Treatment with PH-targeted vasodilators successfully resolved severe pregnancy-induced pulmonary hypertension in a 33-year-old patient with thromboangiitis obliterans.
Case Report (n=1)
Pregnancy may precipitate severe pulmonary hypertension and acute right heart failure in patients with thromboangiitis obliterans, which can be successfully managed with aggressive PH-targeted vasodilator therapy.
Abstract Introduction Thromboangiitis obliterans (Buerger’s disease) is a nonatherosclerotic inflammatory disease of small and medium size blood vessels in the extremities. This disease affects primarily young men and is associated with smoking. Pulmonary hypertension (PH) during pregnancy is associated with high morbidity and mortality. Here we present a case of pulmonary hypertension induced by pregnancy in a patient with thromboangiitis obliterans (TAO). Case presentation A 33-year-old female with TAO, deep vein thrombosis (DVT), pulmonary embolism (PE), tobacco use disorder, and opioid use disorder presented with extremity pain and opioid withdrawal symptoms while pregnant with twins. She was diagnosed with a partially occlusive lower extremity DVT and acute cholecystitis. Her hospital course was complicated by significant thrombocytopenia and was subsequently induced at 32 weeks and 5 days. On post-partum day 5, her clinical status worsened despite percutaneous cholecystostomy tube and antibiotics. She was started on norepinephrine and transferred to the ICU. Transthoracic echocardiogram showed a severely dilated right ventricle (RV), with ventricular septal flattening, moderately reduced RV systolic function, and severe pulmonary hypertension without evidence of intra-cardiac shunt. She was supported with inhaled nitric oxide and right heart catheterization was performed showing severe precapillary pulmonary hypertension (62/31 42 mmHg) and reduced cardiac output (5.04 L/min) yielding a diagnosis of WHO group 1 PH. She was started on furosemide, epoprostenol, ambrisentan, and sildenafil with improvement in her clinical status. As an outpatient, she was started on soteracept. Three months later, a repeat echocardiogram showed normal RV size and function and normal systolic pulmonary artery pressure. She was slowly weaned off epoprostenol infusion to eliminate the need for central venous access. Discussion Pregnancy induces profound cardiovascular changes—markedly increased blood volume, cardiac output, and hormonal shifts—that may precipitate or unmask PH in susceptible individuals. This case illustrates a unique presentation of acute right heart failure and PH in the setting of TAO, a nonatherosclerotic vasculitis with hallmark small- and medium-vessel involvement. We hypothesize that the stress of pregnancy was the inciting event for the development of PH. There has been one case reported previously in the literature of a patient with TAO and PH. Other literature notes that the hypercoagulable and pro-thrombotic state of pregnancy increases thrombotic risk and could worsen pulmonary vasculopathy in TAO. Ultimately, management of PH in this case required hemodynamic stabilization, and initiation of PH-targeted vasodilators. Ongoing contraception counseling and post-discharge follow-up are essential because future pregnancies carry substantial maternal risk. This abstract is funded by: None
Riddle et al. (Fri,) conducted a case report in Pregnancy-induced Pulmonary Hypertension and Thromboangiitis Obliterans (n=1). PH-targeted vasodilators (furosemide, epoprostenol, ambrisentan, sildenafil, soteracept) was evaluated. Treatment with PH-targeted vasodilators successfully resolved severe pregnancy-induced pulmonary hypertension in a 33-year-old patient with thromboangiitis obliterans.