Blood pressure response to close or loose contact between physician and patient during attended office blood pressure measurement.

PURPOSE: Compared to unattended office blood pressure (uOBP), attended office blood pressure (aOBP) is higher. It is not known, however, to what extent distance between physician and patient influences blood pressure (BP) values. MATERIALS AND METHODS: Participants were stable hypertensive patients, followed in the university hospital-based out-patient center. During a session, automated office BP was measured three times after a pre-set five-minute pause, using the Omron 907 device; both aOBP and uOBP were done, in a random order. Simultaneously, beat-to-beat BP measurement was performed using the Finapress device. During aOBP, some participants were in close contact with the physician while others were in loose contact where the doctor was sitting in the room about 2.5 m apart. One year later, the second session with the same protocol was organized, but the close and loose contact were interchanged. The data were analyzed using a paired t-test. RESULTS: Complete data were collected in 32 patients, baseline uOBP was 122.8 ± 14.8/69.5 ± 11.7 mmHg. Systolic and diastolic aOBP with close contact was higher by 4.6 ± 6.9 and 1.9 ± 3.4 mmHg (p < 0.0007 and 0.0039, respectively), while aOBP with loose contact was not different from uOBP. Beat-to-beat BP increased during aOBP by 6.5 ± 8.5/3.3 ± 4.8 mmHg. The increase persisted during all the three aOBP measurements (p < 0.0001 for all systolic and diastolic BP values); the results were similar for close and loose contact. The peak increase during uOBP was of similar magnitude as during aOBP but it lasted shorter: it reached the significance level of p < 0.0001 only during the first uOBP measurement. CONCLUSIONS: Compared to uOBP, aOBP values were higher with close, but not with loose contact between physician and patient. These differences were, however, not detected by beat-to-beat BP measurement.

High leptin status indicates an increased risk of mortality and heart failure in stable coronary artery disease.

BACKGROUND AND AIMS: Leptin is an adipocyte-derived peptide involved in energy homeostasis and body weight regulation. The position of leptin in cardiovascular pathophysiology remains controversial. Some studies suggest a detrimental effect of hyperleptinemia on the cardiovascular (CV) system, while others assume the role of leptin as a neutral or even protective factor. We have explored whether high leptin affects the mortality and morbidity risk in patients with stable coronary heart disease. METHODS AND RESULTS: We followed 975 patients ≥6 months after myocardial infarction or coronary revascularization in a prospective study. All-cause or cardiovascular death, non-fatal cardiovascular events (recurrent myocardial infarction, stroke, or any revascularization), and hospitalizations for heart failure (HF) we used as outcomes. High serum leptin concentrations (≥18.9 ng/mL, i.e., 4th quartile) were associated with worse survival, as well as with a higher incidence of fatal vascular events or hospitalizations for HF. Even after full adjustment for potential covariates, high leptin remained to be associated with a significantly increased 5-years risk of all-cause death [Hazard risk ratio (HRR) 2.10 (95%CIs:1.29-3.42), p < 0.003], CV death [HRR 2.65 (95%CIs:1.48-4.74), p < 0.001], and HF hospitalization [HRR 1.95 (95% CIs:1.11-3.44), p < 0.020]. In contrast, the incidence risk of non-fatal CV events was only marginally and non-significantly influenced [HRR 1.27 (95%CIs:0.76-2.13), p = 0.359]. CONCLUSIONS: High leptin concentration entails an increased risk of mortality, apparently driven by fatal CV events and future worsening of HF, on top of conventional CV risk factors and the baseline status of left ventricular function.

The prognosis and therapeutic management of patients hospitalized for heart failure in 2010-2020.

AIMS: We analyzed the mortality risk and its predictors in patients hospitalized for heart failure (HF). METHODS: Patients discharged from hospitalization for acute decompensation of HF in 2010-2020 and younger than 86 years were followed (n=4097). We assessed the incidence and trends of all-cause death, its main predictors, and the pharmacotherapy recommended at discharge from the hospital. RESULTS: The 30 days all-cause mortality was in discharged patients 3.2%, while 1-year 20.4% and 5-years 55.4%. We observed a modest trend to decreased 1-year mortality risk over time. Any increase of year of hospitalization by one was associated with about 5% lower risk in the fully adjusted model. Regarding predictors of 1-year mortality risk, a positive association was found for age over 65, history of malignancy, and peak brain natriuretic peptide during hospitalization ≥10times higher than normal concentration. In contrast, as protective factors, we identified LDL ≥1.8 mmol/L, treatment with beta-blockers, renin-angiotensin axis blockers, statins, and implanted cardioverter in the same regression model. The ejection fraction category and primary etiology of HF (coronary artery disease vs. others) did not significantly affect the mortality risk in a fully adjusted model. CONCLUSIONS: Despite advances in cardiovascular disease management over the last two decades, the prognosis of patients hospitalized for heart failure remained highly unfavorable.

