Cancer Therapy-Associated Pulmonary Hypertension and Right Ventricular Dysfunction: Etiologies and Prognostic Implications

Figures

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  Fig. 1.. Potential etiologies of pulmonary hypertension among patients with cancer. Patients with cancer are at risk for developing pulmonary hypertension via several different etiologies including cancer therapy toxicity, hypercoaguability leading to increased risk of pulmonary embolism and tumor biology. PTTM, pulmonary tumor thrombotic microangiopathy; PVOD, pulmonary venous occlusive disease.

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  Fig. 2.. Mechanisms of cancer therapy-associated pulmonary hypertension. Cancer therapy can cause pulmonary hypertension via several possible mechanisms including endothelial damage and dysfunction, off-target TK inhibition, systemic inflammation, and inducing a pro-thrombotic state. IFNα, interferon-α; PE, pulmonary embolism; ROS, reactive oxygen species; TK, tyrosine kinase; VTE, venous thromboembolism.

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  Fig. 3.. Proposed algorithm for diagnosis and surveillance of cancer therapy-associated pulmonary hypertension. Symptosm concerning for PH after initiation of cancer therapy should be investigated with blood work and echocardiography. Patients with findings on echocardiography with high-probability of PH should be considered for right heart catheterization for diagnosis of PH. Strong evidence for the safety and efficacy of PH-specific therapy is lacking but can be considered for patients with right heart catheterization-proven PAH. IVC, inferior vena cava; LV, left ventricle; mPAP, mean pulmonary artery pressure; PAH, pulmonary arterial hypertension; PH, pulmonary hypertension; RV, right ventricle; RVOT, right ventricular outflow tract; TRV, tricuspid regurgitation maximum velocity.