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Stress as a Risk-Factor for CVD


  1. Search Strategies

A computerised search of the English-language literature published between 1980 and 2017 was completed. PubMed, National Centre for Biotechnology Information (NCBI) and MEDLINE databases and Cochrane database of systematic reviews were used to inform the literature review process. An initial search was undertaken in June 2017 and a more rigorous search was carried out in July 2017. A final search was performed in August 2017.
To supplement the search, bibliographies of relevant published articles were identified and searched. The abstract of studies and reviews extracted by the search were reviewed for relevance and full text copies of all potential relevant studies were obtained. Few relevant studies, published before 1980, were also included.
Search strategies using MeSH (medical subject headings) and a combination of keyword descriptors were used as listed below:
Stress, heart, CVD, cause, risk-factor, treatment, patient, society, community, perception, belief, prevalence, burden, prevention, management, intervention, diagnosis, rates, patterns, trends, triggers, disease mortality, smoking, obesity, lifestyle, changes, alcohol, effective interventions, psychosocial, self-help, advice, counselling, face to face, therapy, pharmacotherapy, secondary prevention, primary prevention, exercise, combined interventions, occupation, work, marital, acute, chronic, anxiety, depression, behavioural, preventive cardiology, health, management, pathophysiology, biological markers, awareness.
A general search using the same text terms as above was conducted using Google and Google scholar.
Other relevant websites were also searched:

  • Lancet
  • Springer
  • European Society of Cardiology (ESC)
  • World Heart Federation (WHF)
  • American Heart Association (AHA)
  • New England Journal of Medicine (NEJM)
  • Science Direct
  • Journal of Chronic Disease (JCD)
  • Ireland Health Services (IHS)
  • Nature
  • Economic and Social Research Institute (ESRI)
  • Journal of the American Medical Association (JAMA) Articles
  • The National Institute for Health and Care Excellence (NICE)
  • American Journal of Cardiology (AJC)
  • Medical Journal of Australia (MJA)
  • Irish Heart Foundation (IHF)
  • World Health Organisation (WHO)
  • Centres for Disease Control and Prevention (CDCP)
  1. The Burden of Cardiovascular Diseases

CVDs are a group of disorders of heart and blood vessels including CHD, coronary artery disease (CAD), stroke, angina, MI, heart attack and congenital heart disease (WHO 2017). According to the WHO Factsheet May 2017, CVDs are the number one cause of death globally, annually causing death more than any other cause (WHO 2017). An estimated 17.7 million people died from CVDs in 2015, representing 31% of all global deaths (WHO 2017). Of these deaths, an estimated 7.4 million were due to CHD and 6.7 million were due to stroke (WHO 2017). Out of the 17 million premature deaths (under the age of 70) is due to non-communicable diseases in 2015, 82% are in low- and middle-income countries, and 37% are caused by CVDs (WHO 2017). Moreover, it is estimated that by 2030, more than 23.3 million people will die annually from CVD  (Mathers and Loncar 2006).
Worldwide CVD is also estimated to be the leading disability-adjusted life years (DALYs) lost (WHO 2017). DALY represents the ‘healthy years of life lost’ and indicated the total burden of disease as opposed to simply representing the resulting death. It combines years of potential life lost due to premature death with years of productive life lost due to disability. Within the coming decades, the global burden of DALYs estimate for CVD is expected to rise from a loss of 85 million DALYs in 1990 to a loss of 150 million DALYs in 2020, thereby remaining the leading cause of loss of productivity (Vilahur et al. 2014, WHO 2017).
While in the past decades, this epidemic has receded in many developed countries, low- and middle-income countries experience an increase in the prevalence of CVD and 80% of the global burden of CVD occurs there (Vilahur et al. 2014, Yusuf et al. 2004). This also imposes a substantial economic burden at both population and household levels in such countries (Vilahur et al. 2014, Yusuf et al. 2004).

  1. CVD and Associated Risk Factors

Having a risk-factor does not necessarily lead an individual to develop CVD but increases the likelihood of developing such diseases. The presence of multiple risk factors results in a greater likelihood of developing CVD unless actions are taken to modify the risk factors and reduce the exposure to such risk
There are many known risk factors associated with CVDs. The conventional risk factors can be categorized as non-modifiable and modifiable (Pearson 2007, Vilahur et al. 2014).
Table1: Categories of Conventional Risk Factors

Type of Risk-factor Example
Non-Modifiable Advancing Age, Hereditary or Family History, Gender and Ethnicity or Race
Modifiable Behavioural Psychosocial Stress, Tobacco Use, Alcohol Use, Sedentary Lifestyle, Depression and Diet
Physiological or Biological Cholesterol, Hypertension, Diabetes, Certain Medications and Diseases