Prevalence of cancer in patients with superficial vein thrombosis and its clinical importance.

OBJECTIVE: The objective of the present study was to evaluate the prevalence of cancer in patients with superficial vein thrombosis (SVT) of the legs. Moreover, we evaluated the potential determinants of SVT complications by comparing a subgroup with isolated SVT and a subgroup of SVT complicated by concurrent deep vein thrombosis (DVT) and/or pulmonary embolism (PE) with respect to the presence of cancer and other clinical and laboratory characteristics. METHODS: The present single-center, retrospective study of prospectively collected data was conducted in a tertiary care setting. We included patients who had been treated in the thrombosis clinic from 2006 to 2018 for symptomatic SVT of the legs, either isolated SVT or SVT complicated by concurrent DVT/PE. We evaluated the prevalence and type of malignancy (diagnosed ≤12 months before SVT and/or ongoing therapy), demographics, and clinical and laboratory characteristics of the patients. For statistical evaluation, we used the Student t test, Kruskal-Wallis test, Fisher exact two-sided test, and logistic regression. RESULTS: Of 276 patients with SVT (mean age, 58.9 ± 14.7 years; 60.9% women), 191 had had isolated SVT and 85 had had SVT complicated by concurrent DVT/PE. The prevalence of malignancy was 8.7% in the whole group (mainly breast and urinary tract cancer), including 4.2% of those with isolated SVT and 18.8% of those with SVT and concurrent DVT/PE (P < .001). Between the two subgroups, no significant differences were present in the duration of leg symptoms, family or personal history of SVT and/or DVT, SVT location, and smoking. In logistic regression, several factors were significantly associated with the concurrent presence of DVT/PE: age (odds ratio [OR], 1.024; 95% confidence interval [CI], 1.004-1.044), female gender (OR, 0.545; 95% CI, 0.309-0.960), varicose vein SVT (OR, 0.42; 95% CI, 0.194-0.902), thrombophilia (OR, 1.939; 95% CI, 1.089-3.454), and cancer (OR, 4.727; 95% CI, 1.814-12.316). CONCLUSIONS: The prevalence of malignancy in the patients with SVT was 8.7%. Age, thrombophilia, male gender, nonvaricose vein SVT, and cancer were significantly associated with the presence of concurrent DVT/PE. Cancer was the strongest determinant of concurrent DVT/PE.

Myocardial Involvement Detected Using Cardiac Magnetic Resonance Imaging in Patients with Systemic Sclerosis: A Prospective Observational Study.

INTRODUCTION AND OBJECTIVES: Cardiac involvement in systemic sclerosis (SSc) patients affects mortality. Cardiac magnetic resonance (CMR) is capable of detecting structural changes, including diffuse myocardial fibrosis that may develop over time. Our aim was to evaluate myocardial structure and function changes using CMR in patients with SSc without known cardiac disease during a 5-year follow-up and find possible correlations with selected biomarkers. METHODS: A total of 25 patients underwent baseline and follow-up CMR examinations according to a pre-specified protocol. Standard biochemistry, five biomarkers (hsTnI, NT-proBNP, galectin-3, sST2, and GDF-15), and disease-specific functional parameters enabling the classification of disease severity were also measured. RESULTS: After five years, no patient suffered from manifest heart disease. Mean extracellular volume (ECV) and T1 mapping values did not change significantly (p ≥ 0.073). However, individual increases in native T1 time and ECV correlated with increased galectin-3 serum levels (r = 0.56; p = 0.0050, and r = 0.71; p = 0.0001, respectively). The progression of skin involvement assessed using the Rodnan skin score and a decrease in the diffusing capacity of the lungs were associated with increased GDF-15 values (r = 0.63; p = 0.0009, and r = -0.51; p = 0.011, respectively). CONCLUSIONS: During the 5-year follow-up, there was no new onset of heart disease observed in patients with SSc. However, in some patients, CMR detected progression of sub-clinical myocardial fibrosis that significantly correlated with elevated galectin-3 levels. GDF-15 values were found to be associated with disease severity progression.

