Biomedicine & Pharmacotherapy 95 (2017) 487–496

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Review

Psychological sequelae of myocardial infarction Mukesh Kumar, Prasanta Kumar Nayak



MARK

Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, Uttar Pradesh, India

A R T I C L E I N F O

A B S T R A C T

Keywords: Myocardial infarction Depression Anxiety Post-traumatic stress disorder Chronic mild stress Inflammation

Patient with myocardial infarction (MI) are often affected by psychological disorders such as depression, anxiety, and post-traumatic stress disorder. Psychological disorders are disabling and have a negative influence on recovery, reduce the quality of life and causes high mortality rate in MI patients. Despite tremendous advancement in technologies, screening scales, and treatment strategies, psychological sequelae of MI are currently understudied, underestimated, underdiagnosed, and undertreated. Depression is highly prevalent in MI patients followed by anxiety and post-traumatic stress disorder. Pathophysiological factors involved in psychopathologies observed in patients with MI are sympathetic over-activity, hypothalamic–pituitary–adrenal axis dysfunction, and inflammation. Numerous preclinical and clinical studies evidenced a positive association between MI and psychopathologies with a common molecular pathophysiology. This review provides an update on diagnostic feature, prevalence, pathophysiology, clinical outcomes, and management strategies of psychopathologies associated with MI. Moreover, preclinical research findings on molecular mechanisms involved in post-MI psychopathologies and future therapeutic strategies have been outlined in the review.

1. Introduction Myocardial Infarction and psychological disorders are the two major cause of death and disability worldwide [1,2]. MI is the irreversible injury of myocardial tissue due to prolonged ischemia and hypoxia, and manifested by the cardinal symptoms of varying degree of chest pain, sweating, lethargy, and difficulty in breathing [3]. Psychological disorders particularly depression, anxiety, and post-traumatic stress disorders (PTSD) are caused due to abnormality in the central nervous system (CNS) activity and manifested by behavioral or psychological symptoms that impact multiple life areas and create distress in person experiencing these symptoms [4,5]. According to Diagnostic and Statistical Manual of Mental Disorders (DSM-5), psychological disorders are defined as “a syndrome characterized by clinically significant disturbance in an individual's cognition, emotion regulation, or behavior that reflects a dysfunction in the psychological, biological, or developmental process underlying mental functioning” [6,7]. The Global Burden of Disease study launched by the World Health Organization (WHO) predicts coronary heart disease (including MI) and depression will be two of the three most disabling disorders worldwide by 2030 [8]. Over the past 20 years, it has been found that depressed MI patients have a high risk of cardiac morbidity and mortality independent of traditional risk factors [9–11] and a poor prognosis of further adverse cardiac events [12,13]. A great body of literature found that the MI ⁎

survivors are more prone to psychological disorders [14–18]. However, the precise neurobiological mechanisms underlying this association have not been fully described [19]. With the advancement in therapeutic strategy, health-care professionals are becoming more aware of the prevalence and relevance of psychological sequelae of MI, but the complications of MI are understudied, underestimated, underdiagnosed, and undertreated [20–23]. The acute treatment strategy of MI has improved noticeably in the past few decades with the use of pharmacological interventions such as thrombolytic agents and thrombectomy, and by patient awareness. As a result, the mortality rate associated with acute MI has decreased, but on the other hand, psychological sequelae of MI have increased [24]. The post-MI psychopathology causes significant reduction in the quality of life; increase in stress and exhaustion, and often precipitate hospitalization of the patient. Unfortunately, there is no effective treatment strategy available, which can treat both MI and psychological sequelae of MI. This review provides an update on the acute and long-term psychopathologies associated with MI, with an emphasis on the diagnostic feature, prevalence, pathophysiology, clinical outcomes, and management strategies of psychopathologies associated with MI. Moreover, we have also discussed the possible mechanisms (Fig. 2) involved in postMI psychopathologies and therapeutic strategies. All of the relevant databases (PubMed, Science Direct and Google Scholar) were searched for the terms “myocardial infarction”, “post-MI psychopathologies”, post-MI depression, post-MI anxiety and “post-MI

Corresponding author. E-mail addresses: [email protected] (M. Kumar), [email protected] (P.K. Nayak).

http://dx.doi.org/10.1016/j.biopha.2017.08.109 Received 21 June 2017; Received in revised form 8 August 2017; Accepted 23 August 2017 0753-3322/ © 2017 Elsevier Masson SAS. All rights reserved.

