Thyroid storm-induced cardiovascular complications and modalities of therapy: Up-to-date review

A thyroid storm (TS) or thyrotoxic crisis is an infrequent, life-threatening endocrinological emergency due to the worsening of the hyperthyroid state. Thyroid hormones (THs) influence almost all the body cells and tissues' differentiation, growth, and energy metabolism. Consequently, excess THs are expected to lead to profound organ function, regulation, and hemodynamic changes. In addition to their roles in metabolism and thermoregulation, THs play critical role in maintaining cardiovascular homeostasis through both genomic and non-genomic mechanisms. Receptors for THs are expressed in myocardial and vascular endothelial tissues, allowing fluctuations in circulating hormone levels to directly influence cardiovascular function. Excess TS induces a hyper-dynamic cardiovascular state, characterized by increased ventricular contractility and improved systolic and diastolic performance. The chronotropic and inotropic properties of THs result in dysregulation of blood pressure, heart rate, contractility, cardiac output, and systemic vascular resistance. This could lead to serious consequences such as cardiomyopathy, heart failure, and life-threatening arrhythmia, ultimately contributing to cardiocirculatory collapse and cardiac death. The management of TS necessitates a systematic approach that emphasizes the significance of resuscitation and identification of the underlying causes. It is crucial to prioritize assessing cardiac function in patients with TS. This review explores the clinical impact of TS on the heart and its clinical repercussions, emphasizing the intricate molecular and pathophysiological mechanisms and the interplay between TS and key cardiovascular parameters. This review summarizes the current knowledge of pathophysiology, pharmacological and mechanical interventions, ranging from beta-blocker use to the surgical approach.