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.

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.

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.

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.

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.

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.

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 (.

Factors influencing the accuracy of non-invasive blood pressure measurements in patients admitted for cardiogenic shock.

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.

The effects of intrapartum synthetic oxytocin on maternal postpartum mood: findings from a prospective observational study.

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.

Long-term relationship between unattended automated blood pressure and auscultatory BP measurements in hypertensive patients.

AIMS: Unattended automated office blood pressure (uAutoOBP) has attracted more attention since SPRINT trial had been published. However, its long-term relationship to attended office blood pressure (AuscOBP) is not known. MATERIAL AND METHODS: Stable treated hypertensive subjects were examined in four Czech academic hypertension centers. All subjects attended four clinical visits three months apart. uAutoOBP was measured with the BP Tru device; AuscOBP was measured three times with auscultatory method by the physician. 24-hour ambulatory blood pressure monitoring (ABPM) was performed within one week from the second clinical visit. RESULTS: Data on 112 subjects aged 65.6 ± 10.8 years with mean AuscOBP 128.2 ± 12.2/78.5 ± 10.3 mm Hg are reported. Across the four clinical visits, the uAutoOBP was by 10.1/3.7 mm Hg lower than AuscOBP and the mean difference was similar during all four visits (P≥.061). Both uAutoOBP and AuscOBP had similar intra-individual variability during study follow-up as demonstrated by similar intraclass correlation coefficients (ICC, for systolic ICC = 0.50, for diastolic ICC = 0.72). However, the intra-individual variability of the systolic AuscOBP and uAutoOBP difference was high as demonstrated by low ICCs for absolute (ICC = 0.17 [95%CI, 0.09 - 0.25]) and low κ coefficients for categorized differences (κ ≤ 0.16). The main determinant of AuscOBP-uAutoOBP difference was AuscOBP level. The AuscOBP-uAutoOBP difference was poor tool to identify hypertension control categories defined on the basis of AuscOBP and ABPM. CONCLUSIONS: Although mean AuscOBP-uAutoOBP differences were relatively similar across the four clinical visits, intra-individual variability of this difference was high. The AuscOBP-uAutoOBP difference was poor tool to identify hypertension control categories defined on the basis of AuscOBP and ABPM. Therefore, uAutoOBP cannot be used as a replacement for ABPM.

Serum Vitamin D Status, Vitamin D Receptor Polymorphism, and Glucose Homeostasis in Healthy Subjects.

Low vitamin D status has been frequently associated with impaired glucose metabolism. We examined associations between 25-hydroxyvitamin D (25-OH-D) and several parameters of glucose homeostasis in virtually healthy subjects, and explored possible interaction with vitamin D receptor (VDR) polymorphism. Nondiabetic subjects without chronic medication or any known significant manifest disease were selected from large general-population based population survey. Insulin sensitivity and ß cell secretion were calculated by homeostasis model assessment (HOMA) and soluble isoform of receptor for advanced glycation end-products (sRAGE) using commercial ELISA. Subjects were also genotyped for rs2228570 polymorphism of VDR. After adjustment for potential confounders, we observed a significant relationship between 25-OH-D and fasting glycemia (ß coefficient=-5.904; p=0.002) or insulin sensitivity (ß=0.042; p=0.001), but not with ß cell secretion or sRAGE. We found also an interaction with VDR polymorphism. Subjects with low 25-OH-D and AA genotype had significantly lower insulin sensitivity than those with GG genotype plus highest 25-OH-D concentrations (107.3% vs. 183.9%, p=0.021). In conclusion, low vitamin D status was in virtually healthy subjects associated with decreased insulin sensitivity, namely in those with GG genotype of rs2228570 VDR polymorphism.

In the aftermath of SPRINT: further comparison of unattended automated office blood pressure measurement and 24-hour blood pressure monitoring.

AIMS: Several papers reported that unattended automated office blood pressure (uAutoOBP) is closely related to daytime ambulatory blood pressure monitoring (ABPM). In the present study, we aim to study uAutoOBP and its relation to 24-hour ABPM and ABPM variability. MATERIAL AND METHODS: Stable treated hypertensive subjects were examined in two Czech academic hypertension centres. uAutoOBP was measured with the BP Tru device; attended BP three times with auscultatory method (AuscOBP) by the physician. ABPM was performed within one week from the clinical visit. RESULTS: Data on 98 subjects aged 67.7 ± 9.3 years with 24-hour ABPM 120.3 ± 10.6/72.7 ± 7.9 mm Hg are reported. uAutoOBP was lower than 24-hour (by -5.2 ± 11.3/-0.5 ± 6.9 mm Hg) and daytime (by -6.7 ± 12.82.4 ± 8.0 mm Hg) ABPM and the individual variability of the difference was very large (up to 30 mm Hg). The correlation coefficients between ABPM and uAutoOBP were similar compared to AuscOBP (p ≥ .17). Variability of uAutoOBP, but not AuscOBP, readings during one clinical visit was related to short-term blood pressure variability of ABPM. The difference between AuscOBP and uAutoOBP was larger in patients with white-coat effect compared to other blood pressure control groups (25.1 ± 7.0 vs. 2.2 ± 10.3 mm Hg; p = .0036). CONCLUSIONS: Our study shows that uAutoOBP is not good predictor of ambulatory blood pressure monitoring, not even of the daytime values. It might, however, indicate short-term blood pressure variability and, when compared with AuscOBP, also detect patients with white-coat effect.