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Table 1 Common post-MI psycopathologies. Disorder

Prevalence in MI patients (%)

Depression

31–45

Anxiety

24–37

PTSD

4–8.7

Clinical characteristics

Treatment options

• Anhedonia of energy • Loss concentration • Decreased isolation • Social appetite • Decreased thoughts • Suicidal • Insomnia • Guilt • Worry • Pain • Nervousness • Restlessness • Fatigue • Irritation appetite • Decreased • Insomnia mood • Negative and uncontrollable re‐experiences of MI • Unpleasant and flashbacks of MI attack • Nightmares negative emotions • Extreme social interaction • Poor • Persistent avoidance of stimuli associated with the MI

(SSRIs) • Antidepressants therapy • Cognitive-behavioral • Psychotherapy • Exercise programs

(BDZs) • Anti-anxiety therapy • Supportive therapy • Cognitive-behavioral • Internet-based cognitive behavior therapy

therapy • Cognitive-behavioral support • Social • Emotionally Focused Therapy

References [25,88,89,92]

[113,128–130]

[20,158,160]

PTSD” from 1980 to 30th March 2017. Clinical studies including clinical trials, meta-analysis and systematic reviews, and preclinical studies were selected for review. Reference lists of selected studies and review articles were hand searched to identify additional studies that met selection criteria.

Academy of Family Physicians (AAFP) publishes guidelines that includes evidence-based recommendations [40].

2. Depressive disorders

Depressive disorders are much more common in MI patients and increases the risk of an acute MI attack by 4.5-fold, compared with nondepressed patients [41–43]. In a recent nationwide population-based cohort study, Feng et al. reported a high prevalence of anxiety and depressive disorders in MI patients [44]. The comorbid depression with MI is an independent predictor of mortality and rehospitalizations in MI patients. In a systematic review of data more than 14,000 patient-based structured interviews, the prevalence of major depressive disorder (MDD) was found to be 19.8% [45]. Based on the Beck Depression Inventory (BDI) score and Hospital Anxiety and Depression Scale (HADS), the score of MDD in MI patients was found to be 31.1% and 15.5% respectively [45]. In another meta-analysis, Wu and Cling found 2.1% cases of MI due to depression and depression also increases 31% risk of MI in depressed patients [46]. In a longitudinal study, the postMI depressive symptoms were assessed by BDI score and the prevalence of depressive symptoms during hospitalization was reported as 26%, and after 4 and 12 months it was increased up to 38% and 37% respectively [14]. Suicidal thoughts or attempts of suicide are one of the diagnostic symptoms of MDD [6]. Previous studies have reported suicidal ideation in post-MI depressed patients [47–49]. In a study, 886 cardiovascular patients were screened for depression according to American Heart Association (AHA) and American Psychiatric Association (APA) guidelines in which 12% of patients were found to have suicidal ideation [50]. In this context, Larsen et al. performed a population-based casecontrol study in which a total of 19,857 patients were recorded with suicide and among 19,857 patients who committed suicide, 851 (4.3%) had a history of MI compared with 5537 controls (2.9%) [51]. The study reported that the depressive symptoms had increased the suicidal risk 64 times during the month following MI and suicidality risk was highest within the first month after discharge and associated with younger age group patients [51].

