Home » Health & Fitness » Psychosocial Effects of Coronary Heart Disease: Free Research Paper Sample

Psychosocial Effects of Coronary Heart Disease: Free Research Paper Sample

by Suleman
79 views

Introduction

Coronary heart disease (CHD) is the largest cause of premature death in the United States, and atherosclerosis is the disorder precipitating this disease. The characteristic of CHD is atherosclerosis, which is distinguished by the accumulation of atheromatous or fatty plaques in the arterial wall, contributing to a decline in the cross-sectional region of the arteries. As these occur in the coronary arteries, the luminal blood supply into these arteries reduces (Williams, et al., 2002). The actual or relative lack of oxygen and metabolites in the areas supplied by these arteries will result in an acute or relative decline in blood flow across these arteries responsible for blood supply to the cardiac muscles. This is referred to as ischemia, and if the ischemia exceeds the threshold stage of cardiac musculature vitality repair, defined as myocardial infarction, will contribute to death of cardiac muscles (Hemingway and Marmot, 1999). If labelled CHD, the whole continuum of this disease mechanism is known, and there are several known causes that predispose, precipitate, and facilitate this disease. The effects of both CHD variants and their findings are well established, but it is very important to remember that distinct identities exist in the disease (Asbury, Creed, and Collins, 2004). The metabolic mechanisms of cholesterol or lipids are well recognised, and it is identified that the essential pathology that predisposes to CHD is dyslipidemia. There is a large variety of studies on these subjects’ personalities and the psychosocial causes directly linked to this disorder. Such disorders cause persons more vulnerable to coronary heart disease. Researchers also shown that persons who are consistently engaged in an ongoing, relentless battle to accomplish more and more in less and less time are more likely to experience CHD (Sullivan et al., 2001).

Psychosocial Factors

Diabetes, chronic CHD-accompanied hypertension and stress have been linked to depression and are an independent risk factor for CHD. Stress is a feeling that you’re out of control and under painful, almost endless pressure. Many conditions create stress which may be attributed to injury, deprivation, work challenges, job concerns, personal relationships, professional relationships, financial relationships, and other areas of daily life. Depression is typically part of stress that influences all ages of patients (ENRICHD Researchers, 2005, Burg et al.). Unlike blood pressure, cholesterol, weight, blood sugar, or the number of cigarettes that an individual smokes, stress can not be measured. Only the person affected knows how intense the tension is. It’s arbitrary. Stress is adverse to physical well-being and fitness and is detrimental to the spirit. The risk of having angina is improved by these sources of tension. Heart problems may be caused by intense tension. The role of stress in promoting cardiac disease has long been discussed by academics, but there is an increasing body of evidence that it is a risk factor (Denollet and Brutsaert, 2001). Researchers should however, recognise that chronic high levels of stress prompt hormone adjustments that may raise blood pressure and insulin levels and probably encourage inflammation and other changes in the body that increase cardiovascular risk over time. It is not well established yet how stress harms the heart. Tension may also induce depression, one of the neural factors associated with an increased risk of heart failure (Januzzi, Jr. et al., 2000).

Psychosocial Effects of Coronary Heart Disease

Background

CHD cases may also not have any well-known risk factors correlated with them. Depression has been described by several research conducted in recent years as an independent factor that raises the likelihood of a heart attack. Why depression influences cardiac function remains unclear, but the prevention and management of depression is now deemed a significant part of minimising cardiovascular risk (Lett et al., 2005). This is one of the key reasons known to exist in psychosocial terms. While an impressive body of research has been gathered that connects psychological variables and cardiac disease, this association remains an area of ongoing discussion. Even, it is not necessary to disregard the importance of psychological influences and personality, and they may play important roles in CHD precipitation. Health psychology offers certain variables a great deal of weight (Kop et al., 2005). Several tests have shown that heart patients with a stable system of emotional support fare well than someone living alone or without support. Instead, depression will take a toll not just on the depressed user, but also on family members and near associates. To explain this dilemma, the first move is to realise that this condition may be a real problem. Therefore, to find out the current evidence for these psychosocial factors in the etiology of CHD, it was decided to a systemic review of contemporary literature.

Aims

This work aims to conduct a systematic review of contemporary literature to integrate the evidences from all relevant and primary sources, about the psychosocial factors that have been incriminated in causation of CHD. This is a way of integrating research that limits bias. The synthesis of research evidence is an accepted form of research in health psychology. The use of systemic reviews is now widespread and is linked strongly to evidence-based practice. Over time, the results from such reviews have the potential to influence clinical and health psychology practice in different ways.

