Transcatheter pulmonary denervation in patients with left heart failure with reduced ejection fraction and combined precapillary and postcapillary pulmonary hypertension: A prospective single center experience

Abstract

Objectives: The present study was a prospective, single-center, single-arm study to investigate the efficacy of transcatheter pulmonary artery denervation (TPADN) in patients with combined postcapillary and precapillary PH (Cpc-PH) associated with left heart failure with reduced ejection fraction (HF-rEF).Background: Pulmonary hypertension (PH) in patients with left ventricular systolic dysfunction has a negative impact on outcome. Methods:The combination of pulmonary artery systolic pressure (PAPs) ≥60 mmHg, transpulmonary pressure gradient (TPG) ≥12 mmHg, nonreversible mean PAP, and pulmonary vascular resistance (PVR) ≥3.5 Wood Units was considered as too high risk for heart transplantation (HTx). The clinical efficacy endpoint was an improvement in 6-min walking test and the hemodynamic endpoints were changes in PAPs, PVR, and TPG between baseline and 6 months. Circumferential radiofrequency applications were delivered around distal main, left and right pulmonary arteries. At each ablation point temperature was 45 C and energy 10 W.

Clinical features do not identify risk of progression from isolated postcapillary pulmonary hypertension to combined pre‐ and postcapillary pulmonary hypertension

“…Cardiac index (CI) was unchanged between baseline and repeat RHC (2.24 [1.90, 2.67] vs. 2.46 [1.98, 2.91] L/min/m 2 , p = 0.1) in those who progressed to Cpc-PH. Conversely, mPAP (33 [29,37] vs. 40 [33,44] mmHg, p < 0.001), PVR (1.99 [1.63, 2.41] vs. 3.88 [3.49, 4.72] WU, p < 0.001), RA pressure (9 [6,15] vs. 14 [10,19] mmHg, p < 0.01), and the diastolic pressure gradient (DPG, −1 [−3, 2] vs. 4 [1,7] mmHg, p < 0.001) increased in this group. These changes resulted in a 26% increase in mPAP and 11% decrease in CI.…”

“…[3][4][5][6] Distinguishing Cpc-PH from Ipc-PH is important because the former group has worse outcomes 7 and therapies targeted at Cpc-PH are only in the preliminary stages. [8][9][10][11][12][13] Cross-sectional studies have reported the hemodynamic, 5,14 pathologic, 15,16 genetic, 4,17 and cellular changes [18][19][20] behind the pathophysiology of PH-LHD and Cpc-PH, but it remains unclear why some patients transition from Ipc-PH to Cpc-PH, while others remain with Ipc-PH. Although no prior studies describe a conversion from Ipc-PH to Cpc-PH and the development of Cpc-PH at onset of PH-LHD could be possible, the currently accepted pathophysiology of Cpc-PH begins with long-standing elevation in left-sided pressures, which suggests that development of Ipc-PH should precede Cpc-PH.…”

“…Approximately 12%–40% of patients with PH‐LHD develop Cpc‐PH, which is characterized by pulmonary vascular remodeling as evident by elevated pulmonary vascular resistance (PVR) 3–6 . Distinguishing Cpc‐PH from Ipc‐PH is important because the former group has worse outcomes 7 and therapies targeted at Cpc‐PH are only in the preliminary stages 8–13 . Cross‐sectional studies have reported the hemodynamic, 5,14 pathologic, 15,16 genetic, 4,17 and cellular changes 18–20 behind the pathophysiology of PH‐LHD and Cpc‐PH, but it remains unclear why some patients transition from Ipc‐PH to Cpc‐PH, while others remain with Ipc‐PH.…”

Update in approaches to pulmonary hypertension because of left heart disease

“…Small feasibility trials have demonstrated benefit in the PAH and chronic thromboembolic pulmonary hypertension populations [31,32]. A single center series of PADN in 10 patients with HFrEF and CpcPH found a significant reduction in PVR in five patients, from mean 7.2 to 3.7 Woods units at 6 months of follow-up [33]. There was no significant change in the PCWP, and intriguingly right atrial pressure improved as well suggesting improvement in right heart function.…”