Diet, Lifestyle, Smoking

Cardiovascular disease is the leading cause of death globally The past few decades have shown that especially low- and middle-income countries have undergone rapid industrialization, urbanization, economic development and market globalization. Although these developments led to many positive changes in health outcomes and increased life expectancies, they all also caused inappropriate dietary patterns, physical inactivity and obesity. Evidence shows that a large proportion of the cardiovascular disease burden can be explained by behavioural factors such as low physical activity, unhealthy diet and smoking. Controlling these risk factors from early ages is important for maintaining cardiovascular health. Even in patients with genetic susceptibility to cardiovascular disease, risk factor modification is beneficial.

Despite the tremendous advances in the medical treatment of cardiovascular risk factors to reduce overall cardiovascular risk, the modern lifestyle which has led to greater sedentary time, lower participation in active transport and time spent in leisure or purposeful physical activity, unhealthy diets and increased exposure to stress, noise and pollution have diminished the beneficial effects of contemporary medical cardiovascular prevention strategies. Therefore attenuating or eliminating these health risk behaviours and risk factors is imperative in the prevention of cardiovascular diseases.

1. Diet

The evidence that dietary factors influence the development of CVD derives mainly from epidemiological observations and from clinical studies on the impact of dietary changes on traditional risk factors such as plasma lipids, blood pressure or glucose levels.

In fact, epidemiological studies clearly indicate that higher consumption of fruit, non-starchy vegetables, nuts, legumes, fish, vegetable oils, yogurt and whole grains, along with a lower intake of red and processed meats and foods high in refined carbohydrates and salt, is associated with a reduced incidence of cardiovascular events. Moreover, they indicate that the replacement of animal fats, including dairy fats, with PUFAs or other vegetable sources of fats as well as fibre-rich carbohydrate foods can decrease the risk of CVD (Forouhi et al. 2018; Sacks et al. 2017).

Conversely, the evidence from randomized controlled trials (RCTs) is based on few studies that provide, in some cases, conflicting results. In this respect, the difficulties of performing clinical trials that adequately test nutritional interventions for CVD prevention cannot be underestimated since these studies require thousands of participants followed for years or decades. As to the lack of concordance between studies, this is due not only to methodological problems, particularly inadequate sample size or the short duration of many trials, but also to the difficulty of evaluating the impact of a single dietary factor independently of any other change in the diet (Forouhi et al. 2018).

These limitations suggest caution in interpreting the results of RCTs or even meta-analyses of RCTs in relation to the effect of a single dietary change on CVD, particularly where they diverge from the existing global evidence (Catapano et al. 2016). Therefore, in evaluating the role of diet in the prevention of cardiovascular diseases, we will consider not only RCTs on the impact dietary modifications on CVD events but also observational studies and clinical trials on the effects on major CVD risk factors.

1.3. Salt (Table 1)

1.3.1. Effects on CVD Risk Factors

Extensive scientific evidence shows that reducing dietary salt (sodium chloride) intake significantly decreases systolic and diastolic blood pressure in adults with or without hypertension (He et al. 2013; Stamler et al. 2018). Recent data from the international multicentre population INTERMAP study reported a positive association between salt intake and blood pressure values also within the normal range (Zhou et al. 2019). In addition to sodium reduction, an increase in potassium intake is beneficial to prevent and control blood pressure in people with hypertension, with no adverse effects on plasma lipid concentrations (Aburto et al. 2013a). In line with these findings, current nutritional recommendations include a potassium intake of at least 3.5 g per day in adults. Therefore, a diet that combines low sodium and high potassium intakes is more effective in reducing blood pressure and hypertension risk. An example of this type of approach is the DASH diet, recommended for the non-pharmacological management of hypertension. This diet includes also changes in the quality of fat – promoting unsaturated fat and carbohydrates – favouring unrefined ones. Recent results from a systematic review and meta-analyses of RCTs support the beneficial effect of the DASH diet not only on blood pressure but also on other cardiovascular risk factors, including total and LDL cholesterol concentrations (Siervo et al. 2015).

