It has been shown that SIC predominantly affects postmenopausal woman [1]. Although several cases of SIC in young woman have already been described, pregnancy associated SIC (P-SIC) appears to be rather unusual [3‐7].

The pathophysiological mechanism of SIC is still not completely understood. Several possibilities have been discussed but increased levels of catecholamine and vasoconstrictive substances appear to play crucial role in triggering SIC [8]. It can be defined as a catecholamine- triggered myocyte injury caused by catecholamine- induced microvascular spasm or by direct catecholamine- associated myocardial toxicity. Cardiac troponins are elevated in almost all patients with SIC. However the elevation in serum troponin is disproportional in comparison to the extension of the akinetic myocardial regions. The pathophysiology of wall motion abnormalities in SIC is not well established. Reversible ventricular dysfunction may be also the result of epicardial coronary artery spasm and consequently regionally stunned myocardium [9]. This extended stunning is probably correlated with only slight elevation of cardiac necrosis markers. Moreover it has been reported that the risk of SIC can be reduced by blocking α- and β- adrenergic receptors [10, 11]. Furthermore, a difference in the distribution and density of adrenergic receptors in myocardium are responsible for the variance in SIC appearance in either the apical or mid- ventricular wall. Inverted SIC occurs mainly in younger females with higher prevalence of identifiable activating stress and possibly in relation to a larger distribution of adrenergic receptors in the basal segments of LV in this population [2, 12, 13]. The subjective experience of stress by woman in the course of delivery may be an additional factor contributing to occurrence of reverse SIC during caesarean section. SIC in the perioperative setting has been reported yet as well as vasoconstrictive substances such as ephedrine were suggested as triggering factors [14]. In our case, treatment of hypotension associated with spinal anaesthesia with ephedrine also appears to have precipitated SIC. Therefore adrenergic stimulants should be used with caution in treating maternal hypotension after spinal anaesthesia. However it is worth mentioning that hypotension is described as an undesirable result of central blockade and its prevalence is estimated as 30–90 % of all spinal anaesthesia. Standard methods of hypotension treatment in pregnancy are infusion of fluids and intravenous ephedrine administration, the use of corticosteroids is not recommended (their effect of action is too slow and weak). Ephedrine is easily adjustable and has a short duration of action so after all it appears to remain the first line option of treatment of hypotension associated with spinal anaesthesia. Moreover, taking into consideration that main aetiology of SIC appears to be the catecholamine- triggered myocyte injury, exogenous catecholamines in such patients with cardiogenic shock should be avoided. The use of inotropes and further activation of catecholamine receptors may worsen the clinical status and prognosis of these individuals. Unfortunately, due to persistent hypotension LV dysfunction, our patient received inotropic agents. This treatment could probably exacerbate or prolong the acute phase of the disease. According to current state of knowledge on Takotsubo syndrome of the Heart Failure Association of the European Society of Cardiology, in this case, treatment options should include mechanical support such as temporary LV assist devices, extracorporeal membrane oxygenation or if those option are not available low- dose of levosimendan infusion as a catecholamine sparing positive inotrope [15]. In the pathogenesis of SIC it is also suggested that lower estrogen levels may play a role [16]. In late pregnancy placenta produces high amounts of estradiol that decrease rapidly after placenta expulsion favouring a higher myocardium susceptibility to adrenergic stimuli. Consequently woman in the postpartum may represent another vulnerable group for SIC onset, especially inverted SIC.

Minatoguchi et al. identified a total of 18 (8 from Western countries) confirmed cases of symptomatic P- SIC [4]. Most women underwent caesarean delivery. Almost all electrocardiograms showed abnormalities and serum levels of cardiac enzymes were elevated. In 33 % cases, as well as in our, acute cardiopulmonary collapse occurred on the day of labour and symptoms were similar to those in ACS, PE or peripartum cardiomyopathy (PCM). In presented case computed tomography, as a diagnostic test of choice, excluded PE whereas coronary angiography has not confirmed ACS. PCM differs from typical SIC in terms of presentation and outcome and it does not present with a remarkable contraction pattern. Moreover recovery in PCM may be delayed of several months and is prevalent in less than 50 % of patients, whereas repeated TTE, among women with SIC, revealed normalized LV systolic function within 6 months in all reported cases [4, 17]. Furthermore in PCM myocardial late gadolinium enhancement can be present in cardiac magnetic resonance [18]. Therefore multimodality imaging may help to exclude or confirm the diagnosis of SIC. Echocardiography still remains preferred screening method to asses cardiac function. Bedside TTE seems to be a useful, non- invasive readily available diagnostic tool for the differential diagnosis of ACS, PE, PCM and SIC. Instantaneous recognition of SIC in the postpartum period has immediate therapeutic implications. Although SIC generally has a good prognosis, intensive heart failure therapy is required for successful convalescence.