Our study demonstrated a modest reduction in heart rate by approximately 10 beats per minute, accompanied by a slower decrease in noradrenaline requirements com-pared to the control group in the overall population.

This observation suggests that a subset of patients in the intervention group may have experienced a relative reduction in cardiac output, which was not fully compensated by an increase in stroke volume.

We agree that this observation could be attributable to the presence of diastolic dysfunction, or impaired lusitropy, in some patients.

Diastolic dysfunction could limit the heart’s ability to efficiently handle increased filling volumes during a prolonged diastolic phase.

In HFpEF and other conditions with com-promised lusitropic function, the ventricles do not relax adequately.

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