Editor’s Presentation Benefit of healthy lifestyle on cardiovascular risk factor control: Focus on body weight, exercise and sleep quality

It has been shown that adiposity partly explains the inverse association between cardiorespiratory fitness and physical activity arterial stiffness and metabolic health in children and adolescents, suggesting that excess adiposity is a strong mediator in the positive effects of healthy lifestyle on cardiovascular health.1 Now, the associations of changes and persistence of overweight and obesity with blood pressure in over 1500 children aged four years followed up for two years have been investigated. Being overweight or obese at baseline was associated with a larger increase in blood pressure during the follow-up compared with being normal weight at baseline. Moreover, persistent general and abdominal overweight and obesity and becoming overweight or obese during the follow-up was related to a larger increase in blood pressure during the follow-up. Importantly, there were no marked differences in blood pressure between children whose body mass index (BMI) or waist-to-height ratio returned to normal weight category and those who were persistently normal weight, suggesting that normalisation of body weight and adiposity level may also normalize other cardiovascular risk factors. Aerobic exercise exerts a positive effect on reduction in blood pressure.2 Moreover, previous studies investigating the impact of chronic exercise on serum lipoprotein levels revealed an upregulation of high-density lipoprotein (HDL) cholesterol, though this effect may be attenuated when exercise training is added on the top of statin therapy.3 Here is the first study to evaluate the role of HDL in the context of chronic exercise-induced amelioration of vascular function. Specifically, only chronic aerobic exercise downregulated circulating oxidized HDL (oxHDL) and the exercise-induced decrease in oxHDL correlated with the reduction of systolic, as well as diastolic, daytime ambulatory blood pressure. oxHDL has been shown to be characterized by impaired ability to promote cholesterol efflux from macrophage-derived foam cells. This novel finding constitutes one more step in our understanding of the exercise-induced cardiovascular benefits and thereby supports current hypertension guidelines recommending aerobic exercise on a regular basis. The association between reduced sleep duration and/or quality and cardiovascular events has been previously reported,4 as well as a link with abnormalities in the lipid profile. In the present issue, the relationship between sleep duration and quality and hyperlipidaemia was evaluated in 20,712 retired workers enrolled in the Dongfeng–Tongji cohort study, based in a central region of China: subjects with self-reported poor sleep quality as well longer duration (>10 h vs. 9–10 h vs. <8 h) were associated with higher prevalence of hyperlipidaemia also after adjusting for potential confounders. As is the case for all population studies, this study does not sufficiently explain the relationship between longer sleep duration and hyperlipidaemia. Several mechanisms have been advocated, including abnormalities in hormones regulating metabolism, presence of daytime fatigue with consequently sedentary habit, or sympathetic activation, similar to the occurrence of obstructive apnoeas. However, there are few reports of an association between longer sleep duration and abnormal lipid profile. Instead it seems plausible that subjects sleeping for more hours are also those with poorer health status, lower levels of physical activity and possibly also an overall less healthy lifestyle. Further, mood disorders possibly associated with abnormal sleep quality and duration, namely depression, have also been linked to atherosclerosis,5 and most notably to markers of inflammation.6 Third, it is intriguing to consider that cholesterol synthesis is more active during sleep. The Multi-Ethnic Study of Atherosclerosis, a population-based cohort with no known cardiovascular disease, reported the accuracy of coronary artery calcium score in predicting clinical events. A calcium score greater than 300 accurately identified subjects at high risk for future coronary heart disease events, with a hazard ratio of nearly 10.7 Interesting data supporting new approaches to improve subjects’ education toward a healthy lifestyle is here presented based on a sub-analysis from the Dutch Risk Or Benefit IN Screening for CArdiovascular disease (ROBINSCA) trial. The ROBINSCA trial is a large population-based randomized controlled screening trial designed to investigate the difference between the traditional assessment of cardiovascular disease risk, by means of the SCORE risk table, and an evaluation based on coronary artery calcification score performed by computed tomography scanning. The results show that more subjects with a high coronary artery calcium score contacted their general practitioners, seeking advice, compared with those with high SCORE risk alone. Furthermore, a higher percentage of those who sought advice were commenced on risk factor controlling medications, and antihypertensive and cholesterol lowering drugs, compared with controls. Standardized and verbally delivered information alone rarely lead to effective lifestyle change. However, a personalized approach towards highlighting individuals’ risks, race,8 arterial health status and available methods for improving it should have a significant impact on patients’ adherence to clinical, pharmacological and lifestyle instructions.9 In an observational French study, the regional variations in hypertension prevalence were evaluated: 62,247 French adults aged 18 to 69 years, aged 47.9 years and with a normal BMI were recruited in the 16 centres