The current issue of the Journal of Hypertension opens with two challenging articles. A review by Manolis et al. (pp. 2109–2117) shows that, although hypertension frequently coexists with atrial fibrillation thus increasing the risk of stroke and of brain haemorrhage induced by concomitant antithrombotic therapy, the role of blood pressure (BP) remains remarkably unappreciated in atrial fibrillation trials, and very limited, if any, data are provided in trial reports regarding BP, including in-study and final BP levels, BP control and concomitant antihypertensive medication. Unfortunately, this is not new in trials of cardiovascular therapy: years ago, when reviewing early trials of beta-blockers or angiotensin-converting enzyme inhibitors in acute myocardial infarction and in heart failure, I realized that data on BP at randomization and in-treatment were not reported in many trials, thus leaving the question about pleiotropic vs. haemodynamic actions of cardiac drugs unresolved.
In a stimulating editorial, Vito M. Campese (pp. 2118–2122) opens a debate about current definitions of resistant hypertension and raises the point as to whether some of these definitions have the potential to cause overuse and abuse of some new invasive technologies. The suggestion to distinguish between ‘difficult to control hypertension’, that is BP values that can at the end be controlled, say by four or more active drugs, from refractory hypertension (that is, uncontrolled in any way), I feel will stimulate a debate, that our Journal will be delighted to host. Equally challenging is Campese's proposal to limit interventional procedures to really refractory forms of hypertension.
A number of articles in this issue are devoted to epidemiology, some of them with interesting prognostic implications. Völzke et al. (pp. 2142–2150), by using data mining procedures, identify a predictive model for incident hypertension in the 5-year follow-up of a population-based study and confirm the validity of the model in another population cohort. These findings promise applicability in screening settings and clinical practice, as commented in an editorial by Egan (pp. 2123–2124). Wang et al. report that the risk of incident heart failure in a 14-year follow-up of Finnish men and women was lower in hypertensive patients who engaged in healthy lifestyle, but higher in hypertensive people using antihypertensive drug treatment. Salles et al. (pp. 2176–2186) in a 5.75-year follow-up of 565 type-2 diabetic patients found that ambulatory BP monitoring provides more valuable predictive information than clinic BP measurements. Achieved 24-h ambulatory BP values less than 120/75 mmHg were found associated with a significantly lower incidence of cardiovascular events. On the same topic of the predictive values of various kinds of BP measurement, Huang et al. (pp. 2187–2194) report that among 448 consecutive patients receiving contrast media for percutaneous coronary interventions, development of contrast-induced nephropathy and 3-year incidence of major cardiovascular events were significantly more frequent in patients within the highest tertile of central BP.
Another article by Salice et al. (pp. 2165–2175) helps clarifying another issue concerning discrepancies between different types of BP measurement. It has been known for some time that, although in adults office BP is commonly higher than ambulatory BP, in children the relation is reversed, office being commonly lower than ambulatory BP. Salice et al. now find that there is a common relation both in children and adults with ambulatory BP being progressively higher than office BP at office BP lower than 117/73 mmHg, and progressively lower at office BP greater than 117/73 mmHg and suggest that differences between office and ambulatory BP, being bidirectional according to office BP values, are likely to be largely due to regression to the mean rather than to the white-coat effect. A well known expert in children hypertension, Empar Lurbe, in an accompanying editorial, comments on the difficulties of defining hypertension, including white-coat and masked hypertensions, in children and adolescents (pp. 2125–2127).
In this current issue of the Journal, Professor Lurbe and her associates (pp. 2230–2236) contribute interesting data on obesity in children, reporting that prevalence of elevated urinary albumin is not prominent in obese children, and when it occurs it depends mainly on concomitant metabolic factors, suggesting that the concept of ‘metabolic syndrome’ may have some clinical usefulness in children. Also in the area of obesity, Bonfils et al. (pp. 2220–2229) find that 5 days of a high sodium diet, though increasing substantially cardiac output and stroke volume, does not induce any significant BP change, either in morbid obesity (BMI >40 kg/m2) or in lean individuals. These findings are commented by Jordan in an editorial (pp. 2130–2132).
