Clinical Case: Tako-Tsubo Cardiomyopathy vs. Kounis Syndrome vs. Possibly Another Condition Induced by Anaphylactic Shock from a Wasp Sting

Introduction:
Tako-Tsubo cardiomyopathy (TTC) is an acute, reversible heart failure (HF) syndrome typically triggered by stress. It is characterized by transient left ventricular (LV) wall motion abnormalities, particularly apical ballooning. Although TTC is generally considered a reversible condition, it can lead to mortality, with risks similar to myocardial infarction. The mechanisms of TTC are not fully understood and it remains unclear whether elevated catecholamine levels are directly associated with TTC or are a consequence of increased brain activity. 

Clinical Case:
We present the case of a 65-year-old woman who developed HF following an anaphylactic shock triggered by a wasp sting. After her initial hospitalization for anaphylaxis and treatment with adrenaline, she began experiencing symptoms of typical angina pectoris, dynamic troponin elevations, and apical akinesia observed on echocardiography (TTE), with a reduced ejection fraction (EF) of 30%.

Urgent cardiac catheterization ruled out coronary artery disease but revealed myocardial bridging of the medial left anterior descending coronary artery. Cardiac magnetic resonance imaging showed a typical pattern of TTC. Other potential causes were excluded and HF-therapy was initiated.

The first follow-up TTE showed a persistently reduced EF of 30% with continued apical akinesia; troponin levels remained elevated without significant decline. Additionally, elevated inflammatory markers were noted, which were also considered indicative of stress. Interestingly, 2015 myocardial perfusion studies of our patient had shown minimal underperfusion in the apical region and minimal akinesis.

Discussion:
According to the literature, TTC is a rare complication that can follow anaphylactic shock. In this case, TTC may have been triggered either by the allergic reaction itself or by the administration of adrenaline or be the result of  allergic acute coronary syndrome (Kounis syndrome).

Anaphylaxis is typically an IgE-mediated hypersensitivity reaction. Cascading effects results in increased vascular permeability, cardiac and pulmonary vascular constriction, heightened chemokine synthesis, and intravascular coagulation. Epinephrine is a sympathomimetic catecholamine that  increases heart rate and myocardial contractility and induces vasoconstriction. This combination can lead to myocardial ischemia and stunning.  In Kounis syndrome, the inflammatory cytokines released by mast cells can lead to coronary artery vasospasm, atheromatous plaque erosion, or rupture. 

In our case, the condition may be diagnosed as multifactorial. Compared to other cases, this example may represent a very rare combination of the “ATAK complex” (Adrenaline, Tako-Tsubo, Anaphylaxis, and Kounis syndrome), which has been reported only six times in the literature. The multifactorial background of this complex may contribute to worse outcomes, especially in patients with pre-existing conditions.

Conclusion:
We report a patient with acute HF-morphology of TTC following an anaphylactic shock and catecholamine administration. Although only a small number of clinical cases describing this condition have been documented, the actual prevalence is likely underestimated. There is a definite need for further studies on the impact of anaphylactic shock and catecholamine treatment on subsequent HF. In particular, long-term prognosis should be closely examined.

Fig. 1: Illustration of possible reasons for HF in our patients