Very relevant question, eager to acquire the answers of others. Great regards

One our experience we sometimes find decreased ejection fraction during bicycle stress Echocardiography. One of the reason why there is false positive results in supine bicycle stress Echocardiography is decreasing ejection fraction due increased blood pressure induced by the exercise. The cardiac out put is inversely proportional to vascular resistance.

Thank you for your answer: my further Q, if you allow me, have you stratified LV end diastolic volumes; SV and HR of healthy versus diseased individuals' while performing supine bicycle test?

This might help me to relate my data with positive inotropic challenges in swine.

I was able to increase the end-systolic elastance, but unfortunately my end arterial elastance has also increased due to increase of driving LVP, as at this moment I have observed decoupling of heart to aorta with decrease of pulse wave velocity and increase of afterload pressure. Positive inotrope also increased HR but decreased SV with only miniscule decrement of EDV, hence I ended up similar to Dr. Morimont with increased LV inotropy but decreased EF.

Thank you kindly,

Filip

The whole data set during stress Echocardiography can include the volumes of the left ventricular so that. Ejection fraction is derived from end diastolic and the end Systolic volumes. In normal person with excercise end Systolic volume decreases and hence we get increase ejection fraction. But in some normal person who gets hypertensive responses show no changes or increased end Systolic volumes and eventually decrease ejection fraction during excercise. This happens because of increase peripheral vascular resistance ehich causes decrease cardizc out put despite increase cardiac contraction.

Thank you

I have found additional answers I was looking for in the Letter to the editor

PMID: 30312209

There are total of 3 major guiding formulae/equations:

First discusses that at a fixed EDV (limited preload reserve), an increase in ESP/Ees ratio (increase in afterload relative to contractility) must lead to reduction in LVEF.

EF = 1− (ESP / Ees)(1/ EDV) −V0 / EDV

Another corroborates that mathematically at higher Ea/Ees ratio (ventriculoarterial mismatch) or decouplings would result in a lower LVEF.

EF= [Ees/ ( Ees+ Ea)]

And another makes an extra provision that during remodeling the V0 increases, which results in greater reduction in LVEF, which I have to still research and make some translation from math to physiology and model it using my data.

EF= [Ees/(Ees+Ea)] * (1-V0/EDV)

thank you again for answering

A typical example of an increase in contractility and a decrease in EF is asymmetrical septum hypertrophy in hypertrophic cardiomyopathy (HCM). During exercise the adrenergic stimulation causes an increase in subaortic constriction. The increase in afterload can be so high that the patient loses consciousness by the low cardiac output.