Low vitamin K status, high sclerostin and mortality risk of stable coronary heart disease patients.

Aim: We explored whether matrix Gla protein (MGP, natural calcification inhibitor) and sclerostin (glycoprotein responsible for osteoblast differentiation) interact in terms of mortality risk in coronary patients. Methods: 945 patients after myocardial infarction and/or coronary revascularization were followed in a prospective study. All-cause death, fatal or nonfatal cardiovascular events and heart failure hospitalizations were registered. Results: Either high desphospho-uncarboxylated MGP (dp-ucMGP) or high sclerostin were independently associated with 5-year all-cause/cardiovascular mortality. However, we observed an additional mortality risk in the coincidence of both factors. Concomitantly high dp-ucMGP (≥884 pmol/l) plus sclerostin (≥589 ng/l) were associated with increased all-cause mortality risk compared with 'normal' concentrations of both factors (HRR 3.71 [95% CI: 2.07-6.62, p < 0.0001]), or if only one biomarker has been increased. A similar pattern was observed for fatal, but not for nonfatal cardiovascular events. Conclusion: Concomitantly high MGP and sclerostin indicate increased mortality risk, which probably reflects their role in cardiovascular calcifications.

A novel nonsense mutation in the ß-subunit of the epithelial sodium channel causing Liddle syndrome.

PURPOSE: Liddle syndrome is a hereditary form of arterial hypertension caused by mutations in the genes coding of the epithelial sodium channel - SCNN1A, SCNN1B and SCNN1G. It is characterised by early onset of hypertension and variable biochemical features such as hypokalaemia and low plasma concentrations of renin and aldosterone. Phenotypic variability is large and, therefore, LS is probably underdiagnosed. Our objective was to examine a family suspected from Liddle syndrome including genetic testing and evaluate clinical and biochemical features of affected family members. MATERIALS AND METHODS: Thirteen probands from the Czech family, related by blood, underwent physical examination, laboratory tests, and genetic testing. Alleles of SCNN1B and SCNN1G genes were examined by PCR amplification and Sanger sequencing of amplicons. RESULTS: We identified a novel mutation in the ß-subunit of an epithelial sodium channel coded by the SCNN1B gene, causing the nonsense mutation in the protein sequence p.Tyr604*. This mutation was detected in 7 members of the family. The mutation carriers differed in the severity of hypertension and hypokalaemia which appeared only after diuretics in most of them; low aldosterone level (< 0.12 nmol/l) was, however, present in all. CONCLUSIONS: This finding expands the spectrum of known mutations causing Liddle syndrome. Hypoaldosteronemia was 100% sensitive sign in the mutation carriers. Low levels are observed especially in the Caucasian population reaching 96% sensitivity. Assessment of plasma aldosterone concentration is helpful for differential diagnosis of arterial hypertension. CONDENSED ABSTRACT: Liddle syndrome is a hereditary form of arterial hypertension caused by mutations in the genes encoding the epithelial sodium channel's α-, ß- and γ-subunit. It is usually manifested by early onset of hypertension accompanied by low potassium and aldosterone levels. We performed a physical examination, laboratory tests and genetic screening in 13 members of a Czech family. We found a new mutation of the SCNN1B gene which encodes the ß-subunit of the epithelial sodium channel. We describe the variability of each family member phenotype and point out the relevance of using aldosterone levels as a high sensitivity marker of Liddle syndrome in Caucasians.

The prognostic impact of renal function decline during hospitalization for myocardial infarction.

Aim: We analyzed the mortality risk of myocardial infarction (MI) patients according to renal function, observed during hospitalization. Materials & methods: Patients hospitalized for MI between 2006 and 2018 were followed (n = 5659). We divided the sample into four groups by estimated glomerular filtration (eGFR) [ml/min]: normal functions (lowest eGFR during hospitalization >60); transiently moderate insufficiency (lowest eGFR >30 and ≤60, highest >60); permanently moderate insufficiency (highest eGFR >30 and ≤60); severe insufficiency (highest and lowest eGFR ≤30). Results: Permanently moderate renal insufficiency indicates increased 5-years all-cause mortality (hazard risk ratio: 2.27 [95% CIs: 1.87-2.75], p < 0.0001), but a similar risk was found in patients with the only transient decline of renal functions (hazard risk ratio: 2.08 [95% CIs: 1.70-2.55], p < 0.0001). Both moderate insufficiency subgroups (transient/permanent) did not statistically differ regarding mortality risk. Conclusion: Even just fluctuation of eGFR toward moderate insufficiency during hospitalization represents an important prognostic indicator in MI patients.

