Takotsubo cardiomyopathy (TTC), also known as stress-induced cardiomyopathy, is a peculiar reversible cardiovascular disease (CVD) that may mimic an acute coronary syndrome, often affecting postmenopausal women after a stressful event. The prevalence ranges between 1.7 and 2.2% inpatients admittedwith chest pain for suspected acute coronary syndrome [1,2]. Proposed pathophysiological mechanisms include: catecholamine cardiotoxicity, microvascular dysfunction and coronary artery spasm [3,4]. Major depression and comorbid anxiety disorders have been associated with elevated sympathetic activity and diminished reuptake of norepinephrine, which may be responsible for prolonged cardiac sympathetic stimulation [5]. As suggested by Ziegelstein et al. [6], the double impact effect of disproportional high catecholamine responses and increased cardiac sympathetic sensitivity may place depressed patients at higher risk for developing TTC when exposed to stressful situations. Several case reports [7–11] have suggested that the use of SSRIs (in both therapeutic and over dosage scenarios) is associated with TCC, potentially by increasing norepinephrine levels in neuronal tissue via reuptake inhibition. This retrospective descriptive study consisted of 78 patients who met the Modified Mayo criteria [12]: 1) akinesia or dyskinesia of the apical and/or midventricular segments of the left ventricle with regionalwallmotionabnormalities extendingbeyond thedistributionof a single epicardial vessel, 2) absence of obstructive coronary artery disease, 3) new electrocardiographic abnormalities, and 4) absence of pheochromocytomas/myocarditis. The diagnosis of depression and anxiety was made based on clinical criteria by a primary care physician or psychiatrist before being admitted to the hospital. The diagnosis of anxiety included generalized anxiety disorder, panic disorder, post-traumatic stress disorder and social phobia. Clinical outcomes were assessed during the hospital admission and within 6 months after the index event, as follows: in hospital death (all cause-mortality), inpatient acute heart failure (HF), length of stay, and left ventricular ejection fraction (LVEF) determined by 2-D echocardiogram. Chi-squared and paired t-tests were used to assess statistical differences in categorical and continuous variables, respectively. A twotailed P b 0.05 was considered statistical significant. Cox-proportional hazard model was constructed to evaluate mortality. All analyses were performed employing SPSS v 19.0, Chicago IL. This study was approved by the hospital’s institutional review board. Baseline characteristics of the studypopulation aswell as by SSRI use are reported in Tables 1 and 2 respectively. SSRIs use was strongly associatedwith all-causemortality during index hospital admission (OR 7.6; 95% CI 1.1–50.3; P= 0.016). Mean LVEF on admission in patients taking SSRIs was 36.3 ± 11.4% and for patients not taking SSRIs was 36.7 ± 11.0%. Repeated echocardiogram within 6-months revealed statistically significant recovery of LVEF in each group (P b 0.05 for both comparisons) with a relatively lower LVEF in patients taking SSRIs (Fig. 1, P = 0.01). (See Table 3.) Mean LVEF on admission for patients without depressionwas 36.4 ± 11.2% and for patients with depression was 37.2 ± 10.6%. Repeated LVEF within 6-months revealed statistically significant recovery of LVEF in each group (P b 0.05 for both comparisons), although patientswith depression had relatively lower LVEFcompared topatientswithoutdepression (Fig. 2, P=0.02). The survival curve (Fig. 3) showed that SSRIs patients had lower survival rate compared with patients not taking SSRIs (P=0.04). In this study, the prevalence of depression and anxiety (21% and 31%, respectively) was consistent with previous reports [4,13,14] which reported a prevalence ranging between 20 and 40%. Several authors