Accordingly, clinical trials in pulmonary arterial hypertension (PAH) have historically included patients with PAWP ≤15 mmHg (in agreement with the 2016 recommendations on heart failure from the European Society of Cardiology ) and PVR >3 WU. Therefore, taking into account 2 standard deviations, a value ≥14 mmHg should be considered abnormal. In normal individuals, PAWP is close to dPAP, with a mean± sd value of 8.0☒.9 mmHg for a normal DPG between 0 and 2 mmHg.
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What is a normal PAWP and how to measure it? The combination of recent analyses and basic physiology reveals that the haemodynamic definition of PH-LHD relies heavily on the accurate measurement of PAWP. These two distinct haemodynamic phenotypes may be further defined by several variables obtained during diagnostic right heart catheterisation (RHC), none being totally independent from potential limitations.
To date, the haemodynamic definition of PH-LHD stands as: 1) post-capillary PH when mPAP ≥25 mmHg and PAWP >15 mmHg 2) IpcPH, when DPG 3 WU. Pulmonary vascular resistance (PVR) was subsequently reintroduced to better reflect the impact of the right ventricle on outcome. However, this definition was found to be too restrictive and exposed to interpretation, leading to controversies about whether the DPG would or would not predict outcome in patients with group 2 PH. This article summarises these findings, key challenges and proposals for the approach to this condition, with a specific focus on PH due to HFpEF.Īt the 5th WSPH in 2013, a new terminology was adopted to distinguish isolated post-capillary PH (IpcPH) from combined post-capillary and pre-capillary PH (CpcPH), based on the diastolic pressure difference/gradient (DPG) between the diastolic PAP (dPAP) and PAWP. Over the past 5 years since the 5th World Symposium on Pulmonary Hypertension (WSPH) in 2013, significant advances have improved our understanding of PH-LHD. This is especially true in heart failure with preserved ejection fraction (HFpEF). In addition, the function of the right ventricle is often affected independently from the afterload increase, leading to uncoupling of the right ventricle/pulmonary artery unit with further exercise limitation and adverse outcome. In heart failure, recent data even suggest that the severity of PH correlates most strongly with venous and small arteriolar intimal thickening. However, the structure and function of the pulmonary circulation may be further affected by several mechanisms potentially leading to pulmonary arterial and venous remodelling. In most cases, PH-LHD (group 2 PH) is a consequence or an abnormal biomarker of the underlying cardiac disorder. It is currently defined as post-capillary PH, by an increase in mean pulmonary arterial pressure (mPAP) ≥25 mmHg and a pulmonary arterial wedge pressure (PAWP) >15 mmHg. Pulmonary hypertension (PH) is a common complication of left heart disease (LHD), in response to a passive increase in left-sided filling pressures, more specifically left atrial pressure.
Finally, recent clinical trials did not demonstrate a benefit in treating PH due to LHD with pulmonary arterial hypertension-approved therapies. Invasive confirmation of PH-LHD is based on the accurate measurement of pulmonary arterial wedge pressure and, in patients with high probability, provocative testing to clarify the diagnosis. This includes the identification of a specific “left heart” phenotype and a non-invasive probability of PH-LHD. Based on the latest evidence, we propose a new haemodynamic definition for PH due to LHD and a three-step pragmatic approach to differential diagnosis. PH in heart failure with preserved ejection fraction represents the most complex situation, as it may be misdiagnosed with group 1 PH. Significant advances have occurred over the past 5 years since the 5th World Symposium on Pulmonary Hypertension in 2013, leading to a better understanding of PH-LHD, challenges and gaps in evidence. Pulmonary hypertension (PH) is frequent in left heart disease (LHD), as a consequence of the underlying condition.
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