The aims of this study were to determine 24 h blood step-wise regression with age, gender, weight and height showed age to be the best predictor of variation pressure (BP) levels in a sample taken from a normal British population, and to investigate factors contribuin office BP and awake and asleep diastolic BP. However, age accounted for only a small amount of the variting to variation within the sample. Two hundred and eighty-two Caucasian subjects, with no known hyperation and did not contribute towards the variation in systolic BP.

Premature vascular aneurysms and fragility of cerebral arteries are commonly associated with type III collagen mutations and physical signs suggesting a generalized abnormality of connective tissue. Sometimes these traits are clearly genetically transmitted. Here we present seven examples of early cerebrovascular aneurysms or fragility including five examples of carotid cavernous sinus aneurysms. With one exception in which we suspect the mutation is too small to be detected, all of them had easily visible abnormalities of their type III collagen proteins. Further work in progress will eventually allow the characterization of their mutations at gene sequence level and will be followed by the ability to prevent transmission of the mutant genes in these families.

This randomised, double-blind, double-dummy, parallel group, multicentre study compared the efficacy and tolerability of lercanidipine with lacidipine. Elderly patients with isolated systolic hypertension (supine blood pressure X160/o95 mmHg) were enrolled and underwent a placebo run-in period of 14-27 days before random allocation to lercanidipine tablets 10 mg once daily (n ¼ 111) or lacidipine tablets 2 mg once daily (n ¼ 111) for the assessment period (112-160 days). Titration to lercanidipine 20 mg once daily (two 10 mg tablets) or lacidipine 4 mg once daily (two 2 mg tablets) was allowed after 8 weeks, if required. Both treatments decreased supine and standing systolic and diastolic blood pressure between the end of the run-in period and the end of the assessment period (Po0.0001). At the end of the assessment period, the estimated mean treatment difference (95% confidence intervals) in supine systolic blood pressure was À0.81 (À4.45, 2.84) mmHg. These confidence intervals were within the limits specified for equivalence, that is, (À5, 5) mmHg. Ambulatory blood pressure monitoring showed that the antihypertensive effects of both drugs lasted for the full 24-h dosing period and followed a circadian pattern. Both treatments were well tolerated with a low incidence of adverse drug reactions and a low withdrawal rate. Significantly fewer patients withdrew from treatment with lercanidipine (P ¼ 0.015). Neither treatment had any clinically significant effect on pulse rate or cardiac conduction. In conclusion, both treatments were equally effective in controlling supine systolic blood pressure in patients with isolated systolic hypertension.

Within routine clinical practice, white coat hypertension (where blood pressure is persistently higher in the presence of the doctor or nurse but normal outside the medical setting) makes the diagnosis and management of hypertension difficult. There are conflicting data regarding the prevalence and significance of white coat hypertension. This study has used ambulatory blood pressure monitoring to detect the presence of white coat hypertension in 186 patients referred to an out-patient hypertension unit. The presence of white coat hypertension was defined as an average office blood pressure (measured on three occasions over a 2-month period) of >140/90 mm Hg and an ambulatory awake blood pressure < or = 136/86 mm Hg. The prevalence of white coat hypertension in those patients with borderline hypertension (diastolic blood pressure 90-99 mm Hg) and those with mild-to-moderate hypertension (diastolic blood pressure > or = 100 mm Hg) was determined. Echocardiography was used to assess left ventricular mass index in patients with and without white coat hypertension. The prevalence of white coat hypertension in the total group was 23%. However, the prevalence was higher (33%) in those patients with borderline hypertension compared to 9% of those patients with mild-to-moderate hypertension. There was a statistically significant increase in left ventricular mass index in patients with no evidence of white coat hypertension (125 gm/m2) compared to those with white coat hypertension (102 gm/m2). We conclude that, if office blood pressure is used to identify patients with hypertension who may require treatment, some patients will be incorrectly diagnosed and may be treated inappropriately. We recommend that ambulatory blood pressure monitoring is used in the routine assessment of all newly diagnosed hypertensive patients. Furthermore, we recommend echocardiography in patients with borderline hypertension as some will already have an increased left ventricular mass index.

Whether raised blood pressure precedes, follows or develops in parallel with the onset of microalbuminuria, remains unclear. Previous studies, using conventional blood pressure recordings, have yielded discrepant results. Ambulatory blood pressure (ABP) monitoring detects borderline hypertension more reliably, and correlates more closely with end-organ damage. We have therefore compared ABP and left ventricular dimensions in normotensive insulin-dependent diabetic patients with or without microalbuminuria, and matched nondiabetic control subjects. Those diabetic patients with microalbuminuria, and to a lesser extent those without, had higher 24 h mean arterial blood pressure than matched non-diabetic control subjects, with corresponding increases of left ventricular mass, interventricular septal width and posterior wall thickness. These observations suggest that raised arterial blood pressure is present at an early stage of 'incipient' microalbuminuria.