Role of Polypeptide Procalcitonin in Cardiac and Microvascular Injury in Sepsis, Myocardial Ischemia/Reperfusion, Cardiac Arrest, Mixed Shock, and Stress

High mortality in patients with sepsis, acute myocardial infarction (AMI), cardiac arrest (CA), and Takotsubo syndrome (TS) is the main problem of modern medicine. Polypeptide procalcitonin is synthesized and secreted by different cells and tissues. Septic shock (SS), cardiogenic shock (CS), CA, CoronavIrus disease 2019, and TS significantly increase circulating procalcitonin levels. Lipopolysaccharide stimulates the production of procalcitonin through the activation of toll-like receptor-4 and transcription factor nuclear factor of κ light polypeptide gene enhancer in B-cells. Procalcitonin activates the calcitonin gene-related peptide receptor in endothelial cells and an unknown receptor. Procalcitonin causes lung microvessel injury, apoptosis, and pyroptosis of endothelial cells. Procalcitonin antibodies increase survival in animals with sepsis. Exogenous procalcitonin exacerbates sepsis in animals. Procalcitonin is involved in the pathogenesis of SS, CS, and death after CA, and stress-induced cardiac injury. An increase in circulating procalcitonin levels is associated with acute heart failure, but not microvascular injury or intramyocardial hemorrhage in patients with AMI. An increase in circulating procalcitonin levels is a predictor of mortality after SS, CS, and CA. The elevation in the procalcitonin level indicates a worsening of the course of pneumonia. Mixed CS is observed in patients with AMI and TS and is often associated with sepsis and systemic inflammatory response. Hence, calcitonin gene-related peptide receptor antagonists and procalcitonin monoclonal antibody may become the basis for the development of drugs for the treatment of SS, CS, TS, and prevention of death after CA.