Thursday, 28 November 2013

Pulmonary vascular disease – Pulmonary arterial hypertension – The Causes

ulmonary vascular disease is defined as a condition of blood flow to the lung’s artery is blocked suddenly due to a blood clot somewhere in the body, including pulmonary embolism, chronic thromboembolic disease, pulmonary arterial hypertension, pulmonary veno-occlusive disease, pulmonary arteriovenous malformations, pulmonary edema, etc.
Pulmonary arterial hypertension
Pulmonary arterial hypertension is a subgroup of a specific subgroup of pulmonary hypertension (PH) defined as a condition of slowly progressive disorder as a result of abnormally high blood pressure in the blood vessel, including pulmonary artery, pulmonary vein, or pulmonary capillaries, that carries blood from the heart to the lungs due to narrowing in diameter of most of the very small arteries throughout the lungs of that increased resistance to blood flow, leading to right heart failure and death. Because the phrase pulmonary arterial hypertension is long and pulmonary hypertension is a bit shorter the phrase. Pulmonary hypertension is often used in place of pulmonary arterial hypertension(a). According to statistic, approximately over 1,000 new cases of pulmonary arterial hypertension are diagnosed each year, in the United States alone.
A. Causes
1. Mutation of BMPR2 gene
Experimental and clinical studies now converge on the intersection and interactions between a genetic predisposition involving the BMPR2 signaling pathway and an impaired metabolic and chronic inflammatory state in the vessel wall(4). According to the study by the University of Cambridge School of Clinical Medicine, Heterozygous germline mutations in the gene encoding the bone morphogenetic protein type II (BMPR-II) receptor underlie the majority (>70%) of cases of familial pulmonary arterial hypertension (FPAH), and dysfunction of BMP signaling has been implicated in other forms of PAH(5).
2. Pulmonary veno-occlusive disease (PVOD)
Pulmonary veno-occlusive disease (PVOD) is a rare cause of pulmonary hypertension. So far some 200 cases have been published worldwide. Since the latest classification, agreed at a meeting in Venice in 2003, PVOD is included in the group of pulmonary arterial hypertension (PAH)(6).
3. Pulmonary endothelial injury and enhanced inflammatory response
In the study to examine the effect of pulmonary endothelial injury in BMPR2(+/-) mice, with mice with two injections of monocrotaline combined with intratracheal instillation of replication-deficient adenovirus expressing 5-lipoxygenase (MCT+Ad5LO), showed that greater endothelial injury and an enhanced inflammatory response could be the underlying causes of the sensitivity and may work in concert with BMPR2 heterozygosity to promote the development of persistent pulmonary hypertension(7).
4. The role of disturbed blood flow
According to the study by University Medical Centre Groningen-GUIDE, In this concept disturbed blood flow is seen as an important trigger in the development of vascular remodeling. For instance, in PAH associated with congenital heart disease, increased pulmonary blood flow (i.e. systemic-to-pulmonary shunt) is an essential trigger for the occurrence of neointimal lesions and PAH development. Still, questions remain about the exact role of these blood flow characteristics in disease progression(7a)
5. Certain Medication
In the late 1960s, an epidemic of primary pulmonary hypertension (PPH) occurred in Europe shortly after the introduction of aminorex fumarate, a potent anorexigen. According to the study by the McGill University Faculty of Medicinethere is a strong association between aminorex and PPH probably led to a 5-fold increase in PPH incidence, and thus a very noticeable epidemic. The association with dexfenfluramine would result in an increase in incidence of only 20%. Based on the available evidence, a repeat PPH epidemic seems unlikely(7b).
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