2.2. Prevalence

2.1. Diagnostic features MI is a sudden and intense stressor condition, which causes feelings of extreme sadness and despair. Most of the patients with MI develop a prominent and persistent depressed mood and loss of interest in daily activities (anhedonia) [25,26] (Table 1). Depressed mood and anhedonia are the two core symptoms of post-MI depression along with commonly associated symptoms such as social withdrawal, loss of energy and decreased concentration [27,28]. Other symptoms such as feelings of worthlessness or excessive guilt and frequent thoughts of suicide are less occurring symptoms [28,29]. An increasing number of studies have found that there is a strong association between adverse cardiovascular outcomes and depression [30]. The biopsychosocial model proposed that biological, psychological, and social factors altogether responsible for etiology of depression [31,32]. There are accumulated evidence on high cardiac morbidity and mortality independent of traditional risk factors (high cholesterol, atherosclerotic plaque, etc.) [11,24,33] and poor prognosis of further cardiac events [34], in depressed MI patients. Researchers are focusing on the bidirectional association between depression and MI but the precise neurobiological mechanism underlying this association remains unclear [19]. In clinical settings, diagnosis of depression in MI patients is a very crucial step that requires sound clinical judgment and expertise. The use of validated questionnaires and different screening scales provide insights on the depressive symptoms. The health care practitioners assess MI-related depressive symptoms by using a variety of screening scales that includes the Montgomery and Asberg Depression Rating Scale (MADRS) [35], the Hamilton Depression Rating Scale (HDRS) [36], the Hospital Anxiety and Depression Scale (HADS) [37], the Beck Depression Inventory (BDI) [38], and the Mini International Neuropsychiatric Interview (M.I.N.I.) [39]. To harmonize the detection and management of post-MI depression in clinical settings, the American 488

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Fig. 1. The major mechanisms contribute to the development and/or acceleration of MI and MI associated psychopathologies. All mechanisms are interconnected and can negatively affect both cardiac, CNS, and ANS function. Neurohormonal mechanisms include activation of HPA axis which results in release of cortisol and catecholamines from adrenal galnds. Corisol and catecholamines participate in the MI-associated multiple mechanisms that contribute to the development and acceleration of MI. These mechanisms include the abnormal cholesterol metabolism, overactivation of immune system, increased secretion of cytokines, increased platelet activity, vascular endothelial dysfunction low HRV, and cardiac arrythmia. Abbreviations: PTSD, post traumatic disorder; CRH, corticotropin-releasing hormone; ACTH, adrenocorticotropic hormone; HPA, hypothalamic–pituitary–adrenal; MI, myocardial infarction; HRV, heart rate variability.

Consequently, neurohumoral pathway is disturbed which leads to hypertriglyceridemia, hypercholesterolemia, hypertension, and vulnerability to plaque rupture [61–63]. Moreover, the balance between parasympathetic and sympathetic innervation gets disturbed which results in alteration of heart rate variability (HRV) and cardiac rhythm. The change in the HRV leads to fatal ventricular arrhythmia like ventricular fibrillation which might be responsible for high prevalence of sudden cardiac death in post-MI depressed patients [15,61,64–66]. Altered platelet activity is another key mechanism implicated in the pathophysiology of MI and post-MI depression. An increased platelet activity followed by thrombosis and sudden ischemia is the major cause

2.3. Pathophysiology There is a bidirectional link between the heart and the brain via HPA axis. HPA axis connects the emotional and cognitive centers of the brain with peripheral organs including the heart [52,53]. Myocardial infarction leads to secretion of corticotropin-releasing hormone (CRH) from hypothalamus that activates the anterior pituitary gland [5,19] leading to release of adrenocorticotropic hormone (ACTH). Further, ACTH activates the adrenal glands to release cortisol and catecholamines [54–58]. The increased serum level of cortisol results in reduced HPA feedback control [59,60], and finally HPA dysfunction (Fig. 1).

Fig. 2. Depicts the major predictors, treatment, and management strategies of post-MI psychopathologies. MI severity, previous depression, anxiety and social isolation among other factors, worsen the cardiovascular health and the course of psychopathologies. Treatment and management strategies for MI-associated psychopathologies included psychotherapy (CBT, internet-based CBT, and emotionally focused therapy), cardiac rehabilitation programs, exercise, and pharmacological interventions by SSRIs, TCAs, and BZDs. Abbreviations: MI, myocardial infarction; CBT, cognitive behavioral therapy; SSRIs, selective serotonin reuptake inhibitors; TCAs, tricyclic antidepressants; BZDs, benzodiazepines.

