Attack the ATAK; A Challenging Contemporary Complex: Pathophysiologic, Therapeutic, and Preventive Considerations
Nicholas G. Kounis, Virginia Mplani, Cesare de Gregorio, Ioanna Koniari
Abstract
The adrenaline, takotsubo, anaphylaxis, and Kounis (ATAK) complex constitutes a challenging contemporary clinicopharmacological combination of syndrome ATAK. 1 "Αttacking" is needed to elucidate its etiology and pathophysiology and implement preventive and therapeutic measures.Adrenaline is considered the drug of choice for anaphylactic shock; however, its administration, especially in excess doses, could contribute to coronary spasms.Moreover, coronary spasms through direct myocardial stunning can lead to Takotsubo syndrome (TS). 2 During anaphylaxis, the released mediators can also initiate coronary spasms and again TS. 3 Adrenaline administration as hemodynamic support during anaphylactic shock could also increase the plasma catecholamine levels and perpetuate this vicious cycle.Kounis syndrome has also been associated with TS. 4 AdrenalineParadoxically, adrenaline, the drug of choice for anaphylaxis, can induce anaphylaxis by itself.Indeed, commercially available adrenaline contains sodium metabisulfite as a preservative. 5naphylactic reactions secondary to exposure to sulfites found in sparkling water have already been reported. 6This situation poses a therapeutic dilemma in sulfite-sensitive patients who suffer from anaphylactic shock. 7Fortunately, free sulfite adrenaline is currently commercially available for administration to patients with sulfite sensitivity (American Regent Inc., USA).Glucagon is another alternative used successfully for anaphylaxis treatment in patients taking β-blockers. 5,8terestingly, both the appropriate intramuscular adrenaline dose of 0.01 mg/kg of a 1:1,000 (1 mg/mL) solution to a maximum dose of 0.5 mg in adults 5,9 and the appropriately diluted intravenous dose (1:10,000 [0.1 mg/mL] or 1:100,000 [0.01 mg/mL]) may also contribute to coronary spasms.