Global Spotlights Changing the conversation from ‘chronic disease’ to ‘chronic health’ Sophie Cassidy 1 , Imre Hunyor 1,2,3 , Ian Wilcox 1,2,3 , and Luigi Fontana 1,4,5 * 1 Charles Perkins Centre, Faculty of Medicine and Health, John Hopkins Drive, The University of Sydney, Sydney, NSW 2006, Australia; 2 Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, Sydney, NSW 2050, Australia; 3 Central Sydney Cardiology, 407/100 Carillon Ave, Sydney, NSW 2042, Australia; 4 Department of Endocrinology, Royal Prince Alfred Hospital, Camperdown, Sydney, NSW 2050, Australia; and 5 Department of Clinical and Experimental Sciences, Brescia University, Brescia, Italy Despite spectacular advancements in pharmacological and interven- tional treatments for cardiovascular disease (CVD), it remains the leading cause of morbidity, disability, and premature death worldwide, the costs of which are unsustainable in all healthcare systems. Lifetime risk of a first CVD event at age 50 is 65% in men, and it is increasingly affecting younger women and men. Atherosclerosis is the underlying cause of 90% of cases of myocardial infarction, 60% of strokes, most cases of chronic heart failure, peripheral arterial disease, and many cases of dementia. The evidence that an ageing, increasingly sedentary, sleep deprived and psychologically challenged population consuming hypercaloric diets rich in animal and ultraprocessed food since concep- tion is likely responsible for this is substantial. The opportunity to inter- vene exists many years before presentation in middle age and our failure to act effectively is alarming. The current pandemic has dis- rupted health systems worldwide and renewed interest in, and appre- ciation of, the critical importance of lifestyle over an individual’s lifetime to deliver affordable improvements in health and healthy age- ing. Into the frame of the problem comes a renewed focus on digital health and educational solutions delivered with precision in a personal- ized way. Evidence that lifestyle changes markedly improve cardiovascular outcomes including reduced disability and improved longevity in asymptomatic and known CVD is overwhelming. The actual change needed to achieve benefit is remarkably small which makes our failure to achieve it in the real world so much more compelling. The CALERIE trial showed that in non-obese middle aged men and women, a modest 13% calorie restriction maintained adequate nutrition while reducing inflammation, oxidative stress and improved all classical cardiometa- bolic risk factors well below the conventional risk thresholds used in clinical practice. 1 Participants in the Framingham Study with cardiovas- cular factors similar to those achieved by CALERIE volunteers had a 5% risk of developing CVD, whereas those with two or more abnor- mal factors had a 69% probability and lived 11 years less. 2 In lifestyle prevention studies, the UK DiRECT 3 and Cuban trial 4 have shown that remission occurs in 80% of patients affected by type 2 diabetes and NAFLD who lost >10 kg, and in those with diabetic nephropathy small reductions in body weight significantly reduce glo- merular hyperfiltration, albuminuria, inflammation, and multiple other cardiometabolic risk factors. 5 The Pridimed, the Lyon, and Indo-Mediterranean Diet Heart trials have demonstrated a powerful protective effect of a Mediterranean-style diet against major cardiovas- cular events, including stroke in high-risk patients, coronary recurrence rate, and sudden cardiac death in those who already suffered from a prior myocardial infarction. 6 Recent and accumulating work in animal models and humans indicates that specific dietary manipulations (e.g. intermittent fasting, time-restricted feeding, single-nutrient modifica- tions) in conjunction with different forms of exercise training, mindfulness-based stress reduction, and sleep-promoting interven- tions can also play a role in preventing or slowing the accumulation of molecular damage leading to cardiovascular dysfunction. 7 Despite the clear experimental animal, epidemiological, and clinical trial data demonstrating the power of lifestyle to alter cardiometabolic risk factors and events (Figure 1), we see two clear gaps which need to be addressed. First, there is a need for more mechanistic studies to understand the magnitude and temporal effects of different lifestyle interventions on coronary macro- and microvascular structure and function, myocardial inflammation, and fibrosis. Computed tomogra- phy coronary angiography (CTCA) coupled with AI-assisted algorithms and radiomic plaque analysis is emerging as a powerful non- invasive tool to quantify not only the coronary calcium score but also the volume and structure of low attenuation non-calcified plaques, and pericoronary adipose tissue. Several studies have tracked the positive impact of various pharmacological therapies on atheroma volume and characteristics on CTCA, and early evidence suggests that lifestyle intervention may yield changes observable as early as 12 months. 8 Moreover, state-of-the-art MRI techniques can provide quantitative * Corresponding author. Tel: þ61 2 8627 7499, Email: luigi.fontana@sydney.edu.au Published on behalf of the European Society of Cardiology. All rights reserved. V C The Author(s) 2021. For permissions, please email: journals.permissions@oup.com. European Heart Journal (2021) 00, 1–4 doi:10.1093/eurheartj/ehab633 Downloaded from https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehab633/6365856 by guest on 10 September 2021