Strategy of Literature Review

An exhaustive manual search of the medical and psychological literature was performed covering a time span of 2000 till 2008 April. Psychological abstracts were searched on the basis of key words, “cardiovascular disorders”, “coronary heart disease”, “risk factors for coronary heart disease”, “atherosclerosis”, “myocardial infarction”, and “psychosocial factors in coronary heart disease.” Additional articles were located using the bibliographies of the articles already located. Those journals that yielded the largest numbers of appropriate and suitable articles were searched from cover to cover. These journals were Journal of Psychosomatic Medicine, European Heart Journal, British Medical Journal, Archives of Internal Medicine, and Circulation. Similar searches were undertaken in electronic media, especially in different databases. The medical subject headings of “stress”, “mood disorder”, “depression”, “epidemiology”, “mortality”, and “heart disease”, were used to search these databases preliminarily. After locating 293 articles all together, a narrowed search were undertaken among these articles those dealt with “psychosocial factors” and “coronary heart disease.”  Databases, such as Medline, PubMed, Highwire Press, AMED, ASSIA, Ingenta, Science Direct, and Cochrane Databases  were searched, and this narrowed the number of articles to 93. After studying these articles, it was decided that both quantitative and qualitative articles will be reviewed.

Only peer-reviewed articles published in English language were preferred, and the most recent articles would be preferred. It was also decided that preference will be given to the more recent literatures, meaning if adequate numbers of studies are available in the recent time, comparatively older studies would be excluded.

The other criteria of inclusion of these studies were, the study must include at least psychosocial aspect, such as, anger, stress, depression, anxiety, or aggression. These personality variables were included because these are of theoretical interest and have been rigorously studied in relation to coronary heart disease. The studies must have investigated the targeted disease variable, coronary heart disease. The studies would have been any of the following, qualitative or quantitative, although purely descriptive or anecdotal studies were decided to be excluded. The study must contain enough information to allow the estimation of the effect size and the level of significance, since effect size would determine the significance of the effect irrespective of the sample size.

Plan of Systemic Review

For this article, all the articles that have been chosen to be reviewed will be critically evaluated on the basis of essential key elements. Although in each reviewed study, there would be sections such as title, abstract, background information or literature review, methodology, analysis, and discussion of the results, this systemic review will critically examine those with the focus on the evidence presented there. In summary, a reflection of the knowledge gained from these literatures reviewed will be discussed, and any further recommendations considered necessary, useful, or appropriate will be noted.

Methods

The methods can be summarized as below. An initial search of relevant psychosocial features was conducted. These comprised of terms as follows

  1. Depression.                      5. Anger                                          9.  Coping
  2. Mood disorders.              6. Psychosocial stressors            10. Adaptation.
  3. Anxiety.                            7. Epidemiology.                           11. Adjustment
  4. Stress.                               8. Anxiety.                                      12. Tension

The other terms in relevance to coronary heart disease those were included in search strategy were coronary heart disease, symptoms, disease conditions, and pathological terminology. These were as follows

  1. Heart disease.                         4. Risk factors.
  2. Coronary heart disease.       5. Atherosclerosis.
  3. Cardiovascular disorders.    6. Myocardial infarction.

An expanded search terms were created for each of these search terms, and all main permutations and combinations of these terminologies were utilized to search databases as discussed earlier.

  1. Coronary heart disease
9. Heart Disease
  1. Atherosclerosis
10. Risk factors
  1. Psychosocial
11. Myocardial infarction
  1. Stress*
12. Adaptation
  1. Anxiety
13. Tension.
  1. Psychosocial stress
14. Anger
  1. Adjustment.
15. Mood*
  1. Coping
16. Epidemiology
The search was conducted with 1 or 2 or 9 or 11 and/or 10, 3, 4, 5, 6, 7, 8, 12, 13, 14, 15, and/or 16

Review of the abstracts and the methodologies taking in consideration the inclusion criteria, narrowed the search to 6 studies. One study dealt only with depression, and this study was excluded, yielding 5 studies that would be included in this review. The entire method, in the following flow chart of the literature search has been represented.

Initial Search                                               N =   293

Review of Titles                                                     93

Secondary cull by review of abstract                         6

After exclusion following methodology study            5

————————————————————N=5

Mixed Quantitative and Qualitative Design:  N = 5.

Quantitative and semi-structured interview  N= 2

Quantitative and Open-ended questions N= 3

 

Methodology

In the research, the number of participants differed greatly. While the study by Vitiliano et al included only 152 subjects (Vitaliano et al., 2002), the study by Eaker et al. was done as a part of Framingham Offspring Study included a sample size of 3862 patients (Eaker et al., 2005). Inordinately large number of patients have been included in the study by De Bacquer et al., that included 21, 419 subjects (De Bacquer et al, 2005). The age ranges of these participants varied. In the Player study the average of the participants were 45 to 64 (Player et al., 2007), whereas the study by Vitaliano et al. included only people over the age of 60 years (Vitaliano et al., 2002). A far wider range of populations were included in the study by Eaker et al. (Eaker et al., 2005). Attrition rates have been reported in all the studies, except in the study by Eaker et al., and minimal attrition rates were reported in the study by Denollet et al. (Denollet, Vaes, and Brutsaert, 2000) due to mortality and other reasons. The study locations have been mentioned in each of these studies, and they varied from United States (Player et al., 2007; Vitaliano, PP. et al., 2002; Eaker et al., 2005) and Belgium (De Bacquer et al, 2005; Denollet et al., 2000).