Further epidemiological contributions are provided by Brown et al. (pp. 2213–2219), who report that in the Genetic Epidemiology Network of Arteriopathy (GENOA) study, a history of hypertension in pregnancy is associated with elevated C-reactive protein levels later in life, independent of traditional cardiovascular risk factors and BMI, possibly reflecting an inflammatory state. Celi et al. (pp. 2136–2141) have examined the association of hypermagnesemia and SBP in 11 284 ICU patients finding that hypermagnesemia was associated with lower SBP values, in support to the biological importance of magnesium in BP control. Lovic et al. (pp. 2151–2157) present the results of a Serbian Society of Hypertension survey confirming that Serbia belongs to countries with a high prevalence and poor control of hypertension. In Algeria, elderly women have been found to exhibit an increase in arterial stiffness similar to that in elderly men, whereas European elderly women maintain a lower arterial stiffness than men (Temmar et al., pp. 2244–2250). However, in a USA study, elderly hypertensive women are reported to have early left ventricular diastolic dysfunction and higher estimated filling pressure, consistent with their greater susceptibility to heart failure with preserved ejection fraction (Fujimoto et al., pp. 2282–2289).
Arterial stiffness is also the topic of a technical study verifying the accuracy of carotid-femoral pulse wave velocity assessment using novel cuff-based techniques (Butlin et al., pp. 2237–2243). According to Labat et al. (pp. 2251–2258), arterial stiffness and subclinical atherosclerosis are associated with increased levels of inflammatory markers that can also be detected in saliva. Barden et al. (pp. 2195–2202) report that acute consumption of alcohol as red wine results in a relative increase in plasma levels of a vasoconstrictor ecosanoid over 24 h, possibly contributing to the BP elevation associated with binge drinking.
A group of animal experiments with possible clinical and therapeutic implications complete the current issue of the Journal. Gelosa et al. (pp. 2259–2269) summarize experiment findings, suggesting that iron dysmetabolism is involved in the development of hypertensive nephropathy in the stroke-prone spontaneously hypertensive rat. Pushpakumar et al. (pp. 2270–2281) have investigated the role of tissue inhibitor of metalloproteinase-2 (TIMP2) in angiotensin-II-induced renal remodelling in TIMP-2 knockout mice. Chaykovska et al. (pp. 2290–2299) have investigated the effects of telmisartan alone, linagliptin alone or the combination of the two drugs on cardiac and renal function and structure in rats with renovascular hypertension. Honda et al. (pp. 2300–2308) describe that central inhibition of sympathetic activity induced by intracerebroventricular moxonidine attenuated brain oxidative stress, prevented cardiac dysfunction and remodelling, and improved the prognosis in rats with hypertensive heart failure. The possibilities and limitations of extrapolating these observations to the treatment of heart failure in man are discussed by Grassi in an editorial commentary (pp. 2133–2135): he recalls that the only trial testing moxonidine in human heart failure (MOXCON) has reported higher mortality in moxonidine patients. Muñoz-Pacheco et al. (pp. 2309–2319) also report that in a hypertensive heart failure model, the addition of eplerenone to conventional therapy further improves cardiac structure and function delaying the progression of the disease. Finally, Steireif et al. (pp. 2203–2212) have been able to demonstrate the partial genetic independence of albuminuria and endothelial dysfunction in a genetic rat model. In an editorial commentary of this article, Marques et al. (pp. 2128–2129) remark that the consomic strains used by Steireif et al. provide the first level of dissection of the complex genetic background behind both conditions. It is, however, challenging that these experiments point towards oxidative stress as the potential mechanism driving susceptibility to endothelial dysfunction and microalbuminuria.
Conflicts of interest
There are no conflicts of interest.