Reversible HFrEF-The Pattern Five Specialties Missed, Lantern of Sulfur, Concept A, v12.1, February 2026

This preprint defines Terrain-Induced Functional Cardiomyopathy (TIFC), a reversible HFrEF phenotype arising not from structural myocardial damage, but from coordinated physiologic collapse along the Vertical Terrain Axis, including bile stasis, RAAS dysregulation, hyperchloremia-associated non–anion gap metabolic acidosis, mitochondrial energetic suppression, and autonomic sequencing disruption. Across cardiology, nephrology, endocrinology, gastroenterology, and neurology, the individual manifestations appear unrelated. This fragmentation obscures an underlying vertical descent pattern in which neuroendocrine mis-signaling, electrolyte imbalance, acid–base disruption, and metabolic instability unfold in a sequential and interdependent manner, ultimately expressed as suppressed cardiac ejection fraction despite structurally intact myocardium. Unlike structural cardiomyopathy, TIFC demonstrates functional suppression without irreversible tissue damage and shows rapid improvement when upstream physiologic coordination is restored, including normalization of bile flow, electrolyte balance, acid–base buffering, and metabolic stability.Mechanistic interpretation of this phenotype has been further explored in a linked series of standalone hypothesis-generating preprints examining bile-mediated modulation of RAAS and chloride homeostasis, regulatory axis orientation, execution-state divergence, and electrolyte timing dynamics.These observations support reframing a subset of HFrEF presentations as reversible systems-level dysfunction rather than fixed structural disease, providing a basis for physiologic differentiation and recovery-oriented management.VERSION HISTORYVersion 12.1 update (February 2026):Mechanistic continuity references added. No changes were made to the core framework orconclusions.