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patients [99]. The Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) study is the largest psychosocial intervention study that evaluated the efficacy of CBT and selective serotonin reuptake inhibitors (SSRIs) in post-MI depressed patients [98]. This study has revealed mixed outcomes; the antidepressant effect was more in patients receiving SSRIs with CBT, but there was no significant reduction in mortality due to antidepressant therapy. These mixed outcomes may be due to study design issues such as the inclusion of a large number of patients with transient depression and use of traditional end point; morbidity and mortality. In this context, Blumenthal et al. designed a randomized controlled study by replacing traditional endpoints with sophisticated intermediary clinical endpoints such as left ventricular ejection fraction, flow-mediated dilatation, heart rate variability (HRV), and baroreflex sensitivity to assess the effects of exercise and stress management training on markers of cardiovascular risk in patients with MI [88]. Pharmacological interventions such as SSRIs and tricyclic antidepressants (TCAs) have been reported in the management of post-MI depression. However, most of the studies provided strong support for the use of SSRIs [7,91]. In this context, Alvarez & Pickworth have reported the superior cardiovascular safety of SSRIs over TCAs in cardiac patients [90]. SSRIs such as sertraline, fluoxetine, paroxetine, and fluvoxamine have shown good efficacy as well as safety in post-MI depressive patients as compared to TCAs. SSRIs also demonstrated efficacy against other depressive disability and anxiety [7,100–102]. In agreement with these findings, the Sertraline Antidepressant Heart Attack (SADHART) trial demonstrated similar results [91]. In SADHART trial, a total of 369 depressed patients were treated with sertraline or placebo for 24 weeks, where sertraline demonstrated a marked efficacy against severe or recurrent depressive symptoms in post-MI patients [91].

of MI [3,67]. Similarly, an altered platelet activity is also observed in depressed patients [68,69]. The serotoninergic signaling pathway is involved in both depression [70] and platelet aggregation [13,56,71]. It has been reported that serotonin through 5-HT2 receptors induces both platelet aggregation and coronary vasoconstriction which further aggravate the ongoing MI [72]. The contribution of inflammation to the development of MI is well documented [22,23]. Activation of pro-inflammatory cytokines might be one of the cellular mechanisms in the development of post-MI depressive disorders [22,73]. The peripherally produced pro-inflammatory cytokines in MI induces expression of the same cytokines in the brain. The increased level of brain cytokines (specifically IL-1, IL-6, and TNF-α), both in patients with and without a history of cardiovascular disease are responsible for the development of sickness behavior and/or depression [74–77]. The cardinal symptoms of sickness behavior are depressed mood, altered cognition, fatigue, and sleep disorders. On the other hand, two major findings by Kop et al. and Vacacarino et al. evidenced that the inflammation related with elevated depressive symptoms results in the progression of the disease as well as mortality of cardiac patients [76,78]. 2.4. Clinical course and outcome The Agency for Healthcare Research and Quality (AHRQ) reported that most episodes of post-MI depression begin during initial hospitalization (7.2%–41.2%) and remains high after one month (35.4%) [40,79]. Forrester et al. reported that 19% of the patients had MDD within ten days of MI [80]. Parashar et al. reported the prevalence of depressive symptoms during initial hospitalization and 1-month after discharge as 20.6% and 13.1% respectively [81]. On 6-month follow-up study, depressed patients had higher rates of morbidity and mortality as compared with non-depressed patients [81]. A meta-analysis on depressed MI patients revealed 2.4-fold increased risk of mortality in postMI depressed patients [82]. Post-MI depression also has a negative effect on cardiac outcomes and quality of life [83]. The hospital readmissions and increased mortality are particularly prominent in patients with other comorbidities, smoking, alcohol use, less physical exercise, and poor medication compliance [26,84,85].

