Reflections on wave reflections in chronic thromboembolic pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a surgically curable form of severe pulmonary hypertension. However, in 10% of the patients, the procedure may not be successful, because of persistent pulmonary hypertension after removal of proximally located thromboembolic material. This complication is of particularly poor prognosis. In the present issue of the European Heart Journal, Hardziyenka et al. report on its prediction by the analysis of Doppler pulmonary arterial waves. The authors defined a time to notching expressed as a notch ratio (NR), or the ratio of time from onset of flow to maximum flow deceleration to time from maximum flow deceleration to end of flow. This NR was found to be associated with in-hospital mortality and increased systolic pulmonary artery pressure at 3 months. The authors explain these results by the effects of proximal as opposed to distal wave reflection. Thus an increased NR would allow for the identification of peripheral small vessel disease that is not amenable to surgery. The report of Hardziyenka is remarkable, because it introduces a simple measurement that is easily integrated into routine echocardiography, for great clinical relevance and a lot of physiological sense. The pulmonary circulation is a low resistance and high compliance circuit with little wave reflection. Therefore, normal pulmonary arterial flow and pressure waves present with rounded contours and are superposable, in contrast to aortic pressure and flow waves where wave reflection determines a phase lag and early systolic peaking of flow with late systolic peaking of pressure. Patients with pulmonary hypertension present with a right ventricular pressure wave with a sharp initial upstroke, followed by a short plateau, and a late systolic peaking, a pulmonary wave with a huge pulse pressure, and a flow wave with a shortened time to peak velocity and a late or midsystolic deceleration. All these changes are largely determined by wave reflections. The effects of wave reflection on pulmonary artery pressure and flow waves can be shown experimentally by the comparison of the effects of proximal and distal obstruction, respectively by pulmonary arterial banding and injected of small glass beads, to produce the same increase in mean pulmonary artery pressure. As illustrated in Figure 1, proximal obstruction causes a midsystolic deceleration of flow even when mean pulmonary artery pressure is only moderately increased. This can be further analysed in the frequency domain to decompose waves into their forward and backward components. In the case of the example shown in Figure 1, midsystolic notching is clearly caused by the substraction of an early returned reflected wave on the forward wave. Wave reflection explains previously reported shorter time to notching on pulmonary arterial flow waves in embolic pulmonary hypertension when compared with pulmonary arterial hypertension (PAH), in spite of lower mean pulmonary artery pressures. This result would not be affected by the adjustment of time to notching to heart rate, which is inherent to the NR as calculated by Hardziyenka et al. While a proximal site of reflection on thromboembolic material is an obvious cause for an earlier return of a reflected wave, this can also be caused by an increased wave speed, or, as shown in the initial report of pulmonary artery flow patterns to evaluate pulmonary hypertension, by a longer preceding R–R interval in an arrhythmic patient. Pulmonary arterial wall distension with decreased compliance as a consequence of high pressures increases wave speed. This is why midsystolic deceleration of pulmonary flow is also seen in patients with severe PAH, in spite of a site of resistance and wave reflection that is at the periphery of the pulmonary arterial tree. These physiological notions were recently challenged by the report of a close correlation between systolic, mean, and diastolic pulmonary artery pressures in pulmonary hypertension of various severities. The implication of this observation is that any pulmonary artery pressure can be predicted from any other, with for example mean pulmonary artery pressure reliably estimated from 0.6 times systolic pulmonary artery pressure plus þ2 mmHg. While it is The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society Cardiology.