Three studies used along with other means semi-structured interviews over telephone and pre-sent questionnaires by mail (Player, King, Mainous, III, and Geesey, 2007; Denollet, Vaes, and Brutsaert, 2000) and the three other used open-ended questions on different scales of assessment. Purely quantitative data were parts of all the papers in terms of clinical assessment and health record coding by blinded data recorders (Vitaliano et al., 2002; De Bacquer et al., 2005; Eaker et al., 2005).

Several standardized and validated scales and measures were used in all these studies, and all of them have been tabulated in the summary table. These are Lubben social network scale, Maastricht Questionnaire, Spielberger Trait Anger Scale, Mini-Mental Status Examination, Record of Independent Living, Revised Ways Of Coping Checklist, Anger Expression Scale, Interpersonal Support Evaluation List, The Hassles and Uplifts Scales, Puckett’s criteria, Karasek and Theorell’s expanded demand-control model of Job Strain, The Health Complaints Scale (HCS), the Global Mood Scale (GMS), and the Rose questionnaire. Depression was assessed by Zung Depression Scale and/or the State Anxiety Scale. Chronic emotional distress was assessed with Type D Scale 16.

Several of these studies also developed questionnaires specific for the study. Self-administered  psychosocial questionnaire was utilized to assess satisfaction with life (Player, King, Mainous, III, and Geesey, 2007). Health habits of diet were assessed using diet dairy (Vitaliano et al., 2002). The despondency scores were assessed at 5-year followup in the study (Denollet, Vaes, and Brutsaert, 2000) Denollet at al by phone interviews that used developed questionnaires. The study by Eaker et al., however, assessed the psychosocial questionnaires that were mailed to the participants before the followup checkup (Eaker, Sullivan, Kelly-Hayes, D’Agostino, Sr, and Benjamin, 2005).

Quantitative data analyses were performed using statistical methods that included multivariate analysis, latent variable partial least square estimation, chi-square statistic, Cox modeling, Kaplan-Meier Survival Estimates, and bivariate chi-square analyses. Only one study mentioned the statistical software used; SUDAAN 9.0.1 statistical software was used in the study by Player et al (Player, King, Mainous, III, and Geesey, 2007). None other reported the statistical software used.

All the studies have qualitative components, and information about the raters was provided in only two studies. Vitaliano et al. reported blinded coders assessing CHD by Puckett’s criteria (Vitaliano et al., 2002). In the study by Eaker et al., they determined assessment end-points by physician-administered history (Eaker et al., 2005).

Study Participants Study Type and Relevant Measures and Procedure Main Findings
Player, King, Mainous, III, and Geesey, 2007, Psychosocial Factors and Progression From Prehypertension to Hypertension or Coronary Heart Disease The Atherosclerotic Risks in Communities Study involving 15, 792 men and women of ages 45 to 64, recruitment was by random probability sampling.  2334 of this previous study population included in the ARIC study was included in this study. Type: Prospective epidemiologic study designed to investigate the origin and progression of various atherosclerotic diseases.

Measures: Random probability sampling from the population lists and area sampling in communities. Done by interview.

Data Collection: Done by annual telephone interviews and three triennial visits, following up the cohort through the end of the study period.

Procedure: From the second clinical visit, the baseline measurements as well as psychosocial factors of interest were assessed. By application of exclusion criteria of established CHD, the initial cohort was reduced to 2334 participants who had prehypertension but were free of established cardiovascular disease.

Followups were done through each of the remaining scheduled clinical examination. Annual morbidity and mortality assessment were done by annual followups for up to a period of 4 to 8 years.

Predefined criteria were used to assess development of hypertension and CHD, and hospital discharge data and death certificates were used to corroborate findings. Demographic predictors were assessed. Cardiovascular risk variables such as BMI and lipid profiles were used as predefined markers.  The physical activity was also assessed.

Psychosocial variables were measured by three standardized self-administered  psychosocial questionnaires

i) Satisfaction with life.

ii) Lubben social network scale

iii) Long-term psychological stress by Maastricht Questionnaire

iv) Spielberger Trait Anger Scale (10 questions) to assess levels of anger and hostility.

Bivariate and multivariate statistical regression analyses were performed of the collected data.