While, non-modifiable risk factors are useful in risk assessment, behavioural risk factors may be direct causes of CVD but may also contribute to physiological risk factors. Physiological risk factors are those which are measured in a clinical setting. They might be addressed with behavioural change advice but often require pharmacologic interventions as well.
Two major studies conducted in late 20th century, INTERHEART and EUORASPIRE, made significant contribution in identification of major risk factors of CVD (Kotseva 2011, Yusuf et al. 2004). The large international INTERHEART study, conducted from 1990 to 2010, concludes that conventional risk factors account for over 75% of CVD, with dyslipidaemia and smoking the two most important risk factors for CHD around the globe, with abdominal obesity, diabetes, and hypertension also noted as significant  (Yusuf et al. 2004).
In terms of behavioural risk factors of heart disease and stroke unhealthy diet, physical inactivity, tobacco use and alcohol misuse have been identified as the most significant factors in this category (WHO 2017). The effects of behavioural risk factors may present as raised physiological markers such as raised BP, blood glucose, blood lipids, and body mass index (BMI) (WHO 2017). These risks factors can in turn be measured, indicating an increased risk of developing a heart attack, stroke, heart failure and other complications (WHO 2017).
Apart from these, there are also a number of other factors which are known to impact on CVDs often referred to as “the causes of the causes” for example, globalisation, urbanisation and population ageing (Kreatsoulas and Anand 2010). It is suggested that these factors also impact upon the conventional physiological risk factors associated with CVD (Kreatsoulas and Anand 2010). Other determinants such as stress, socioeconomic  and environmental factors are also highlighted  (Kreatsoulas and Anand 2010). Additional research suggests that psychosocial risk substantially magnify risk associated with physiological factors, resulting in risk elevations that are comparable to those associated with hypercholesterolemia, hypertension, and other major risk factors for CAD (Rozanski et al. 1999).
In light of the current, and growing, burden of CVD, prevention and control of CVD and associated risk factors are gaining increased attention (Dimsdale 2008, Mathers and Loncar 2006, Pearson 2007, Vilahur et al. 2014). Biological risk factors can be managed with medicines and other treatments, while behavioural risk factors require various lifestyle interventions (Dimsdale 2008, Pearson 2007, Vilahur et al. 2014). WHO suggests that most CVDs can be prevented by addressing behavioural risk factors such as tobacco use, unhealthy diet and obesity, physical inactivity and harmful use of alcohol using population-wide strategies (WHO, 2017).
In this sense, Joint European Societies, gathered under the auspices of the European Society of Cardiology (ESC), conducts cross-sectional European surveys (the EUROASPIRE surveys) to raise clinical standards in secondary prevention against CHD. EUROASPIRE I, II, and III (1997–2009) demonstrate inadequate use of drug therapies to achieve CVD prevention in CHD patients and people at high risk of developing CVD in Europe (Euroaspire 1997, Euroaspire 2001, Kotseva 2011, Kotseva et al. 2009). Critically EUROASPIRE III time trends survey show a compelling need for more effective lifestyle management of patients with CHD (Kotseva 2011, Kotseva et al. 2009). The survey concludes that, despite a substantial increase in prescription of anti-hypertensive and lipid-lowering drugs, BP management remained unchanged, and almost half of all patients remain above the recommended lipid targets. This is primarily because the benefits of medicines are mitigated by poor lifestyle habits (Kotseva et al. 2009). The presentation of EUROASPIRE IV (ESC Congress 2013) primary results highlight the pressing need for modern preventive cardiology programmes with lifestyle changes at their core (ESC 2013, Vilahur et al. 2014).
While the importance of psychosocial factors in the development and expression of CAD has been debated extensively, the literature now provides clear and convincing evidence of the significant contribution of psychosocial factors to the pathogenesis and expression of CAD (Rozanski et al. 1999). It has also been reported that psychosocial factors are independently associated with CHD, with stress being an important risk-factor (Rosengren et al. 2004).
However, compared with other major risk factors, psychosocial variables such as stress are difficult to define objectively, besides stress also consists of several different (and inter-related) elements (Rosengren et al. 2004). Therefore, measurement of stress is complex and difficult, as a result of which there is limited focus on SM as a primary preventive intervention (Roohafza et al. 2012). SM programs and psychosocial interventions are mainly recommended as part of secondary prevention (Euroaspire 1997, Euroaspire 2001, Kotseva et al. 2009) or cardiac rehabilitation programs (Dusseldorp et al. 1999, Linden et al. 1996, Rees et al. 2004).
Current clinical practice guidelines recommend the need to target SM and coping as primary intervention programs (Roohafza et al. 2012) and long-term preventive approach (Tofler and Muller 2006). Nevertheless, whether it is implemented effectively or not is still unclear, as discussed in further sections.

