# Aortic Stenosis as a Mechanical Stressor and Tissue Energetics: Consistent Clue with Hypertensive Stress Septal Sign

## TL;DR

The paper explores how aortic stenosis causes specific heart muscle changes and metabolic patterns, offering a new way to assess cardiac stress.

## Contribution

Introduces the 'Triple S' imaging paradigm to unify the assessment of cardiac stress across different causes.

## Key findings

- Chronic aortic stenosis leads to basal septal hypertrophy and hypermetabolic activity.
- Apical regions show reduced metabolic activity and hypokinesis in severe aortic stenosis.
- Triple S identifies adaptive remodeling linked to advanced stages requiring intervention.

## Abstract

Background: Hemodynamic overload induces left ventricular remodeling and heart failure across various clinical presentations. While geometric remodeling is classically associated with increased vascular resistance in hypertension, distinct patterns emerge under the mechanical stress of aortic stenosis (AS). Concept: The “Stress Septal Sign” (Triple S) represents a marker of stress-mediated hemodynamic overload driven by diverse stimuli, ranging from mechanical stress in AS to emotional triggers in acute stress cardiomyopathy. Within this spectrum, Stressed Heart Morphology describes a specific phenotype characterized by a predominant and hyperdynamic LV septal base. Results: Chronic hemodynamic stress in severe AS results in prominent basal septal hypertrophy. This remodeling is characterized by distinct tissue energetics: hypermetabolic activity at the basal septum contrasted with reduced metabolic activity or hypokinesis in the apical regions. These findings on myocardial geometry, function, and energetics align with the adaptive phase of LV remodeling. Conclusions: The presence of adaptive myocardial basal tissue suggests an advanced remodeling stage that may require timely therapeutic intervention in severe AS. Therefore, identifying these specific tissue characteristics offers a unifying imaging paradigm (Triple S) for assessing cardiac stress, independent of the primary etiology.