  • In the bivariate analysis, demographic parameters, cardiac risk parameters, Maastricht score, Spielberger anger score had unadjusted p value of less than 0.2.
  • These were included in the multivariate regression analysis for progressive hypertensive disease.
  • Current smoking status and Lubben social network scores were unassociated with statistical significance for development of hypertensive heart disease in the unadjusted analysis.
  • Approximately 7% of the population with prehypertension had a high trait anger score.
  • Of these 7%, about 65% would develop hypertension.
  • These individuals would be with 1.5 times greater odds for developing hypertension that those with low or moderate scores.
  • Stratification by sex indicated high trait anger scores were associated with progression, in men only.
  • Long-term stress was not associated with higher risk of progression to develop disease in both sexes.
  • Significant differences between these participants developing CHD for each risk factor and who did not develop for both long-term psychosocial stress and trait anger.
  • These two categories also varied in terms of demographic and cardiac risk factor variables.
  • High trait angers were associated with 90% increase in the risk of progression to CHD.
Vitaliano et al., 2002.  A Persistent Stress, Metabolic Syndrome, and Coronary Heart Disease Path Model. Testing a theoretical stress model in a study involving 47 older adult men, 64 older adult women not using hormone replacement therapy, and 41 older adult women using hormone replacement therapy. Total sample size was 152. Recruitment was from several sources. This is a prospective cross-sectional study that examined whether relationships of chronic stress, psychophysiology, and CHD varied in these groups of individuals.

 

Structural equations examined influence and relationship of development and progression of CHD with chronic stress, vulnerability expressed by anger and hostility, social resources, psychological distress manifested by burden, sleep problem, or low uplifts, poor health and dietary habits, and metabolic syndrome. The following measuring tools were utilized.

  • Chronic stress was measured by mental status examination by a Mini-Mental Status Examination.
  • Functioning was measured by Record of Independent Living.
  • The Revised Ways Of Coping Checklist was used to assess problem-focused coping, and this measured the personal resources.
  • The Anger Expression Scale was utilized to measure vulnerability, complemented by the Trait Anger Scale to measure anger proneness and hostility.
  • The Interpersonal Support Evaluation List included 4 scales. These were Appraisal, Belonging, Tangible, and Self-esteem. The Social Support Questionnaire assessed the degree of satisfaction with support.
  • The Hassles and Uplifts Scales were used to examine the psychological distress. The Hamilton Depression Rating Scale was utilized to assess depressive symptoms using a structured interview. The Sleep Problems Questionnaire derived from Sleep Disorders Questionnaire assessed problems with sleeping.
  • Health habits of diet were assessed from a diet diary, and a self-reported 10-item scoring was used to assess exercise habits.
  • The  metabolic syndromes were assessed by laboratory tests.
  • CHD was measured by Puckett’s criteria from medical records with coder blinded about the status of the subject.

Statistical analysis of the data was performed by structural equation modeling.

  • There were no demographic differences among the participants in terms of level of stress.
  • Male participants were noted to be more obese and reported more depression, less social support, more burden, fewer uplifts, less problem-focused coping, and less education.
  • Women not using HRT reported less exercise.
  • This group also was found to have more depressed mood, sleep problems, burden, and fewer uplifts.
  • In all strata, positive relationships between chronic stress and distress were very strong.
  • Vulnerability and social resources were related negatively in women. Negative correlation between social resources and distress was more in women not using HRT.
  • The positive relationship of vulnerability with distress was significant in men.
  • Six of the 12 paths from chronic stress and distress were significantly correlated to health habits.
  • The variability of mental status was explained by distress and poor health habits.
  • The pathways from mental status to CHD were significant in men and women, men being twice than the women, and all these women were not on HRT. It was, however, insignificant in case of women with HRT.
  • The significant pathways were chronic stress to distress, distress to mental status, and mental status to CHD.
  • Extensive modification occurred for poor health habits with mental status. In men this was driven by sedentary habits, and in women this was significantly associated with sedentary behaviors in presence of no HRT use, obesity, and insulin use on the face of hyperglycemia.
De Bacquer, Pelfrene, Clays, Mak, Moreau, de Smet, Kornitzer, and De Backer, 2005.  Perceived Occupational Burden and Heart Accidents Incidence:: 3-Year Follow-up of the Belgian Job Stress Project Cohort. The sample comprised of middle-aged individuals from both sexes in 25 large industries.  This is study to assess the association between work-related psychosocial stress and the incidence of clinically manifest coronary heart disease.  Without any formal exclusion criteria, and a total of 21, 419 participants consisting of 16, 329 men and 5,090 women participated in the study. This is a prospective cohort study design to examine the independent role of perceived job stress on the short-term incidence of clinically manifest coronary artery disease in a large occupational cohort. It measured the work-related characteristics, and self-administered questionnaires directed to information on sociodemographic characteristics, lifestyle-related factors, medical history, health perceptions, and psychosocial scales for depression and anxiety.

·  Stress at work was measured using Karasek and Theorell’s expanded demand-control model of Job Strain. The scales used were psychological job demand in the areas of quantity of work, mental requirements, and time constraints; job control or decision latitude using subscales of skill discretion and decision authority; and social support at workplace. These scales were derived from Job Content Questionnaire. Using a 4-point Likert scale, each object was scored.

·  The clinical data was collected using clinical examination and laboratory studies.

· To ascertain a coronary event, the clinical diagnosis was confirmed with a formal diagnostic algorithm of cardiac enzymes and electrocardiographic data.

