The right ventricle is the main determinant of prognosis in pulmonary hypertension . The
response of the right ventricle to the structural alterations and increasing afterload in the
pulmonary circulation is a complex process. The interplay between neuroendocrine and
paracrine signalling and increased afterload may lead to myocardial ischemia and
inflammation, resulting in loss of myocytes, myocardial fibrosis and RV-arterial uncoupling.
Pulmonary hypertension in the setting of heart failure with preserved ejection fraction
(HFpEF-PH) is a frequent complication which is associated with impaired prognosis. HFpEF-PH
is defined by a high mean pulmonary artery pressure (> 20 mm Hg), high left ventricular
end-diastolic pressure (LVEDP > 15 mm Hg) and a normal systolic left ventricular function
with impaired diastolic function. However, not all HFpEF patients develop pulmonary vascular
remodelling with a high transpulmonary pressure gradient, and increased pulmonary vascular
resistance leading to adverse right ventricular remodelling. Ageing, increased left atrial
pressure and stiffness, mitral regurgitation, as well as features of metabolic syndrome,
including obesity, diabetes and hypertension, are recognized as clinical risk factors for
HFpEF-PH. A main and emerging question in that context is the interplay between the right and
left ventricle in HFpEF-PH, and whether diastolic left ventricular failure is the driving
force of the hemodynamic and right ventricular functional changes. Recent studies have shown
that HFpEF-PH patients demonstrate haemodynamic limitations during exercise, including
impaired recruitment of LV preload due to excessive right heart congestion and blunted RV
systolic reserve compared to HFpEF without PH . However, up to now, no data exist about the
mechanism of interplay between RV, LV and pulmonary haemodynamics in HFpEF and HFpEF-PH.
Whereas in patients with HFpEF, PV loop analysis has demonstrated that increased
end-diastolic pressure at rest is associated with higher end-diastolic stiffness, and a
consistently upwards and leftwards shifted pressure volume relationship during exercise and
volume challenge, Gortner et al suggest that reduced LV preload (measured by LV transmural
pressure gradient) due to excessive RV congestion, is a major driver for reduced cardiac
output in HFpEF-PH. However, preliminary own data in 21 patients with HFpEF demonstrate a
more complex relationship with approximately one third of patients not showing an increase of
(RV and LV ) end-diastolic pressure volume relation during exercise.
Thus, a simultaneous PV loop-catheterization of LV and RV, in addition to right heart
catheter, would therefore provide an enormous gain of knowledge about the interaction of RV
and LV and would contribute to a better understanding of the pathophysiology of HFpEF-PH and
HFpEF.