3. Anxiety disorders 3.1. Diagnostic features Anxiety disorders are common after MI and play a critical role in the development of depression and MI [23,32,103,104]. Anxiety is highly prevalent and approximately 50% of MI patients experienced anxiety immediately after the MI [62,63]. Surprisingly, as compared to depression, the prevalence and role of anxiety in MI patients is understudied [32]. Generalized anxiety disorder (GAD) characterized by long-lasting anxiety and other somatic or cognitive symptoms has a significant association with MI and is manifested in the MI patients during the first 24 h [6,105–107]. In addition to its independent role in MI, anxiety in co-occurrence with post-MI depression increases the mortality rate [108]. Phillips et al. reported that MI patients with both generalized anxiety disorder and MDD were at utmost risk of cardiac mortality, also suggested the synergistic activity of anxiety and depression in cardiac mortality [104]. Several studies suggested that anxiety symptoms are highly prevalent over the first 12 months after MI and associated with recurrent cardiac events in the long term follow-up [14,66,109]. The comorbidity of anxiety needs more attention and further preclinical and clinical studies to unravel underlying pathophysiology and management strategies of anxiety in MI patients.

2.5. Management and treatment In general, management of post-MI depression includes cardiac rehabilitation programs [40,86], social support [87], exercise programs [88], psychotherapy [48], cognitive behavior therapy [89], and pharmacological treatment by antidepressants [7,90–92] (Fig. 2). Cardiac rehabilitation programs which includes reassurance, education, and exercise have a great impact on emotional, psychosocial, and physical sequelae of MI, thus, prevent the progression of post-MI depression and improve the quality of life [44,86,93]. Recently, it has been shown that social support has significant association with reduced mortality in post-MI patients [87]. Further Netanela et al. recommended clinicians to assess post-MI psychosocial status to identify high-risk patients [87]. Previous reports evidenced the positive outcomes of exercise on MIassociated depression. Patients who were physically active after MI had lower depression score than physically inactive MI patients [94]. Also, on long term basis, exercise have shown similar effectiveness in reducing depressive symptoms to that of antidepressant treatment [95]. Cognitive behavior therapy (CBT) is one of the important strategies in the management of depression which helps in reducing stress and dysfunctional thoughts [96]. However, there were a small impact of CBT on MI patients, suggested the need for optimization of therapy [89]. On the other hand, CBT with other treatment strategies such as exercise [97] and pharmacological interventions [90,98] have demonstrated efficacy in reducing depressive symptoms. Despite high prevalence of post-MI depression and advancement in the treatment strategies, depression remained underdiagnosed and undertreated in MI

3.2. Prevalence The prevalence of anxiety symptoms in MI patients ranging from 24% to 31% [32,110–116]. In a meta-analysis of 12 observational studies comprising of 5750 patients with MI, anxiety was found to increase the risk of new cardiovascular events or mortality by 36% [117]. Researchers also reported the role of anxiety disorder in the progression of MI in younger men 490

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4. Post-traumatic stress disorder

[118] and mortality in older male population [119]. Roest et al. reported the relationship between GAD and cardiovascular prognosis [120]. In this study, 438 patients with acute MI were assessed for GAD and endpoint of cardiac mortality and cardiovascular-related readmissions. After the follow-up, 5.5% patients were found to be affected by GAD with 2-fold increase in the risk of cardiac mortality and rehospitalizations [120]. In a recent longitudinal cohort study, 540 MI patients were included in the study and found that anxiety was directly related to poorer quality of life [5].

4.1. Diagnostic features It is now clear that MI is an experience of the unexpected lifethreatening traumatic event and causes serious anxiety disorders. Furthermore, the fear of next MI attacks may apparently increase the psychological trauma and could result in PTSD. There is lack of extensive information on post-MI PTSD as most of the studies on post-MI PTSD are vague in nature. Post-MI PTSD is characterized by various unpleasant symptoms such as the feeling of danger to his or her life, feel intense fear and helplessness, dreams, psychological distress, decreased interest in activities, and feeling of detachment [130,131]. Post-MI PTSD symptoms if remained underdiagnosed or unrecognized can impart negative impact on cardiovascular health and increase cardiovascular morbidity and mortality [132,133]. Prior identification of risk factors of PTSD may help healthcare professionals to assess the vulnerable patients of PTSD and may prevent the complication of it [130,134]. The Posttraumatic Diagnostic Scale (PDS) [135], General Health Questionnaire-28 (GHQ-28) and the Modified PTSD Symptom Scale Self-Report (MPSS-SR) [136,137] are commonly used measurement scales for the screening of PTSD patients.

