( supported by SVV 02684, PROGRES Q39 and AZV 15-27109 grants ).

Postpartum depression (PPD) affects up to 19% of all mothers, with detrimental effects on both mother and child. The antidepressant and anxiolytic effects of plasma oxytocin are well-documented, but it is still disputable whether synthetic oxytocin (synOT) may protect women against postpartum mood alterations. The current study examined the association between synOT intrapartum and maternal mood postpartum using a prospective design. Two hundred sixty women were screened for depressive symptoms in the last trimester of pregnancy and then again 6 weeks and 9 months postpartum using the Edinburgh Postnatal Depression Scale. They also completed Maternity Blues Questionnaire in the first postpartum week. The data concerning the intrapartum interventions and health status of the newborn were extracted from the medical records. Cox proportional hazards regression adjusted for a history of depression, mode of delivery, and childbirth experience showed that synOT predicted a significantly lower risk of PPD (HR = 0.65, 95% CI 0.45–0.95, p = 0.025). The risk factors for PPD included a history of depression (HR = 3.20, 95% CI 2.33–4.40, p < 0.001) and negative childbirth experience (HR = 1.39, 95% CI 1.01–1.90, p = 0.040). Logistic regression adjusted for the same covariates found no significant effect of synOT on maternity blues (OR = 0.64, 95% CI 0.31–1.32, p = 0.23). While synOT administered intrapartum does not affect maternal mood immediately, it may come to effect some weeks after childbirth to protect mothers from developing PPD symptoms.