·         At the analysis stage, exclusion criteria for myocardial infarction events were applied to the subjects, and these were ascertained using Rose questionnaire.

After manipulation and categorization of the data, statistical analysis was performed by power calculations. Cox potential hazard modeling was used to determine hazard ratios. Kaplan-Meier survival estimates were used to calculate the assumption of proportionality of odds.

 

  • In the male population free from overt CHD, the incidence of new coronary events was 1.93 per 1000 persons per year of observation.
  • About 50% of the events were acute myocardial infarction.
  • 26% of the employees were experiencing low job strain.
  • 17% of the employees were categorized as high strain category.
  • 11% of the employees were isostrain, having a high job strain exposure and low level of social support.
  • The probability of a coronary event was found to be not significantly associated with the decision latitude scale.
  • Higher job strains were associated with higher CHD rates, although the statistical significance is questionable after adjustments with hazard ratios of other associated demographic and risk factor parameters.
  • Lower social support at work place was found to be associated with a greater risk of experiencing a coronary event with more than twice as frequent risk for those in the lowest support groups.
  • There was no significant difference in incidences of coronary events between job strain categories according to the quadrant definitions.
  • The coronary risk in the high strain group was 38% higher than in the complementary group with statistically insignificant risk elevations after multivariate analysis.
  • There were no synergistic effects between job demands and decision latitudes.
  • There was a significant inverse association between social support at work and the risk of a coronary event.
Denollet, Vaes, and Brutsaert, 2000. Inadequate Response to Treatment in Coronary Heart Disease: Adverse Effects of Type D Personality and Younger Age on 5-Year Prognosis and Quality of Life. In this study, 322 subjects, comprising of 297 men and 25 women with age ranges 35v to 70 years and mean age 56.7 years were recruited from a consecutive series of patients attending a cardiac rehabilitation program in Antwerp. The eligibility criteria were precise in that if the subjects have experienced myocardial infarction or coronary bypass or angioplasty in a period of 2 months before the study. The numbers of subjects in these categories were 162 and 160.  The patients will major comorbidity such as cancer were excluded. All subjects underwent a standardized treatment regimen for 36 sessions as per outpatient rehabilitation protocols. The final sample consisted of 319 patients. In this prospective analysis, prognostic factors included left ventricular activity and resistance to exercise as measures of disease intensity. Such biomedical considerations examined included myocardial infarction thrombolysis, aspirin therapy, beta-blockade therapy, ACE inhibitors following release from the recovery unit, smoking abstinence relapse, history of hypertension or dyslipidemia.

In this review, indicators of both episodic and persistent depression were used. Because signs of depression and anxiety are the most prominently correlated indicators of episodic suffering with CHD, Zung Depression Scale and/or State Anxiety Scale tests of despondency scale were used. Form D Scale 16 measured persistent mental disorder. To distinguish patients, a median split on the DS16 negative affectivity and social inhibition scales was used.

In this prospective analysis, prognostic factors included left ventricular activity and resistance to exercise as measures of disease intensity. Such biomedical considerations examined included myocardial infarction thrombolysis, aspirin therapy, beta-blockade therapy, ACE inhibitors following release from the recovery unit, smoking abstinence relapse, history of hypertension or dyslipidemia.

In this review, indicators of both episodic and persistent depression were used. Because signs of depression and anxiety are the most prominently correlated indicators of episodic suffering with CHD, Zung Depression Scale and/or State Anxiety Scale tests of despondency scale were used. Form D Scale 16 measured persistent mental disorder. To distinguish patients, a median split on the DS16 negative affectivity and social inhibition scales was used.The main end points were cardiac events and impaired quality of life. The secondary end point was revascularization during followup. The Health Complaints Scale (HCS) and the Global Mood Scale (GMS) were utilized to measure quality of life psychometrically. The HCS comprises of 12 somatic and 12 items of perceived disability that are frequently reported by CHD patients. All these items were rated on a 5 point scale of distress.

The GMS consists of 10 negative and 10 positive mood terms that were rated on a 5-point scale of intensity.

Depressive affect was characterized by the interaction of high negative and low positive moods; a median split on the positive and negative scales was used to assess the depressive affect at followup.

The outcome data were summarized using a multicategorical index.

At entry, the subjects filled out the emotional distress and type D scales. After 5 years telephone and mail followup were used to determine the end points. Mortality and infarction data were derived from the hospital records. The followup questionnaire contained the quality of life scales. Multiple logistic regression analysis was used to determine the best independent predictors of cardiac events and impaired quality of life. The subjects were stratified by number of prognostic factors to examine the effect of convergence of risk factors.

