Letter to the Editor

The paper by Hieda and al. describes the beneficial effects of prolonged exercise training on cardiac structure and function in HFpEF.

These findings are encouraging and align with prior studies focusing on the effect of exercise in more advanced stages of CHF, in regard to maximal oxygen uptake (CO2 max) and hemodynamic changes which strengthens the belief that aerobic exercise and cardiac rehab in heart diseased patients may be beneficial^{1 2 3}.

However, we would like to draw attention to a few additional points regarding this paper.

First, we noticed the focus patients with stage B HFpEF, which is suggestive of a chronic stage of LV remodeling, and which would require inclusion of the left atrial (LA) volume index. LA size is an important diagnostic and prognostic marker in HFpEF.

Indeed, one of the hemodynamic consequences of chronically elevated LV filling pressure is the concurrent rise in LA pressure, causing adverse heart remodeling with enlargement and stiffness of the LA chamber and impairment of its function, aka “atrial cardiomyopathy”.

Secondly, we were surprised that Atrial Fibrillation (AF), which is known to be an important factor in HFpEF pathogenesis⁴, was not mentioned in the baseline characteristics of the study population.

Third, the factors contributing to LVH are highly heterogeneous and, even though the paper took care to exclude some known diseases contributing to LVH, no further mention regarding the potential mechanism of LVH in the studied population was provided.

Fourth, we noticed that the BMI was different between the control group (32 kg/m2) and the exercise group (29kg/m2) in the baseline population characteristics, which falls respectively into the range of obesity and overweight. Considering that higher BMI may predispose to a more advanced degree of HFpEF and a stiffer LV at baseline⁵, it is surprising that the study did not address the significance of the BMI baseline difference.

Furthermore, the one year exercise intervention did not contribute to a change in body composition of the exercise group, which, in addition to the difference in baseline characteristics, led us to suspect that the population chosen as the exercise group were already less sedentary than the control group prior to the experiment and thus question the premise and findings of this study.

Lastly, given the lack of long term follow up, it may be hasty to suggest that these punctual hemodynamics changes may reverse the LV remodeling and protect against the development of HFpEF.

In summary, we would suggest further evaluation of the hemodynamic changes, a long-term follow-up of the effects of these initial changes, and inclusion of LA volume index and AF which are essential markers in the course of HFpEF.