A multicentre study on unattended automated office blood pressure measurement in treated hypertensive patients.

AIMS: Unattended automated office blood pressure (uAutoOBP) may eliminate white-coat effect. In the present study, we studied its relationships to attended office blood pressure (BP) and ambulatory BP monitoring (ABPM). MATERIAL AND METHODS: Stable treated hypertensive subjects were examined in four Czech academic hypertension centres. uAutoOBP was measured with the BP Tru device; attended BP was measured six times: three times with auscultatory method (AuscOBP) by the physician followed optionally by three oscillometric measurements (OscOBP). ABPM was performed within one week from the clinical visit. RESULTS: Data on 172 subjects aged 63.7 ± 12.4 years with AuscOBP 127.6 ± 12.1/77.6 ± 10.0 mm Hg are reported. uAutoOBP was by 8.5 ± 9.0/3.0 ± 6.1 mm Hg lower than AuscOBP. The AuscOBP-uAutoOBP difference increased with the AuscOBP level and it did not depend on any other factor. OscOBP differed by 8.6 ± 8.6/1.9 ± 5.7 mm Hg from uAutoOBP. 24-hour mean BP was by 4.2 ± 12.1/3.5 ± 7.8 mm Hg lower than AuscOBP and by 4.3 ± 11.0/0.5 ± 6.9 mm Hg higher than uAutoOBP; the correlation coefficients of 24-hour mean BP with AuscOBP and with uAutoOBP did not differ (p for difference ≥.13). In the lowest BP group (systolic AuscOBP <120 mm Hg or diastolic AuscOBP <70 mm Hg), both AuscOBP and uAutoOBP were lower than 24-hour mean BP, while in the highest BP group (systolic AuscOBP ≥140 mm Hg or diastolic AuscOBP ≥90 mm Hg), they were higher. CONCLUSIONS: Compared to uAutoOBP, attended BP measurement gives higher values, both when measured with auscultatory or oscillometric method. Inter-individual variability of AutoOBP - uAuscOBP difference, as well of uAutoOBP - ABPM difference, is large. We did not prove that uAutoOBP would be associated to 24-hour ambulatory BP more closely than attended BP.

[Risk factors for cardiovascular diseases in the descendants of patients after early myocardial infarction]. / Rizikové faktory kardiovaskulárních onemocnení u potomku nemocných po casném infarktu myokardu.

GOAL: The cardiovascular diseases (CVDs) developing as the result of atherosclerosis are among the most frequent causes of morbidity and mortality within the Czech Republic and elsewhere. Genetic predisposition for cardiovascular diseases is amplified in the presence of routine risk factors which can be influenced. Our aim was to establish whether the level of the risk factors for ICHS already differs in the population of healthy descendants of the patients after early myocardial infarction, as opposed to the control group of examined individuals. METHODOLOGY: We approached adult children (n = 127; age 28.7 ± 6.5 years) of the patients with early manifestation of ICHS, who were examined within the study EUROASPIRE IV. The examination of both the descendants and the control group (n = 199; age 28.9 ± 5.3 years) focused on identifying the risk factors for ICHS. RESULTS: Descendants presented arterial hypertension more often (18.9 vs 8.0 %, p = 0.003) and there were more smokers among them compared to the control group (37 vs 24.1 %, p = 0.01). The levels of triglycerides (1.13 vs 0.99 mmol/l, p = 0.05) and LDL-cholesterol (2.7 vs 2.45 mmol/l, p = 0.01) were higher in the descendant group, HDL-cholesterol was similar in both groups (1.6 vs 1.67 mmol/l, p = 0.17). Increased fasting glycemia occurred more frequent in the descendant group (5.5 vs 1.5 %, p = 0.05). None of the examined participants met the criteria for the diagnosis of diabetes mellitus. Aortic stiffness was higher in the descendant group as opposed to the control group (6.2 vs 5.8 m/s, p = 0.001). The total calculated cardiovascular risk based on the SCORE system was also higher in the descendant group as compared to the control group - the current risk related to the age of 40 years: 0.35 (0.19-0.64) vs 0.20 (0.13-0.47), p < 0.0001 and the risk related to the age of 60 years: 3.35 (2.23-5.36) vs 2.40 (1.58-4.11), p < 0.0001. CONCLUSION: The population of the descendants includes, based on our results, a greater number of smokers and hypertensive patients. They also have higher levels of LDL-cholesterol, triglycerides and impaired fasting glycemia more frequently. Unfavourable genetic predisposition along with unfitting lifestyle contributes to a higher likelihood of accumulation of risk factors, and therefore to a higher risk of a cardiovascular disease manifestation. In practice we should try, with regard to these predisposed individuals, to lower their cardiovascular risk and implement a healthy lifestyle.Key words: atherosclerosis - cardiovascular disease - lifestyle - myocardial infarction - primary prevention - risk factors for CVD.