  1. Stress as a Risk-Factor for CVD

Homeostasis, a combination of two Greek words: ‘homeo,’ meaning ‘similar,’ and ‘stasis,’ meaning ‘stable’, is a property of an organism to that helps an individual to maintain their body within normal parameters and hence stay healthy (Cannon 1929). Stress poses a serious threat to an individual’s homeostasis, and prolonged exposure to stress can result in tissue damage and various diseases, including increased CV risk (Lucini et al. 2002). This is consistent with the ‘Flight or Fight’ response theory to stress, a term which was coined in 1915 by an American physiologist, Walter Bradford Cannon (Cannon 1929). According to the theory, when we feel danger, the hormone norepinephrine (adrenaline) floods through every tissue in our bodies. Adrenaline exerts several important effects in different body organs. Cannons ideas demonstrated that the body tries to maintain inner consistency in order to maintain balance when confronted with stress. This balance is known as homeostasis.
Stress can also characterise itself as various stress-related behaviours including stress-eating, smoking, alcohol consumption, lethargy and lack of exercise, many more leading to a milieu of health issues (Hunt et al. 2000, Parrott 1995). These can present as biological determinants in terms of raised physiological markers like BP, blood glucose, lipid levels, etc. (WHO 2017).
The relationship between psychosocial stressors and chronic disease is complex and may be reflective of the nature, number, and persistence of the stressors as well as by the individual’s biological vulnerability (i.e., genetics, constitutional factors), psychosocial resources, and learned patterns of coping affect it (Schneiderman et al. 2005).
Health-related behaviours, like unhealthy diet, physical inactivity, tobacco use and harmful use of alcohol, have been identified as important risk factors for coronary disease at both a population and individual level (Hunt et al. 2000, WHO 2017). However there appears to be many research studies that do not yet include psychosocial factors – especially stress and stress-related behaviours (Yusuf et al. 2004).

  1. Sources of Stress

The effect of stress is largely consistent across geographic regions, ethnic groups, age groups, and in men and women but it can exhibits itself in different ways (Rosengren et al. 2004, Yusuf et al. 2004). For example, in women aged 30 to 65 years marital stress, not work stress, predicts a poor prognosis with CHD according to Stockholm Female Coronary Risk Study (Orth-Gomer et al. 2000). Work stress, on the other hand, has been particularly associated with increased CHD incidence and poorer prognosis in men (Orth-Gomer et al. 2000).
Work-related stress is the most extensively studied chronic stress. Studies  regarding presence of stress at work and subsequent CAD development suggest a strong causal relationship between this form of chronic stress and development of atherosclerosis (Bosma et al. 1998, Johnson et al. 1996, Karasek et al. 1981, Lynch et al. 1997, Ritchie et al. 1994, Rosengren et al. 1991, Rozanski et al. 1999, Siegrist et al. 1990, Undén et al. 1991).
Low socioeconomic status combined with low levels of perceived emotional support confer an increased risk for future cardiac events, not just in patients with established CAD, but in healthy individuals (Kaplan and Keil 1993, Karasek et al. 1981, Winkleby et al. 1990). An inverse relationship has been established between the magnitude of social support and the incidence of CAD and/or future cardiac events (Rozanski et al. 1999). Patients classified as being socially isolated and having a high degree of life stress had more than four times the risk of death of the men with low levels of both stress and isolation (Ruberman et al. 1984).
Like other psychosocial factors, social support also influences the extent to which individuals engage in high-risk behaviours such as smoking, fatty diet intake, and excessive alcohol consumption, leading to adverse effects on the heart (Rozanski et al. 1999).
There is experimental and clinical evidence of emotional stress and anxiety triggering as severe, reversible left ventricular dysfunction in patients without coronary disease (Wittstein et al. 2005). Physical exertion and anger or emotional upset are triggers associated with first acute MI in all regions of the world, in men and women, and in all age groups, with no significant effect modifiers (Smyth et al. 2016). Mental stress causes increased sympathetic activity (Iso et al. 2002), which could lead to increased ambulatory BP levels and pulse rates (Robert M. Kelsey 2007), reduced insulin sensitivity (Moberg et al. 1994), increased platelet aggregation (Grignani et al. 1992), and endothelial dysfunction (Ghiadoni et al. 2000). These effects, individually or in combination, may contribute to increased risk of CVD. Psychosocial stressors are also linked to increased risk of acute MI (Rosengren et al. 2004).