Serum biomarkers, skin autofluorescence and other methods. Which parameter better illustrates the relationship between advanced glycation end products and arterial stiffness in the general population?

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.

The coincidence of low vitamin K status and high expression of growth differentiation factor 15 may indicate increased mortality risk in stable coronary heart disease patients.

BACKGROUND AND AIMS: Matrix Gla protein (MGP) is a natural inhibitor of vascular calcification critically dependent on circulating vitamin K status. Growth differentiation factor 15 (GDF-15) is a regulatory cytokine mainly of the inflammatory and angiogenesis pathways, but potentially also involved in bone mineralization. We sought to determine whether these two circulating biomarkers jointly influenced morbidity and mortality risk in patients with chronic coronary heart disease (CHD). METHODS AND RESULTS: 894 patients ≥6 months after myocardial infarction and/or coronary revascularization at baseline were followed in a prospective study. All-cause and cardiovascular mortality, non-fatal cardiovascular events (myocardial infarction, stroke, any revascularization), and hospitalization for heart failure (HF) were followed as outcomes. Desphospho-uncarboxylated MGP (dp-ucMGP) was used as a biomarker of vitamin K status. Both, increased concentrations of dp-ucMGP (≥884 pmol/L) and GDF-15 (≥1339 pg/mL) were identified as independent predictors of 5-year all-cause or cardiovascular mortality. However, their coincidence further increased mortality risk. The highest risk was observed in patients with high dp-ucMGP plus high GDF-15, not only when compared with those with "normal" concentrations of both biomarkers [HR 5.51 (95% CI 2.91-10.44), p < 0.0001 and 6.79 (95% CI 3.06-15.08), p < 0.0001 for all-cause and cardiovascular mortality, respectively], but even when compared with patients with only one factor increased. This pattern was less convincing with non-fatal cardiovascular events or hospitalization for HF. CONCLUSIONS: The individual coincidence of low vitamin K status (high dp-ucMGP) and high GDF-15 expression predicts poor survival of stable CHD patients.

The Prognostic Importance of Impaired Fasting Glycemia in Chronic Coronary Heart Disease Patients.

OBJECTIVES: Impaired glucose metabolism represents one the most important cardiovascular risk factors, with steeply raising prevalence in overall population. We aimed to compare mortality risk of impaired fasting glycaemia (IFG) and overt diabetes mellitus (DM) in patients with coronary heart disease (CHD). STUDY DESIGN: prospective cohort study METHODS: A total of 1685 patients, 6-24 months after myocardial infarction and/or coronary revascularization at baseline, were followed in a prospective cohort study. Overt DM was defined as fasting glucose ≥ 7 mmol/L and/or use of antidiabetic treatment, while IFG as fasting glucose 5.6-6.99 mmol/L, but no antidiabetic medication. The main outcomes were total and cardiovascular mortality during 5 years of follow-up. RESULTS: During follow-up of 1826 days, 172 patients (10.2%) deceased, and of them 122 (7.2%) from a cardiovascular cause. Both exposures, overt DM (n=623, 37.0% of the whole sample) and IFG (n=436, 25.9%) were associated with an independent increase of 5-year total mortality, compared to normoglycemic subjects [fully adjusted hazard risk ratio (HRR) 1.63 (95%CI: 1.01-2.61)]; p=0.043 and 2.25 (95%CI: 1.45-3.50); p<0.0001, respectively]. In contrast, comparing both glucose disorders one with each other, no significant differences were found for total mortality [HRR 0.82 (0.53-1.28); p=0.33]. Taking 5-years cardiovascular mortality as outcome, similar pattern was observed [HRR 1.96 (95%CI: 1.06-3.63) and 3.84 (95%CI: 2.19-6.73) for overt DM and IFG, respectively, with HRR 0.63 (95%CI: 0.37-1.07) for comparison of both disorders]. CONCLUSIONS: Impaired fasting glycaemia adversely increases mortality of CHD patients in the same extent as overt DM.