1.3.2. Effects on CVD Events

Two recent meta-analyses of cohort studies showed a direct relationship between sodium intake and stroke, CVD and CHD mortality; a higher sodium intake was significantly associated with an increased risk of CVD (12%) and CHD (32%) mortality, in addition to a much higher risk of stroke mortality (63%) (Aburto et al. 2013b; Poggio et al. 2015). Consistently, two recent meta-analyses of clinical trials showed that dietary salt reduction induces a significantly lower incidence (−20%) of CVD (Adler et al. 2014; He and MacGregor 2011).

Actually, in many parts of the world, the average sodium consumption (mainly derived from dietary salt intake and food additives, such as sodium glutamate) is above that recommended by guidelines: less than 5 g of salt/day (equivalent to about 2.3 g of sodium daily) (WHO Guidelines Approved by the Guidelines Review Committee 2012).

In the last decades, the science of human nutrition has shifted from a reductionistic approach focused on specific nutrients to a broader view emphasizing the role of food groups/dietary patterns (van Horn et al. 2016). This paradigm change is due to convincing scientific evidence showing that human health is indeed influenced by single nutrients but also by their complex interactions and by their interplay with other bioactive substances present in foods. These are likely to act synergistically, and, therefore, their impact on human health may not be appreciated unless evaluated within the context of the whole diet. Furthermore, characteristics other than nutrient combinations (i.e. physical features of the foods, technological processes, cooking procedures) may influence the absorption and bioavailability of nutrients and in turn modulate their metabolic effects. Therefore, there is growing attention to the identification of dietary patterns associated to the risk of disease or death. The Mediterranean diet is one of dietary patterns for which strong evidence from observational and intervention studies has accumulated on the benefits in the primary and secondary prevention of cardiovascular disease and other major chronic diseases, such as type 2 diabetes, cancer and probably cognitive impairment (de Lorgeril et al. 1999; Estruch et al. 2018; Sofi et al. 2014).

The Mediterranean diet is characterized by a food pattern resembling the healthy food choices outlined above and, in particular, by the regular consumption of plant foods – including vegetables, pulses, nuts, fruits and unrefined cereals – and fish as well as a low intake of red and processed meats and whole fat dairy products; the main source of fat is extra virgin olive oil (Table 1). The optimal nutrient distribution and the balanced food choices of this dietary pattern have supported it as a useful model for the implementation of a healthy diet at the population level. Its strengths are not only the evidence in support of its beneficial impact on cardiovascular disease prevention but also its very deep cultural roots that are the source of the large body of culinary recipes to make a healthy choice a gastronomical adventure (Catapano et al. 2016) (Table 2).

Table 1

Summary of the effects of dietary fatty acids, carbohydrates and salt on cardiovascular risk factors and cardiovascular events

Table 2

Summary of lifestyle measures and healthy food choices for managing total cardiovascular risk

2. Physical Activity

Having a sedentary life is a cardiovascular risk factor in itself. The amount of time spent being sedentary is increasing all over Europe even in young people. Watching TV, being stationary in front of a computer and using vehicles for transportation are the disadvantages of modern living. Especially in middle-aged females, sedentary lifestyle is almost as risky as smoking (Brown et al. 2015). Several studies have shown that sedentary behaviour increases cardiovascular risk. One of the largest prospective registries was the PURE study where physical activity was recorded in 130, 843 participants without existing CVD for 6.9 years. Compared with low physical activity (<600 metabolic equivalents [MET]  ×  minutes per week or <150 min per week of moderate-intensity physical activity), moderate (600–3,000 MET  ×  minutes or 150–750 min per week) and high physical activity (>3,000 MET  ×  minutes or >750 min per week) were associated with graded reduction in mortality and major cardiovascular events (Lear et al. 2017).

Experimental studies that mimicked sedentary behaviour have shown greater postprandial glucose and insulin levels during bouts of prolonged sitting compared with individuals taking frequent standing or walking breaks (Pulsford et al. 2017). Compared with prolonged sitting, breaking up sitting time with intermittent, even light-intensity activity, can increase expression of anti-inflammatory and antioxidative pathway modulators (Latouche et al. 2013). A recent meta-analysis investigated the association between sedentary behaviour and incident CVD events using data from nine prospective cohort studies and showed that risk increased with increased sedentary time, with the highest risk being in more than 10 h a day of sedentary time (Pandey et al. 2016). A recent study has shown that sustained physical activity but not weight loss was associated with improved survival in coronary heart disease (Moholdt et al. 2018).