  1. Stress and Other Risk Factors

One question that arises is the importance of stress in comparison to more traditional risk factors like elevated cholesterol or adverse behaviours like smoking and obesity. Many of the stressor studies reviewed show risk gradients comparable to or steeper than that of elevated cholesterol (Dimsdale 2008). For severe global prevalence of stress, this risk gradient was less than that for smoking but comparable with that of hypertension and abdominal obesity (Rosengren et al. 1991).
In line with that, studies show that psychosocial factors interact synergistically with conventional CAD risk factors to heighten the risk for cardiac events. For example, depressed patients who smoke have a substantially higher risk of cardiac events than depressed patients who do not smoke (Anda et al. 1993). Low socioeconomic status cluster together with other psychosocial risk factors and often magnifies the risk of cardiac events (Kaplan and Keil 1993).
Moreover, stress and stress-related behaviours embody a vicious cycle. Once people are addicted to tobacco, it becomes enormously difficult for them to stop once their life stress and depression levels are elevated (Siahpush and Carlin 2006). In addition, many of the larger epidemiologic studies contended for risk-enhancing stress behaviours such as smoking and obesity (Dimsdale 2008). Thus, a valid hypothesis could be that stress can be dealt with by modifying other health behaviours (Charles H Hennekens 2017, Murray et al. 2012, NICE 2016).
Although the harmful physiological effects of acute “stressors” as significant triggers of CV events is well documented, the role of chronic “stressors” in the onset and prognosis of CVD may substantially differ from acute effects (Rosengren et al. 2004). The effects of acute stress on heart disease is supported by epidemiological studies regarding natural life stressors like bereavement (Kaprio et al. 1987, Parkes 1964). Cardiac event rates also increase in the immediate aftermath of other acute life stressors, such as earthquakes (Leor et al. 1996) and terrorist activities (Meisel et al. 1991). However, the discussion in terms of distinction between acute and chronic stress is arbitrary (Dimsdale 2008). For instance, an acute distress can reverberate for years or, the “stressor” may be instant (public criticism by a boss), but the patient may continue thinking about the distress for weeks or longer.
A systematic review of an expert working group of the National Heart Foundation of Australia (NHFA) concluded that there is consistent evidence of an independent causal association between depression and prognosis of CVD (Bunker et al. 2003, Lahiri et al. 2007). In contrast, there is no consistent evidence for a causal association between chronic life events, work-related stressors, and behaviour patterns like hostility, anxiety disorders or panic disorders and CVD (Bunker et al. 2003).
Thus, it is difficult to study and quantify the magnitude of stress.

  1. Stress and Temporality

The temporal sequence of events of psychosocial factors and “stressful” event remains to be determined, as does the exact pathophysiological nature of the influence.
Findings of a case-control study shows that experience of one or more life event during the year preceding an acute MI, and dissatisfaction with one’s financial situation, was twice more common in cases than controls (Welin et al. 1995). In a Danish registry-based study, an extreme external stressor, such as the death of a child, is shown to be associated with increased risk of future acute MI (Li et al. 2002). These are consistent with findings of a study, in which business failure, major intra-family conflict, job loss, death of spouse, and violence were associated with increased CV risk (Rosengren et al. 1991).
On the other hand, another study shows that optimism predicts a lower rate of rehospitalisation after coronary artery bypass graft (CABG) surgery (Scheier et al. 1999). Hence, fostering positive expectations promotes better recovery from the disease.
The outstanding question here is whether stress that triggers the event; or was the stress triggered by the event, in turn worsening the prognosis of the disease. In either case, management of stress becomes more important since stress, as seen from evidence provided up till now, is undoubtedly linked to CVD events.
There is overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects (Dimsdale 2008).