The role of advanced glycation end products in vascular aging: which parameter is the most suitable as a biomarker?

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) [ß 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.

Adherence to cardiovascular prevention principles in subjects at high risk.

BACKGROUND: Asymptomatic high-risk individuals represent one of the highest priorities of cardiovascular prevention, in clinical practice frequently overlooked. We analyzed the real adherence to recommended principles of cardiovascular prevention in primary care subjects. METHODS: Our analysis is based on random general population sample, examined in the frame of post-MONICA survey in 2016/17. Each subject was categorized with regard to its individual cardiovascular risk (based on Sixth Joint European Guidelines) and the real adherence to recommended targets was ascertained. RESULTS: In total 898 subjects aged 25-75 years (47% males) were analyzed. Of them, 16.7% were classified into “very high risk“ and 36.8% into “high risk“ subgroup; remaining 46.5% were only at moderate or low risk. Regarding adherence to recommended principles, in “very high risk“ category only 58.7% abstain from any form of tobacco, 38% reported appropriate physical activity (150 minutes of at least moderate activity weekly), 16.7% had recommended body constitution (BMI 20-25 kg/m2 ), 39.3% appropriate blood pressure (.

Is There Really an Association of High Circulating Adiponectin Concentration and Mortality or Morbidity Risk in Stable Coronary Artery Disease?

Adiponectin has several beneficial properties, namely, on the level of glucose metabolism, but paradoxically, its high concentrations were associated with increased mortality. We aimed to clarify the impact of high serum adiponectin on mortality and morbidity in patients with stable coronary artery heart disease (CAD). A total of 973 patients after myocardial infarction and/or coronary revascularization were followed in a prospective cohort study. All-cause and cardiovascular (CV) death, non-fatal cardiovascular events, and hospitalizations for heart failure (HF) were registered as outcomes. High serum adiponectin levels (≥8.58 ng/ml, i. e., above median) were independently associated with increased risk of 5-year all-cause, CV mortality or HF [with HRR 1.57 (95% CI: 1.07-2.30), 1.74 (95% CI: 1.08-2.81) or 1.94 (95% CI: 1.20-3.12), respectively] when adjusted just for conventional risk factors. However, its significance disappeared if brain natriuretic peptide (BNP) was included in a regression model. In line with this, we observed strong collinearity of adiponectin and BNP. Additionally, major adverse cardiovascular event (i. e., CV death, non-fatal myocardial infarction or stroke, coronary revascularization) incidence risk was not associated with high adiponectin. In conclusion, the observed inverse association between adiponectin concentrations and mortality risk seems to be attributable to concomitantly increased BNP, rather than high adiponectin being a causal factor.

Synergistic effect of sclerostin and angiotensin II receptor 1 polymorphism on arterial stiffening.

Aim: 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. Methods: 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. Results: 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). Conclusion: Sclerostin concentrations were associated with an accelerated natural course of arterial stiffening, but only in interaction with renin-angiotension system.

The prognostic importance of subclinical heart failure in stable coronary heart disease patients.

Background: In stable coronary heart disease (CHD) patients we aimed to assess the predictive potential of only mild increase of brain natriuretic peptide (BNP) in subjects free from symptoms or diagnostic criteria of heart failure (HF).Methods: We examined 967 patients, at least 6 months after myocardial infarction or coronary revascularization and divided them into three categories: 'overt HF' (NYHA II-IV, objective signs of HF, chronic treatment with furosemide and/or spironolactone or history of hospitalisation for HF), 'subclinical HF (BNP over 150 ng/mL, but no criterion of overt HF)' and 'no HF' (no above mentioned criterion present). Follow-up was done to assess 5-years all-cause mortality.Results: Overt and subclinical HF (by definition) had 38.8% and 9.6% of patients, respectively. In analyses adjusted for classical risk factors and other possible covariates, both overt and subclinical HF were independently associated with increased mortality compared to no HF subjects [hazard risk ratio 1.99 (95%CI:1.02-3.91) and 3.01 (95%CI:1.90-4.78), respectively. The risk of total mortality was similar in overt and subclinical HF patients [HRR 1.30 (95%CI: 0.72-2.36)]. Within overt HF group, those with BNP >150 ng/mL had also higher mortality risk than those with low BNP levels [HRR 2.79 (95%CI: 1.67-4.68)]. The addition of left ventricle ejection fraction into definition of HF groups did not affect main results.Conclusions: Mild increase of BNP in generally stable and asymptomatic CHD patients identifies high individual mortality risk in the same extend that presence of clinically manifest HF.

