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 Table of Contents 
Year : 2018  |  Volume : 7  |  Issue : 6  |  Page : 1592-1593  

Grand Coeur, Grand Ecoeurement! Depression and the Heart!

Al-Manara CAP Centre, Kuwait Centre for Mental Health, State of, Kuwait

Date of Web Publication30-Nov-2018

Correspondence Address:
Dr. Ahmed Naguy
Al-Manara CAP Centre, KCMH, Jamal Abdul-Nassir St., Shuwaikh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jfmpc.jfmpc_267_18

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How to cite this article:
Naguy A, Alrashidi F. Grand Coeur, Grand Ecoeurement! Depression and the Heart!. J Family Med Prim Care 2018;7:1592-3

How to cite this URL:
Naguy A, Alrashidi F. Grand Coeur, Grand Ecoeurement! Depression and the Heart!. J Family Med Prim Care [serial online] 2018 [cited 2021 Jun 24];7:1592-3. Available from: https://www.jfmpc.com/text.asp?2018/7/6/1592/246491


The prevalence rates of depression in cardiovascular disease (CVD) range from 17% to 27%. It is three times more common in patients after myocardial infarction (MI). Women are particularly at high risk. Depression is a risk factor for CVD; it approximately doubles the risk. Depression, especially treatment-resistant (TRD), independently portends poor prognosis in patients with CVD.[1] As such, there seems to be a dose–response relationship between severity of depression and cardiac mortality. Post-MI depression increases mortality by two to three times. It has been shown that somatic/neurovegetative symptom cluster of depression has a stronger association with CVD prognosis than the cognitive cluster. Possible mechanisms for this bidirectional relationship include both biological and behavioral links. Biological links include shared risk factors, metabolic syndrome, increased platelet activation, procoagulant states, hypothalamic–pituitary–adrenal axis dysregulation, dysautonomia, impaired immune function, vascular dysfunction, and inflammation.[2] Moreover, shared genetic effects might be contributory as demonstrated in a Swedish twin study,[3] with age-adjusted hazard ratio of 1.3. Recently, a systematic review and meta-analysis found a 27% increase in the risk of venous thromboembolism with antidepressant use class effect.[4] Psycho-social links include unhealthy lifestyle and treatment nonadherence. The relationship between depressive symptoms and multiple health risk factors begins in the adolescence calling for early intervention long before CVD sets in the middle age. Furthermore, a growing body of evidence connects childhood abuse to depression and other health outcomes including CVD in later years, mediated chiefly through inflammatory process.[5]

Screening for depression for patients with CVD is recommended by American Heart Association. The Patient Health Questionnaire (PHQ)-2 provides two screening questions and can be followed by PHQ-9 if either answer is positive. Likewise, patients with depression should be closely monitored and treated for risk factors for CVD.

Despite this link, studies failed to demonstrate reduced CVD by treating depression.[6] The major trials for treating depression in the setting of CVS include the following[7]:

  • SADHART – demonstrated safety of sertraline
  • ENRICHD – cognitive behavioural therapy improved depression and social isolation
  • CREATE – citalopram was efficacious
  • MIND-IT – mirtazapine was safe in patients after MI
  • K-DEPACS – escitalopram was effective.

Selective serotonin reuptake inhibitors are generally considered first-line treatment for demonstrated safety. Besides, they might be advantageous for blood-thinning actions. Sertraline and escitalopram are commonly preferred due to minimal pharmacokinetic interactions. Food and Drug Administration recommended a ceiling dose of 40 mg of citalopram due to concerns of dose-dependent QTc prolongation. Tricyclic antidepressants (e.g., nortriptyline) are best avoided due to quinidine-like action, prolongation of QTc interval, and possible torsadogenecity. Serotonin-norepinephrine reuptake inhibitors (e.g., venlafaxine) and norepinephrine reuptake inhibitors (e.g., reboxetine) are notorious for hypertension as these agents boost norepinephrine drive. Cases of Takotsubo cardiomyopathy have been reported in literature.[8] Bupropion (norepinephrine–dopamine reuptake inhibitor) has been associated with supine hypertension. Monoamine oxidase inhibitors (e.g., tranylcypromine) cause orthostasis and use is fraught with potential cheese reaction (hypertensive crisis) and serotonin syndrome. Finally, electro-convulsive therapy (ECT) generally can be performed safely in most patients with underlying cardiac conditions, whenever indicated (e.g., failed pharmacotherapy, depressive symptoms pose a significant barrier to care, patient's preference), as long as these patients are identified ahead of time and are closely monitored for potential complications.[9] Interestingly, Magid et al.[10] have reported on a successful ECT in a patient 10 days after MI.

Of note, suggestions of psychiatric adversity with commonly prescribed cardiac medications generally have not been substantiated. B-blockers are not depressogenic (even pindolol has been anecdotally deployed to augment antidepressants in TRD) and statins do not appear to increase suicidality, as was once thought.[11]

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Conflicts of interest

There are no conflicts of interest.

  References Top

Hare DL, Toukhsati SR, Johansson P, Jaarsma T. Depression and cardiovascular disease: A clinical review. Eur Heart J 2014;35:1365-72.  Back to cited text no. 1
Dhar AK, Barton DA. Depression and the link with cardiovascular disease. Front Psychiatry 2016;7:33.  Back to cited text no. 2
Kendler KS, Gardner CO, Fiske A, Gatz M. Major depression and coronary artery disease in the Swedish Twin Registry. Arch Gen Psychiatry 2009;66:857-63.  Back to cited text no. 3
Kunutsor SK, Seidu S, Khunti K. Depression, antidepressant use, and risk of venous thromboembolism: Systematic review and meta-analysis of published observational evidence. Ann Med 2018;12:1-17.  Back to cited text no. 4
Taylor SE, Lehman BJ, Kiefe CI, Seeman TE. Relationship of early life stress and psychologic functioning to adult C-reactive protein in the Coronary Artery Risk Development in Young Adults Study. BiolPsychiatry 2006;60:819-24.  Back to cited text no. 5
Fiedorowicz JG. Depression and cardiovascular disease: An update on how course of illness may influence risk. Curr Psychiatry Rep 2014;16:492.  Back to cited text no. 6
Yekehtaz H, Farokhnia M, Akhondzadeh S. Cardiovascular considerations in antidepressant therapy: An evidence-based review. J Tehran Heart Cent 2013;8:169-76.  Back to cited text no. 7
Naguy A, Al-Mutairi H, Al-Tajali A. Al-Mutairi H, Al-Tajali A. Atomoxetine-related Takotsubo cardiomyopathy. J Psychiatr Pract 2016;22:232-3.  Back to cited text no. 8
Zielinski RJ, Roose SP, Devanand DP, Woodring S, Sackeim HA. Cardiovascular complications of ECT in depressed patients with cardiac disease. Am J Psychiatry1993;150:904-9.  Back to cited text no. 9
Magid M, Lapid MI, Sampson SM, Mueller PS. Use of electroconvulsive therapy in a patient 10 days after myocardial infarction. J ECT 2005;21:182-5.  Back to cited text no. 10
Hallas J. Evidence of depression provoked by cardiovascular medication: A prescription sequence symmetry analysis. Epidemiology 1996;7:478-84.  Back to cited text no. 11


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