Editorial

Isolated systolic hypertension (ISH), defined as systolic blood pressure (BP) greater than 140 mmHg and diastolic BP less than 90 mmHg, is the most common hypertensive phenotype above 50 years of age. Although ISH is less common in adolescents and younger adults, its prevalence is increasing. Based on the HEalthy LIfe in an Urban Setting database, a prevalence of ISH of 2.7% (5.2% in men and 1.0% in women) was found, with the highest prevalence in individuals of African descent, but with a substantial heterogeneity within the ISH population, associated with both normal and increased central systolic BP. This may have important implications for cardiovascular risk, because central BP is a strong predictor for future cardiovascular disease (CVD).1 Genetic factors can also play a role as genetic variations associated with raised systolic BP in adulthood appear to be related to high systolic BP levels in children.2 Endothelial dysfunction estimated by reactive-hyperaemia peripheral-arterial tonometry (RH-PAT), which correlates inversely with various cardiovascular risk factors, predicted the risk of repeated coronary angiography due to recurrent angina after successful angioplasty. This suggests the opportunity for a more intense treatment including intense risk factor control and preventive intervention (such as exercise training)3 in patients with lower RH-PAT index values. The rising burden of atrial fibrillation (AF) confronts healthcare systems with enormous costs and the importance of primary prevention.4 Previous investigations have identified conditions associated with an increased burden, such as coffee intake,5 or exercise. Here a large prospective population-based cohort study has shown that normal weight, currently not smoking and low alcohol intake across all ages, sex, education levels and social classes in a free-living population was associated with an estimated 2.8-fold difference in the risk of AF.6 Interestingly, being physically inactive showed no significant association, which is in contrast with recent evidence.7 Furthermore, a meta-analysis involving 29 prospective studies (22 publications) suggested that smoking also is associated with an increased risk of AF in a dose-dependent manner, but the association is weaker among former smokers compared to current smokers.8 Loneliness is associated with poor health status,9 while psychological interventions are associated with favourable results.10 Here prospective follow-up data from the English Longitudinal Study of Ageing confirmed that also in aging loneliness was associated with coronary heart disease and stroke, independently of traditional CVD risk factors. Social factors are powerful determinants of cardiovascular outcomes in the general population, and the neurobiological basis of loneliness, including cardiovascular, inflammatory and neuroendocrine mechanisms may well explain its relationship with CVD.11,12 Elevated fast food density in the urban residential environment (<1000 m) was related to an increased incidence of CVD and coronary heart disease in a study involving a cohort of 2,472,004 healthy adults and living at the same address for over 15 years. Recent years have witnessed the development of changes in the food environment towards large-scale, inexpensive and calorie-dense food production, and this has influenced the population’s food consumption, which has been hypothesised to affect the development of CVD.13 High physical fitness, current smoking and younger age were associated with a lower incidence of Parkinson’s disease. These findings parallel those of several epidemiological studies focusing on physical activity and the onset of Parkinson’s disease. Together, these observations provide strong support for recommending physical activity to diminish the risk not only of CVD14 and risk factors,15 but also of neurological disease. How autonomic nervous system activity can be altered by chronic stressors, and how this may affect individual cardiomyocytes by altering the neuro-cardiac junction are reviewed.16 In particular, the alterations of metabolism and circadian rhythms of cardiomyocytes, leading to an imbalance of the cross-talk between cardiomyocytes and cardiac fibroblasts are discussed. Through these mechanisms, chronic stress can make individuals more prone to arrhythmias and myocardial fibrosis not only in the diseased17,18 but also in the healthy heart. The author(s) declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article. The author(s) received no financial support for the research, authorship and/or publication of this article.