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Traditionally, we have used age, gender, body mass index, blood pressure, lipids, smoking, and diabetes to assess cardiovascular (CV) risk. However, up until recently, the CV risk provided by environemental hazards such as pollution,1–3 noise,4–6 temperature,7 sleep duration8, and air quality,9,10 among others, have been overlooked. Indeed, ambient air pollution is a major health risk, leading to respiratory and cardiovascular mortality, as outlined the FAST TRACK ‘Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions’ by Thomas Münzel and colleagues from the Johannes Gutenberg Universität in Mainz, Germany.11 The authors calculated excess CV mortality attributed to air pollution in Europe with a novel global exposure–mortality model. Their calculated annual excess mortality rate from ambient air pollution in Europe averaged 790 000, and 659 000 in the EU-28 (Figure 1). In Europe, they estimate that 48–80% of such deaths are due to CV events. The upper limit includes events attributed to other non-communicable diseases which are currently not specified. These estimates exceed recent analyses, such as the Global Burden of Disease for 2015, by more than a factor of two. Based on these data, the authors estimate that air pollution reduces mean European life expectancy by 2.2 years. The annual, attributable per capita mortality rate in Europe was calculated to be 133 per 100 000 inhabitants, thereby exceeding the global mean. Thus, this novel analysis supports the statement of the European Court of Auditors in 2018 that European citizens are insufficiently protected against harmful air. Replacing fossil fuels by clean, renewable energy sources could prevent around half of the attributable deaths in Europe. These provocative and indeed alarming findings are put into further perspective in a balanced Editorial by Rachel Nethery from the Harvard University T.H. Chan School of Public Health in Boston, Massachusetts, USA.12
Another environmental factor affecting health is air temperature. Indeed, air temperture has been associated with blood pressure13 and mortality, but evidence of temporal changes in the risk of myocardial infarction is lacking. In their article entitled ‘Temporal variations in the triggering of myocardial infarction by air temperature in Augsburg, Germany, 1987–2014’, Kai Chen and colleagues from the Helmholtz Centre Munich for Environement and Health in Germany estimated the relationship between temporal variations in air temperature and myocardial infarction in Augsburg, Germany over 28 years.14 In that time, 27 310 cases of myocardial infarction and coronary deaths were recorded. They observed a non-significant decline in cold-related myocardial infarction risk. Heat-related myocardial infarction relative risk significantly increased from 0.93 in 1987–2000 to 1.14 in 2001–2014. The same trend was also observed for recurrent and non-ST segment elevation myocardial infarction events. This increasing susceptibility of the population to heat was more evident in diabetics and those with hyperlipidaemia. Thus, exposure to heat should be considered as a hitertho unrecognized environmental trigger of myocardial infarction.
Pain is a common symptom of many diseases and associated with discomfort, anxiety, and sympathetic nerve activation. Of note, widespread pain has received a separate diagnostic code in the ICD-11 and is also common in patients with acute and chronic coronary syndromes,15 as well as in Takotsubo syndrome.16 It has been suggested that widespread pain increases the risk of CV disease. However, studies on mortality risk in individuals with widespread pain have reported inconsistent results. In their article ‘Widespread pain is a risk factor for cardiovascular mortality: results from the Framingham Heart Study’, Jonas Tesarz and colleagues from the Heidelberg University in Germany investigated whether there is increased mortality in individuals with widespread pain and establish potential determinants of mortality risk in 4746 participants in the Framingham Heart Study over 15 years.17 A total of 14.5% of the subjects fulfilled criteria for widespread pain. When adjusting for age and sex, all-cause mortality was increased by ∼16% in subjects with widespread pain. Individuals with widespread pain had an increased hazard ratio of 1.45, particularly for CV cause of death (Figure 2). Thus, widespread pain is associated with increased risk for CV death, underlining the need for pain assessments in CV practice. These novel findings are put into perspective in an informative Editorial by Christian Templin from the University Hospital Zurich in Switzerland.18
