Abstract

This report highlights the complex interplay between cardiac func8on, metabolic disorders, and the impact of Oshtoran Syndrome on overall health. Par8cular emphasis is placed on the implica8ons of a le? ventricular ejec8on frac8on (LV-EF) decline, PDH cytopathy, and the resultant metabolic dysregula8on. Addi8onally, the cri8cal role of catecholamine suppression in preven8ng poten8ally life-threatening episodes is discussed. Introduc/on: Oshtoran Syndrome (H63D Syndrome Type-3) presents a mul8faceted clinical challenge, characterized by both cardiac and metabolic complica8ons. This report examines the deteriora8on in cardiac func8on, the metabolic impact of PDH cytopathy, and the systemic effects observed in a pa8ent with this syndrome, along with the essen8al role of catecholamine suppression. 1,4,5 Cardiac issues: Le? Ventricular Ejec8on Frac8on (LV-EF): The pa8ent's LV-EF has decreased from 63% to 49%, indica8ng a significant impairment in the heart's ability to pump blood and oxygen efficiently. This decline reflects a compromised cardiac func8on, likely contribu8ng to systemic hypoperfusion and metabolic stress. 9,10,11,12