BackgroundOslo University Hospital, Norway, had by autumn 2016, accumulated a waiting list of 101 patients with obsessive-compulsive disorder (OCD) who had a legal right to receive treatment by a specialized OCD team. In this challenging situation, the Bergen OCD-team suggested to solve the problem by offering all patients an option for the rapid Bergen 4-day treatment (B4DT). The B4DT is an individual treatment delivered during four consecutive days in a group of six patients with the same number of therapists. The approach has previously shown a post-treatment response rate of 90% and a 3-month remission rate of 70%.MethodsNinety-seven of the wait-list patients were available for the scheduled time slots, and 90 received the 4-day format during 8 days (45 patients each week). The therapists were recruited from 22 different specialized OCD-teams from all over Norway, and 44 (68%) had not previously delivered the 4-day format.ResultsPost-treatment; 91.1% of the patients were classified as responders, and 72.2% were in remission. At 3-month follow-up; 84.4 were classified as responders and the remission rate was 67.7%. Oslo University Hospital now offers the 4-day treatment as standard treatment for OCD.ConclusionsWe conclude that the B4DT is an acceptable and potentially effective OCD-treatment.

Arterial plasma noradrenaline at baseline, as an index of sympathetic activity, predicts LV mass at follow-up independently of systolic blood pressure and body build in middle-aged men who developed hypertension over a period of 20 years.

Atrial fibrillation is the most frequent occurring sustained cardiac arrhythmia and it is related to common cardiac disease conditions. Hypertension increases the risk of atrial fibrillation by approximately two-fold and, because of the high prevalence of hypertension, it accounts for more cases of atrial fibrillation than any other risk factor. In recent years, there are two large hypertension trials (LIFE and VALUE) and two large heart failure trials (CHARM and Val-HeFT) reporting the beneficial effect of angiotensin II-receptor blockers (ARBs) on new-onset atrial fibrillation, beyond the blood pressure-lowering effect. Blockade of the renin-angiotensin system may prevent left atrial dilatation, atrial fibrosis, dysfunction and conduction velocity slowing. Some studies also indicate direct anti-arrhythmic properties. This review aims to consider the preventive effect of ARBs on new-onset atrial fibrillation observed in recent reports from these trials, and to discuss possible mechanisms of the beneficial effect of angiotensin II-receptor blockade.

Our data suggest that arterial adrenaline is involved in the development of hypertension over 20 years in middle-aged men. Men with sustained normotension may have an inherent protection against sympathetic overactivity. Furthermore, screening BP at baseline in normotensive men differentiated between those who developed hypertension and those who remained normotensive at follow-up.

The authors investigated the relationship between serum phosphate (S-phosphate) and the metabolic syndrome in a group of middle-aged hypertensive and normotensive men during 20-year follow-up. Fifty-six men participated. Of the original 34 normotensive men, hypertension developed in 17. In the group as a whole and in those in whom hypertension developed, there was a significant negative relationship between S-phosphate at baseline and mean blood pressure (MBP) at follow-up. A significant relationship was observed between S-phosphate at baseline and components of the metabolic syndrome in the group as a whole, in individuals with hypertension, and in individuals with the lowest S-phosphate levels at follow-up. S-phosphate at baseline predicted MBP 20 years later in a group of hypertensive and normotensive men. When grouped according to the number of components of the metabolic syndrome, individuals with the lowest serum phosphate levels had the highest number of risk factors. These findings may suggest a role of low S-phosphate in the development of hypertension and the metabolic syndrome. J Clin Hypertens (Greenwich). 2008;10:814-821. Reduction of serum phosphate levels could therefore theoretically contribute to the pathogenesis of the syndrome by leading to disturbances in energy metabolism resulting in insulin resistance, hyperglycemia, disturbed lipid metabolism, increased weight, and hypertension. It was suggested for the first time in 1926 that hypophosphatemia might contribute to impaired glucose tolerance. 4 More recently, hypophosphatemia has been linked to impaired glucose utilization, insulin resistance, and hyperinsulinemia 1,5,6 in patients with the metabolic syndrome; a negative correlation between serum phosphate and body mass index (BMI) has been observed.