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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.

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.

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

Background: The aim of this study was to analyze medication non-adherence by measuring serum drug levels (SDL) in patients presenting with acute decompensated heart failure (ADHF). Methods: Included in the study were chronic heart failure patients presenting with signs of acute decompensation. Blood sampling for the measurement of SDL was performed shortly after presentation. SDL were measured using liquid chromatography coupled with mass spectrometry. The estimation of SDL was calculated from the recommended chronic cardiac medications with the exception of drugs administered as part of the acute treatment prior to blood sampling. The patients were labeled as non-adherent when any one of the evaluated medications was not found in the serum. Results: Fifty patients with ADHF were prospectively enrolled. All of the evaluated drugs were detected in the sera of 28 (56%) patients. Non-adherence was diagnosed in the remaining 22 (44%) patients. None of the evaluated medications was detected in the sera of 5 (10%) patients. Conclusion: The estimation of SDL indicates that non-adherence to the recommended chronic therapy is a common problem among patients presenting with ADHF. This method should be an essential aspect of routine clinical evaluation in these 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. [ABSTRACT FROM AUTHOR]

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.

Mutations in KCNJ5 , ATP1A1 , ATP2B3 , CACNA1D , and CTNNB1 are thought to cause the excessive autonomous aldosterone secretion of aldosterone-producing adenomas (APAs). The histopathology of KCNJ5 mutant APAs, the most common and largest, has been thoroughly investigated and shown to have a zona fasciculata-like composition. This study aims to characterize the histopathologic spectrum of the other genotypes and document the proliferation rate of the different sized APAs. Adrenals from 39 primary aldosteronism patients were immunohistochemically stained for CYP11B2 to confirm diagnosis of an APA. Twenty-eight adenomas had sufficient material for further analysis and were target sequenced at hot spots in the 5 causal genes. Ten adenomas had a KCNJ5 mutation (35.7%), 7 adenomas had an ATP1A1 mutation (25%), and 4 adenomas had a CACNA1D mutation (14.3%). One novel mutation in exon 28 of CACNA1D (V1153G) was identified. The mutation caused a hyperpolarizing shift of the voltage-dependent activation and inactivation and slowed the channel's inactivation kinetics. Immunohistochemical stainings of CYP17A1 as a zona fasciculata cell marker and Ki67 as a proliferation marker were used. KCNJ5 mutant adenomas showed a strong expression of CYP17A1, whereas ATP1A1 / CACNA1D mutant adenomas had a predominantly negative expression ( P value =1.20×10 -4 ). ATP1A1 / CACNA1D mutant adenomas had twice the nuclei with intense staining of Ki67 than KCNJ5 mutant adenomas (0.7% [0.5%-1.9%] versus 0.4% [0.3%-0.7%]; P value =0.04). Further, 3 adenomas with either an ATP1A1 mutation or a CACNA1D mutation had >30% nuclei with moderate Ki67 staining. In summary, similar to KCNJ5 mutant APAs, ATP1A1 and CACNA1D mutant adenomas have a seemingly specific histopathologic phenotype., (© 2017 American Heart Association, Inc.)