Post-MI Heart Failure Rodent Model

Post-MI Heart Failure Model for Preclinical Efficacy Studies

Post-myocardial infarction heart failure is driven by ischemic injury, adverse ventricular remodeling, progressive loss of cardiac function, fibrosis, inflammation, and compensatory changes in surviving myocardium. At IPST, post-MI heart failure models are used to evaluate therapeutic candidates designed to preserve cardiac function, limit adverse remodeling, reduce fibrosis or inflammation, and improve long-term functional outcomes after myocardial infarction.

The model can be adapted to the sponsor’s therapeutic strategy, including early intervention after infarction, delayed treatment during the remodeling phase, or chronic efficacy assessment in established post-MI heart failure. Functional, biochemical, and histological endpoints can be integrated to provide a translational assessment of treatment effect.

Post-MI Heart Failure - Methodology

Species: mice, rats, rabbits, or pigs
Induction: permanent ligation of the left anterior descending coronary artery
Disease phase: acute ischemic injury followed by chronic ventricular remodeling
Typical follow-up: in-life monitoring can extend up to approximately 26 weeks depending on the study objective
Treatment design: prevention, early intervention, delayed intervention, or chronic treatment protocols can be implemented
Applications: efficacy testing, cardiac remodeling assessment, regenerative medicine studies, device-based approaches, and mechanism-of-action support

Permanent LAD ligation produces reproducible myocardial injury followed by progressive ventricular remodeling and functional impairment. The model is suitable for evaluating therapies intended to improve cardiac performance, reduce infarct expansion, limit fibrosis, modulate inflammation, or preserve viable myocardium during the post-infarction remodeling phase.

Post-MI Heart Failure - Readouts & Application

Echocardiography: left ventricular ejection fraction, fractional shortening, ventricular dimensions, wall motion, and remodeling
Infarct assessment: infarct size, infarct expansion, and viable myocardium
Invasive hemodynamics / PV loops: systolic and diastolic performance, pressure-volume relationships, contractility, relaxation, and cardiac output
Histology: H&E, Picrosirius Red, collagen area, scar remodeling, and tissue architecture
Cardiac remodeling: ventricular dilation, hypertrophy, fibrosis, and wall thinning
Inflammation and biomarkers: cytokine panels, tissue or plasma biomarkers, and mechanism-specific endpoints
Functional outcomes: survival, clinical observations, body weight, activity or exercise-related endpoints when appropriate

The post-MI heart failure model is widely used to evaluate pharmacological agents, biologics, cell therapies, regenerative approaches, and device-based interventions intended to preserve cardiac function or prevent further deterioration after myocardial infarction. The model is particularly valuable when treatment effects must be assessed across multiple levels, including cardiac function, ventricular remodeling, scar formation, inflammation, fibrosis, and tissue repair.

At IPST, the study design can be adapted to the sponsor’s therapeutic hypothesis, treatment window, species preference, and endpoint requirements.