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Exploring the Role of Sildenafil in Acute Pulmonary Embolism
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A3785 - Exploring the Role of Sildenafil in Acute Pulmonary Embolism
Author Block: H. Hall, C. Orton, R. Mirza, E. Shaw, B. P. Madden; St George's Hospital, London, United Kingdom.
Rationale Acute pulmonary embolism (PE) related right ventricular (RV) strain attributes significant risk of adverse outcomes. Even in haemodynamically stable patients, mortality rates may be as high as 13.7% at 3 months. The combined effects of direct occlusion of the vascular bed and release of vasoactive mediators cause a dramatic rise in pulmonary vascular resistance, which may precipitate cardiovascular decompensation and potential catastrophic circulatory collapse. Therapeutic options aiming to stabilise this physiological response are therefore desirable. Sildenafil is a widely used pulmonary vasodilator, with evidence supporting it’s application in chronic thromboembolic pulmonary hypertension (CTEPH). Animal models and case report literature suggest Sildenafil may stabilise the haemodynamic responses seen in acute PE. We describe our experience in the early initiation of Sildenafil in this context.
Methods Patients referred to the pulmonary hypertension team with acute PE and associated RV strain were identified. All were verbally consented to receive Sildenafil in addition to standard care. Patients were monitored to discharge and underwent repeat 2D echocardiogram and CT pulmonary angiography at 3 months.
Results 20 patients received Sildenafil in the context of acute PE; 45% (9/20) were male, mean age 54 (±16 SD) years. All had clinical, biochemical or radiological evidence of acute RV strain. 35% (7/20) required systemic thrombolysis at presentation. None required advanced haemodynamic support or invasive ventilation. All patients were alive at 3 months. 3 patients had incomplete follow-up data and one stopped treatment prematurely due to intolerable side effects. Of those remaining, 62.5% (10/16) had full resolution of thrombus and no evidence of pulmonary hypertension. 2 were diagnosed with CTEPH and 4 had either residual thrombus of no clear clinical significance or persistent pulmonary hypertension in the absence of residual PE. Ongoing follow-up continued for median 9 months (range 4 - 28). Two patients subsequently died due to underlying malignancy.
Conclusion In this small review of patients with high-risk pulmonary embolism, the addition of Sildenafil appears to be well tolerated with only a single dropout due to adverse side effects. In spite of the presence of poor prognostic features in this group, all patients survived to discharge and were alive at 3 months. Sildenafil appears to be safe when used judiciously in this setting, and may have a role in stabilising the haemodynamic impact of PE in the acute phase. Our data supports the need for larger, randomised trials to better ascertain the benefits of Sildenafil in this context.
Author Block: H. Hall, C. Orton, R. Mirza, E. Shaw, B. P. Madden; St George's Hospital, London, United Kingdom.
Rationale Acute pulmonary embolism (PE) related right ventricular (RV) strain attributes significant risk of adverse outcomes. Even in haemodynamically stable patients, mortality rates may be as high as 13.7% at 3 months. The combined effects of direct occlusion of the vascular bed and release of vasoactive mediators cause a dramatic rise in pulmonary vascular resistance, which may precipitate cardiovascular decompensation and potential catastrophic circulatory collapse. Therapeutic options aiming to stabilise this physiological response are therefore desirable. Sildenafil is a widely used pulmonary vasodilator, with evidence supporting it’s application in chronic thromboembolic pulmonary hypertension (CTEPH). Animal models and case report literature suggest Sildenafil may stabilise the haemodynamic responses seen in acute PE. We describe our experience in the early initiation of Sildenafil in this context.
Methods Patients referred to the pulmonary hypertension team with acute PE and associated RV strain were identified. All were verbally consented to receive Sildenafil in addition to standard care. Patients were monitored to discharge and underwent repeat 2D echocardiogram and CT pulmonary angiography at 3 months.
Results 20 patients received Sildenafil in the context of acute PE; 45% (9/20) were male, mean age 54 (±16 SD) years. All had clinical, biochemical or radiological evidence of acute RV strain. 35% (7/20) required systemic thrombolysis at presentation. None required advanced haemodynamic support or invasive ventilation. All patients were alive at 3 months. 3 patients had incomplete follow-up data and one stopped treatment prematurely due to intolerable side effects. Of those remaining, 62.5% (10/16) had full resolution of thrombus and no evidence of pulmonary hypertension. 2 were diagnosed with CTEPH and 4 had either residual thrombus of no clear clinical significance or persistent pulmonary hypertension in the absence of residual PE. Ongoing follow-up continued for median 9 months (range 4 - 28). Two patients subsequently died due to underlying malignancy.
Conclusion In this small review of patients with high-risk pulmonary embolism, the addition of Sildenafil appears to be well tolerated with only a single dropout due to adverse side effects. In spite of the presence of poor prognostic features in this group, all patients survived to discharge and were alive at 3 months. Sildenafil appears to be safe when used judiciously in this setting, and may have a role in stabilising the haemodynamic impact of PE in the acute phase. Our data supports the need for larger, randomised trials to better ascertain the benefits of Sildenafil in this context.
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