between 2012 and 2015. The prevalence of hypertension (defined as a blood pressure of greater than 140/90 and/or taking antihypertensive medications) was 30.1% and was higher in men than in women. The prevalence rates of hypertension decreased in a north–east–south gradient. BMI was the highest contributor to the differences between the centres, followed by socio-economic variables and a family history of hypertension. Interestingly, the levels of education, occupation and residential deprivation were relatively unimportant factors in the prevalence of hypertension, but this was attributed to the highly selected study population, which included a volunteer population that probably was healthier, more highly educated and more health conscious than the non-volunteers who were not included. A recent study on a much smaller but more representative sample of the whole population from northern Sweden reported that low level of education was correlated with the prevalence of hypertension after adjustment for age, male sex, higher BMI and being born in a Nordic country.10 Also, ethnic differences, which are well recognized factors in the prevalence of hypertension and hypertension-mediated cardiovascular complication, were not considered here.11 The majority of familial hypercholesterolaemia cases result from pathogenic variants in the low-density lipoprotein receptor (LDLR) gene (>90%), with pathogenic apolipoprotein B variants (5–10%) and proprotein convertase subtilisin/kexin type 9 variants (1–3%) being less common. Here, a systematic review and meta-analysis of available literature has addressed the impact of a molecular diagnosis of familial hypercholesterolaemia on screening and diagnosis, outcomes and cardiovascular risk, and found that: The diagnostic yield varied widely, from 28% to 80%, depending on diagnostic criteria, method used and country. The authors concluded that a molecular diagnosis should be reserved principally for patients meeting the low-density lipoprotein cholesterol (LDL-C) criteria with at least one additional criterion for familial hypercholesterolaemia. Very little information on the impact of genetic testing prognosis is available, while the major impacts have been in increasing proportions of individuals initiated on lipid lowering therapy, referrals to a specialized clinic, and adherence to medication. Cardiovascular risk is, in great part, dependent on the type of mutation and in particular the risk for atherosclerotic cardiovascular disease is approximately 4.4-fold in patients with a hypomorphic LDLR change and 6.8-fold in those with a complete loss-of-function. In conclusion, a molecular testing for familial hypercholesterolaemia is used in many countries, and has been proven to be of great utility in identifying patients with familial hypercholesterolaemia who were at increased risk and for whom a clinical diagnosis is not always well defined.12 When the LDL-C criterion is not met, but the patient has a strong family history of premature atherosclerotic cardiovascular disease or familial hypercholesterolaemia or the presence of xanthomas, DNA diagnosis may be considered. A recently published meta-analysis highlighted the prognostic importance and favourable outcomes of heart failure patients with improved left ventricular ejection fraction (LVEF) under optimal medical therapy, compared with those with persistently reduced ejection fraction.13 The prognostic value of LVEF is here confirmed in patients referred for coronary artery percutaneous intervention, independently of the clinical presentation, either acute or stable. This study is based on a patient-level data analysis from 6198 subjects enrolled in five randomized clinical trials: irrespective of the clinical setting, patients in the reduced and mid-range LVEF groups displayed higher all-cause and cardiac mortality and were at increased risk for the composite of cardiac death, stroke and myocardial infarction along a five-year follow-up. Assessment of left ventricular (LV) systolic function is proposed to remain a key element in patient prognostication in the coming years. In this respect, a refinement in the evaluation of LV systolic function could be achieved by using global longitudinal strain, overcoming some limitations linked to LVEF measurements such as geometric assumptions and technical issues, such as apical foreshortening and difficulties in proper delineation of endocardial borders.14,15 REACH-HF (Rehabilitation EnAblement in CHronic Heart Failure) is a home-based cardiac rehabilitation programme delivered over 12 weeks by a trained healthcare professional, co-developed with patients, caregivers and clinicians to include core components of comprehensive cardiac rehabilitation (i.e. education, psychological support and exercise training).16 Previously, the REACH-HF randomized controlled trial demonstrated the beneficial effect of REACH-HF intervention on quality of life with a reduction in total Minnesota Living with Heart Failure Questionnaire score by –5.7 points. Now, the cost-effectiveness of this intervention has been explored: a cost of £1721/quality-adjusted life-year (QALY) was demonstrated, with a 78% likelihood of being cost-effective at the willingness to pay threshold of £20,000 per QALY gained used by policymakers in UK and many developed healthcare economies. These findings, which are in keeping with a previous report demonstrating the cost-effective of home-based cardiac rehabilitation in coronary patients,17 should encourage also healthcare providers and stake-holders to promote access and participation in cardiac rehabilitation for people with heart failure and thereby to improve the health related quality of life and morbidity of this population.18 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.