Treating exercise oscillatory ventilation in heart failure: the detail that may matter

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Over the last 15 yrs, cardiologists have had to face a progressive recognition that abnormalities in the ventilatory response to exercise are relevant features of the heart failure syndrome [1]. Prior pathophysiology studies have defined the mechanistic role of the lung (impaired perfusion and increased minute ventilation ( V ′E)) [2] and of the periphery (increased chemo/metaboreflex sensitivity) [3] as determinants of the inefficient ventilatory response and early exercise termination. A wealth of literature has indeed brought evidence that, whatever the predominant substrate, the increase in V ′E relative to carbon dioxide production ( V ′CO2), primarily measured as the slope of this relationship, is a powerful indicator of disease severity [1, 4] that extends beyond peak oxygen uptake ( V ′O2), since its prognostic power is retained even when peak V ′O2 is near the normal range [5]. The consistency of these observations has substantially contributed to broadening the use of exercise gas exchange analysis for the clinical assessment and estimation of prognosis for the wide spectrum of heart failure populations [6]. As ventilation inefficiency has become an established matter of interest for heart failure specialists, further details have emerged as part of the picture, the most remarkable being exertional oscillatory ventilation (EOV) [7–12], a phenomenon originally described as anecdotal [13–15], and now considered a marker of disease severity even stronger than …