Key result
Experimental MI reduces LVEF by ~31%, closely correlating with increased arterial elastance.
Why the study?
The mechanisms determining cardiac pumping function during recovery after myocardial infarction, particularly the role of arterial wall elasticity, are not fully understood.
Does arterial elasticity determine the degree of left ventricular pumping dysfunction in a rat model of chronic heart failure following myocardial infarction?
Does arterial elasticity determine the degree of left ventricular pumping dysfunction in a rat model of chronic heart failure following myocardial infarction?
Effect estimate: 31% reduction
Absolute Event Rate: 49% vs 71%
p-value: p=<0.01
In a preclinical model of myocardial infarction, cardiac pumping function is significantly determined by aortic wall elasticity independent of myocardial contractile function, suggesting that limiting reactive fibrosis is an important therapeutic target.
Supports arterial elastance as determinant of LV dysfunction in rat MI; hypothesis-generating and leaves open clinical translation.
Aim To study the left ventricular (LV) contractile and pumping function during the recovery phase following ligation of the anterior descending coronary artery (CA).Material and methods Cardiodynamic parameters were studied in Wistar rats 2-4 weeks after experimental myocardial infarction (MI). MI was induced by ligation of the anterior descending CA under zoletil anesthesia. LV catheterization was performed with a standard FTH-1912B-8018 PV catheter inserted into the LV through the right carotid artery.Results After the induction of MI, the mortality rate of animals was 50%. Survived animals developed significant LV dilatation and a decrease in ejection fraction (EF) by an average of 31%. However, major indexes of the pumping function, including minute volume, heart work, and maximum ejection velocity, were within a normal range whereas the maximum filling velocity was almost doubled. Approximately 50% of hearts with dilated LV had normal EF, delayed relaxation, and increased LV diastolic pressure, which qualified this group as a diastolic dysfunction group. The systolic dysfunction group with EF less than 50% of normal had similar values of myocardial contractility and relaxation but differed from the diastolic dysfunction group in more than 50% reduced maximum LV ejection velocity and 1.7 times increased elasticity of the arterial wall. A close inverse correlation was found between these values (r= -0.91).Conclusion The study results showed that, with a similar myocardial contractile function, the cardiac pumping function is determined by the elasticity of the aortic wall. Therefore, restriction of reactive fibrosis during MI is an important task of modern cardiology.
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Lakomkin et al. (2023) studied Myocardial Infarction (n=38). Coronary artery ligation (Experimental myocardial infarction) vs. Intact control was evaluated on Left ventricular ejection fraction (31% reduction, p=<0.01). Experimental myocardial infarction reduced left ventricular ejection fraction by an average of 31% compared to control, and revealed that severe pump dysfunction strongly inversely correlates with increased arterial wall elastance (r = -0.91).
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