Sleep is an essential part of human life, allowing us to recover from the physical and psychological stress endured during the daytime. In their article entitled ‘Association of estimated sleep duration and naps with mortality and cardiovascular events: a study of 116 632 people from 21 countries’, Chuangshi Wang and colleagues from the Population Health Research Institute in Hamilton, Canada investigated the association of estimated total daily sleep duration and daytime nap duration with deaths and CV events in 116 632 individuals over a period of 8 years.19 They found that, after adjustment for age and gender, both shorter (≤6 h/day) and longer (>8 h/day) estimated total sleep durations were associated with an increased risk. After adjustment for demographic characteristics, lifestyle behaviours, and health status, a J-shaped association was noted. Compared with sleeping 6–8 h/day, those who slept ≤6 h/day had a non-significant trend for increased risk of the composite outcome, with a hazard ratio of 1.09. As estimated sleep duration increased, a significant trend for a greater risk with a hazard ratio of 1.05, 1.17, and 1.41 for 8–9 h/day, 9–10 h/day, and >10 h/day was observed. Daytime nap duration was associated with an increased risk of the events in those with >6 h of nocturnal sleep duration, but not in shorter nocturnal sleepers (≤6 h). Thus, sleep duration of 6–8 h per day is associated with the lowest risk of deaths and CV events. Daytime napping was associated with increased risks of CV events and deaths in those with >6 h of night-time sleep but not in those sleeping <6 h per night. The study is further discussed in a comprehensive Editorial by Dominik Linz from the University of Adelaide in Australia.8
So far, cardiorespiratory fitness has been mainly indirectly assessed in studies on its relationship with CV disease.20,21 In their article ‘Peak oxygen uptake and incident coronary heart disease in a healthy population: the HUNT Fitness Study’, Bjarne Martens Nes and colleagues from the Norges Teknisk-Naturvitenskapelige Universitet Fakultet for Medisin og Helsevitenskap in Trondheim, Norway examined the associations between VO2 peak measured by the gold-standard method of cardiopulmonary exercise testing and coronary heart disease in 4527 healthy and fit adults over a period of 9 years.22 Average VO2 peak was 36.0 mL/kg/min and 44.4 mL/kg/min among women and men, respectively. Multi-adjusted Cox regression showed a 15% lower risk for the primary endpoint per one metabolic equivalent task (MET) higher VO2 peak, with a hazard ratio of 0.85. The highest quartile of VO2 peak had half of the events compared to the lowest quartile. Thus, VO2 peak is strongly and inversely associated with coronary heart disease across the whole fitness continuum in a healthy population. Increasing VO2 peak may have substantial benefits in reducing the burden of coronary heart disease, an interpretation that is further discussed in an infromative Editorial by Sanjay Sharma from St George’s University of London in the UK.23
Non-coding RNAs have evolved as important regulators of gene expression and body function.24,25 Furthermore, they have been shown to predict outcomes in a number of diseases, including acute coroanry syndromes.26 In their review article entitled ‘Circulating non-coding RNAs in biomarker-guided cardiovascular therapy: a novel tool for personalized medicine?’, Thomas Thum and colleagues from the Hannover Medical School in Germany remind us that biomarker-guided CV therapy is an increasingly established approach to tailor treatment decisions and monitor efficacy and outcomes.27 Recently, the non-coding human transcriptome has emerged as a new guide for novel therapeutic strategies and biomarker discovery. Non-coding RNA signatures provide molecular fingerprints of patient phenotypes, and complement traditional markers and clinical variables. Importantly, non-coding RNAs are present in body fluids, and their concentrations differ in health and disease. Here, the authors summarize current methodological and conceptual limitations and propose future steps for their incorporation into personalized cardiology. Despite the lack of robust population-based studies and technical barriers, circulating non-coding RNAs will eventually emerge as a promising tool for biomarker-guided therapies.
The editors hope that readers of this issue of the European Heart Journal will find it of interest.