  1. Pathophysiology of Stress

Pathophysiological mechanisms underlying relationships between entities like depression, anxiety, stress, social factors, etc. and CVD can be categorised into two groups – behavioural mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviours, such as smoking, unhealthy dietary habits, excessive alcohol consumption, poor patient compliance (Bunker et al. 2003, Delaney M. 2010-2019, Rozanski et al. 1999); and direct pathophysiological effects, as delineated in experimental animal studies and/or investigations in humans, like adverse effects on BP, blood glucose, lipid levels, BMI, etc. (WHO 2017).
In a longitudinal study, conducted in 2002, it was revealed that in healthy medical students experiencing real-life stressor resulted in raised resting arterial pressure, in addition, induced important humoral changes, and impaired autonomic regulation (Lucini et al. 2002).
Other reactions to stressful life situations include alterations in the rate, rhythm, force and magnitude of cardiac contraction, change in the configuration of the heart’s action potential, and modification in the peripheral circulatory resistance (Wolff 1950). Moreover, ventilatory function is dramatically modified and efficiency impaired (Wolff 1950). Changes in the visceral parenchymal circulation, notably in the kidney, may affect other vital functions, further jeopardizing the health and survival of the organism (Wolff 1950). Many of these alterations cause the heart to work uneconomically and give rise to sensations and complaints (Wolff 1950). This becomes of special importance if the valves or myocardium are already damaged, which leads on the one hand to a faulty appraisal of the heart’s potential effectiveness, and on the other to an extra burden upon an already heavily laden organ (Wolff 1950).
An extensive body of evidence, from animal models studies (especially the cynomolgus monkey, Macaca fascicularis), reveals that chronic psychosocial stress can lead, via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis (Kaplan et al. 1983, Kaplan et al. 1982, Manuck et al. 1997, Skantze et al. 1998, Williams et al. 1993, Williams et al. 1994). In the presence of underlying atherosclerosis (example, in CAD patients), acute stress also causes coronary vasoconstriction (Rozanski et al. 1999, Smyth et al. 2016). Other studies link sympathetic hyper-responsivity to the induction of ischemia during exercise (Kral et al. 1997, Smyth et al. 2016), anger or emotional upset (Smyth et al. 2016) and mental stress (Krantz et al. 1991), and to the development of hypertension (Everson et al. 1996, Matthews et al. 1993, Palatini et al. 1997). However, because the literature relating psychosocial factors to CAD is multidisciplinary, there may be an under-appreciation of the strength of some of the epidemiological and pathophysiological observations that are reported (Rozanski et al. 1999).
Social factors may also exert direct pathophysiological effects, like hypercortisolemia, as demonstrated by animal studies (Sapolsky et al. 1997, Stanton et al. 1985). Human studies have demonstrated an inverse relationship between the degree of social support and resting heart rates (Undén et al. 1991). The presence of social support may also temper BP and heart rate responses to stressful stimuli in humans (Kamarck et al. 1990).
From a pathophysiological point of view, the increase in cardiac events associated with clustering of psychosocial stresses suggests that this clustering compounds the health-damaging effects of individual psychosocial stresses (Anda et al. 1993, Kaplan and Keil 1993, Kim et al. 2005, Rozanski et al. 1999, Ruberman et al. 1984). However, because psychosocial stresses and behavioural risk factors in humans change over time and cluster together in variable fashion, it is difficult to study the potential mechanisms by which they exert their pathophysiological effects (Rozanski et al. 1999).

  1. Perceptions and Beliefs Surrounding Stress as a Risk-Factor for CVD

One facet of illness representation is belief about the factors that individuals typically attribute to the development of their illness. Throughout the history of medicine, “stress” reveals as one of the most common patient complaints (Dimsdale 2008). In cardiology, complaints of stress take on special prominence because the links between brain and heart are well established (Dimsdale 2008).
From a patient’s perspective, stress can imply that they have become embroiled in an unpleasant or challenging new life circumstance, but sometimes it can also refer to challenging new circumstances that are not exactly unpleasant but still demand attention (e.g., a promotion). Sometimes patients are able pinpoint an exact event (“death in the family”); other times they might refer to their overall life experience (“job stress,” “poverty”).  As the complaint is entirely subjective, one either relies totally on the patient’s self-report or else applies generally agreed upon rules for how stressful a given event is for most people (Dimsdale 2008). Alternatively, one can expose subjects to a stressor, and then measure physiological responses and observe behavioural responses.
While several studies establish a clear association between symptoms of depression and CVD (Anda et al. 1993, Lesperance et al. 2002, Suarez 2004), INTERHEART for the first time establishes large-scale evidence in terms of the importance of perceived psychosocial stress by patients (Lahiri et al. 2007).
In a study by Hunt et al., most respondents ascribe a high importance to `lifestyle’ (aspects like smoking, drinking and diet’) in the aetiology of heart disease (Hunt et al. 2000). It is of interest that the majority of the all respondents regard `stress’ as being an important cause of heart disease and also accord similar importance to family history. Housing and living conditions is rated as having less importance than the above. However, it is of note that the vast majority in all groups agree that for `someone with a family history of heart disease’ it is `particularly important’ for them `not to smoke’, `to take exercise’ and `to eat a healthy diet’. ‘Whether they get heart disease or not is out of their hands’ (Hunt et al. 2000).
Findings from a study revealed that stress was perceived to be a major cause of hypertension (Kusuma 2009). In terms of stroke, other studies reveal participant’s perceptions of the factors that may increase a person’s chances of having a stroke.
Table 2: Perception of Stroke Risk Factors

Risk Factors National Stroke Association (NSA) survey (NSA 1996) (Pancioli et al. 1998) (Kothari et al. 1997)
Hypertension 43% 57% 27%
Stress 21% 22%
Cholesterol 14% 17%
Smoking 11% 35% 11%
Diabetes 1% 13%
Alcohol use 1%

