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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Sources
(a) http://pulmonaryhypertensionrn.com/ph-vs-pah/
(4) http://www.ncbi.nlm.nih.gov/pubmed/23202738
(5) http://www.ncbi.nlm.nih.gov/pubmed/16497988
(6) http://www.ncbi.nlm.nih.gov/pubmed/18814100
(7) http://www.ncbi.nlm.nih.gov/pubmed/18552156
(7a) http://www.ncbi.nlm.nih.gov/pubmed/23624788
(7b) http://www.ncbi.nlm.nih.gov/pubmed/9539893
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