TAC-Induced Heart Failure Model | Pressure Overload Cardiac Hypertrophy

TAC-Induced Pressure Overload Heart Failure Model

Transverse aortic constriction (TAC) is a well-established model of left ventricular pressure overload used to study cardiac hypertrophy, fibrosis, remodeling, and progression toward heart failure.

By adjusting constriction severity and study duration, the TAC model can support evaluation of compensated hypertrophy, diastolic dysfunction, ventricular dilation, systolic impairment, and treatment effects on cardiac remodeling.

IPS Therapeutique uses TAC models to evaluate cardioprotective, anti-remodeling, anti-fibrotic, and heart failure-directed therapies using integrated functional, hemodynamic, biochemical, and histological endpoints.

TAC Model Methodology

Available species

Mouse
Rat

Disease induction

Partial ligation of the aortic arch
Constriction between the 1st and 2nd or 2nd and 3rd aortic branch, depending on study design
Progressive left ventricular pressure overload
Cardiac hypertrophy, fibrosis, and remodeling

Typical study design

In-life phase: approximately 6–8 weeks
Total study duration: approximately 11 weeks
Preventive or therapeutic dosing designs
Adjustable disease severity based on constriction site and study timeline
Serial echocardiography, when required
Terminal hemodynamics, tissue collection, and histology

Model design considerations

Suitable for pressure-overload cardiac remodeling studies
Can model compensated or decompensated cardiac dysfunction
Timing is critical for distinguishing hypertrophy, fibrosis, dilation, and heart failure progression
Best interpreted using integrated echo, hemodynamic, morphometric, and histological endpoints

TAC Readouts & Application

Hemodynamic readouts

Systemic arterial pressure
Left ventricular systolic pressure
Left ventricular end-diastolic pressure
Mean arterial pressure
Pressure-volume loop analysis
Contractility and relaxation parameters

Echocardiographic readouts

Left ventricular dimensions
Ejection fraction and fractional shortening
Stroke volume and cardiac output
Wall thickness
LV mass and hypertrophy indices
Diastolic function parameters, when applicable

Histological and morphometric readouts

Heart weight and organ weight ratios
Fulton index / RVFWT, when applicable
Cardiomyocyte hypertrophy
Cardiac fibrosis
Ventricular dilation
Morphometric analysis
H&E and fibrosis staining

Drug development applications

Pressure-overload heart failure studies
Cardiac hypertrophy evaluation
Anti-fibrotic therapy testing
Anti-remodeling therapy assessment
Dose-response studies
Mechanism-of-action support
Candidate selection for heart failure programs