3.3. Pathophysiology Post-MI anxiety is triggered by chronic dysregulation of neurohormonal systems involved in the two main arms of the physiological stress response, i.e., the sympathetic nervous system and the HPA axis [32,64,106]. Due to decreased vagal tone and increased sympathetic activity, patients with anxiety disorders exhibit reduced heart rate variability (HRV) and arrhythmic response [15]. Platelet aggregation is one of the main factors in the development of MI, which results in ischemia (poor blood supply to the myocardium). In anxiety, the platelet activity is altered which may lead to thrombus formation [83] and can provoke the next MI attack. Increased level of thromboxane B2 was found in patients with post-MI anxiety which also contributes to thrombus formation [121,122].

4.2. Prevalence The estimated lifetime prevalence rate of PTSD in general population is 4.4% whereas, the prevalence of post-MI PTSD is twice of the prevalence found in the general population [73]. Studies using selfadministered questionnaires reported the prevalence rate of PTSD in MI patients ranging from 4% to 25% [73,138–141]. The prevalence rates of PTSD tend to decrease with time, in a study, out of 24% of PTSD-positive MI patients only 15% remained after nine months [141]. Sociodemographic factors such as young age and female sex have a great influence on the pathophysiology of PTSD, young age and female sex individuals are more prone to PTSD in MI [141]. In addition, previous MI, depression or mental disorders, and previous traumatization are the predictors of post-MI PTSD [141]. Pedersen et al. reported personality as an important factor for susceptibility to PTSD, as the distressed personality also called Type D personality (extreme negative emotions with poor social interaction) were associated with a 4-fold increased risk of PTSD in MI patients than controls [142].

3.4. Clinical course and outcome Post-MI anxiety is more prevalent in women (11%) as compared to men (7%) [123]. Previous reports have demonstrated increased adverse cardiovascular events in women with co-occurrence of post-MI depression and anxiety than depressed women with low anxiety [83,124]. Several studies also reported an independent association of depression and anxiety with cardiovascular morbidity and mortality. The symptoms of anxiety are more intense as compared to depression and are associated with reduction in the health-related quality of life and increase in rehospitalization of MI patients [83,109,125,126] 3.5. Management and treatment Early diagnosis and effective treatment strategy of anxiety in MI patients may decrease cardiac morbidity and mortality. Management of anxiety disorder in MI patients includes patient education, lifestyle modifications, and pharmacological and non-pharmacological treatments [44]. Antidepressant medications are also used in the post-MI anxiety, but few studies have been conducted to examine their efficacy for treating anxiety in MI patients. Among all antidepressant SSRIs are the best studied and most frequently used drugs in cardiac patients [90] while selective noradrenergic reuptake inhibitors (SNRIs) such as venlafaxine and duloxetine are not well studied drug for the management of post-MI anxiety disorders [44]. Moreover, TCA and SNRIs are not recommended in patients with cardiovascular disease because they lead to adverse cardiovascular outcomes [93,127]. Pharmacological treatments by anti-anxiety drugs have shown efficacy in the management of post-MI anxiety symptoms [44]. Anti-anxiety drugs used in the management of post-MI anxiety are lorazepam, diazepam, chlordiazepoxide hydrochloride, midazolam hydrochloride, alprazolam, temazepam, and diphenhydramine hydrochloride [128]. In addition to anti-anxiety drugs, MI patients are also prescribed with pain medication, because pain is also an important aggravating factor in anxiety. The non-pharmacological anxiety management strategy includes supportive therapy, CBT, internet-based cognitive behavior therapy, and reassurance [48,128–129] (Fig. 2). In a recent study, internet-based cognitive behavior therapy was found efficacious and suggested future prospects of CBT as an easily accessible treatment option for post-MI anxious patients [48].

