• Users Online: 190
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
SPECIAL ARTICLE
Year : 2020  |  Volume : 9  |  Issue : 2  |  Page : 84-89

Psychosocial impact of COVID-19 on cardiovascular health


1 Society for Continuing Medical Education and Research, Kerala Institute of Medical Sciences, Trivandrum, Kerala, India
2 Society for Continuing Medical Education and Research, Kerala Institute of Medical Sciences; Department of Cardiology, Kerala Institute of Medical Sciences, Trivandrum, Kerala, India

Date of Submission13-May-2020
Date of Decision16-May-2020
Date of Acceptance19-May-2020
Date of Web Publication01-Aug-2020

Correspondence Address:
Dr. M T Manoj
Society for Continuing Medical Education and Research, Kerala Institute of Medical Sciences, Anayara PO, Trivandrum - 695 029, Kerala
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JCPC.JCPC_30_20

Rights and Permissions

How to cite this article:
Manoj M T, Vijayaraghavan G. Psychosocial impact of COVID-19 on cardiovascular health. J Clin Prev Cardiol 2020;9:84-9

How to cite this URL:
Manoj M T, Vijayaraghavan G. Psychosocial impact of COVID-19 on cardiovascular health. J Clin Prev Cardiol [serial online] 2020 [cited 2020 Aug 10];9:84-9. Available from: http://www.jcpconline.org/text.asp?2020/9/2/84/291226




  Introduction Top


The outbreak of the 2019 novel Coronavirus (COVID-19) originated in the Wuhan province of China in December 2019[1] and spread across the world within 4 months, infecting over 4,355,456 people and resulting in the death of 2,93,090 individuals (at the time of penning this article).[2] The contagiousness of the disease with limited effectiveness in the efforts to curtail the spread, explosiveness, and severity of the attack rates and minimal population immunity has forced many countries to introduce various stringent measures such as lockdown of all services, social distancing, quarantine, and isolation. These measures, which are indispensable in curtailing the infection, have debilitated the social and economical stability of all the affected countries including the developed nations and resulted in a wide range of emotional and mental disturbances in people.[3] These disturbances are closely associated with an increased prevalence of psychological and social problems across all age groups[4],[5] which can have a negative impact on the physical health of individuals,[1],[6],[7] especially on the cardiovascular health.[8] Identification of people exposed to negative psychosocial factors and thus susceptible and at-risk for ill-health is important for timely intervention to prevent secondary mental and physical health issues.[9] Studies that examined the impact of psychosocial factors of the COVID-19 pandemic are very limited.[8] As the impact on cardiovascular health is still not ascertained, we explore the various psychosocial problems that can result from COVID-19 and how these could affect cardiovascular health.


  Psychosocial Factors Associated With Covid-19 Top


The current outbreak of COVID-19 can cause a wide spectrum of psychosocial stress on human lives. A mental breakdown may happen in anyone who fears of getting infected and thereby falling ill or dying. They may experience helplessness and hopelessness and thus feel uneasy in coming in contact with others owing to fear of acquiring infection.[10] People who are uncomfortable of being quarantined may feel isolation, discrimination, frustration, exhaustion, shame, guilt, and anger which could all lead to depression, anxiety, stress, insomnia, denial, and fear.[1],[7] They also experience weepiness, nightmares, and poor concentration.[11] People requiring a longer duration of quarantine have a higher prevalence of posttraumatic stress disorder (PTSD).[12] Factors influencing PTSD include quality of treatment received, accessibility to medical care and medications, the environmental condition of the quarantined place, and emotional and mental support that has been received.[6],[12] The infected and quarantined people could also notice stigma and discrimination from society. These emotions fueled by preexisting psychological problems, if any, may negatively affect them and bring about remodeling of their behavior and social life.[8]

The viral infection has also taken a toll on the psychosocial health of medical and allied staff. Longer working hours in isolation wards, the possibility of directly being exposed to the infected patients, the uneasiness of wearing personal protective equipment and inadequacy of protection, all of them may result in heightened anxiety. The fear of contracting infection or transmitting infection to their family members or loved ones, could have adverse psychiatric outcomes.[13] These individuals may become highly stressful, emotionally imbalanced, and traumatized which all can also result in depression, anxiety, PTSD, anger, and disgust.[14]

The elderly and people with chronic illnesses such as heart disease, cancer, and kidney diseases are severely affected by virus infection. They may be exposed to emotional disturbances, anxiety, fear of infection or death, confusion, and depression[6] because of isolation, financial strain, limited accessibility to medical treatment or medications, and the uncertainty of the disease status.[9] Those who are experiencing emotional trauma from a sudden loss of a loved one often find it difficult to cope with the loss and have anger, grief, and resentment.[15] The family members of patients with COVID-19 may also face discrimination and stigmatization from others.

