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Published on: September 2, 2021
Development of a novel large animal model of ischemic heart failure using autologous platelet aggregates
Pawel Kwiatkowski1, Chittoor Sai-Sudhakar, Angela Philips
1Department of Surgery, The Ohio State University Medical Center, Columbus, OH, USA. Pawel.Kwiatkowski@osumc.edu
Insights
Researchers developed a new animal model for heart failure using platelet aggregates to mimic human myocardial infarction. This model shows promise for studying ischemic cardiomyopathy and improving research translation.
Area of Science:
- Cardiovascular Research
- Animal Models
- Ischemic Cardiomyopathy
Background:
- Existing animal models inadequately replicate the thrombus biomass seen in human myocardial infarction.
- A novel model of ischemic cardiomyopathy is proposed using autologous platelet aggregates.
Purpose of the Study:
- To develop and validate a new animal model for ischemic cardiomyopathy.
- To mimic the thrombus formation and cardiac insufficiency observed in human heart failure patients.
Main Methods:
- Autologous platelets were isolated, aggregated, and injected into the coronary circulation of sheep.
- Cardiac tissue injury was assessed via Troponin I levels; heart failure progression was monitored using echocardiography.
- Histopathology confirmed coronary artery obstruction using mepacrine-labeled platelets.
Main Results:
- All animals developed heart failure with elevated Troponin I levels.
- A significant decrease in ejection fraction was observed, confirming cardiac insufficiency.
- The model successfully replicated ischemic cardiac insufficiency.
Conclusions:
- Sequential injection of aggregated platelets induces progressive ischemic cardiac insufficiency in an animal model.
- This model closely mimics human ischemic heart failure, offering new research avenues.
- The model bridges the gap between basic science and clinical practice in heart failure research.
Background:
Current animal models of heart failure lack the biomass of thrombus that occurs in patients undergoing myocardial infarction. We propose a novel animal model of ischemic cardiomyopathy developed by sequential direct injections of autologous platelet aggregates into the coronary circulation resulting in development of ischemic cardiac insufficiency.
Methods:
Autologous platelets from adult sheep were isolated and aggregated. Aggregated platelets were then injected into the coronary circulation of anesthetized animals under fluoroscopic guidance. Troponin I levels were monitored for first three days after embolization to validate cardiac tissue injury. Progression of heart failure was corroborated by monitoring changes in echo-based assessment of ejection fraction and left ventricular end-systolic and end-diastolic dimensions. Thrombus-based obstruction of coronary artery was confirmed with histopathology review by mepacrine labeling of pre-aggregated platelets.
Results:
All experimental animals developed heart failure-like cardiac insufficiency confirmed by elevated levels of troponin I and associated with significant drop in the ejection fraction.
Conclusions:
Sequential injections of aggregated platelets into coronary circulation lead to progressive development of ischemic cardiac insufficiency. This phenomenon seems to mimic development of ischemic heart failure seen in human patients and opens multiple research opportunities to fill the existing gap between basic research and clinical practice.