  • Only 0% patients were lost to followup.
  • 2% of the patients had 5-year cardiac death.
  • Cardiac events were significantly associated with LV failure, poor exercise tolerance, symptoms of depression, type D personality, and age.
  • No drug treatment variables were related to outcome.
  • Type D patients have greater risks of death and nonfatal myocardial infarction.
  • 6% of the type D patients had cardiac death and 0.5% non-type D patients had cardiac deaths.
  • 13%  of the type D patients had nonfatal myocardial infarction and 2%  non-type D patients had the same.
  • Poor exercise tolerance had no significant association.
  • Symptoms of anxiety had significant associations.
  • Low left ventricular ejection fraction and type D personality were independent predictors of total CHD events.
  • Poor quality of life at the end of 5-year followup was associated with female sex, age greater than or equal to 55, poor exercise tolerance, failure to quit smoking, symptoms of depression and anxiety, type D personality, and nonfatal myocardial infarction including cardiac revascularization.
  • Psychosocial factors were estimated to be having a prognostic power above and beyond that of standard biomedical factors in predicting quality of life.
  • 4 independent prognostic factors for poor outcome as opposed to good outcome were recognized. These were type D personality, left ventricular ejection fraction less than or equal to 50%, age less than or equal to 55, and symptoms of depression at baseline.
Eaker, Sullivan, Kelly-Hayes, D’Agostino, Sr, and Benjamin, 2005.  Tension and Anxiety and the Prediction of the 10-Year Incidence of Coronary Heart Disease, Atrial Fibrillation, and Total Mortality: The Framingham Offspring Study. This is a prospective longitudinal community-based study on the offspring and their spouses of the Original Framingham Heart Study cohort.  This study was done on the 3873 offspring participants returning for their third followup examinations. Completed Psychosocial questionnaires that were mailed to the participants a few weeks before the clinic examinations were collected.

Clear exclusion and inclusion criteria were predetermined, and they were used to certify inclusion into the study.

About 95% of the participants attended subsequent examinations.

Tension and anxiety were assessed using scales that were developed in the original Framingham Study.

These two scales are highly correlated, but they measure distinct psychological traits.

The three outcomes of interest were 10-year incidence of CHD, AF, and total mortality.

The assessment of endpoints included physician administered history blinded to psychological data, routine ascertainment of outside physician and hospitalization records, and detailed adjunctions of all cardiovascular events by written criteria.

Potential confounders were ascertained in the index examination. These were selected for their known relations to the outcomes of interest.

Multivariate models predicting 10-year incidence of CHD were studied in terms of different criteria.

All analyses were sex specific.

The relation of psychosocial measures to education and CHD risk factors classified at the baseline were examined with Pearson correlations and analysis of variance for continuous and discrete variables.

Cox proportional hazards regression was used to estimate 10-year age-adjusted rates and CHD.

For each significant psychological predictor variable in the age-adjusted analysis, the effects were examined after adjustment using Cox proportional hazards model.

  • For causes of death, 25% of men and 12% of women died of CHD.
  • 48% of the study population were men with an age range of 18-77 years and with a mean age of 48.5.
  • Women scored higher on the tension and anxiety scales compared with men.
  • Except for total cholesterol and current cigarette smoking, men had less healthy risk profile compared with women.
  • The two psychological scales were positively associated with current cigarette smoking in both sexes.
  • In both sexes, tension and anxiety were negatively associated with education.
  • Anxiety was positively associated with body mass index in both sexes and with diabetes in women.
  • Increased tension was significantly related to CHD and total mortality.
  • Increased symptoms of anxiety were associated with total mortality in both the sexes.
  • Men with increased tension were at significantly higher risk of developing CHD.

 

The summary of the findings have been tabulated below.

Results

Overall Risks

The results indicate that the CHD has a potent psychosocial reasons that can be an independent risk factor apart from the other well-known health-related and behavior related risk factors. High level of trait anger in middle-aged prehypertensive men is associated with increased risk of progressing to hypertension and CHD may result from this. Long-term stress is also associated with increased risk of CHD in both sexes (Player et al., 2007). While attempting to study the causative role, job-related stress, the study by De Bacquer et al., however, could not find any evidence in favor of the putative causal associations between psychosocial work characteristics and health outcomes in relationship with progression of or cardiac events from CHD (De Bacquer et al., 2005). In older men, there is a stress pathway to development of CHD in relation to chronic stress to distress to the metabolic syndrome that in turn predicted CHD, almost similar to that in the older women without HRT, although the pathways were fewer. The observation was that over time distress, mental stress, and CHD. No such distant correlation existed in women on HRT (Vitaliano et al., 2002). The conclusion from adverse events from type D personality and younger age was interesting in the sense that decreased LV ejection fraction, type D personality, and younger age increases the risk of cardiac events. When all these factors converge in the same individual, this leads to nonresponse to treatment. Emotionally stressed younger individuals represent high-risk groups (Denollet, Vaes, and Brutsaert, 2000). The study by Eaker et al. demonstrated tension and anxiety are independent risk factors for CHD and mortality (Eaker et al., 2005).