A survey conducted during the initial stage of the COVID-19 outbreak found that 53.8% of respondents had moderate-to-severe symptoms of psychosocial problems associated with the outbreak.[1] Among them, 16.5% had moderate-to-severe symptoms of depression, 28.8% had moderate-to-severe symptoms of anxiety, and 8% had moderate-to-severe symptoms of stress. Studies carried out during the severe acute respiratory syndrome (SARS) epidemic had observed acute psychosis among a few patients,[16] and the psychosocial impact was persisting even after the outbreak had subsided. In another study, 13%–32% of patients reported moderate-to-severe levels of anxiety, 18%–26% reported moderate-to-severe levels of depression, and around 4% reported PTSD even after their discharge from hospital.[17],[18] Even though data on the impact of psychosocial factors on the health of the SARS survivors on a longer follow-up are unavailable, studies have shown that these psychosocial disturbances evolve over time. SARS survivors 3 months after their discharge from hospital have reported diminished symptoms of anxiety and posttraumatic intrusion and posttraumatic hyperarousal, but depression and posttraumatic avoidance symptoms remained constant.[18]

The longest follow-up study examining the prevalence of PTSD, anxiety, and depression among SARS survivors reported that 36.5% of them had PTSD, 36.5% had sleep problems, 34.9% had anxiety, and 30.2% had depression. Patients who were on ventilators or with family members who died from SARS infection had a higher prevalence of PTSD, anxiety, and depression than those without such history.[19] These studies suggest that patients who are affected by COVID-19 may also experience psychosocial problems for over a period of time.


  How Can Psychosocial Factors Influence Cardiovascular Health? Top


Psychological variables can affect the physiological mechanism of an individual either directly or indirectly and have a significant impact on the health or illness conditions of a person. Individuals who are prone to negative psychological conditions can have unfavorable cardiovascular outcomes and a very poor cardiovascular profile.[20],[21]

Plausible mechanisms

An important link between emotions and heart is provided by the hypothalamic–pituitary–adrenal (HPA) axis and the stress hormone cortisol. The HPA axis discharges the hormones into the blood for preparing the body to react to various threats. The mechanism controls the levels of the hormones, depending on the threat levels.[22],[23] Constant exposure to cortisol can result in hypercortisolemia, impairment of platelet function, elevated heart rate, and reduced heart rate variability and is thus detrimental to the heart and the entire cardiovascular system and may contribute to cardiovascular diseases (CVDs).[24],[25] Cortisol also slows down growth hormone and gonadal axes[7],[8] leading to increased visceral fat causing dyslipidemia, hypercortisolism, and hyperinsulinism, increasing the risk for CVDs and other disorders.[26] Stress can accelerate the atherosclerotic process leading to arterial occlusion,[27] plaque rupture and thrombosis resulting in myocardial infarction (MI), or cerebral stroke.[28]

Depression causes sympathetic hyperactivity, increased platelet reactivity,[29],[30] pro-inflammatory processes, and an elevation of interleukin-6, which is a primary pro-inflammatory cytokine.[31],[32] A pro-inflammatory condition can accelerate atherosclerosis and lead to increased cardiovascular events.[33] There are also other factors linking depression with CVDs. Depression can result in nonadherence with medical treatments,[34] higher rates of smoking without cessation,[35] and greater risk for obesity because of a sedentary lifestyle.[36]

Anxiety can contribute to a chain reaction in the body, most likely mediated by the sympathetic nervous system and culminating in the sensitization of cardiac sympathetic nerves.[37] Constant anxiety can predispose an individual to cardiac rhythm changes and risk for coronary artery spasm.[37] Individuals whose sympathetic nervous system response to stress is exaggerated and prolonged are at a higher risk for atherosclerosis and subsequent coronary artery diseases (CADs).[4]

Socially isolated people may have a different mood state or disturbing complex emotional experience which could result in dejection or demoralization and physical problems.[38] It is also related to health risk behaviors such as reduced physical activity, reduced sleep quality, smoking, and poor mental health[39],[40] which could all eventually cause physical illness. Social support can offer a protective effect against progression of CVDs and death by facilitating greater adherence to medical therapies and lifestyle modifications and reducing negative emotional interferences.[41] Social support also provides protection from various stressors, disengages people from risky behaviors such as excessive consumption of nicotine, alcohol, or narcotic drugs, and reinforces healthy behaviors and better mental health.[42]

