The largest number of articles in the current issue of the Journal of Hypertension are focused on lifestyle and therapeutic interventions to prevent and control hypertension.
Li et al. (pp. 2210–2214) have investigated the association of hypertension with passive smoking in rural areas where the proportion of men who smoke at home is high, whereas the proportion of smoking among women is very low. After adjusting for age, BMI, education, occupation, drinking status, physical activity, and menopause, passive smoking was found to confer an approximately two-fold increase of the risk of hypertension. In an accompanying commentary, De Buyzere (pp. 2200–2203) acknowledge that Li et al.'s article adds an important piece of evidence to answer the question ‘is there hypertension where there's smoke?’, but underlines that the effects of passive smoking of tobacco (at home or wherever) should be disentangled from the contributions of passive smoking unrelated to tobacco use (e.g. smoke from traffic, workplaces, and industrial air pollution). Borgi et al. (pp. 2231–2238) have analyzed data from three large longitudinal cohort studies of initially nonhypertensive individuals and found that long-term intake of meat and poultry was associated with increased risk of developing hypertension. In contrast with common belief, they report a weak but significant trend toward an increased risk of hypertension with increasing seafood consumption also. Another unexpected observation is reported by Jiang et al. (pp. 2223–2230), who have evaluated the association of concordance with the Dietary Approaches to Stop Hypertension (DASH) diet with blood pressure trajectories and incidence of hypertension in the Framingham Offspring cohort. Although the DASH diet is commonly considered to lower blood pressure, in the Framingham Offspring population, long-term concordance with the DASH diet was not associated with a decreasing blood pressure trajectory over time or with decreased incidence of hypertension. Exercise blood pressure is often taken as a marker of future cardiovascular morbidity: Prasad et al. (pp. 2239–2244) have investigated the blood pressure response to submaximal exercise in individuals with different levels of cardiovascular fitness and found the lowest submaximal SBPs among men with fair or good cardiorespiratory fitness and the highest values among those with poor fitness. Higher mortality from cardiovascular disease in winter is partly explained by increased blood pressure caused by cold exposure. Saeki et al. (pp. 2338–2343) have investigated whether suitable instructions about home heating are able to increase home temperature and decrease blood pressure. After conducting an open, randomized, controlled trial in winter, they report that intervention with suitable instructions raised living room temperature and also significantly reduced ambulatory SBPs and DBPs.
Although the presence of anxiety or depression in hypertensive patients has been associated with higher cardiovascular mortality, Ho et al. (pp. 2215–2222) in a retrospective analysis of a longitudinal study report that hypertensive patients with anxiety or depression had a greater healthcare utilization and obtained significantly faster rates of hypertension control. In the Mitchelstown cohort, O’Flynn et al. (pp. 2257–2264) find that the absolute blood pressure level, better than the dipping status categorization, is an early marker of organ damage. In a large cross-sectional survey of treated hypertensive patients in Eastern European countries, Grassi et al. (pp. 2250–2256) report that within-visit blood pressure variability is associated with increased cardiovascular risk, history of previous cardiovascular events, metabolic disturbances, and poor blood pressure control. Visit-to-visit blood pressure variability is reported by Howard et al. (pp. 2359–2367) to be dramatically larger in patients with more background medications prescribed. The authors argue that if this is due to variable adherence to treatment, then future trials of renal denervation in resistant hypertension, when multiple drugs are administered, would benefit from measures to guarantee adherence.
Nelson et al. (pp. 2331–2337) have explored the ‘legacy’ of presence or absence of previous antihypertensive treatment by examining differences in fatal events at 10 years between those who entered the Second Australian National Blood Pressure study previously on therapy and those who did not. They found no long-term ‘legacy’ adverse effect on mortality associated with treatment naivety in their elderly hypertensive cohort. However, as acknowledged by the authors, their results are likely confounded by a higher in-trial adverse cardiovascular risk in the previous treatment group. In a thoughtful accompanying commentary, Gueyffier and Cucherat (pp. 2207–2209) review available evidence in favor and against the reality of legacy, and suggest the only unbiased approach is to test the impact of withdrawing preventive treatment. The readers of the Journal of Hypertension will remember an article published in 2014, with a post-hoc subanalysis of the Hypertension in the Very Elderly Trial (HYVET) , showing that those patients who were under antihypertensive treatment at baseline and had this treatment withdrawn because randomized to placebo had significantly higher mortality and morbidity than those patients who continued antihypertensive treatment being randomized to active treatment.
