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Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat
Published on: November 18, 2018
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Hematological disorders and pulmonary hypertension.
Rajamma Mathew1, Jing Huang1, Joseph M Wu1
1Rajamma Mathew, Department of Physiology, New York Medical College, Valhalla, NY 10595, United States.
World Journal of Cardiology
|January 11, 2017
Summary
Pulmonary hypertension (PH) in blood disorders stems from hemolysis, endothelial dysfunction, and altered iron levels. Understanding these mechanisms is crucial for improving patient outcomes and managing this serious condition.
Area of Science:
- Hematology
- Cardiology
- Pulmonology
Background:
- Pulmonary hypertension (PH) is a severe condition linked to systemic diseases, particularly hematological disorders like sickle cell disease and thalassemia.
- PH in these conditions exacerbates prognosis due to oxidant injury, vascular inflammation, and endothelial dysfunction.
Approach:
- This review examines the mechanisms linking hematological disorders to PH, including nitric oxide (NO) scavenging by free hemoglobin and arginase activity.
- It also explores the role of treatments for hematological disorders in PH development.
- The impact of deregulated iron homeostasis and iron deficiency in PH, especially idiopathic pulmonary arterial hypertension (PAH), is also discussed.
Key Points:
- Hemolysis in blood disorders reduces nitric oxide (NO) bioavailability and impairs endothelial function.
- Arginase released during hemolysis competes with NO synthase for L-arginine.
- Iron deficiency is increasingly recognized as a risk factor for pulmonary arterial hypertension (PAH).
Conclusions:
- Hematological disorders contribute to PH through complex mechanisms involving hemolysis, endothelial dysfunction, and altered iron metabolism.
- Therapeutic strategies targeting these pathways, including iron homeostasis, may offer new avenues for managing PH in these patients.
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