4.3. Pathophysiology Previous research reports clearly demonstrated several predictors of PTSD after an MI attack such as fear at the time of the attack, more awareness of threat to life, psychiatric history; sociodemographic factors, and lack of social support [20,21]. The pathophysiological mechanisms of post-MI PTSD are multifactorial and remain unclear. However, HPA axis and sympathetic nervous system (SNS) deregulation are believed to be a major pathway involved in the pathogenesis of post-MI PTSD. The deregulation of the HPA axis results in increased stress, memory impairment, and diminished immune function [20,143,144]. On the other hand, deregulation of the SNS results in high blood pressure, low HRV, and baroreflex abnormalities [145,146]. Chronic physiological stress in PTSD causes over activation of SNS which inturn leads to massive release of catecholamine, epinephrine. The increased level of epinephrine has been reported to be involved in peripheral vasoconstriction, endothelial dysfunction, abnormal platelet activation, and myocardial injury [147,148]. The prevalent behavioral manifestations of PTSD such as smoking, drug abuse, physical inactivity, and non-adherence to medication also play an important role in the adverse cardiac outcomes in MI patients [149]. Another pathway that is associated with PTSD and MI is the immune/inflammatory pathway. PTSD patients have shown an elevated level of inflammatory biomarkers such as interleukin-6 (IL-6), tumor 491

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cardiovascular dysregulation [168,169]. Results exhibited an elevated sympathetic innervation as the potential autonomic and cardiac mechanisms underlying these cardiovascular dysregulation in the CMS model. Likewise, CMS model of depression has been used to evaluate the vulnerability to ventricular arrhythmias in depression [169]. Results have reconfirmed that depression increases susceptibility to ventricular arrhythmias as the larger percentage of animals in the CMS group exhibited ventricular tachycardia as compared to control group [170]. Physical inactivity and fatigue are the two common features observed in MI and depression may be due to changes in autonomic and cardiovascular functions. Depleted sodium ions (hyponatremia) has also been reported clinically in CHF patients [171]. In an animal model of interrupted sodium homeostasis, via two injections of a loop diuretic (furosemide) combined with a sodium-deficient diet, the role of RAAS in behavioral signs of depression (anhedonia) and cardiovascular dysfunction have been evaluated [172]. Animal models involving manipulation of 5-HT and 5-HT1A receptors have been developed to evaluate the role of the serotoninergic pathway in behavioral, neuroendocrine, autonomic, and cardiovascular functions. Pharmacological interventions by SSRI such as fluoxetine changes the level of 5-HT in the brain. In a recent study, the effect of fluoxetine on electrophysiological characteristics of heart in post-MI depression has been evaluated [127]. Fluoxetine treatment reduced the incidence of ventricular arrhythmia in rats with post-MI depression [127]. Fluoxetine has also been evaluated in CMS model of depression, where it reduced the anhedonia and partially prevented the cardiovascular morbidity [173]. These findings suggested a major role of the 5-HT in mediating depressive symptoms and cardiovascular morbidity. In a rodent model of disturbed sympathetic activity, Moffitt and Johnson evaluated the effect of fluoxetine in reducing sympathetic overactivity frequently observed in post-MI depression [174]. The restoration of the autonomic balance by fluoxetine through reduction in sympathetic overactivity confirmed a connection between the 5-HT transporter and autonomic activity of the heart [174]. Grippo et al. also investigated the relationship between 5-HT receptor and HPA axis in CMS model of depression [166]. Results demonstrated that activation of 5-HT1A receptor in the hypothalamus caused marked the corresponding ACTH response [166]. Brain-derived neurotrophic factor (BDNF) might be one of the connections between MI and psychological sequelae. Depression has been strongly and consistently linked to low levels of BDNF [175] and it is thought that BDNF signaling mediates the hippocampal neurogenesis that has been linked to depression recovery [176]. Indeed, SSRIs has been associated with increased levels of BDNF and hippocampal neurogenesis. BDNF also has an important role in several physiologic processes including cardiovascular health [177,178]. BDNF is expressed by endothelial cells, and it leads to angiogenesis and survival of endothelial cells (primarily mediated via the phosphatidylinositol-3-kinase-Akt pathway) [179]. Endothelial cells are vital to vascular health, and as noted, endothelial function is independently associated with cardiac outcomes. Furthermore, BDNF expression is upregulated by neural signals from the heart after experimentally induced MI (Interestingly, BDNF expression is increased in the brain but not in heart) and such expression was linked with reduced cardiomyocyte death [179]. Apoptosis is a cascade of active non-inflammatory cell death that depends on various apoptotic proteins, among them, Bcl-2 is one member of a family of genes [180]. On the basis of fate on apoptosis, proteins in Bcl-2 family can be divided into two categories a) apoptosis promoters (Bax, Bak, Bad, and Bcl-xS) and b) apoptosis inhibitors (Bcl-2 and Bcl-xl) [180,181]. On chronic stress, Bcl-2 family proteins accumulate at the mitochondrial outer membrane and regulate apoptosis. The Bax/Bcl-2 ratio is a measure of a cell’s susceptibility to apoptosis, in apoptotic conditions Bax/Bcl-2 ratio is increased [182,183]. Previous studies have demonstrated that antidepressant drugs can reverse the elevated level of apoptotic proteins in the myocardium and hippocampus of rats with CMS [184,185]. This suggests a nexus of the pro-