Relationship between hsTnI and coronary stenosis in asymptomatic women with rheumatoid arthritis.

BACKGROUND: Rheumatoid arthritis (RA) is a condition associated with accelerated progression of atherosclerosis in affected individuals. Myocardial assessment using exercise testing in such patients, however, is often difficult to perform. Our objective was to determine the factors associated with severe coronary stenosis using computed tomography (CT) angiography of the coronary arteries in asymptomatic patients with RA. METHODS: Forty-four women with RA were examined using CT angiography to detect atherosclerotic involvement and significant coronary stenosis (>50 %). CT findings were correlated with the cardiovascular risk score, and with classical and most recent parameters of atherosclerosis. RESULTS: CT angiography of the coronary arteries revealed severe stenosis (>70 %) in 9 % of patients. High-sensitivity troponin I level was associated with severe coronary stenosis (odds ratio 6.37; 95 % confidence interval 1.53 - 26.48; P = 0.011). Adjustment for confounders did not alter this result (P = 0.039). In contrast, classical and modified Systemic Coronary Risk Evaluation scores had no value in predicting severe stenosis (P ≥ 0.49). CONCLUSION: The present study showed the possible benefits of a coronary CT angiography in women with RA and asymptomatic ischemic coronary heart disease. Increased levels of high-sensitivity troponin I may be a potential indication for this type of examination. However, further studies are needed to confirm these results.

Automated compared to manual office blood pressure and to home blood pressure in hypertensive patients.

We studied the relationships of automated blood pressure (BP), measured in the healthcare centre, with manual office BP and home BP. Stable outpatients treated for hypertension were measured automatically, seated alone in a quiet room, six times after a 5 min rest with the BpTRU device, and immediately afterwards using the auscultatory method. Home BP was measured in a subgroup during 7 days preceding the visit. The automated, office and home BP values were 131.2 ± 21.8/77.8 ± 12.1 mmHg, 146.9 ± 20.8/85.8 ± 12.4 mmHg and 137.7 ± 17.7/79.4 ± 8.2 mmHg, respectively. Limits of agreement between office and automated BP (2 SDs in Bland-Altman plots) were +42.6 to -12.6/+22.6 to -6.6 mmHg for systolic/diastolic BP; for home and automated BP they were +45.8 to -25.8/+20.8 to -12.6 mmHg. For patients with two visits, intraclass correlation coefficients of BP values measured during the first and second visits were 0.66/0.72 for systolic/diastolic automated BP and 0.68/0.74 for systolic/diastolic office BP. Automated BP was lower than home BP and no more closely related to home BP than to office BP. It did not show better repeatability than office BP. Whether automated BP and the "white-coat effect", calculated cas the office BP-automated BP difference, have clinical and prognostic importance deserves further studies.

Prolonged Corrected QT Interval as a Predictor of Clinical Outcome in Acute Ischemic Stroke.

BACKGROUND: This study aimed to investigate changes of corrected QT (QTc) interval during acute ischemic stroke and its correlation with high-sensitivity troponin I (hsTnI), brain natriuretic peptide (BNP), neurological outcome, and 1-year mortality. METHODS: We registered electrocardiogram in 69 patients immediately after admission to the intensive care unit and then after 24 and 48 hours. Computed tomography was performed on admission to determine brain infarct size and localization. Neurological outcome was assessed by modified Rankin scale (mRS) at discharge. RESULTS: Forty-five (65.2%) patients had prolonged QTc at baseline; only 18 (26.1%) patients had prolonged QTc after 48 hours. Baseline QTc was not associated with neurological outcome (P = .27). However, prolonged QTc after 48 hours was associated with worse mRS at discharge (4.5 [4.0-6.0] versus 2.0 [1.0-3.0]; P < .0001). Patients who deceased during hospitalization (n = 7 [10.1%]) as compared with survivors had more frequently prolonged QTc after 48 hours (38.9 versus 0%; P < .0001), higher level of hsTnI (48.4 [36.1-75.0] versus 8.6 [3.4-26.5]; P = .003), and BNP (334 [224-866] versus 109 [30-190]; P = .014). In univariate analysis, 1-year mortality was associated with prolonged QTc after 48 hours, hsTnI, and BNP. In multivariate analysis, only BNP remained to be associated with 1-year mortality (odds ratio 3.41, 95% confidence interval 1.06-11.03). CONCLUSIONS: QTc interval in patients with acute ischemic stroke is a dynamic parameter. Prolonged QTc after 48 hours, but not baseline QTc, correlated with neurological outcome and 1-year mortality. Patients with prolonged QTc had higher level of hsTnI.