People who are exposed to societal discrimination have negative cardiovascular health outcomes such as alterations in blood pressure,[43] heart rate/heart rate variability,[44] and changes in the body levels of CVD biomarkers.[45] Those who are unemployed or have job insecurity have multiple health problems such as autoimmune disorders, certain types of cancers, metabolic syndrome (including abdominal obesity, dyslipidemia, high blood pressure, insulin resistance, and prothrombotic state), and increased cardiovascular morbidity and mortality.[46],[47],[48],[49]

Moreover, long-term financial problems owing to unemployment directly affect cardiovascular health by limiting access to good quality food, increased negative habits such as smoking, lower physical activity, and indirectly through psychological pathways: higher prevalence of depression, anxiety, exhaustion, or hostility. These increase the risk for coronary heart diseases (CHDs) and poor prognosis, by bringing about acute or chronic physiological changes.[50],[51]

Current evidences

Despite some heterogeneity of findings, a large amount of evidence supports the notion that psychosocial factors are risk factors for all-cause mortality from CVDs as well as for composite outcomes including nonfatal cardiac events.[52] A meta-analysis of 293 studies comprising 1 813 733 participants from 35 countries has revealed a relative risk of mortality of 1.52 (95% confidence interval [CI] = 1.45–1.59) in depressed people compared to nondepressed ones.[53] The authors concluded that patients with depressive symptoms were at increased risk of mortality from cardiac events. Another meta-analysis with a total of 3, 23, 709 participants reported a total of 8447 patients with MI and coronary deaths during follow-up which ranged from 4 to 37 years. The pooled adjusted hazard ratios (HRs) for patients with depression versus those without depression were 1.22 (95% CI: 1.13–1.32) for MI and 1.31 (95% CI: 1.09–1.57) for deaths from CHD.[54] Studies have also identified that patients with CVD have a higher prevalence of depressive symptoms when compared to a normal population[55] and that they are likely to have MI or heart failure.[52] This finding was reaffirmed in another study by May et al.[56] who reported that patients who had depressive disorders after an angiographically confirmed diagnosis of CAD were at two-fold risk of death. In this study, among 24,137 patients with angiographically determined CAD, 3646 were diagnosed as depressed. The authors reported that depression after CAD was strongly associated with death (HR = 2.00, P < 0.0001).

The potential relationship between anxiety and CVD is revealed in a meta-analysis of 37 studies which included 15, 65, 699 participants.[57] The analysis revealed that anxiety was associated with 52% of increased incidence of CVD (HR: 1.52; 95% CI: 1.36–1.71), and the association remained significant even after adjusting for publication bias (HR: 1.41; 95% CI: 1.26–1.57). The authors concluded that anxiety is an independent risk factor for CVD. Anxiety not only increases the risk for CHD but also death from CVD as well.[58] This is indicated in a meta-analysis of 21 prospective studies. The authors found that anxiety increased the risk for CHD by 26% and anxious persons were at 48% more risk for cardiac mortality as compared to nonanxious persons. There are also studies that suggest that anxiety causes nearly two-fold increased risk for adverse cardiac events in patients with stable CAD over 2 years[59] and a two-fold risk for death in the next 10 years after the first event.[60]

A population-based controlled cohort study in siblings consisting of 136,637 patients in the Swedish National Patient Register revealed that stress-related disorders were more robustly related to early onset of various types of CVD.[61] Researchers have also found that perceived social stress is also significantly associated with incidence of MI.[62] Stressful life events such as the death of the spouse or natural disasters also can lead to MI and sudden cardiac death.[63] Stressful working environments with high demands and low decision latitude are also related to high blood pressure and the risk for CHD.[64],[65],[66]

Several studies indicate that socially isolated people are prone to a higher risk of developing CHD. A systematic review and meta-analysis of 16 longitudinal datasets aimed at finding the relationship between loneliness or social isolation and incident CHD reported 4628 CHD events during a follow-up of 3–21 years.[67] The authors reported that people with poor social relationships or who are socially isolated have a 29% increased risk of CHD. Another study found that individuals with low social support or who are socially isolated have higher odds for MI as compared to those with higher social support.[68] Loneliness has a potentially negative effect on our biological stress responses and would be injurious to one's health.[69] This was identified in a study aimed at determining the health risk factors of loneliness or social isolation in 240 working men and women aged 47–59 years. Lonely or socially isolated individuals had a higher level of fibrinogen (P = 0.038) and cortisol levels were also found to be increased (P = 0.046).