Physical activity has a positive effect on body weight, blood pressure, blood glucose, lipid levels, endothelial function, autonomous regulation and coagulation. The summary of all these effects leads to a decrease in cardiovascular disease incidence and mortality. Physical activity has both acute and chronic effects on blood pressure. With increased physical activity, blood pressure is lowered especially in subjects with prehypertension compared to those with normal blood pressure (Physical Activity Guidelines Advisory Committee 2018). Physical activity combined with calorie restriction can contribute to weight loss and supports the maintenance of weight loss. The risk of type 2 diabetes mellitus is greatly reduced with physical activity, and this benefit is observed irrespective of body weight. Engaging in 150–300 min a week of moderate-intensity physical activity can reduce the risk of developing type 2 diabetes mellitus by 25–35% (Physical Activity Guidelines Advisory Committee 2018). Regular physical activity or exercise can affect serum lipid levels favourably. Men and women who exercise regularly have significantly lower LDL-C and VLDL and higher HDL-C levels compared to age- and gender-matched sedentary controls (Vodak et al. 1980; Wood et al. 1976). Similarly, moderate physical exercise decreases LDL-C and triglycerides and increases HDL in male survivors of myocardial infarction (Ballantyne et al. 1982). The effect of exercise on lipids varies in exercise intervention studies, and there appears to be a minimum exercise volume to increase HDL-C (Kodama et al. 2007). There are additional antiatherogenic effects of physical activity besides those affecting traditional cardiovascular disease risk factors (Green et al. 2017). Exercise intensity improves vascular endothelial function in a dose-dependent manner for aerobic activities (Ashor et al. 2015). Endothelial function is improved with exercise even in the absence of changes in classical risk factors like lipids levels, blood pressure, glucose or BMI (Green et al. 2008). Acute- and moderate-intensity exercises increase shear stress, which stimulates endothelium-dependent vasodilatation through the increased synthesis of nitric oxide (Erkens et al. 2017). Regular exercise training also leads to increased coronary artery size and dilatation capacity (Haskell et al. 1993) and increased luminal diameter of conduit arteries (Green et al. 2008). Exercise training can reduce the wall thickness of conduit arteries and increases the development of coronary collateral blood vessels (Thijssen et al. 2012). Unhealthy gut microbiota has recently been shown to increase the risk of CVD (Fu et al. 2015; Lanter et al. 2014). Regular physical activity or endurance exercise training can positively alter the human gut microbiota by increasing bacterial diversity, increasing faecal concentrations of short-chain fatty acids and increasing the proportion of healthy bacterial species (Allen et al. 2018; Bressa et al. 2017; Estaki et al. 2016). A recent study on endurance training has shown that exercise increases telomerase activity and length, whereas resistance training did not show these effects (Werner et al. 2019). Ideally, a combination of resistance and endurance training should be implemented (Reiner et al. 2019).

Physical activity is any activity that moves the skeletal muscles and consumes energy, whereas systematic physical activity, like swimming and running, is described as exercise. In healthy individuals, regular physical activity decreases all-cause and cardiovascular mortality by 20–30% (Lollgen et al. 2009; Moore et al. 2012; Sattelmair et al. 2011). Regular physical activity increases cardiorespiratory fitness (The American College of Sports Medicine 2014). Cardiorespiratory fitness is associated with reduced prevalence of CVD risk factors and improves prognosis (Harber et al. 2017). A meta-analysis of 33 studies in over 100, 000 individuals observed that every 1 estimated MET increase in CRF was associated with 13 and 15% reductions in all-cause and CVD mortality (Nauman et al. 2017). Cardiorespiratory fitness is important even in the presence of other risk factors and shown to be protective even in men with metabolic syndrome (Katzmarzyk et al. 2004) and obesity (Moholdt et al. 2017).

Although all agree that any level of physical activity is better than none, there is controversy about the optimal dose of physical activity for CVD prevention. The intensity and frequency of exercise should be personalized and adapted to a person’s needs as well as lifestyle. We also need to keep in mind that there is a high degree of interindividual variation in cardiorespiratory fitness responses to exercise.

