Pulmonary hypertension secondary to left-sided valvular disease (VHD-PH) is associated with high morbidity and mortality. Angiotensin-receptor neprilysin inhibitor (ARNI) is a novel pharmacotherapy, which reduces afterload with natriuresis and peripheral vasodilation. Whether ARNI can also reduce pulmonary vasculature resistance is unknown. We present two cases of VHD-PH that improved after treatment with ARNI.
Case 1: Ms. M is a 63-year-old woman with past medical history of rheumatic mitral valve (MV) stenosis (mean gradient = 12 mm Hg at a heart rate = 69 beats/minute) who presented with New York Heart Association (NYHA) Class IIIB symptoms. The initial workup showed normal left ventricular function (LV) but severe combined pre- and post-capillary PH (Cpc-PH). She was deemed to be a high-risk surgical candidate given the severity of PH. Subsequently, she was treated with ARNI for three months, and repeat right heart catheterization showed significant improvement in Cpc-PH (see Table). Case 2: Mr. S is a 59-year-old man with past medical history of MV endocarditis s/p remote bovine MV replacement in 1984 complicated by paravalvular leak and redo replacements who presented with worsening shortness of breath. The workup demonstrated a well-functioning MV prosthesis and normal LV function, but elevated filling pressures. After two months of diuresis, Mr. S continued to have NYHA Class IIIB symptoms with persistent Cpc-PH. He was subsequently started on ARNI, and two months later had complete resolution of his symptoms. Repeat evaluation showed normalization of pulmonary vascular resistance (PVR, see Table).
This report is the first to describe treatment of VHD-PH with ARNI along with invasive hemodynamic data showing successful reduction in PVR. In these two cases, treatment with ARNI led to reduction in not only mean pulmonary arterial pressures but also PVR. Future prospective trials are needed to evaluate role of ARNIs in treatment of VHD-PH.
|Right heart catheterization (RHC) results before and after ARNI initiation and up-titration|
|Case 1||RHC initial conditions||RHC after ARNI|
|Mean mitral valve gradient||12 mm Hg||4 mm Hg|
|Right atrial pressure||7 mm Hg||5 mm Hg|
|Pulmonary arterial pressure||117/33 (66) mm Hg||65/32 (46) mm Hg|
|Pulmonary capillary wedge pressure||25 mm Hgg||21 mm Hg|
|Transpulmonary gradient||41 mm Hg||25 mm Hg|
|Diastolic pulmonary gradient||8 mm Hg||11 mm Hg|
|Pulmonary vascular resistance||11.4 woods units||6.1 woods units|
|Cardiac output, cardiac index||3.6 L/min, 1.8 L/min/m2||4.1 L/min, 2.0 L/min/m2|
|Case 2||RHC initial conditions||RHC after diuresis||RHC after ARNI|
|Right atrial pressure||19 mm Hg||9 mm Hg||10 mm Hg|
|Pulmonary arterial pressure||112/44 (67) mm Hg||77/31 (46) mm Hg||49/21 (24) mm Hg|
|Pulmonary capillary wedge pressure||30 mm Hg||20 mm Hg||17 mm Hg|
|Transpulmonary gradient||37 mm Hg||26 mm Hg||7 mm Hg|
|Diastolic pulmonary gradient||14 mm Hg||11 mm Hg||4 mm Hg|
|Pulmonary vascular resistance||6.7 woods units||4.3 woods units||1.1 woods units|
|Cardiac output, cardiac index||6.2 L/min, 2.8 L/min/m2||6.1 L/min, 2.8 L/min/m2||6.5 L/min, 3.0 L/min/m2|
© 2022 Published by Elsevier Inc.