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This letter suggests that future trials of pulmonary vasodilators in left-sided heart disease should focus on patients with truly impaired right ventricular-pulmonary circulation coupling rather than just elevated pulmonary pressures.
I read with great interest the manuscript titled ‘Sildenafil for improving outcomes in patients with corrected valvular heart disease and persistent pulmonary hypertension (SIOVAC)’ by Drs Bermejo et al. 1 which provided important data on the role of pulmonary vasodilators in patients with pulmonary hypertension (PH) and left-sided heart disease. The authors concluded that phosphodiesterase 5 inhibitors (PDE5i) can be harmful in such patients, something the accompanying editorial emphasized.2 Pulmonary vasodilators improve outcomes by recoupling the dysfunctional right ventricle (RV) with an unfavourable pulmonary circulation (PC).3 In this study, the RV-PC units were clearly coupled as evidenced by normal RV size and function (RV ejection fraction, normal cardiac index, and right atrial to pulmonary capillary wedge pressure ratio of 0.5) as well as borderline elevated pulmonary vascular resistance (PVR) of 3.4 WU, and a normal diastolic pressure gradient (DPG) of 2.0 mmHg. Yes, by definition this group represented ‘combined’ pre- and post-capillary physiology, but PC involvement was only modest. More importantly, the RV has perfectly adapted to these mild derangements. Drs Galiè’ et al. 2 eloquently stated that the main abnormality here was elevated left-sided filling pressures, and it is true that this should be the main target of therapy, whenever possible. The caveat here is the ‘whenever possible’. It is interesting that even with supposedly normally functioning prosthesis, left atrial pressure remained so elevated (sometimes to over 40 mmHg). This, in itself, is a topic worthy of further investigation since it is frequently encountered in clinical practice. However, in my humble opinion, a different way of selecting patients for SIOVAC may have provided a much-needed answer for those of us who have similar patients in whom we struggle to further reduce left-sided filling pressures, but who in fact have truly impaired RV-PC coupling. Such a trial would have likely had implications for a wide variety of cardiac patients including advanced heart failure ones. Shifting attention from pulmonary arterial pressure to RV function (the elephant in the room) as the main predictor of response to pulmonary vasodilators (just as it is the main predictor of outcomes in precapillary PH) may allow us to design similarly strong studies that may in fact change clinical guidelines and help us manage these complex patients. Conflict of interest: none declared.
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Hayan Al Maluli (2018) studied this question.
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