  What Needs to Be Done? Top


As indicated earlier, the severity, longevity, and broad spectrum of psychosocial problems lead to diseases[70] depending on the effects of several factors such as the kind of traumatic event, length of the trauma, and available supports. Similarly, COVID-19-induced negative psychosocial problems could facilitate the initiation, progression, and perpetuation of cardiac problems or function as a trigger for reoccurrence of cardiac problems in patients with previous history[71] and could also create an situation conducive for the initiation and perpetuation of atrial fibrillation.[72] Depression, anxiety, PTSD, and social isolation could precipitate ventricular arrhythmia and MI even among individuals with or without any history of CHD.[68], 71, [73],[74],[75]

Comprehensive psychosocial assessment

Therefore, it is advisable that the high-risk groups in any community are identified and health workers conduct initial psychosocial assessments so that appropriate interventions can be undertaken early to limit psychosocial morbidity associated with the outbreak of COVID-19. The assessment could focus on the pandemic-related stressors such as the possibility of exposure to infection, death of family members or loved ones and disconnectedness with the external world, psychological problems such as depression, anxiety, fear, grief, and PTSD, as well as social problems including unemployment, isolation, substance abuse, and domestic violence. Preexisting disease conditions also needs assessment.[3]

Proper communication

Evidence-based genuine communication is to be provided to the public to reduce the incidence of psychosocial problems associated with the infection.[76] Health authorities may ensure the communication process. They have also to provide instructions regarding what people should do if they develop any health problems and proper follow-up of patients in the high-risk category is to be ensured. This could reassure those in quarantine and thus lessen the impact of the outbreak.[6]

Education and training

Appropriate education and training to evaluate and handle psychosocial problems could be provided to all first-level responders and health-care professionals including general practitioners and emergency care physicians. They are to screen along with physiological problems, the psychosocial aspects of patients with COVID-19, and address to the best of their ability psychosocial concerns that are identified. Patients may be referred to mental health professionals as necessitated by seriousness of the problems.[3] To prevent the possibility of health-care providers themselves becoming victims of mental health problems, there should be support from the hospital management, superiors, and co-workers. Proper training for infection control practices and other precautionary measures and monitoring could facilitate adaptive stress responses.[8],[11]

Creation of social support networks

Social media platforms can be used to provide social support networks and improve social belongingness.[77] Interventions could involve more frequent telephone contact with close family and friends, voluntary organizations, and health-care professionals or community outreach programs, which provide peer support throughout enforced isolation. Further, cognitive and behavioral therapies could also be delivered online to decrease the effects of loneliness and improve mental wellbeing.[78]

Monitoring and follow-up

The health authorities are expected to ensure constant monitoring of psychosocial problems and initiation of suitable interventions during the post-COVID-19 pandemic period as well. These could reduce the after-effects of psychosocial impact on the mental and physical health of the affected and advance their return to normal life.


  Conclusion Top


The psychosocial impact of the COVID-19 outbreak could be enormous. The pandemic has debilitated the social and economical stability of all countries. Although the impact of the outbreak has the potential to affect all, it is likely to be more among vulnerable populations such as children, the elderly, those with a history of mental illness, socially isolated people, and low-income group. The outbreak could result in several psychological and social problems including depression, anxiety, PTSD, fear, anger, grief, stigmatization, and social isolation. These psychological and social problems, though may often be transient, could produce a negative impact on the physical health of individuals including increased risk for CVDs and adverse cardiovascular outcomes.

There is necessity to rein in the psychosocial impact of the outbreak by developing and implementing a timely, comprehensive, and balanced intervention strategies as a post-COVID-19 increase in incidence of psychosocial problems could lead to poor mental health of a large proportion of vulnerable people and further debilitate both economical and social structure of the society. There is certainly an urgent need for studies related to the psychosocial impact of COVID-19 and on their long-term effects on individual's physical health, particularly on cardiovascular health.



Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Wang C, Pan R, Wan X, Tan Y, Xu L, Ho CS, et al. Immediate Psychological responses and associated factors during the initial stage of the 2019 coronavirus disease (COVID-19) epidemic among the general population in China. Int J Environ Res Public Health 2020;17:1729.  Back to cited text no. 1
    
2.
Coronavirus Update (Live): 3,741,276 Cases and 258,511 Deaths from COVID-19 Virus Pandemic-Worldometer. Available from: https://www.worldometers.info/coronavirus/?utm_campaign=homeAdvegas1? [Last accessed on 2020 May 06].  Back to cited text no. 2
    
3.
Pfefferbaum B, North CS. Mental Health and the Covid-19 Pandemic [published online ahead of print, 2020 Apr 13]. N Engl J Med. 2020;10.1056/NEJMp2008017. doi:10.1056/NEJMp2008017.  Back to cited text no. 3
    
4.
Matthews KA, Owens JF, Kuller LH, Sutton-Tyrrell K, Lassila HC, Wolfson SK. Stress-induced pulse pressure change predicts women's carotid atherosclerosis. Stroke 1998;29:1525-30.  Back to cited text no. 4
    
