Grand Coeur, Grand Ecoeurement! Depression and the Heart!

Abstract

Sir, 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] Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.