Systemic Consequences of Pulmonary Hypertension and Right-Sided Heart Failure
Pulmonary hypertension (PH) is a feature of a variety of diseases and continues to harbor high morbidity and mortality. The main consequence of PH is right-sided heart failure which causes a complex clinical syndrome affecting multiple organ systems including left heart, brain, kidneys, liver, gastr...
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| Published in | Circulation (New York, N.Y.) Vol. 141; no. 8; pp. 678 - 693 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
by the American College of Cardiology Foundation and the American Heart Association, Inc
25.02.2020
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 1524-4539 |
| DOI | 10.1161/CIRCULATIONAHA.116.022362 |
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| Abstract | Pulmonary hypertension (PH) is a feature of a variety of diseases and continues to harbor high morbidity and mortality. The main consequence of PH is right-sided heart failure which causes a complex clinical syndrome affecting multiple organ systems including left heart, brain, kidneys, liver, gastrointestinal tract, skeletal muscle, as well as the endocrine, immune, and autonomic systems. Interorgan crosstalk and interdependent mechanisms include hemodynamic consequences such as reduced organ perfusion and congestion as well as maladaptive neurohormonal activation, oxidative stress, hormonal imbalance, and abnormal immune cell signaling. These mechanisms, which may occur in acute, chronic, or acute-on-chronic settings, are common and precipitate adverse functional and structural changes in multiple organs which contribute to increased morbidity and mortality. While the systemic character of PH and right-sided heart failure is often neglected or underestimated, such consequences place additional burden on patients and may represent treatable traits in addition to targeted therapy of PH and underlying causes. Here, we highlight the current state-of-the-art understanding of the systemic consequences of PH and right-sided heart failure on multiple organ systems, focusing on self-perpetuating pathophysiological mechanisms, aspects of increased susceptibility of organ damage, and their reciprocal impact on the course of the disease. |
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| AbstractList | Pulmonary hypertension (PH) is a feature of a variety of diseases and continues to harbor high morbidity and mortality. The main consequence of PH is right-sided heart failure which causes a complex clinical syndrome affecting multiple organ systems including left heart, brain, kidneys, liver, gastrointestinal tract, skeletal muscle, as well as the endocrine, immune, and autonomic systems. Interorgan crosstalk and interdependent mechanisms include hemodynamic consequences such as reduced organ perfusion and congestion as well as maladaptive neurohormonal activation, oxidative stress, hormonal imbalance, and abnormal immune cell signaling. These mechanisms, which may occur in acute, chronic, or acute-on-chronic settings, are common and precipitate adverse functional and structural changes in multiple organs which contribute to increased morbidity and mortality. While the systemic character of PH and right-sided heart failure is often neglected or underestimated, such consequences place additional burden on patients and may represent treatable traits in addition to targeted therapy of PH and underlying causes. Here, we highlight the current state-of-the-art understanding of the systemic consequences of PH and right-sided heart failure on multiple organ systems, focusing on self-perpetuating pathophysiological mechanisms, aspects of increased susceptibility of organ damage, and their reciprocal impact on the course of the disease.Pulmonary hypertension (PH) is a feature of a variety of diseases and continues to harbor high morbidity and mortality. The main consequence of PH is right-sided heart failure which causes a complex clinical syndrome affecting multiple organ systems including left heart, brain, kidneys, liver, gastrointestinal tract, skeletal muscle, as well as the endocrine, immune, and autonomic systems. Interorgan crosstalk and interdependent mechanisms include hemodynamic consequences such as reduced organ perfusion and congestion as well as maladaptive neurohormonal activation, oxidative stress, hormonal imbalance, and abnormal immune cell signaling. These mechanisms, which may occur in acute, chronic, or acute-on-chronic settings, are common and precipitate