5.
Elovainio M, Hakulinen C, Pulkki-Råback L, Virtanen M, Josefsson K, Jokela M, et al. Contribution of risk factors to excess mortality in isolated and lonely individuals: An analysis of data from the UK Biobank cohort study. Lancet Public Health 2017;2:e260-6.  Back to cited text no. 5
    
6.
Brooks SK, Webster RK, Smith LE, Woodland L, Wessely S, Greenberg N, et al. The psychological impact of quarantine and how to reduce it: Rapid review of the evidence. Lancet 2020;395:912-20.  Back to cited text no. 6
    
7.
Banerjee D. The COVID-19 outbreak: Crucial role the psychiatrists can play. Asian J Psychiatry 2020;50:102014.  Back to cited text no. 7
    
8.
Ho CS, Chee CY, Ho RC. Mental health strategies to combat the psychological impact of COVID-19 beyond paranoia and panic. Ann Acad Med Singapore 2020;49:155-60.  Back to cited text no. 8
    
9.
Kang M, Wu J, Ma W, He J, Lu J, Liu T, et al. Evidence and characteristics of human-to-human transmission of SARS-CoV-2. Epidemiology; 2020. Available from: http://medrxiv.org/lookup/doi/10.1101/2020.02.03.20019141. [Last accessed on 2020 May 06].  Back to cited text no. 9
    
10.
Hall RC, Hall RC, Chapman MJ. The 1995 Kikwit Ebola outbreak: Lessons hospitals and physicians can apply to future viral epidemics. General Hosp Psychiatry 2008;30:446-52.  Back to cited text no. 10
    
11.
Chua SE, Cheung V, McAlonan GM, Cheung C, Wong JW, Cheung EP, et al. Stress and psychological impact on SARS patients during the outbreak. Canadian J Psychiatry 2004;49:385-90.  Back to cited text no. 11
    
12.
Hawryluck L, Gold WL, Robinson S, Pogorski S, Galea S, Styra R. SARS control and psychological effects of quarantine, Toronto, Canada. Emerg Infect Dis 2004;10:1206-12.  Back to cited text no. 12
    
13.
Naushad VA, Bierens JJ, Nishan KP, Firjeeth CP, Mohammad OH, Maliyakkal AM, et al. Systematic review of the impact of disaster on the mental health of medical responders. Prehospital Disaster Med 2019;34:632-43.  Back to cited text no. 13
    
14.
McAlonan GM, Lee AM, Cheung V, Cheung C, Tsang KW, Sham PC, et al. Immediate and sustained psychological impact of an emerging infectious disease outbreak on health care workers. Canadian J Psychiatry 2007;52:241-7.  Back to cited text no. 14
    
15.
Shear MK. Grief and mourning gone awry: Pathway and course of complicated grief. Dialogues Clin Neurosci 2012;14:119-28.  Back to cited text no. 15
    
16.
Lee DT, Wing YK, Leung HC, Sung JJ, Ng YK, Yiu GC, et al. Factors associated with psychosis among patients with severe acute respiratory syndrome: A case-control study. Clin Infect Dis 2004;39:1247-9.  Back to cited text no. 16
    
17.
Cheng SK, Wong CW, Tsang J, Wong KC. Psychological distress and negative appraisals in survivors of severe acute respiratory syndrome (SARS). Psychol Med 2004;34:1187-95.  Back to cited text no. 17
    
18.
Wu KK, Chan SK, Ma TM. Posttraumatic Stress after SARS. Emerg Infect Dis 2005;11:1297-300. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320475/. [Last accessed on 2020 May 06].  Back to cited text no. 18
    
19.
Shin J, Park HY, Kim JL, Lee JJ, Lee H, Lee SH, et al. Psychiatric morbidity of survivors one year after the outbreak of middle east respiratory syndrome in Korea, 2015. J Korean Neuropsychiatr Assoc 2019;58:245.  Back to cited text no. 19
    
20.
Cohen S, Wills TA. Stress, social support, and the buffering hypothesis. Psychol Bull 1985;98:310-57.  Back to cited text no. 20
    
21.
Rozanski A, Blumenthal JA, Kaplan J. Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation 1999;99:2192-217.  Back to cited text no. 21
    
22.
Kupper N, Denollet J. Type D personality as a prognostic factor in heart disease: Assessment and mediating mechanisms. J Pers Assess 2007;89:265-76.  Back to cited text no. 22
    
23.
Pedersen S, Denollet J. Is type D personality here to stay? Emerging evidence across cardiovascular disease patient groups. Curr Cardiol Rev 2006;2:205-13.  Back to cited text no. 23
    
24.
Kop WJ. The integration of cardiovascular behavioral medicine and psychoneuroimmunology: New developments based on converging research fields. Brain Behav Immun 2003;17:233-7.  Back to cited text no. 24
    
