According to the results of the validation study based on the European Society of Hypertension International Protocol the Omron M5-I, R5-I, and HEM-907 may be recommended for clinical use in elderly individuals, without atrial fibrillation or frequent ectopic beats.

A fructose-enriched diet induces an increase in blood pressure associated with metabolic alterations in rats. Our hypothesis was that an increase in protein kinase C (PKC) activation, reported in the acute period of fructose overload, and an impaired vessel's response to vasoactive substances contribute to maintain elevated blood pressure levels in the chronic period. The aims of this study were to investigate in this animal model of hypertension: (1) if the increase in PKC activation was also found in the chronic stage; (2) the involvement of nitric oxide and insulin in the vessel's response; and plasma atrial natriuretic factor and nitrites/nitrates (nitric oxide metabolites) behavior. We evaluated the effects of: PKC-stimulator 12,13-phorbol dibutyrate, phenylephrine, insulin, nitric oxide synthase-inhibitor NG-nitro-L-arginine methyl esther (L-NAME) and PKC-inhibitor Calphostin C on aortic rings responses of Sprague-Dawley rats: fructose-fed and control. The fructose-fed group showed higher contractility to 12,13-phorbol dibutyrate than the control group in aortic rings pre-incubated with insulin, and this difference disappeared with L-NAME. The response to phenylephrine in rings pre-incubated with Calphostin C was decreased in the fructose-fed group and increased with Calphostin C plus L-NAME. Fructose-fed rats showed higher levels of plasma atrial natriuretic factor and nitrites/nitrates than controls. In conclusion, chronic fructose feeding seems to develop an impaired response to insulin, dependent on nitric oxide, suggesting a PKC alteration. Vasorelaxant agents, such as atrial natriuretic factor and nitric oxide, would behave as compensatory mechanisms in response to high blood pressure.

The electrocardiogram (ECG) of athletes, especially in those that are endurance-trained, frequently shows some alterations; however, abnormalities of athlete’s ECG may be an expression of an underlying heart disease, which carries a risk of sudden death during sport. It is important that ECG abnormalities are correctly distinguished. We report a case of an ultramarathon athlete who arrived in Emergency Department, after a 100-kilometer race, showing ECG alterations that required further investigations to rule out a cardiac disease. ECG trace showed anterior repolarization abnormalities with ST-segment elevation in V1 to V3 leads. He was admitted to the Cardiology Department and underwent a coronary study that was normal. A cardiac magnetic resonance was also performed. The final diagnosis was athlete’s heart.