A number of studies focus on cultural differences and beliefs related to cause in individuals with established CHD (Farooqi et al. 2000, French et al. 2001, Fukuoka et al. 2004, Webster et al. 2002). In the majority of these studies the findings indicate that patients most commonly believe that stress, worry, tension, smoking, diet and overwork caused their CHD. A systematic review by French et al, identifies that 41% of studies found stress is listed by participants as the most important cause of their CHD, whereas lifestyle behaviours is reported in 31% of studies (French et al. 2001). Stress and lifestyle factors are the most frequently cited causes for CHD irrespective of ethnic grouping, although older European participants frequently cite family history (Darr et al. 2008).
Finding from Darr et al. study report approximately half of the participants’ describing stress as contributing to the development of their CHD. Furthermore, South Asian and European participants describe events in their families’ lives that they thought caused them considerable worry and tension. Some of the patients believe that their CHD develop because of the stress they experience, for example, the sudden death of a family member. Participants recall such incidents bringing on feelings of extreme remorse and grief that they had found difficult to control. Other participants report that they had been living under stressful circumstances for a prolonged period and that as a result, stress had accumulated over time. Individuals who had been caring for family members with ill health for a prolonged period, those experiencing work-related problems, and those dealing with stressful family situations thought that this had had a negative impact on their health.
In light of such evidence and the growing burden of CVD, as previously outlined, there is a need to assess the current trend in patient perception of CV risk-factor (Mathers and Loncar 2006). More specifically within an Irish context it has been highlighted that CVD remains the most common cause of death in Ireland, currently accounting for and one in five premature deaths (Delaney M. 2010-2019).
In terms of perception and gender, women are four-to-eight times more likely to die of CVD than of any other disease, yet they are under-diagnosed and under-treated for their diseases and associated risk factors (Prendergast et al. 2004). This is mainly because most women do not perceive heart disease as a substantial health concern and report that they are not well informed about the risk (Mosca et al. 2000, Mosca et al. 2010, Prendergast et al. 2004, Robertson 2001). Despite increasing medical education and media time spent on women’s health issues, up to 87% of women in the urban population do not know the leading cause of death for their gender (Prendergast et al. 2004).

  1. Management of Stress

The experience of the acute MI could theoretically alter a patient’s perceptions about recent stress and mood (Rosengren et al. 2004). Previous studies have shown that although perception of risk-factor status may change, confirmatory search after the discovery of disease only moderately influences the recollection of symptoms in the month preceding disease (Croyle and Sande 1988).
It is now generally accepted that effective communication is as essential to high-quality medical practice as is clinical knowledge (Wallis and Guly 2001). Evidence suggests that participation of the patient in all stages of the clinical encounter promotes resolution of emotional and physical symptoms, greater treatment compliance, improved satisfaction, and fewer repeated consultations, referrals, and investigations (Griffin et al. 2004). Despite this evidence, practitioners often fail to listen, to elicit patients’ concerns, or to negotiate treatment options (Elwyn et al. 1999, Stewart et al. 1979). This failure may be in part because skills are not effectively taught (Silverman et al. 2004), but there may remain scepticism about the importance of partnership with patients in the consultation (Elwyn et al. 1999, Stewart 1995).
Further to that, barriers like, misconceptions and optimistic biases, hamper the implementation of treatment recommendations in patients (Elwyn et al. 1999, Griffin et al. 2004, Stewart 1995, van Steenkiste et al. 2004a). There is a mismatch between patients’ actual CV risk and their risk perceptions (van der Weijden et al. 2007). If people do not perceive themselves as vulnerable to a disease or condition, they are less likely to adopt recommended behavioural treatments (Griffin et al. 2004, Stewart 1995, van Steenkiste et al. 2004a). This leads to conflicts between the GPs intended management and patients’ expectations (Griffin et al. 2004, Kaplan et al. 1989, Stewart 1995). Knowing patients’ fears and risk perceptions and bringing them into line with the actual risk becomes a prerequisite for effective management (Griffin et al. 2004, Stewart 1995). Involving the patients in decision making on high-risk management may improve patients’ satisfaction, well-being, and even lifestyle and health outcomes (Kaplan et al. 1989, Stewart 1995). Thus, it is important for effective CV risk management that GPs have a clear view of patients’ actual CV risk, their risk perceptions, and their preferences and expectations regarding risk management. In the end, given that the majority of patients suffering CVD would name stress as a major cause there is clearly a need to assess the role of stress and CVD to develop effective and feasible (i.e., not time-consuming) instruments for the explanation of risk and for reassuring and counselling the patients (van der Weijden et al. 2007).