25.
Steptoe A, Hamer M, Chida Y. The effects of acute psychological stress on circulating inflammatory factors in humans: A review and meta-analysis. Brain Behav Immun 2007;21:901-12.  Back to cited text no. 25
    
26.
Gold PW, Chrousos GP. Organization of the stress system and its dysregulation in melancholic and atypical depression: High vs low CRH/NE states. Mol Psychiatry 2002;7:254-75.  Back to cited text no. 26
    
27.
Gersh BJ, Bassendine MF, Forman R, Walls RS, Beck W. Coronary artery spasm and myocardial infarction in the absence of angiographically demonstrable obstructive coronary disease. Mayo Clin Proc 1981;56:700-8.  Back to cited text no. 27
    
28.
Schwartz AR, Gerin W, Davidson KW, Pickering TG, Brosschot JF, Thayer JF, et al. Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease. Psychosom Med 2003;65:22-35.  Back to cited text no. 28
    
29.
Brown AD, Barton DA, Lambert GW. Cardiovascular abnormalities in patients with major depressive disorder: Autonomic mechanisms and implications for treatment. CNS Drugs 2009;23:583-602.  Back to cited text no. 29
    
30.
Musselman DL, Evans DL, Nemeroff CB. The relationship of depression to cardiovascular disease: Epidemiology, biology, and treatment. Arch Gen Psychiatry 1998;55:580-92.  Back to cited text no. 30
    
31.
Kiecolt-Glaser JK, Glaser R. Depression and immune function: Central pathways to morbidity and mortality. J Psychosom Res 2002;53:873-6.  Back to cited text no. 31
    
32.
Maes M, Bosmans E, De Jongh R, Kenis G, Vandoolaeghe E, Neels H. Increased serum IL-6 and IL-1 receptor antagonist concentrations in major depression and treatment resistant depression. Cytokine 1997;9:853-8.  Back to cited text no. 32
    
33.
Bot I, de Jager SC, Zernecke A, Lindstedt KA, van Berkel TJ, Weber C, et al. Perivascular mast cells promote atherogenesis and induce plaque destabilization in apolipoprotein E-deficient mice. Circulation 2007;115:2516-25.  Back to cited text no. 33
    
34.
DiMatteo MR, Lepper HS, Croghan TW. Depression is a risk factor for noncompliance with medical treatment: Meta-analysis of the effects of anxiety and depression on patient adherence. Arch Intern Med 2000;160:2101-7.  Back to cited text no. 34
    
35.
John U, Meyer C, Rumpf HJ, Hapke U. Depressive disorders are related to nicotine dependence in the population but do not necessarily Hamper smoking cessation. J Clin Psychiatry 2004;65:169-76.  Back to cited text no. 35
    
36.
Stapelberg NJ, Neumann DL, Shum DH, McConnell H, Hamilton-Craig I. A topographical map of the causal network of mechanisms underlying the relationship between major depressive disorder and coronary heart disease. Aust N Z J Psychiatry 2011;45:351-69.  Back to cited text no. 36
    
37.
Esler M. The sympathetic system and hypertension. Am J Hypertens 2000;13:99S-105S.  Back to cited text no. 37
    
38.
de Figueiredo JM. Depression and demoralization: Phenomenologic differences and research perspectives. Compr Psychiatry 1993;34:308-11.  Back to cited text no. 38
    
39.
Cornwell EY, Waite LJ. Social disconnectedness, perceived isolation, and health among older adults. J Health Soc Behav 2009;50:31-48.  Back to cited text no. 39
    
40.
Coyle CE, Dugan E. Social isolation, loneliness and health among older adults. J Aging Health 2012;24:1346-63.  Back to cited text no. 40
    
41.
Krumholz HM, Butler J, Miller J, Vaccarino V, Williams CS, Mendes de Leon CF, et al. Prognostic importance of emotional support for elderly patients hospitalized with heart failure. Circulation 1998;97:958-64.  Back to cited text no. 41
    
42.
Umberson D. Family status and health behaviors: Social control as a dimension of social integration. J Health Soc Behav 1987;28:306-19.  Back to cited text no. 42
    
43.
Matheson K, Gill R, Kelly O, Anisman H. Cortisol and cardiac reactivity in the context of sex discrimination: The moderating effects of mood and perceived control. Open Psychol J 2008;1:1-10.  Back to cited text no. 43
    
44.
Utsey SO, Hook JN. Heart rate variability as a physiological moderator of the relationship between race-related stress and psychological distress in African Americans. Cultur Divers Ethnic Minor Psychol 2007;13:250-3.  Back to cited text no. 44
    
