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Background— Most cardiovascular events associated with hypertension are complications of atherosclerosis. Some antihypertensive agents influence experimental models of atherosclerosis through mechanisms independent of blood pressure lowering. Methods and Results— The European Lacidipine Study on Atherosclerosis (ELSA) was a randomized, double-blind trial in 2334 patients with hypertension that compared the effects of a 4-year treatment based on either lacidipine or atenolol on an index of carotid atherosclerosis, the mean of the maximum intima-media thicknesses (IMT) in far walls of common carotids and bifurcations (CBM max ). This index has been shown by epidemiological studies to be predictive of cardiovascular events. A significant ( P max progression of −0.0227 mm (intention-to-treat population) and −0.0281 mm (completers). The yearly IMT progression rate was 0.0145 mm/y in atenolol-treated and 0.0087 mm/y in lacidipine-treated patients (completers, 40% reduction; P =0.0073). Patients with plaque progression were significantly less common, and patients with plaque regression were significantly more common in the lacidipine group. Clinic blood pressure reductions were identical with both treatments, but 24-hour ambulatory systolic/diastolic blood pressure changes were greater with atenolol (−10/−9 mm Hg) than with lacidipine (−7/−5 mm Hg). No significant difference between treatments was found in any cardiovascular events, although the relative risk for stroke, major cardiovascular events, and mortality showed a trend favoring lacidipine. Conclusion— The greater efficacy of lacidipine on carotid IMT progression and number of plaques per patient, despite a smaller ambulatory blood pressure reduction, indicates an antiatherosclerotic action of lacidipine independent of its antihypertensive action.

The controlled, open, cross-over study reported in this article demonstrates that sotalol and propranolol administered twice daily to 20 patients provide an equally satisfactory control of moderately elevated blood-pressure for 24 hours. The average daily dose of sotalol and propranolol required to achieve this effect was 200 +/- 95 mg and 154 +/- 90 mg respectively. No important side-effects were observed.

Blood pressure variability over a 24-hour period was compared between subjects with labile and those with established hypertension. For this purpose, a computer analysis of the blood pressure tracings, obtained with continuous unrestricted monitoring, was adopted, which characterizes the blood pressure variability in a quantitative manner. The following parameters were employed: the mean, the standard deviation, the coefficient of variation, the indexes of skewness and of kurtosis. No significant differences could be found between the two groups except for the mean value of the blood pressure. It is concluded, therefore, that the term 'labile hypertension' in inappropriate.

ECG and cinecoronary angiography of two patients with Prinzmetal's variant angina are reported. A pathologic study was performed on both. In one case, a transient luminal obstruction of the left circumflex coronary artery became apparent during selective coronary arteriography. Histologic examination of the corresponding coronary segment revealed a severe concentric atherosclerotic process with a normal-sized muscular layer, so that the angiographic transient occlusion might be attributed to an arterial spasm. In the second case no angiographic narrowings were demonstrated by cinecoronary angiography. Nevertheless, histologic examination revealed significant obstructive atherosclerotic narrowing in some coronary segments. It is suggested that atherosclerotic disease may be present also in cases with variant angina who have apparently normal coronary angiograms.

A WHO-coordinated study of the community control of hypertension in six countries (Cuba, Finland, France, Italy, Mongolia and Portugal) has shown that a comprehensive approach clearly improves the care of hypertensives in various populations. Hypertension control programmes were individually designed in each country and were implemented in defined communities. The intervention strategies varied between countries, the major components being: establishment of hypertension clinics and hypertension registers, involvement of health care personnel, and health education of the entire community. As a result of this programme, the blood pressure in the age group 30-59 years decreased on average by 3/2 mmHg among men and by 6/3.5 mmHg among women; the mean blood pressure level decreased twice as much in hypertensive subjects as in the entire population in the intervention areas of the study.

Prognostic gene expression signatures have been proposed as clinical tools to clarify therapeutic options in acute myeloid leukemia (AML). However, these signatures rely on measuring large numbers of genes and often perform poorly when applied to independent cohorts or those with older patients. Long intergenic non-coding RNAs (lincRNAs) are emerging as important regulators of cell identity and oncogenesis, but knowledge of their utility as prognostic markers in AML is limited. Here we analyze transcriptomic data from multiple cohorts of clinically annotated AML patients and report that (i) microarrays designed for coding gene expression can be repurposed to yield robust lincRNA expression data, (ii) some lincRNA genes are located in close proximity to hematopoietic coding genes and show strong expression correlations in AML, (iii) lincRNA gene expression patterns distinguish cytogenetic and molecular subtypes of AML, (iv) lincRNA signatures composed of three or four genes are independent predictors of clinical outcome and further dichotomize survival in European Leukemia Net (ELN) risk groups and (v) an analytical tool based on logistic regression analysis of quantitative PCR measurement of four lincRNA genes (LINC4) can be used to determine risk in AML.

It has been proposed, therefore, that hyperinsulinemia may favor the development of hypertension through sodium retention, sympathetic nervous system activation, and vascular hypertrophy. In insulin-resistant hypertensive subjects, insulin infusion during euglycemic clamp promotes a transient sodium retention by stimulating proximal tubular Na+ reabsorption, but chronic hypertension usually is not associated with extracellular fluid and plasma volume expansion. In essential hypertensive subjects, intracellular potassium is decreased and intracellular sodium increased, which is consistent with insulin resistance. The latter is also associated with high red blood cell Li+/Na+ exchange, and chronic insulin treatment in insulin-dependent diabetics induces a slight increase in Li+/Na+ CT. This is a functioning mode of the Na+/H+ exchange, and its increase may reflect either an increased number of transport units or abnormal kinetic properties. Experiments in vitro and in vivo suggested that any change in insulin concentration and insulin sensitivity may affect Li+/Na+ and Na+/H+ counter-transport. High Li+/Na+ and Na+/H+ CT are associated with a significant cardiac and vascular remodeling in essential hypertension, insulin-dependent diabetes, and familiar hypertrophic cardiomyopathy. Reduced insulin sensitivity is associated with salt-sensitive hypertension. Finally, insulin potentiates the effects of other agonists (eg, thromboxane A2, angiotensin II) on vascular contraction and cell growth. These data indicate that insulin may play a role in the pathogenesis of hypertension and its major complications by amplifying the effects of sodium, vasoconstrictors, and growth factors.