  1. Stress Management: Prevention, Lifestyle Changes and Challenges

Disease prevention actions/management programmes for healthy individuals is termed as primordial prevention (Kones 2011). Primordial prevention is described as focusing on an individual’s behavioural lifestyle characteristics to achieve a level of health that does not permit CV risk factors to appear in the first place itself (Kones 2011). The AHA incorporated the powerful principle of primordial prevention in defining “ideal CV health” as a goal in reducing cardiac and stroke mortality 20% by the year 2020 (Lloyd-Jones et al. 2010).
Primary prevention traditionally works by delaying or limiting the first event in high-risk individuals, who have yet not been formally diagnosed with the disease but may still be symptomatic for example have high BP (Kones 2011). Prevention also may generally refer to screening and immunizations to detect, forestall, or limit serious disease (Kones 2011). Secondary prevention classically seeks to prevent, postpone, or limit recurrence of a clinical event, or death, in patients who have been previously diagnosed with CVD (Kones 2011).
A more recent approach is to stratify people on the basis of risk is done by using tools like AHA guidelines and the more recent SCORE (Systemic Coronary Risk Evaluation) total CVD risk assessment tool recommended by the ESC (Pearson 2007). According to SCORE, a small (but growing) number of people would be at high risk (arbitrarily defined as more than 20 percent risk per ten years), demanding aggressive risk-factor management, prophylactic medications, and treatment of symptoms of CVD (Pearson 2007). A larger group would be considered to be at moderate risk (10–20 percent risk), benefiting from risk-factor management with less costly drugs and devices (Pearson 2007). Finally, low-risk people (less than 10 percent risk) would benefit from health education, modification of harmful health behaviour, and a healthier environment, at little direct personal cost (Pearson 2007).
The various levels of prevention, identifies at least three approaches for intervention to reduce CVD mortality: modification of harmful risk behaviour at the population level to prevent the onset of risk factors themselves; treatment of behavioural and physiologic risk factors to reduce risk of disease onset or progression in individuals; and treatment of the symptomatic patient (Pearson 2007). In reality, this illustrates the contribution of a broad and balanced CVD prevention effort, rather than one focused on a single risk-factor or stage of disease (Pearson 2007).
Guidelines for primordial prevention are directed at the social and physical environment, not just the medical care system or even public health agencies (Pearson et al. 2003). Recommendations include targeting behaviour needs, including diet, sedentary lifestyle, tobacco use; approach in dealing with screening and treatment for BP and cholesterol; and early recognition of symptoms of heart attack and stroke for improving CV health at community level (Pearson 2007).
Primary prevention guidelines, aimed at symptomatic or high-risk adults who have yet not experienced a CV event, are much more extensive. The American, European and British guidelines demonstrate numerous methods to reduce CVD risk profile with strong consensus regarding smoking and exercise, whilst the fine details may vary slightly for other factors (Charles H Hennekens 2017, Stewart et al. 2017). ESC (Fuster et al. 2001) and NICE (Excellence 2011, NICE 2016) guidelines provides advice on exercise, diet, smoking, alcohol, weight management. The AHA Primary Prevention Guidelines contains identical recommendations for smoking, BP, physical activity, weight management, and diabetes management (Pearson et al. 2002). One important difference between other guidelines and secondary prevention guidelines is the need to assess risk through risk-factor screening and global-risk estimation (Pearson 2007).
Goals of secondary prevention for adults with coronary and other vascular diseases include smoking cessation, BP control, lipid, weight and diabetes management, physical activity and pharmacotherapies according to 2006 AHA/American College of Cardiology (ACC) guidelines (Smith et al. 2006). Pharmaceutical options have developed over the years whilst lifestyle advice remains largely unchanged (Stewart et al. 2017).
As discussed previously, there are wide ranging adverse effects of psychosocial stress on CV health and large studies like INTERHEART establish importance of perceived stress on CV health of a patient. However, in reference to the evidence outlined in this section it is noteworthy that applications of the ‘stress concept’ (the understanding of stress as a risk-factor and the use of SM) in the clinical settings have been relatively limited, although the importance of SM is highlighted in European guidelines for CVD prevention (Steptoe and Kivimaki 2012).
Data collected by Yusuf et al. suggests that lifestyle modification is of substantial importance in both men and women, at all ages, in individuals from all geographic regions of the world, and in those belonging to all major ethnic groups (Yusuf et al. 2004). Therefore, lifestyle modifications, including SM, should be the cornerstone of prevention of CHD in all populations worldwide.
Further reductions in CVD mortality will likely need to involve the entire range of new approaches to prevent CVD. Secondary prevention programs have driven case-fatality rates to extremely low levels, which suggests that there are relatively limited opportunities to make inroads on mortality through this approach alone (Smith et al. 2006). Primary prevention will require expansion of risk-factor assessments and global-risk scoring, with prioritization of cost-effective interventions in moderate- and high-risk people (Pearson 2007, Pearson et al. 2002). The best opportunity to reduce CVD may be at the community and societal levels, where improvements in SM, diet, exercise, and tobacco use have recently been elusive (Pearson 2007).
Up till recently, the evaluation of CHD-related health effects of individual programmes relevant to psychosocial prevention of CHD have been done as secondary preventive trials (Peovska 2013). The evidence for the feasibility of such programmes in primary prevention is accordingly indirect and recommendations have been made at primordial level for total population (Peovska 2013).
Hypertension as one of the established CHD risk factors, has been used as an outcome variable in various intervention trials. Studies assessing SM or similar techniques as secondary prevention in people with CVD, showed reductions in psychological stress factor was associated with reductions in BP (Linden et al. 2001) and other risk factors (Schneider et al. 2012). However a study by Batley et al., assessing the  efficacy of SM as primary prevention for hypertension in healthy individual, showed SM to be an unlikely candidate (Batey et al. 2000).
Psychological interventions like SM also form part of comprehensive cardiac rehabilitation programmes. Meta-analyses of SM trials, as part of comprehensive cardiac rehabilitation programmes, found mixed results with some showing reductions of recurrent cardiac events and death (Blumenthal et al. 2002, Linden et al. 1996, Nunes et al. 1987) while others did not (Frasure-Smith et al. 1997, Jones and West 1996).
Nevertheless, more recent studies, such as EUROACTION (Wood et al. 2008) and EUROACTION Plus (Jennings et al. 2014), and GlObal Secondary Prevention strategiEs to Limit (GOSPEL) (Giannuzzi et al. 2008), provide contemporary scientific evidence for a comprehensive and sustained approach to preventive and rehabilitative care in which structured programmes achieve healthier lifestyles and more effective risk-factor control compared with usual care.
Although, EUROASPIRE IV survey reveals a large majority of coronary patients in Europe failing to achieve the lifestyle, risk-factor and therapeutic targets set by the Journal of Endocrine Society (JES) guidelines (Graham et al. 2007, Perk et al. 2012). There is a large variation between European countries both in lifestyle and risk-factor management, the use of cardio protective medications, the provision of cardiac prevention and rehabilitation and other preventive services (Kotseva et al. 2016).