Association between endothelial NO synthase polymorphisms and arterial properties in the general population.

OBJECTIVE: Nitric oxide plays an important role in vascular biology. Several single nucleotide polymorphisms (SNP) in the endothelial nitric oxide gene (NOS3) have been previously associated with arterial hypertension. We investigated whether these SNPs might be associated with arterial phenotypes in the Czech general population. METHODS: We genotyped three NOS3 SNPs in 426 subjects not treated for arterial hypertension (mean age, 49.1 years; 55.9% women). Arterial properties were measured using applanation tonometry. In multivariate-adjusted analyses, we assessed the gene effects of rs3918226 (-665 C>T), rs1799983 (glu298asp G>T) and rs2070744 (786 T>C) on augmentation index (AIx), central augmentation pressure (AP) and aortic pulse wave velocity (PWV). RESULTS: Carriers of rs3918226 mutated T allele had marginally higher AIx (145.3 ± 2.5 vs. 140.2 ± 1.1%; P = 0.064) and significantly higher AP (12.7 ± 0.7 vs. 11.1 ± 0.3 mm Hg; P = 0.033). These associations were independent of potential confounding factors. Aortic PWV was not different in the two rs39182226 genotypes groups (P = 0.35). In single gene analyses, we did not observe any association between measured phenotypes and rs1799983 or rs2070744 (P ≥ 0.11). In haplotype analysis, we observed trend for higher PWV in haplotypes containing rs3918226 mutated T allele compared with other allelic combination (P ≤ 0.079). CONCLUSION: Mutated T allele of rs3918226 polymorphism in NOS3 gene was associated with parameters reflecting central arterial stiffness and wave reflection. We hypothesize that genetic modulation of intermediate arterial phenotypes might lead to higher blood pressure.

Differential effect of metabolic syndrome on various parameters of arterial stiffness.

Metabolic syndrome (MetSy) is associated with a high risk of cardiovascular complications. Arterial stiffness is an independent predictor of cardiovascular morbidity and mortality. This study investigated the effect of individual MetSy risk factors on central and peripheral parameters of aortic stiffness. In the Czech post-MONICA study, we measured aortic pulse-wave velocity (aPWV), lower extremity pulse-wave velocity (lePWV), augmentation index (AIx) and central augmentation pressure (cAP) in 936 subjects. Based on the definition of MetSy, we divided subjects according to number of risk factors. We used univariate and multivariate linear regression analysis to assess the association between number of risk factors and aPWV, lePWV, AIx and cAP. In analyses adjusted for age, gender, heart rate and mean arterial pressure, aPWV was higher in subjects with MetSy (MetSy+ group) than in those without (MetSy + group) (8.3 vs. 7.7 m/s; p < 0.0001), but lePWV was not significantly different between the groups (11.0 vs. 11.2 m/s; p = 0.2037). After adjustment for covariates, AIx in MetSy+ was lower than in MetSy- respondents (143.2 vs. 146.8; p = 0.014). In adjusted analysis, aPWV rose with increasing number of MetSy risk factors (7.3 ± 0.1 vs. 9.0 ± 0.1 m/s; p for trend < 0.0001). The number of MetSy risk factors did not affect lePWV (p = 0.11). AIx decreased with higher number of MetSy risk factors (148.3 vs. 141.5; p = 0.020). This finding confirms the fact that PWV and AIx may have different associations with risk factors and AIx should not be used as an isolated parameter of arterial stiffness. The individual MetSy risk factors have only a small effect on lower extremity arterial stiffness.

[Renal denervation for treatment of arterial hypertension - the unanswered questions]. / Renální denervace pro lécbu arteriální hypertenze - nezodpovezené otázky.

Despite the extensive armamentarium of antihypertensive medication available, the control of hypertension remains poor. Therefore any possibilities of non-pharmacological treatment of resistant hypertension are welcome. Recently, close attention was paid to renal denervation. Present work summarizes the scientific reports and clinical trials related to this topic published so far and addresses the unanswered questions. Moreover, it also contains brief summary of authors own experience with the method.