Noninvasive pulmonary artery wave intensity analysis in pulmonary hypertension

Abstract

Pulmonary wave reflections are a potential hemodynamic biomarker for pulmonary hypertension (PH) and can be analyzed using wave intensity analysis (WIA). In this study we used pulmonary vessel area and flow obtained using cardiac magnetic resonance (CMR) to implement WIA noninvasively. We hypothesized that this method could detect differences in reflections in PH patients compared with healthy controls and could also differentiate certain PH subtypes. Twenty patients with PH (35% CTEPH and 75% female) and 10 healthy controls (60% female) were recruited. Right and left pulmonary artery (LPA and RPA) flow and area curves were acquired using self-gated golden-angle, spiral, phase-contrast CMR with a 10.5-ms temporal resolution. These data were used to perform WIA on patients and controls. The presence of a proximal clot in CTEPH patients was determined from contemporaneous computed tomography/angiographic data. A backwards-traveling compression wave (BCW) was present in both LPA and RPA of all PH patients but was absent in all controls (P = 6e(-8)). The area under the BCW was associated with a sensitivity of 100% [95% confidence interval (CI) 63-100%] and specificity of 91% (95% CI 75-98%) for the presence of a clot in the proximal PAs of patients with CTEPH. In conclusion, WIA metrics were significantly different between patients and controls; in particular, the presence of an early BCW was specifically associated with PH. The magnitude of the area under the BCW showed discriminatory capacity for the presence of proximal PA clot in patients with CTEPH. We believe that these results demonstrate that WIA could be used in the noninvasive assessment of PH.

Keywords: cardiac magnetic resonance imaging; hemodynamics; pulmonary hypertension; wave intensity.

Fig. 1.

Wave intensity analysis (WIA) in representative pulmonary hypertension (PH) patient (A–D) and control (E–H). Three types of waveforms were found to arise during early and mid systole in study participants using wave separation analysis: 1) a forward compression wave: characterized by increasing area and increasing flow representing cardiac ejection (* in C and G); 2) a backwards compression wave: increasing area [pressure] and decreasing flow († in C); and 3) backwards expansion wave: decreasing area [pressure] and/or increasing flow (‡ in G). The identification of the backwards compression and expansion waves can be seen from examination of D and H, showing the dA ± plots. The dotted line across A–D shows the timing of peak flow used to measure acceleration time (AT), demonstrating it arises as a consequence of the arrival of the backwards compression wave overcoming the forward compression wave (arrow). Time = 0 corresponds to the onset of data acquisition as triggered by the R wave on cardiac magnetic resonance (CMR) vectorcardiography.

Fig. 2.

Scatter diagrams of WIA metrics in patients and controls. A: mean acceleration time (AT_mean). B: mean forward compression wave (FCW_mean) area. C: mean backward compression wave (BCW_mean) area. D: mean backward expansion wave (BEW_mean) area.

Fig. 3.

Receiver operating characteristics analysis for the detection of proximal pulmonary artery (PA) clot: sensitivity (y-axis) and 1-specificity (x-axis). BCW area (black solid line) area under the curve (AUC): 0.97; AT (gray dashed line) AUC: 0.84. Interrupted black line: line of identity.

Fig. 4.

Right PA WIA in 2 patients with chronic thromboembolic pulmonary hypertension (CTEPH). Patient with proximal clot in right lower lobe artery (A) and patient with disease limited to distal vessels. Note larger BCW in patient A (B). PVR, pulmonary vascular resistance; WU, wood units.

Fig. A1.

Bland-Altman of bias (black solid line) and 95% limits of agreement (gray broken lines). Data are presented as difference between flow-area (QA) method and minimization of net wave energy method (y-axis) vs. the average of both (x-axis).