45.
Lucas T, Lumley MA, Flack JM, Wegner R, Pierce J, Goetz S. A preliminary experimental examination of worldview verification, perceived racism, and stress reactivity in African Americans. Health Psychol 2016;35:366-75.  Back to cited text no. 45
    
46.
Quinlan M, Bohle P. Overstretched and unreciprocated commitment: Reviewing research on the occupational health and safety effects of downsizing and job insecurity. Int J Health Serv 2009;39:1-44.  Back to cited text no. 46
    
47.
Heaney CA, Israel BA, House JS. Chronic job insecurity among automobile workers: Effects on job satisfaction and health. Soc Sci Med 1994;38:1431-7.  Back to cited text no. 47
    
48.
Lee S. Prospective study of job insecurity and coronary heart disease in US women. Ann Epidemiol 2004;14:24-30.  Back to cited text no. 48
    
49.
Muenster E, Rueger H, Ochsmann E, Letzel S, Toschke AM. Association between overweight, obesity and self-perceived job insecurity in German employees. BMC Public Health 2011;11:162.  Back to cited text no. 49
    
50.
Gilman SE, Kawachi I, Fitzmaurice GM, Buka SL. Socioeconomic status in childhood and the lifetime risk of major depression. Int J Epidemiol 2002;31:359-67.  Back to cited text no. 50
    
51.
Lorant V, Deliège D, Eaton W, Robert A, Philippot P, Ansseau M. Socioeconomic inequalities in depression: A meta-analysis. Am J Epidemiol 2003;157:98-112.  Back to cited text no. 51
    
52.
Lichtman JH, Froelicher ES, Blumenthal JA, Carney RM, Doering LV, Frasure-Smith N, et al. Depression as a risk factor for poor prognosis among patients with acute coronary syndrome: Systematic review and recommendations: A scientific statement from the American Heart Association. Circulation 2014;129:1350-69.  Back to cited text no. 52
    
53.
Cuijpers P, Vogelzangs N, Twisk J, Kleiboer A, Li J, Penninx BW. Comprehensive meta-analysis of excess mortality in depression in the general community versus patients with specific illnesses. Am J Psychiatry 2014;171:453-62.  Back to cited text no. 53
    
54.
Wu Q, Kling JM. Depression and the risk of myocardial infarction and coronary death: A meta-analysis of prospective cohort studies. Medicine 2016;95:e2815.  Back to cited text no. 54
    
55.
Goldstein BI, Carnethon MR, Matthews KA, McIntyre RS, Miller GE, Raghuveer G, et al. Major depressive disorder and bipolar disorder predispose youth to accelerated atherosclerosis and early cardiovascular disease: A scientific statement from the American Heart Association. Circulation 2015;132:965-86.  Back to cited text no. 55
    
56.
May HT, Horne BD, Knight S, Knowlton KU, Bair TL, Lappé DL, et al. The association of depression at any time to the risk of death following coronary artery disease diagnosis. Eur Heart J 2017;3:296-302.  Back to cited text no. 56
    
57.
Batelaan NM, Seldenrijk A, Bot M, van Balkom AJ, Penninx BW. Anxiety and new onset of cardiovascular disease: Critical review and meta-analysis. Br J Psychiatry 2016;208:223-31. Available from: https://www.cambridge.org/core/product/identifier/S0007125000279373/type/journal_article. [Last accessed on 2018 Jul 21].  Back to cited text no. 57
    
58.
Roest AM, Martens EJ, de Jonge P, Denollet J. Anxiety and risk of incident coronary heart disease: A meta-analysis. J Am Coll Cardiol 2010;56:38-46.  Back to cited text no. 58
    
59.
Frasure-Smith N, Lespérance F. Depression and anxiety as predictors of 2-year cardiac events in patients with stable coronary artery disease. Arch Gen Psychiatry 2008;65:62-71.  Back to cited text no. 59
    
60.
Roest AM, Zuidersma M, de Jonge P. Myocardial infarction and generalised anxiety disorder: 10-year follow-up. Br J Psychiatry 2012;200:324-9.  Back to cited text no. 60
    
61.
Song H, Fang F, Arnberg FK, Mataix-Cols D, Fernández de la Cruz L, Almqvist C, et al. Stress related disorders and risk of cardiovascular disease: Population based, sibling controlled cohort study. BMJ 2019;365:L1255.  Back to cited text no. 61
    
62.
Gupta R, Kishore J, Bansal Y, Daga M, Jiloha R, Singal R, et al. Relationship of psychosocial risk factors, certain personality traits and myocardial infarction in Indians: A case–control study. Indian J Community Med 2011;36:182-6.  Back to cited text no. 62
[PUBMED]  [Full text]  
63.
Krantz DS, McCeney MK. Effects of psychological and social factors on organic disease: A critical assessment of research on coronary heart disease. Annu Rev Psychol 2002;53:341-69.  Back to cited text no. 63
    
