At the time of her acute pulmonary embolism, the echocardiogram revealed LVEF 50%, RV hypokinesis, RV pressure overload with PASP 40–45 mmHg. She did not require thrombolytic therapy. Troponins were negative. Lower extremity duplex dopplers were negative for acute deep vein thrombosis. She was placed on anticoagulation with enoxaparin and bridged to rivaroxaban. The PE was thought to be provoked from a long car trip. She complained of shortness of breath carrying her children and groceries. She had difficulty climbing stairs, though denied chest pain, lower extremity edema and presyncope.

During her initial clinic evaluation, vital signs showed BP 115/82, heart rate 103, respiratory rate of 24, oxygen saturation 96% on room air. Physical examination was unremarkable. Laboratories were notable for BNP 5 pg/mL, complete blood count and comprehensive metabolic panel were within normal limits. Imaging was significant for a V/Q scan (Fig. 8.2) with perfusion defects in left lower lobe, lingula and right upper lobe.

Her echocardiogram showed normal LV and RV size and systolic function, TAPSE 1.8 cm. PASP 35 mmHg, saline contrast study mildly positive for right to left shunt most consistent with a patent foramen ovale (PFO). Six minute walk test revealed a distance of 1050 ft and no desaturations with concluding Borg Score of 2. Pulmonary function testing was significant for reduced DLCO 44% predicted. Given that the acute pulmonary embolism was only 2 months prior and the echocardiogram did not show features of pulmonary hypertension or right heart enlargement, the perfusion defects seen on V/Q scan were felt to be due to her acute PE. Therefore, the decision was made to continue anticoagulation and repeat imaging 6 months after her acute pulmonary embolism.

At the follow up appointment, 6 months after acute PE, the patient continued to complain of dyspnea on exertion and impaired exercise tolerance. No signs of right heart failure. Repeat VQ scan (Fig. 8.3) demonstrated multiple perfusion defects, unchanged from prior scintigraphy.

CT angiogram of the chest (Fig. 8.4) showed resolution of larger more central filling defects within the pulmonary arteries, now with residual linear appearing peripheral filling defects consistent with pulmonary artery webs at the segmental level, particularly in the right lower lobe and left lower lobe pulmonary arteries, mosaic attenuation and mild enlargement of the right ventricle. Repeat echocardiogram showed upper normal RV size and mild RV hypokinesis (RV global longitudinal strain −13.7%), PASP 25 mmHg, normal IVC size.

Due to her young age, persistence of symptoms 6 months post acute PE, with chronic changes consistent with chronic thromboembolic disease on CTA chest and V/Q scan, she was referred to CTEPH Center for evaluation and consideration of pulmonary thromboendarterectomy (PTE). A right heart catheterization was performed to evaluate for chronic thromboembolic pulmonary hypertension (CTEPH). Resting pulmonary hemodynamics: RA 10, PA 42/19 (mean 29), PCWP 14, thermodilution cardiac output 5.4 L/min, cardiac index 2.5 L/min/m², PVR 2.8 Wood Unit, PA saturation 64%. Using weights, her upper extremities were exercised resulting in an increase in her thermodilution cardiac output to 8.1 L/min, PA pressure was 72/30 (mean 49), PCWP 17. She was diagnosed with chronic thromboembolic disease (CTED), characterized by persistent pulmonary thromboembolic occlusion with mild pulmonary hypertension at rest and significant rise in pulmonary artery pressures with a modest increase in cardiac output. As a result of her dissatisfaction with her functional status, and with her exercised induced pulmonary hypertension, she elected to proceed with surgery.

She underwent pulmonary thromboendarterectomy 1 year after diagnosis of her acute pulmonary embolism. She was found to have level 1 disease on the right and level 2 disease on the left (Fig. 8.5). Her post-operative hemodynamics off vasopressors showed a mean PA pressure 19 mmHg with cardiac index 3.1 L/min/m² and PVR < 2 Wood units. She was discharged on post-operative day 7 with the recommendation for life-long anticoagulation.

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