Tako-Tsubo cardiomyopathy is a syndrome first described by Sato et al. in 1991[
1] consisting of transient wall motion abnormalities most often involving the apical ventricle. Abnormalities of the electrocardiogram (ECG) and myocardial enzyme release may mimic acute coronary syndrome (ACS) in the angiographic absence of coronary artery disease[
2]. The estimated prevalence is 2.5% in patients with ACS and post-menopausal women are most often affected[
2,
3]. Usually, TTC subsides rapidly without somatic complications[
4]. But a growing number of recent reports demonstrate that TTC is not entirely benign[
5,
6]. For example, prolongation of the QT-interval is a well known finding in patients with acute TTC[
7]. In a subgroup of patients, the severe prolongation of the QT-interval (QTc > 500 ms) may be a marker for the risk of sudden death[
7]. Furthermore, in patients with pre-existing long QT syndrome or concomitant psychiatric diseases and respective medication, TTC may lead to lethal arrhythmias[
8]. The in-hospital mortality rate is 1.1% and incidence of recurrence is recently reported to be 2.9 – 10%[
4,
9,
10]. Left ventricular thrombus occurs in about 5% of patients, 1.6% suffer from nonfatal cardioembolic outcomes[
11]. In a subgroup of patients, cardiac MRI late enhancement may be present and last over time[
12]. Late enhancement consistent with myocardial scarring has been reported sporadically and scars were not associated with adverse long term outcomes[
5,
13]. The exact pathomechanisms of TTC have not been elucidated[
14,
15]. Five different etiological mechanisms of TTC are discussed[
16]. There is evidence for (1) multi-vessel epicardial spasms[
17], (2) microcirculatory dysfunction[
18], (3) obstruction of the left ventricular outflow[
19] and (4) endocrine effects like increased vulnerability of postmenopausal women to hormonal and sympathetic stimuli[
20]. Most pathophysiological models point to (5) elevated catecholamine levels in TTC patients which are higher compared to patients with myocardial infarction of corresponding Killip classes[
21]. In latest reports, a hypothetical association of concurrent sympathetic over activity and vagal withdrawal has been proposed[
22]. As acute episodes of physical or mental stress antecede an event in 7 out of 10 cases, stress induced peaks of catecholamine levels acting on differently localized and sensitized adrenergic receptors are thought of setting off an event[
2,
23‐
27]. In several recent reports, a high prevalence of anxiety and depression (21 – 66%) has been found in TTC patients[
28‐
32]. Furthermore, anxiety and depression show effects on catecholamine metabolism. For example, levels of systemic and cardiac catecholamines are elevated and noradrenaline reuptake is reduced in depressed patients[
33]. Additionally, noradrenaline responses to emotional stress are correlated with the extent of depressive symptoms[
34]. In patients with panic disorders, epinephrine is released from the heart at rest and during spontaneous attacks[
35]. Due to a norepinephrine transporter impairment, patients with panic disorder show a reduced uptake of nor-/epinephrine during transit to the heart[
36,
37]. In sum, the high prevalence of psychological illnesses in TTC patients led to the assumption that psychosocial stress concomitant with abnormalities in catecholamine signaling may be a risk factor whereas acute physical or emotional stress may ultimately trigger the event[
28,
30‐
32,
38‐
40]. But the key question of cause and effect of psychiatric disorders in the context of TTC remains. Most of the studies could not determine the timeline of psychiatric disorders, and it may well be that the circumstances after the onset of TTC led to psychiatric comorbidity. In an unprecedented study, a high prevalence (56%) of chronic anxiety disorder anteceding TTC has been reported[
32]. The authors hypothesized that premorbid chronic psychiatric conditions may not only be risk factors for TTC but also for recurrences[
32].
There is very little documentation of posttraumatic stress disorder (PTSD) in the context of TTC are very rare. At the same time, stressful events antecede the first onset of PTSD and symptoms are often chronic (>90%) and unremitting (>30%)[
41]. Hyperarousal is one major clinical sign and the condition is closely linked to neuroendocrine alterations[
42,
43]. To our knowledge, there is only one case report of TTC in a postmenopausal patient with a 5 year history of PTSD[
44]. The patient recovered fully and there was no report of recurrences or complications[
44]. We present a unique case of recurrent TTC with complications in a pre-menopausal woman. Furthermore, it is the first description of chronic symptoms of posttraumatic stress peaking right before the first onset of TTC.