necrosis factor-α (TNF-α), and C-reactive protein [30,150]. The increased inflammatory markers may further aggravate the endothelial dysfunction and plaque stability, which could lead to increase in morbidity and mortality [30] (Fig. 1). 4.4. Clinical course and outcome PTSD has a negative effect on mental health and quality of life. It is reported that non-adherence to medication in PTSD patients may have a deleterious effect on the overall health and existing MI [28,133,151]. PTSD in MI patients also affect health status [152], psychological state [60,153], disease prognosis and social interaction [71,133,154]. 4.5. Management and treatment Evidence-based psychotherapy approaches such as CBT in PTSD have shown good efficacy in the management of post-MI PTSD [20,155]. There is increasing evidence on the association of two social factors viz. social isolation and partner’s support with the prediction of PTSD in cardiac patients [156]. In this context, Uchino reported that individuals with greater social support following MI have high survival rate than individuals with less social support [157]. In addition to CBT, emotionally focused therapy (EFT), which aimed to boost the emotional bonds between partners could be a treatment strategy for PTSD in MI patients [20,158,159]. However, further clinical trials are required to evaluate the effectiveness of CBT and EFT in post-MI PTSD patients. 5. Preclinical research on molecular mechanisms and therapeutic strategies In spite of high prevalence of both MI and depression the pathophysiological mechanisms underlying the association remains unclear. The use of animal models to examine possible mediators of post-MI psychological sequeale can provide a greater understanding of the association between MI and psychological disorders. Till date, few preclinical investigations elucidating the neurobiological mechanisms underlying the link between cardiovascular disease and mood disorders have been reported. Currently used preclinical models for the understanding of the pathophysiology of both the diseases are chronic mild stress (CMS) model, congestive heart failure (CHF) model, and pharmacological manipulation models (manipulation of body fluid, sodium balance, and central serotoninergic system). The CMS model of depression is a well-controlled, validated, and reliable animal model for evaluation of the effects of chronic stress on cardiovascular activity [160,161]. Willner and his colleagues using CMS model of depression have reported the role of stressor responsiveness, behavior, oxidative stress, neuroendocrine dysfunction, and immune alterations in depression and MI [161,162]. Similar observations have been made in experimental CHF models of rodents [163,164]. Mercanoglu et al. reported the role of sympathetic hyperactivity and oxidative stress in the pathogenesis of post-MI morbidity and mortality in CMS model of depression [165]. An increased sympathetic tone was observed in CMS model that resulted in increased oxidative stress, nitrosative stress, and infarct size of the myocardium [165]. In another set of experiment, Grippo et al. reported the role of neuroendocrine HPA axis dysfunction, activation of the renin angiotensin aldosterone system (RAAS), and immune dysfunction (activation of proinflammatory cytokines) in depression [166]. In a rat model of CHF using left descending coronary artery (LAD) occlusion, the causal relationship of inflammatory cytokine, TNF-α, in mediating a depression-like behavior has been examined [167]. The increased TNF-α level resulted in anhedonic behaviors in rats. The CMS model of depression has also been used for investigating autonomic and cardiac dysfunction associated with depressive symptoms. Recent studies with the CMS model suggested the association of stress and autonomic mechanisms in the pathogenesis of depression and 492

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Psychological sequelae of myocardial infarction.

Patient with myocardial infarction (MI) are often affected by psychological disorders such as depression, anxiety, and post-traumatic stress disorder...
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