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Low-dose aspirin improves in vivo hemodynamics in conscious, chronically infarcted rats
R G Schoemaker1, P R Saxena, E A Kalkman
1Department of Pharmacology, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands.
Insights
Low-dose aspirin therapy in rats with myocardial infarction normalized heart rate and improved stroke volume, suggesting beneficial cardiac remodeling effects beyond its antiplatelet action.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Myocardial Infarction Studies
Background:
- Low-dose aspirin (antiplatelet) inhibits collagen deposition in non-infarcted myocardium post-myocardial infarction in rats.
- The in vivo hemodynamic effects of daily low-dose aspirin in conscious, instrumented, infarcted rats were investigated.
Purpose of the Study:
- To investigate the in vivo hemodynamic consequences of daily low-dose aspirin administration in rats following myocardial infarction.
- To assess the impact of aspirin on cardiac function and remodeling markers.
Main Methods:
- Rats received 25 mg/kg aspirin daily from pre-infarction to 3 weeks post-coronary artery ligation.
- Chronic instrumentation recorded cardiac output and blood pressure in conscious rats.
- Isolated hearts assessed left ventricular stiffness, maximal perfusion, and beta-adrenergic responsiveness; plasma catecholamines were measured.
Main Results:
- Aspirin normalized elevated heart rate post-infarction while maintaining cardiac output.
- Stroke volume increased non-significantly with unchanged cardiac loading.
- Reduced intrinsic heart rate, not sympathetic activation, explained lower heart rate; circulating catecholamines and beta-adrenergic responsiveness remained unaffected.
- Improved stroke volume was not attributed to decreased ventricular stiffness or increased maximal perfusion.
Conclusions:
- Low-dose aspirin demonstrates favorable hemodynamic effects in myocardial infarction, including a lower heart rate for preserved cardiac output, potentially linked to cardiac remodeling.
- These findings suggest a clinically relevant beneficial effect of aspirin beyond its antithrombotic properties.
- Further investigation is warranted to elucidate the underlying mechanisms of these observed hemodynamic benefits.
Objective:
The equivalent of the clinically used low (= antiplatelet)-dose aspirin, inhibited collagen deposition in the non-infarcted myocardium in rats with myocardial infarction. In the present study, the in vivo hemodynamic consequences of this daily low-dose aspirin were investigated in conscious, chronically instrumented, infarcted rats.
Methods:
Rats, treated with 25 mg/kg aspirin daily from 2 days before to 3 weeks after coronary artery ligation, were chronically instrumented with an electromagnetic flow-probe and arterial and venous catheters, to record cardiac output, and arterial and venous blood pressure, respectively, in the conscious freely moving animal. In parallel, isolated hearts were studied with regard to left ventricular stiffness (pressure/volume relationships), maximal cardiac perfusion (adenosine), and in vitro heart rate and beta-adrenergic responsiveness. Plasma catecholamine levels were measured.
Results:
Aspirin normalized the increased heart rate after infarction, at a preserved cardiac output. This was accompanied by a (non-significant) increase in stroke volume, at unchanged cardiac loading conditions. The lower heart rate after aspirin was due to reduced intrinsic heart rate rather than to lower sympathetic activation of the heart, since similar effects were observed in isolated perfused hearts, while circulating levels of catecholamines and beta-adrenergic responsiveness were not influenced. The improved stroke volume was not explained by reduced left ventricular stiffness or increased maximal perfusion after aspirin.
Conclusion:
In addition to the antithrombotic action, effects of low-dose aspirin on cardiac remodeling could be associated with favorable hemodynamic effects, as reflected by a lower heart rate for the same cardiac output. Although the underlying mechanisms are still unknown, it suggests a clinically relevant beneficial effect which deserves further investigation.