Quality of Life

Psychosocial factors were recognized to be a powerful prognostic factor above and beyond that of standard biomedical factors in prediction of poor quality of life in relation to CHD (Denollet, Vaes, and Brutsaert, 2000). The four other studies mentioned here did not deal with quality of life as a parameter.

Education and Occupation

There is certain impact of education in modification of psychosocial factors while enumerating the risks of CHD. Although Vitaliano et al. found that women with HRT were slightly better educated than women without HRT in their study, this factor was unrelated to the development of cardiac anatomical lesions. Personal resources were related in this study with better health habits, and these socioeconomic status indicators (SES) of education and income were associated with better physical health (Vitaliano et al., 2002). Educational level was insignificant in terms of outcome in the study by De Bacquer et al. Tension and anxiety were negatively associated with education in both sexes leading to a pathway for development of CHD (Eaker et al., 2005). The three other studies do not refer to education. Except the study of  Vitaliano et al., none of the studies mention income as a risk factor.

Discussion and Conclusion

From these studies, it is apparent that various lifestyle behaviors promote and influence the development of clinical manifestations of CHD. Emotional factors and the experience of chronic stress also promote atherosclerosis and cardiac events. Psychosocial factors that promote CHD can be categorized as emotional factors and chronic stressors. Emotional factors include affective disorders such as depression as well as hostility and anger. Chronic stressors include low social support, low socioeconomic status, work stress, and caregiver strain.

There is much we have yet to learn about the complex brain-body interaction. But it is well documented that stress and excessive anger perceived in certain parts of the brain lead to complex hormonal changes. In turn, these hormonal changes can have a very profound influence on cardiovascular function, blood pressure, heart rate, circulation, and the ECG (Thurston et al, 2005). Stress also appears to play a significant role in the health of patients with other classic risk factors and/or diagnosed heart disease. To bolster this contention, thousands of interviews with heart attack patients have pinpointed common traits, behavioral responses, and stress reactions that may increase their cardiovascular risk (Writing Committee for the ENRICHD Investigators, 2003).

It is impossible to remove all stress from one’s life; indeed, a certain amount of stress is desirable and is an integral part of many pleasurable and worthwhile activities. Stress prompts the pituitary and adrenal glands to release stimulatory hormones, which ready the body to fight or flee. The heartbeat quickens, blood pressure rises, and blood rushes to the large muscles and brain. These responses can set the stage for increased strain on the heart and result in relatively reduced blood flow to the heart muscle, a cause of angina. There are many ways to modify the harmful effects of stress. Regular exercise, especially at the beginning of the day, is an excellent way of countering stress and at the same time improving heart health. In certain instances medication may be required to counter stress and anxiety. Building a network of supportive relationships is critical. So if stress, depression, and certain types of anxiety raise cardiovascular risk, it may well be that more positive psychological factors—for example, hope and optimism—are protective.