64.
Hagström E, Norlund F, Stebbins A, Armstrong PW, Chiswell K, Granger CB, et al. Psychosocial stress and major cardiovascular events in patients with stable coronary heart disease. J Internal Med 2018;283:83-92. Available from: http://doi.wiley.com/10.1111/joim. 12692. [Last accessed on 2018 Jul 21].  Back to cited text no. 64
    
65.
Moosavi M, Eslami M, Bagloo OS, Birashk B. Mental strain, more important than stressful life events in myocardial infarction. Acta Med Iranica 2004;42:6.  Back to cited text no. 65
    
66.
Rosengren A, Hawken S, Ounpuu S, Sliwa K, Zubaid M, Almahmeed WA, et al. Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): Case-control study. Lancet 2004;364:953-62.  Back to cited text no. 66
    
67.
Valtorta NK, Kanaan M, Gilbody S, Ronzi S, Hanratty B. Loneliness and social isolation as risk factors for coronary heart disease and stroke: Systematic review and meta-analysis of longitudinal observational studies. Heart 2016;102:1009-16.  Back to cited text no. 67
    
68.
Manoj M, Joseph K, Vijayaraghavan G, Joseph A. Association of social support and myocardial infarction: A case-control study. Ann Clin Cardiol 2019;1:15. Available from: http://www.onlineacc.org/text.asp?2019/1/1/15/273005. [Last accessed on 2020 May 06].  Back to cited text no. 68
    
69.
Steptoe A, Owen N, Kunz-Ebrecht SR, Brydon L. Loneliness and neuroendocrine, cardiovascular, and inflammatory stress responses in middle-aged men and women. Psychoneuroendocrinology 2004;29:593-611.  Back to cited text no. 69
    
70.
Klaric M, Lovric S, Kresic Coric M, Galic K, Coric S, Franciskovic T. Psychiatric comorbidity and PTSD-related health problems in war veterans: Cross-sectional study. Eur J Psychiat 2017;31:151-7. Available from: http://www.elsevier.es/en-revista-european-journal-psychiatry-431-articulo-psychiatric-comorbidity-ptsd-related-health-problems-S0[Last accessed on 2020 May 06].  Back to cited text no. 70
    
71.
Lampert R, Jamner L, Burg M, Dziura J, Brandt C, Liu H, et al. Triggering of symptomatic atrial fibrillation by negative emotion. J Am Coll Cardiol 2014;64:1533-4.  Back to cited text no. 71
    
72.
Patel D, McConkey ND, Sohaney R, McNeil A, Jedrzejczyk A, Armaganijan L. Systematic review of depression and anxiety in patients with atrial fibrillation: The mind-heart link. Cardiovasc Psychiatry Neurol 2013;2013:1-11. Available from: https://www.hindawi.com/archive/2013/159850/. [Last accessed on 2020 May 06].  Back to cited text no. 72
    
73.
Manoj M, Joseph K, Vijayaraghavan G. Association of depression, anxiety, and stress with myocardial infarction: A case–control study. J Clin Prevent Cardiol 2018;7:86. Available from: http://www.jcpconline.org/text.asp?2018/7/3/86/236330. [Last accessed on 2018 Jul 21].  Back to cited text no. 73
    
74.
Peacock J, Whang W. Psychological distress and arrhythmia: Risk prediction and potential modifiers. Prog Cardiovasc Dis 2013;55:582-9.  Back to cited text no. 74
    
75.
Liang J, Huang C, Yang B, Huang H, Wan J, Tang Y, et al. Depressive symptoms and risk factors in Chinese patients with premature ventricular contractions without structural heart disease. Clin Cardiol 2009;32:E11-7.  Back to cited text no. 75
    
76.
Rubin GJ, Wessely S. The psychological effects of quarantining a city. BMJ 2020;368:m313.  Back to cited text no. 76
    
77.
Newman MG, Zainal NH. The value of maintaining social connections for mental health in older people. Lancet Public Health 2020;5:e12-3.  Back to cited text no. 77
    
78.
Käll A, Jägholm S, Hesser H, Andersson F, Mathaldi A, Norkvist BT, et al. Internet-based cognitive behavior therapy for loneliness: A pilot randomized controlled trial. Behavior Ther 2020;51:54-68. Available from: https://linkinghub.elsevier.com/retrieve/pii/S0[Last accessed on 2020 Apr 25].  Back to cited text no. 78
    




 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Introduction
Psychosocial Fac...
How Can Psychoso...
What Needs to Be...
Conclusion
References

 Article Access Statistics
    Viewed41    
    Printed0    
    Emailed0    
    PDF Downloaded16    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]