Previous studies have shown that hyperoxia-induced deactivation of carotid body chemoreceptors reduces sympathetic activity in hypertensive patients but it does not affect blood pressure. The maintenance of blood pressure can be explained by the direct, vasoconstrictive effect of hyperoxia, which offsets diminished sympathetic activity. This study compares the effect of acute hyperoxia on hemodynamic parameters between hypertensive and normotensive subjects. Twelve males with hypertension (age 39.4±2.4 years; body mass index 27.4±1.1 kg m⁻²) and 11 normotensive males (age 39.9±2.7 years; body mass index 25.4±0.7 kg m⁻²) received, via non-rebreathing mask ventilation, ambient air, followed by 100% oxygen for 20 min. The stroke volume, heart rate, cardiac output, blood pressure, total peripheral resistance, respiratory rate, baroreceptor control of heart rate and oxygen saturation were recorded continuously. Several 30 s periods were analyzed before, during and after inducing hyperoxia. At baseline, the hypertensive subject’s blood pressure was higher and their baroreflex control of heart rate was lower when compared with the normotensive control group. After the first 30 s of hyperoxia, systolic, diastolic and mean blood pressures, as well as the total peripheral resistance, decreased significantly in hypertensives but not in normotensives. After 20 min of 100% oxygen ventilation, systolic and mean blood pressures and total peripheral resistance was increased in hypertensive patients, and the cardiac output and stroke volume had decreased in both groups. The results of this study confirm that deactivation of carotid body chemoreceptors can acutely decrease blood pressure in humans.

Beyond lipid-lowering properties, statins decrease sympathetic nervous activity. Due to the limited number of studies and included participants, a meta-analysis of randomized, placebo-controlled studies using microneurography (MSNA) was performed to assess sympatholytic effect of statins.

Introduction : Childhood hypertension is defined based on the normative distribution of blood pressure (BP), but from the age of 18 years high BP is diagnosed using adult criteria. We compared the rates of diagnosis of hypertension in a group of 18-year-old subjects using BP percentiles and...

The aim was to assess the control of negative emotions in treated patients with hypertension in comparison with normotensive individuals and to evaluate the association between suppression of negative emotions, control of blood pressure (BP) on ambulatory blood pressure monitoring (ABPM) and blood pressure variability (BPV). We studied 195 patients (women/men: 89/106); mean age 45.4 ± 15.9 years. All patients had ABPM and completed the Courtauld Emotional Control Scale (CECS). The total CECS score and scores for subscales for anger, depression and anxiety were analyzed together with mean BP values from ABPM, and their SD and coefficient of variation as BPV measures. The mean CECS score was 54 ± 12 in all subjects; highest in uncontrolled hypertension 56 ± 11, intermediate 53 ± 12 in controlled hypertension and lowest 48 ± 12 in normotensive subjects. The reference value for the Polish population is 50 ± 11. Significant differences of mean CECS scores among groups were observed (p = 0.0165) also in multivariate analysis. The difference between uncontrolled hypertension and normotension was significant (p = 0.0262). Few significant, weak correlations were observed between CECS score or its subscales and ABPM derivates in all subjects. Conclusion. Suppression of negative emotions may adversely affect BP control in treated hypertensive patients and it should be considered a cause of uncontrolled hypertension.

Primary hyperaldosteronism may be associated with elevated 24-hour urinary potassium excretion. We evaluated the diagnostic value of spot urine (SU) potassium as an index of 24-hour urinary potassium excretion. We measured SU and 24-hour urinary collection potassium and creatinine in 382 patients. Correlations between SU and 24-hour collections were assessed for potassium levels and potassium/creatinine ratios. We used the PAHO formula to estimate 24-hour urinary potassium excretion based on SU potassium level. The agreement between estimated and measured 24-hour urinary potassium excretion was evaluated using the Bland-Altman method. To evaluate diagnostic performance of SU potassium, we calculated areas under the curve (AUC) for SU potassium/creatinine ratio and 24-hour urinary potassium excretion estimated using the PAHO formula. Strongest correlation between SU and 24-hour collection was found for potassium/creatinine ratio (r = 0.69, P<0.001). The PAHO formula underestimated 24-hour urinary potassium excretion by mean 8.3±18 mmol/d (95% limits of agreement -28 to +44 mmol/d). Diagnostic performance of SU potassium/creatinine ratio was borderline good only if 24-hour urinary potassium excretion was largely elevated (AUC 0.802 for 120 mmol K⁺/24 h) but poor with lower values (AUC 0.696 for 100 mmol K⁺/24 h, 0.636 for 80 mmol K⁺/24 h, 0.675 for 40 mmol K⁺/24 h). Diagnostic performance of 24-hour urinary potassium excretion estimated by the PAHO formula was excellent with values above 120 mmol/d and good with lower values (AUC 0.941 for 120 mmol K⁺/24 h, 0.819 for 100 mmol K⁺/24 h, 0.823 for 80 mmol K⁺/24 h, 0.836 for 40 mmol K⁺/24 h). Spot urine potassium/creatinine ratio might be a marker of increased 24-hour urinary potassium excretion and a potentially useful screening test when reliable 24-hour urine collection is not available. The PAHO formula allowed estimation of the 24-hour urinary potassium excretion based on SU measurements with reasonable clinical accuracy.

The aim of the study was to compare short and long-term mortality and readmissions in patients with non-ruptured abdominal aortic aneurysm (AAA) treated with endovascular aortic repair (EVAR) or open aneurysm repair (OAR). Retrospective survival analysis based on prospectively collected medical records of the national Polish public health insurer. In the National Health Fund database we identified all patients who underwent elective open or endovascular treatment of AAA between January 1^st 2011 and March 22^nd 2016. The data on mortality, selected concomitant diseases and readmissions were collected. A total of 7805 patients (mean age 70.9±8.1 yrs, 85.8% males) underwent OAR (n = 2336) or EVAR (n = 5469). A median follow up was 27.5 months (IQR range 10.0–38.4 months). The primary outcome variable was all-cause mortality, secondary outcomes included 30-day mortality and readmissions. Kaplan–Meier (K-M), Cox proportional-hazards and propensity score analyses were performed for primary and secondary outcomes adjusting for repair type of AAA (OAR vs. EVAR), age, sex and concomitant diseases. EVAR patients had higher all-cause mortality (6.4% vs. 4.6% P = 0.002, adjHR 1.34, 95%CI 1.07–1.67, P = 0.010) compared with OAR. The mortality risks for OAR patients decreased below those for EVAR patients after 9.9 months. Of all the tested confounding factors only age independently and significantly influenced long-term mortality. Readmissions occurred more often in EVAR than in OAR (16.5% vs. 8.4% P<0.001, adjHR 2.15, 95%CI 1.84–2.52, P<0.001) independently from other covariants. Survival and readmissions Kaplan-Meier curves remained statistically different between OAR and EVAR patients after propensity score matching. Survival benefit of EVAR over OAR disappeared early during the first year after procedure, particularly in patients below 70 years of age, accompanied by an increased frequency of readmissions of EVAR patients. Our data suggest re-evaluation of the strategy for AAA management in vascular units in the country.