The 2016 ESC prevention guideline recommends (Piepoli et al. 2016) for healthy adults of all ages to perform at least 150 min a week of moderate-intensity or 75 min a week of vigorous-intensity aerobic physical activity (PA) or an equivalent combination. For additional benefits in healthy adults, a gradual increase in aerobic PA to 300 min a week of moderate-intensity or 150 min a week of vigorous-intensity aerobic PA, or an equivalent combination thereof, is recommended. Multiple sessions of PA should be considered, each lasting ≥10 min and evenly spread throughout the week. Clinical evaluation, including exercise testing, should be considered for sedentary people with cardiovascular risk factors who intend to engage in vigorous PAs or sports.

Even low-level physical activity, such as low-dose running or commuting to work by bicycle, has been associated with a lower incidence of obesity, arterial hypertension, dyslipidaemia and diabetes mellitus (Grontved et al. 2016). The most recent Physical Activity Guidelines for Americans from the US Department of Health and Human Services has stated that benefits related to physical activity start even earlier and are easier to obtain than was previously thought according to recent evidence (Physical Activity Guidelines Advisory Committee 2018). These guidelines state that although one should try to get to guideline-recommended goals, the threshold at which health benefits begin to start is less than 150 min a week for most outcomes. There is no lower limit to the benefits of physical activity in reducing cardiovascular disease risk. However, getting to goal helps in obtaining benefits for the greatest number of outcomes. Additional physical activity confers additional benefits, and health risk does not seem to increase with high amounts of physical activity, even beyond 3–5 times the 150 min a week recommendation in healthy individuals. Compared with inactive adults, meeting the goals is associated with a 14% reduced risk of developing coronary heart disease (Physical Activity Guidelines Advisory Committee 2018).

2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease (Arnett et al. 2019) also recommends that adults should engage in at least 150 min per week of accumulated moderate-intensity or 75 min per week of vigorous-intensity aerobic physical activity to reduce atherosclerotic cardiovascular disease. For adults unable to meet the minimum physical activity recommendations, engaging in some moderate- or vigorous-intensity physical activity, even if less than this recommended amount, and decreasing sedentary behaviour can be beneficial to reduce CVD risk.

Although some exercise is beneficial for all, for those with known cardiovascular disease, the dose of exercise needs to be individualised to prevent adverse outcomes. The risk of having an adverse cardiovascular event during exercise is very low, especially during light exercise. However, it is best to do a risk assessment and tailor the exercise program according to the need of the individual. Light- and moderate-intensity exercise can be done with minimal risk, whereas intensive exercise should be preceded by a medical evaluation, especially for middle-aged people. The cardioprotective effects of regular PA, whether performed in low or high volumes, are clear and extend across all ages, gender and race (El Saadany et al. 2017; Nes et al. 2017; O’Donovan et al. 2018). Whether overexercising in healthy individuals can have unfavourable consequences has been questioned. In some studies, long-term strenuous exercise has been shown to increase the risk of atrial fibrillation (Gorenek Chair et al. 2017). It is never too late to start exercising. The Aerobics Center Longitudinal Study has shown that men who were in the lowest percentile of CRF at their first examination but fit at the time of their second examination years later had a 52% reduction in CVD mortality compared with men who remained unfit (Blair et al. 1995). For every one estimated MET increase, all-cause and CVD mortalities were reduced by 15% and 19%, respectively (Lee et al. 2011).

3. Smoking

Smoking is one of the most important modifiable risk factors for CVD. Furthermore, stopping smoking is the most cost-effective prevention intervention. It is well known that smoking and using all forms of tobacco products cause CVD and increase mortality (Mons et al. 2015; Teo et al. 2006). Because tobacco use even in small amounts increases cardiovascular risk, reducing the number of cigarettes or the amount of tobacco consumption is not sufficient. Even smoking one cigarette per day carries a risk (Hackshaw et al. 2018). Therefore there is no safe level of smoking and quitting is mandatory. Passive smoking also increases cardiovascular risk, and studies have shown that second-hand smoke exposure increases CVD and triggers adverse events in non-smokers (Lv et al. 2015).

