Role of Phosphodiesterase-5 Inhibitors in Acute Right Ventricular Failure Due to Pulmonary Embolism

Sharma, Munish; Suero-Abreu, Giselle Alexandra; Neupane, Ritesh; Kim, Bernard

doi:10.12659/ajcr.915832

Cited by 2 publications

(4 citation statements)

References 12 publications

(15 reference statements)

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“…A large variety of case reports have been published on the use of iNO, ranging from iNO administered to patients with RV failure (including PE-induced) as primary indication; as bridge to embolectomy or thrombolysis; with acute-on-chronic PE; during PE-induced cardiac arrest; on extra-corporal membrane oxygenation (ECMO) support or in case of contraindication to thrombolysis. 92–98 Some cases describe the use of iNO to treat increased PAP after embolectomy of acute PE 99–101 though not all with impressive hemodynamic responses. 102 iNO has been used in children and even infants with PE without success.…”

Section: Resultsmentioning

confidence: 99%

“…Sildenafil showed promising effects in both acute post-operative PE and acute-in-chronic PE. 98,135–137 In a patient with congenital heart disease and acute-in-chronic PE, sildenafil dramatically improved oxygenation. 109 The use of sildenafil made withdrawal of inotropes possible shortly after treatment, 135,138 whereas another case report measures the effects of sildenafil on the following day.…”

Section: Resultsmentioning

confidence: 99%

“…18 PE cases with mostly positive effects [92][93][94]96,108 Five cases in combination with thrombolysis, thrombectomy or embolectomy 97,[99][100][101][102] Five cases of post-operative PE 98 Note: Summary of review of the NO-sGC-cGMP pathway to induce pulmonary vasodilation in acute pulmonary embolism. Divided by treatment option, animal or clinical data and guideline recommendation.…”

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

“…106 A number of case reports describe significant or even dramatic positive hemodynamic effects of iNO, and the effects seem to be present shortly after beginning of treatment 47,[93][94][95]99,[107][108][109] and at low doses. [97][98][99]108 Whether these temporal improvements represent the direct effect of iNO remain uncertain.…”

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

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Pulmonary vasodilation in acute pulmonary embolism – a systematic review

et al. 2020

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Acute pulmonary embolism is the third most common cause of cardiovascular death. Pulmonary embolism increases right ventricular afterload, which causes right ventricular failure, circulatory collapse and death. Most treatments focus on removal of the mechanical obstruction caused by the embolism, but pulmonary vasoconstriction is a significant contributor to the increased right ventricular afterload and is often left untreated. Pulmonary thromboembolism causes mechanical obstruction of the pulmonary vasculature coupled with a complex interaction between humoral factors from the activated platelets, endothelial effects, reflexes and hypoxia to cause pulmonary vasoconstriction that worsens right ventricular afterload. Vasoconstrictors include serotonin, thromboxane, prostaglandins and endothelins, counterbalanced by vasodilators such as nitric oxide and prostacyclins. Exogenous administration of pulmonary vasodilators in acute pulmonary embolism seems attractive but all come with a risk of systemic vasodilation or worsening of pulmonary ventilation-perfusion mismatch. In animal models of acute pulmonary embolism, modulators of the nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway, endothelin pathway and prostaglandin pathway have been investigated. But only a small number of clinical case reports and prospective clinical trials exist. The aim of this review is to give an overview of the causes of pulmonary embolism-induced pulmonary vasoconstriction and of experimental and human investigations of pulmonary vasodilation in acute pulmonary embolism.

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