adverse functional and structural changes in multiple organs which contribute to increased morbidity and mortality. While the systemic character of PH and right-sided heart failure is often neglected or underestimated, such consequences place additional burden on patients and may represent treatable traits in addition to targeted therapy of PH and underlying causes. Here, we highlight the current state-of-the-art understanding of the systemic consequences of PH and right-sided heart failure on multiple organ systems, focusing on self-perpetuating pathophysiological mechanisms, aspects of increased susceptibility of organ damage, and their reciprocal impact on the course of the disease. Pulmonary hypertension (PH) is a feature of a variety of diseases and continues to harbor high morbidity and mortality. The main consequence of PH is right-sided heart failure which causes a complex clinical syndrome affecting multiple organ systems including left heart, brain, kidneys, liver, gastrointestinal tract, skeletal muscle, as well as the endocrine, immune, and autonomic systems. Interorgan crosstalk and interdependent mechanisms include hemodynamic consequences such as reduced organ perfusion and congestion as well as maladaptive neurohormonal activation, oxidative stress, hormonal imbalance, and abnormal immune cell signaling. These mechanisms, which may occur in acute, chronic, or acute-on-chronic settings, are common and precipitate adverse functional and structural changes in multiple organs which contribute to increased morbidity and mortality. While the systemic character of PH and right-sided heart failure is often neglected or underestimated, such consequences place additional burden on patients and may represent treatable traits in addition to targeted therapy of PH and underlying causes. Here, we highlight the current state-of-the-art understanding of the systemic consequences of PH and right-sided heart failure on multiple organ systems, focusing on self-perpetuating pathophysiological mechanisms, aspects of increased susceptibility of organ damage, and their reciprocal impact on the course of the disease. |
| Author | Gomberg-Maitland, Mardi Howard, Luke S. Rosenkranz, Stephan Hoeper, Marius M. |
| AuthorAffiliation | Clinic III for Internal Medicine (Cardiology) and Cologne Cardiovascular Research Center (CCRC), Heart Center at the University of Cologne, Germany (S.R.). Center for Molecular Medicine Cologne (CMMC), University of Cologne, Germany (S.R.). National Pulmonary Hypertension Service, Imperial College Healthcare NHS Trust, London, United Kingdom (L.S.H.). Department of Medicine, George Washington University, Washington, DC (M.G.M.). Department of Respiratory Medicine, Hannover Medical School, Germany (M.M.H.). German Center for Lung Research (DZL), Hannover, Germany (M.M.H.) |
| AuthorAffiliation_xml | – name: Clinic III for Internal Medicine (Cardiology) and Cologne Cardiovascular Research Center (CCRC), Heart Center at the University of Cologne, Germany (S.R.). Center for Molecular Medicine Cologne (CMMC), University of Cologne, Germany (S.R.). National Pulmonary Hypertension Service, Imperial College Healthcare NHS Trust, London, United Kingdom (L.S.H.). Department of Medicine, George Washington University, Washington, DC (M.G.M.). Department of Respiratory Medicine, Hannover Medical School, Germany (M.M.H.). German Center for Lung Research (DZL), Hannover, Germany (M.M.H.) |
| Author_xml | – sequence: 1 givenname: Stephan surname: Rosenkranz fullname: Rosenkranz, Stephan organization: Clinic III for Internal Medicine (Cardiology) and Cologne Cardiovascular Research Center (CCRC), Heart Center at the University of Cologne, Germany (S.R.). Center for Molecular Medicine Cologne (CMMC), University of Cologne, Germany (S.R.). National Pulmonary Hypertension Service, Imperial College Healthcare NHS Trust, London, United Kingdom (L.S.H.). Department of Medicine, George Washington University, Washington, DC (M.G.M.). Department of Respiratory Medicine, Hannover Medical School, Germany (M.M.H.). German Center for Lung Research (DZL), Hannover, Germany (M.M.H.) – sequence: 2 givenname: Luke surname: Howard middlename: S. fullname: Howard, Luke S. – sequence: 3 givenname: Mardi surname: Gomberg-Maitland fullname: Gomberg-Maitland, Mardi – sequence: 4 givenname: Marius surname: Hoeper middlename: M. fullname: Hoeper, Marius M. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32091921$$D View this record in MEDLINE/PubMed |
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