  1. Challenges for Stress Management in CVD

Earlier randomised controlled trials (RCTs) employing SM approaches in CHD patients have had important methodological limitations with larger RCTs failing to demonstrate a benefit for SM therapy over usual care, (Jones and West 1996, Rees et al. 2004) raising questions about the value of SM therapy for patients with CHD (Blumenthal et al. 2010).
Despite the well-established benefits of exercise, nutritional counselling SM and other lifestyle behavioural interventions, among some physicians, there is a perception that psychosocial factors do not merit much attention (Rozanski et al. 1999). Reasons for this may be multi-fold (Rozanski et al. 1999). First, many physicians are not aware of the strength of association between psychosocial risk factors and CAD development. Second, the lack of consensus regarding the measurement of some psychosocial risk factors may be confusing to clinical practitioners. Third, physicians who regard psychosocial factors as potentially important may nonetheless lack expertise to assist patients in modifying these factors. Fourth, even when physician motivation and training are present, such interventions are often time-consuming and labour-intensive. Finally, available evidence showing the effectiveness of psychosocial interventions often suffers from methodological limitations, such as “soft” clinical end points, and inconsistent results (Blumenthal et al. 2010, Rozanski et al. 1999).
Future research focusing on the effectiveness of SM interventions for CHD, need not only address the use of SM techniques to reduce the stress or distress associated with a cardiac event, but also needs to address procedures which aim to reduce the risk of further clinical events (Parrott 1995, Rees et al. 2004).
The magnitude of the problem – pervasive poor CV health and its importance – has not been fully appreciated. Psychosocial aspects of behaviour in embracing and adhering to primordial, primary, and secondary prevention are receiving greater attention (Kones 2011, Mosca et al. 2010, Norcross et al. 2011, Pancioli et al. 1998, Ritchie et al. 1994, Webster and Heeley 2010).
For truly effective improvements in CV risk, primordial prevention appears necessary as an adjunct to the high-risk strategy traditionally offered to individual patients (Kones 2011). Studies designed to assess the effectiveness of SM training in improving the ability of coping with stress in a large population have shown positive results (Roohafza et al. 2012). SM programs could improve coping strategies at the community level and can be considered in designing behavioural interventions.

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