Cigarette smoke contains more than 4,000 chemicals and toxins like nicotine, carbon monoxide, cadmium and oxidants (Smith and Fischer 2001). Exposure to these chemicals affects all stages of atherosclerotic vascular disease unfavourably. Endothelial dysfunction due to reduced NO bioavailability and activation of NF-kB will lead to functional and eventually physical damage to the endothelium (Collins 1993; Rahman and Laher 2007). Nicotine has been shown to promote MMP expression in smooth muscle cells and decreased collagen synthesis in the arterial wall impairing the stability of the plaque (Carty et al. 1996; Raveendran et al. 2004) Cigarette smoke increases systemic inflammation (Csordas et al. 2008). The catecholamines are increased in the circulation triggering vasospasm (Zhu and Parmley 1995). Smoking also alters the balance between pro- and anticoagulant factors towards procoagulation. Plaque thrombogenicity is increased with increased plasma tissue factor, VWF, thrombin and thrombomodulin and activated platelets (Markuljak et al. 1995; Miller et al. 1998). Upon smoking cessation, several of these prothrombotic changes revert to normal. Blood viscosity is also increased with smoking (Lowe et al. 1980). All of these effects contribute to plaque formation, vulnerability and thrombus development. Interestingly, there is a genetic susceptibility to the atherothrombotic effects of smoking. Different variants have been described that alter one’s susceptibility to the negative effects of smoking (Wang et al. 1996).

Smoking dependence is a chronic disease that needs to be managed with patience, expertise and time. The ESC prevention guidelines recommend the following strategy for smoking cessation (Piepoli et al. 2016): systematically inquire about smoking status at every opportunity; unequivocally urge all smokers to quit; determine the person’s degree of addiction and readiness to quit; agree on a smoking cessation strategy, including setting a quit date, behavioural counselling and pharmacological support; and arrange a schedule of follow-up (“five As” for a smoking cessation strategy for routine practice – ask, advise, assess, assist, and arrange). In case where advice and motivational interventions fail, drug-based interventions can be used to aid quitting smoking. Nicotine replacement therapies, bupropion and varenicline, have been shown to be helpful in increasing quitting (Cahill et al. 2013; Hughes et al. 2014; Stead et al. 2012). Electronic cigarettes emitting an aerosol containing nicotine have been developed to aid quitting; however, they may also emit toxic gases that may increase the risk of cardiovascular and pulmonary diseases, arrhythmias and hypertension (Benowitz and Fraiman 2017). Patients often are concerned about weight gain after smoking cessation. However a recent study from the cohorts of the Nurses’ Health Study (NHS), (NHS II) and the Health Professionals Follow-Up Study (HPFS) has shown that even if the smoking cessation was accompanied by substantial weight gain, this did not decrease the benefits of quitting smoking on reducing cardiovascular and all-cause mortality and cardiovascular mortality decreased in all weight-change groups (Hu et al. 2018).

Modern lifestyles expose us to air pollution and occupational noise which also have a negative impact on cardiovascular diseases. It has been shown that the risk of STEMI rises within hours of exposure to air pollutants (Sahlen et al. 2019). Furthermore, several investigations support that inhalation of ambient particulate matter triggers pulmonary and systemic inflammation resulting in metabolic syndrome and cardiopulmonary disease (Clementi et al. 2019). Exposure to high occupational noise is also associated with increase in hypertension, cardiovascular disease and cardiovascular mortality (Skogstad et al. 2016; Teixeira et al. 2019).

A healthy lifestyle is critically important to improve cardiovascular health and increase the control of risk factors. Healthy lifestyles should be adapted from birth to childhood and maintained throughout the lifespan. This can be possible only with creating health-promoting environments and improving healthcare policies, the interaction between the patient and the physician and education of the patient and the public about healthy lifestyles.

The WHO has put together a global action plan for the prevention and control of non-communicable diseases (WHO 2013). The goal is to reduce the risk of premature non-communicable disease deaths by 25% by 2025. According to this plan, reductions in tobacco use, salt intake, physical inactivity, harmful use of alcohol, raised blood pressure as well as stopping the diabetes and obesity epidemics are the goals. Early action and aggressive implementation of this plan may decrease the cardiovascular disease epidemic if the individual WHO targets are met and healthcare systems are strengthened. At the individual level, it is important for us to promote healthy lifestyles to everyone, including patients who already have CVD since it is never too late to benefit from a healthy lifestyle.

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