Mood disorders impaired quality of life but not the mortality or morbidity risk in stable coronary heart disease patients.

Background: It was suggested that depression and anxiety might be associated with increased cardiovascular risk in both primary and secondary prevention. In stable coronary heart disease (CHD) patients, we aimed to assess prevalence of depression and anxiety, its relations to conventional risk profile and mortality or morbidity and to quality of life (QoL).Methods: We examined 969 patients, at least 6 months after myocardial infarction or coronary revascularisation. Depression or anxiety was assessed using a standard HADS (Hospital Anxiety and Depression Scale), while QoL by SF-36 (Short-Form-36 Questions) questionnaires. Follow-up was done to assess mortality in incidence of non-fatal cardiovascular event.Results: Both mood disorders were rather frequent; borderline depression or anxiety (HADS score 8-10) had 14.8 or 10.9% of patients, respectively; moderate-to-severe depression or anxiety (HADS score ≥11) had another 8.2 or 6.7% of patients. After adjustment for potential covariates impaired QoL (SF-36 score <40) was independently associated with depressive mood [odds ratio (OR) 6.08 (95%CI: 2.92-12.7) or anxiety [OR 8.66 (95%CI: 3.77-19.89)], as well as with combination of both disorders [OR 33.58 (95%CI: 15.5-72.6)]. Conventional risk characteristics remained virtually unrelated to mood disorders (with exception of angina pectoris). We found significantly higher incidence of major cardiovascular events in patients with anxious mood and marginally significant inferior survival in patients with depression, but any cardiovascular risk disappeared if adjusted for potential covariates (conventional risk factors, natriuretic peptides, angina pectoris.)Conclusions: Mood disorders severely affected QoL of stable CHD patients, but not their global cardiovascular risk.

Soluble receptor for advanced glycation end-products independently influences individual age-dependent increase of arterial stiffness.

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.

Soluble RAGEs and cardiovascular risk factors in adult offspring of patients with premature coronary heart disease.

Purpose: Advanced glycation end products (AGEs) are a heterogeneous group of highly oxidant compounds which can potentiate microvascular and macrovascular complications through the formation of irreversible cross-links between molecules in the basal membrane and also by engaging the receptor for AGEs (RAGE). Soluble receptor for AGEs (sRAGE) is suggested to have a protective role neutralizing the toxic action of AGEs. We aimed to investigate differences in plasma levels of sRAGE alongside with classic cardiovascular risk factors between offspring of patients with early onset of coronary heart disease (CHD) and healthy controls.Materials and methods: In a cross-sectional design, we examined 114 adult offspring of patients with premature CHD and 194 controls. Concentrations of soluble RAGE were quantified by ELISA methods. Aortic PWV was measured using Sphygmocor device. Multivariate logistic regressions were used to compare differences between the offspring and controls.Results: In the offspring group there were more men (p = 0.023), both groups had similar age (28.5 vs. 28.9 years; p = 0.51). After adjustment for covariates, we observed significantly higher aPWV (6.17 vs. 5.82 m s-1; p = 0.001) and lower sRAGE (1308.11 vs. 1475.59; p = 0.009) in the offspring group compared to controls. The significant determinants of the intergroup difference were sRAGE (p = 0.0017), aPWV (p = 0.011) and current smoking (p = 0.0053).Conclusion: Offspring of patients with early onset of CHD compared to age-matched healthy controls had significantly lower sRAGE levels suggesting a shift in the oxidative balance between stressors and defence mechanisms that may influence a higher cardiovascular risk in the future. The measurement of sRAGE might be a valuable predictor for more precise stratification of cardiovascular risk.

To what extent can the chosen blood pressure measurement technique affect the outcomes of an observational survey?

Aim: We analyzed to what extent measurement protocol influenced individual blood pressure (BP) and achievement of treatment target in patients with coronary heart disease. Methods: 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). Results: 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). Conclusion: Per-protocol oscillometric technique was not equivalent to conventional auscultatory measurement and seriously over-rated the real nonachievement of BP target in observational surveys.