References:
Included Studies
  • De Bacquer, D., Pelfrene, E., Clays, E., Mak, R., Moreau, M., de Smet, P., Kornitzer, M., and De Backer, G., 2005.  Perceived Job Stress and Incidence of Coronary Events: 3-Year Follow-up of the Belgian Job Stress Project Cohort. Am. J. Epidemiol.; 161: 434 – 441.
  • Denollet, J., Vaes, J., and Brutsaert, DL., 2000.  Inadequate Response to Treatment in Coronary Heart Disease : Adverse Effects of Type D Personality and Younger Age on 5-Year Prognosis and Quality of Life. Circulation; 102: 630 – 635.
  • Eaker, ED., Sullivan, LM., Kelly-Hayes, M., D’Agostino, RB., Sr, and Benjamin, EJ., 2005.  Tension and Anxiety and the Prediction of the 10-Year Incidence of Coronary Heart Disease, Atrial Fibrillation, and Total Mortality: The Framingham Offspring Study. Psychosom Med; 67: 692 – 696.
  • Player, MS., King, DE., Mainous, III, AG., and Geesey, ME., 2007. Psychosocial Factors and progression From Prehypertension to Hypertension or Coronary Heart Disease. Ann. Fam. Med; 5: 403 – 411.
  • Vitaliano, PP. et al., 2002.  A Path Model of Chronic Stress, the Metabolic Syndrome, and Coronary Heart Disease. Psychosom Med; 64: 418.
Excluded Studies
  • Horsten, M., Mittleman, M.A , Wamala, S.P , Schenck-Gustafsson, K., and Orth-Gomér, K., 2000.  Depressive symptoms and lack of social integration in relation to prognosis of CHD in middle-aged women. The Stockholm Female Coronary Risk Study. Eur. Heart J.; 21: 1072 – 1080
Other References and Parallel Readings
  • Asbury, EA, Creed, F., and Collins, P., 2004.  Distinct psychosocial differences between women with coronary heart disease and cardiac syndrome X. Eur. Heart J.; 25: 1695 – 1701.
  • Burg, MM. et al. for the ENRICHD Investigators, 2005. Low Perceived Social Support and Post–Myocardial Infarction Prognosis in the Enhancing Recovery in Coronary Heart Disease Clinical Trial: The Effects of Treatment. Psychosom Med; 67: 879 – 888.
  • Denollet, J. and Brutsaert, DL., 2001.  Reducing Emotional Distress Improves Prognosis in Coronary Heart Disease: 9-Year Mortality in a Clinical Trial of Rehabilitation. Circulation; 104: 2018 – 2023.
  • Eng, PM., Fitzmaurice, G., Kubzansky, LD., Rimm, EB., and Kawachi, I., 2003.  Anger Expression and Risk of Stroke and Coronary Heart Disease Among Male Health Professionals. Psychosom Med; 65: 100.
  • Goyal, TM., Idler, EL., Krause, TJ., and Contrada, RJ., 2005.  Quality of Life Following Cardiac Surgery: Impact of the Severity and Course of Depressive Symptoms. Psychosom Med; 67: 759 – 765.
  • Hemingway, H. and Marmot, M., 1999. Evidence based cardiology: Psychosocial factors in the aetiology and prognosis of coronary heart disease: systematic review of prospective cohort studies. BMJ; 318: 1460 – 1467.
  • Januzzi, Jr, JL, Stern, TA., Pasternak, RC., and DeSanctis, RW., 2000. The Influence of Anxiety and Depression on Outcomes of Patients With Coronary Artery Disease. Arch Intern Med; 160: 1913 – 1921.
  • Kop, WJ. et al., 2005.  Social Network and Coronary Artery Calcification in Asymptomatic Individuals. Psychosom Med; 67: 343 – 352.
  • Lett, HE et al., 2005.  Social Support and Coronary Heart Disease: Epidemiologic Evidence and Implications for Treatment. Psychosom Med; 67: 869 – 878.
  • Lett, HS. et al., 2004.  Depression as a Risk Factor for Coronary Artery Disease: Evidence, Mechanisms, and Treatment. Psychosom Med; 66: 305 – 315.
  • Lavie, CJ and Milani, RV., 2006.  Adverse Psychological and Coronary Risk Profiles in Young Patients With Coronary Artery Disease and Benefits of Formal Cardiac Rehabilitation. Arch Intern Med; 166: 1878 – 1883.
  • McAlister, FA., Lawson, FME., Teo, KK., and Armstrong, PW., 2001. Randomised trials of secondary prevention programmes in coronary heart disease: systematic review. BMJ; 323: 957 – 962.
  • Nicholson, A., Kuper, H., and Hemingway, H., 2006.  Depression as an aetiologic and prognostic factor in coronary heart disease: a meta-analysis of 6362 events among 146 538 participants in 54 observational studies. Eur. Heart J.; 27: 2763 – 2774.
  • Orth-Gomér, K. et al., 2000.  Marital Stress Worsens Prognosis in Women With Coronary Heart Disease: The Stockholm Female Coronary Risk Study. JAMA; 284: 3008 – 3014.
  • Rozanski, A., Blumenthal, JA., Davidson, KW., Saab, PG., and Kubzansky, L., 2005. The epidemiology, pathophysiology, and management of psychosocial risk factors in cardiac practice: The emerging field of behavioral cardiology. J. Am. Coll. Cardiol.; 45: 637 – 651
  • Rozanski, A., Blumenthal, JA., and Kaplan, J., 1999.  Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy. Circulation; 99: 2192 – 2217.
  • Sullivan M, LaCroix A, Spertus J, Hecht J., 2000. Five-year prospective study of the effects of anxiety and depression in patients with coronary artery disease. Am J Cardiol; 86 :1135-8. 248
  • Sullivan, MD., LaCroix, AZ., Russo, JE., and Walker, EA., 2001.  Depression and Self-Reported Physical Health in Patients With Coronary Disease: Mediating and Moderating Factors. Psychosom Med; 63: 248.
  • Thurston, RC, Kubzansky, LD, Kawachi, I., and Berkman, LF., 2005.  Is the Association between Socioeconomic Position and Coronary Heart Disease Stronger in Women than in Men? Am. J. Epidemiol.; 162: 57 – 65.
  • Williams, JE et al., 2000.  Anger Proneness Predicts Coronary Heart Disease Risk : Prospective Analysis From the Atherosclerosis Risk In Communities (ARIC) Study. Circulation; 101: 2034 – 2039.
  • Williams, MA. et al., 2002.  Secondary Prevention of Coronary Heart Disease in the Elderly (With Emphasis on Patients >=75 Years of Age): An American Heart Association Scientific Statement From the Council on Clinical Cardiology Subcommittee on Exercise, Cardiac Rehabilitation, and Prevention. Circulation; 105: 1735 – 1743.
  • Writing Committee for the ENRICHD Investigators, 2003.  Effects of Treating Depression and Low Perceived Social Support on Clinical Events After Myocardial Infarction: The Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Randomized Trial. JAMA; 289: 3106 – 3116.

You may also like

Leave a Comment