Imprialos et al. (pp. 2185–2197) review the blood pressure effects of a novel class of agents for the treatment of type 2 diabetes mellitus, the inhibitors of the sodium–glucose cotransporter 2 in the renal proximal tubule, and conclude that although with some differences between individual agents, all of the approved sodium-glucose cotransporter 2 inhibitors provide a mild but meaningful reduction in office SBP and DBP, and, probably, an even larger effect on ambulatory blood pressure. In an accompanying editorial comment Ruiz-Hurtado and Ruilope (pp. 2198–2199) remember that a limitation of this class of drugs is the loss of the effect in the presence of a decreased renal function and that, although we must welcome the arrival of this new class of antidiabetic drugs, we need to wait for the results of large ongoing trials of cardiovascular outcomes to see whether this class of drugs really differs from other classes of antidiabetic drugs by salutary effects on macrovascular disease in diabetes. Two other therapeutic articles focus on invasive interventional approaches in resistant hypertension: Beige et al. (pp. 2344–2349) publish preliminary data showing that baroreflex activation therapy reduces blood pressure in patients with end-stage renal disease and resistant hypertension, and Lambert et al. (pp. 2350–2358) report that lowering blood pressure by renal denervation is accompanied by a sustained improvement in mental health-related aspects of quality of life.
Three other articles focus on hypertension-related organ damage. Angeli et al. (pp. 2322–2330) analyze data from their own cohort (Massa Ventricolare Sinistra nell’Ipertensione, MAVI study) and conduct a cumulative meta-analysis with other studies, and conclude that risk of cardiovascular events is higher in patients with left ventricular hypertrophy regression than in those with persistently normal left ventricular mass. In an experimental work in spontaneously hypertensive rats, Ayme-Dietrich et al. (pp. 2310–2321) identify a cardioprotective function of the serotonin 5-HT2B receptor on diastolic dysfunction with preserved ejection fraction. Aissopou et al. (pp. 2303–2309) revisit the controversial problem of the clinical usefulness of detecting mild hypertensive retinopathy, either according to the classical Keith–Wagener–Barker classification or the more recent Mitchell–Wong classification. They find that mild retinal microvascular changes, such as arteriolar narrowing, arteriovenous crossing, and increased arteriolar reflexes, are more closely correlated to blood pressure levels and organ damage in younger than in older hypertensive patients. In their commentary, Cuspidi et al. (pp. 2204–2206) remark that as consequence, the search for mild hypertensive retinopathy in the elderly fraction of the hypertensive population has a limited value in refining cardiovascular risk stratification, because of the impact of age on retinal vessels.
Other articles report data on other areas of hypertension research. Adiyaman et al. (pp. 2245–2249) find that only a part of the blood pressure differences between home and office can be attributed to the presence of the physician, and think that the major part should be attributed to the hospital environment. Polonikov et al. (pp. 2265–2277) have assessed the effects of polymorphisms in genes associated with hypertension on the variation of erythrocyte membrane proteins in hypertensive patients, and Gong et al. (pp. 2278–2285) identify PTPRD as a novel locus potentially associated with blood pressure response to atenolol and resistant hypertension in multiple ethnic groups. Thomsen et al. (pp. 2294–2302), studying the Norwegian Preeclampsia Family Biobank, identify the heritability of a range of health-related conditions in preeclampsia families. Finally, in a retrospective analysis of a single-center cohort of 59 patients who underwent a urinary clonidine suppression test, Goupil et al. (pp. 2286–2293) conclude the test appears to be highly accurate to detect pheochromocytomas and paragangliomas.
Conflicts of interest
There are no conflicts of interest.