Search

Background Aortic stiffness is an independent predictor of cardiovascular events in patients with arterial hypertension. Resistant hypertension is often linked to hyperaldosteronism and associated with adverse outcomes. Spironolactone, a mineralocorticoid receptor antagonist, has been shown to reduce both the arterial blood pressure (BP) and aortic stiffness in resistant hypertension. However, the mechanism of aortic stiffness reduction by spironolactone is not well understood. We hypothesized that spironolactone reduces aortic stiffness in resistant hypertension independently of BP change. Methods and Results Patients with uncontrolled BP (≥140/90 mm Hg) despite use of ≥3 antihypertensive medications (including diuretics) were prospectively recruited. Participants were started on spironolactone at 25 mg/d, and increased to 50 mg/d at 4 weeks while other antihypertensive medications were withdrawn to maintain constant mean BP. Phase‐contrast cardiac magnetic resonance imaging of the ascending aorta was performed in 30 participants at baseline and after 6 months of spironolactone treatment to measure aortic pulsatility, distensibility, and pulse wave velocity. Pulse wave velocity decreased (6.3±2.3 m/s to 4.5±1.8 m/s, P P P Conclusions Our results suggest that spironolactone improves aortic properties in resistant hypertension independently of BP, which may support the hypothesis of an effect of aldosterone on the arterial wall. A larger prospective study is needed to confirm our findings.

The authors investigated whether a genetic risk score (GRS) constructed of 32 single nucleotide polymorphisms would predict incident hypertension and blood pressure (BP) change over time in a population cohort during an 11-year follow-up (n=5402 at baseline, 3266 at follow-up). In multivariable models, GRS was associated with higher systolic/diastolic BP values at baseline (β±standard error [SE], 1.04±0.14/1.11±0.13 mm Hg; P

Aim A decrease of systolic blood pressure in excess of 20 mmHg during haemodialysis treatment (IDD) is common for haemodialysis patients. Intradialytic hypotension (IDH) is symptomatic IDD by definition. Overproduction of nitric oxide (NO) is a possible cause of IDD. Dialysate nitrate and nitrite amount can be used as an indicator of intradialysis NO production. Our aim was to find the predictor of NO production in IDD patients. Methods Partial dialysate samples were collected during the whole haemodialysis session and total dialysate nitrate and nitrite amount was measured to assess the association of intradialysis NO production with blood pressure change. Results There were 31 IDD patients and 71 patients who did not develop IDD (NIDD) included in the study. Among the IDD patients, 13 were IDH patients with a mean systolic blood pressure lower than that of the other 18 symptomless IDD patients (96.6 ± 3.4 mmHg vs 125.0 ± 3.8 mmHg, P

A group of 297 building labourers from the northernmost province of Sweden was monitored for 2 years in order to register health changes associated with unemployment. Blood pressure before and after the observation period was compared with the subjects' experience of unemployment during that period. More than 60% of the men were unemployed during the period studied. At the beginning of the study period no differences in blood pressure levels were observed between groups of subjects who remained employed and those who later became unemployed. However, the blood pressure change during the follow-up period was significantly greater among individuals who were unemployed during the period than among those who were not. Longer periods of unemployment were associated with greater increases in systolic and diastolic blood pressure. The number of symptoms reported at the start of the study and unemployment at the end of the study were also correlated with a greater increase in blood pressure during the study.

The current study examined the effects of pulse transit time feedback on systolic and diastolic blood pressure. Three subjects were given feedback designed to increase or decrease transit times. Eleven-twelve one-hour training sessions were provided over a two-week period. The results showed that during increase training, significant increases in systolic pressure and heart rate were observed, while pulse transit time showed a significant decrease. Diastolic blood pressure increases were moderate and only inconsistently observed. During decrease training, diastolic pressure and heart rate declined significantly below baseline. Pulse transit time increases were consistent but lower in magnitude than observed for the opposite training condition. Moderate systolic blood pressure decreases were inconsistently observed.

Skin conductance responses (SCR, "sympatho-galvanic reflex") were measured before and during spinal analgesia in 17 patients scheduled for transurethral surgery. Responses were provoked by standardized electrical stimulation over the clavicle opposite to the recording side; alternatively, a short deep breath, pinching, verbal stimuli or sharp sounds were used. Measuring sites (two electrodes 6 cm apart) were the hand, levels T5, T9, T12-L1 and the foot. Spinal analgesia reached a median cephalad level of T4 (mean T4, range +/- 3 segments) 20-25 min after injection. SCR was markedly depressed in the foot in 15 of 17 patients, at T12-L1 in 12 of 17, at T9 in 10 of 17, at T5 in 9 of 16 and in the hand in 6 of 17. Total abolition of the SCR in the foot was accomplished in only seven cases and sympathetic activity reappeared long before regression of analgesia or motor blockade was observed. In four cases of five with an analgesic level T1-T2, the SCR was preserved in the hand. No consistent correlation between blood pressure change and SCR-change was seen. The conclusion from this study is that preganglionic sympathetic B-fibres are more difficult to block than A-fibres during spinal analgesia. The duration of sympathetic blockade was far shorter than analgesia and motor blockade. Thus, sympathetic blockade during spinal analgesia seems to be far less extensive than that described in the literature.