Pulmonary vasodilation in acute pulmonary embolism – a systematic review
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, bu...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2020-03-01
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| Series: | Pulmonary Circulation |
| Online Access: | https://doi.org/10.1177/2045894019899775 |
| _version_ | 1811329962751295488 |
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| author | Mads Dam Lyhne Jeffrey Allen Kline Jens Erik Nielsen-Kudsk Asger Andersen |
| author_facet | Mads Dam Lyhne Jeffrey Allen Kline Jens Erik Nielsen-Kudsk Asger Andersen |
| author_sort | Mads Dam Lyhne |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-13T15:53:11Z |
| format | Article |
| id | doaj.art-70ef024947c842dfb62a5246439fe7b0 |
| institution | Directory Open Access Journal |
| issn | 2045-8940 |
| language | English |
| last_indexed | 2024-04-13T15:53:11Z |
| publishDate | 2020-03-01 |
| publisher | Wiley |
| record_format | Article |
| series | Pulmonary Circulation |
| spelling | doaj.art-70ef024947c842dfb62a5246439fe7b02022-12-22T02:40:47ZengWileyPulmonary Circulation2045-89402020-03-011010.1177/2045894019899775Pulmonary vasodilation in acute pulmonary embolism – a systematic reviewMads Dam Lyhne0Jeffrey Allen Kline1Jens Erik Nielsen-Kudsk2Asger Andersen3Department of Cardiology, Aarhus University Hospital and Institute of Clinical Medicine, Aarhus University, Aarhus, DenmarkDepartment of Emergency Medicine, Indiana University School of Medicine, Indianapolis, IN, USADepartment of Cardiology, Aarhus University Hospital and Institute of Clinical Medicine, Aarhus University, Aarhus, DenmarkDepartment of Cardiology, Aarhus University Hospital and Institute of Clinical Medicine, Aarhus University, Aarhus, DenmarkAcute 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.https://doi.org/10.1177/2045894019899775 |
| spellingShingle | Mads Dam Lyhne Jeffrey Allen Kline Jens Erik Nielsen-Kudsk Asger Andersen Pulmonary vasodilation in acute pulmonary embolism – a systematic review Pulmonary Circulation |
| title | Pulmonary vasodilation in acute pulmonary embolism – a systematic review |
| title_full | Pulmonary vasodilation in acute pulmonary embolism – a systematic review |
| title_fullStr | Pulmonary vasodilation in acute pulmonary embolism – a systematic review |
| title_full_unstemmed | Pulmonary vasodilation in acute pulmonary embolism – a systematic review |
| title_short | Pulmonary vasodilation in acute pulmonary embolism – a systematic review |
| title_sort | pulmonary vasodilation in acute pulmonary embolism a systematic review |
| url | https://doi.org/10.1177/2045894019899775 |
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