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What is PVOD (PVOD)?

Dec 19, 2019 · Pulmonary veno-occlusive disease (PVOD), a subgroup of pulmonary arterial hypertension (PAH), is a rare and devastating condition histologically characterized by occlusion of pulmonary veins and venules with widespread …

Is there a diagnosis for PVOD?

May 01, 2016 · In an explanatory approach, different forms of chronic pulmonary vascular diseases such as PAH, PVOD or chronic thromboembolic PH have traditionally been labelled by their anatomical site of predilection, e.g. muscular pulmonary arteries, pulmonary venules or larger elastic type arteries.

What is the pathophysiology of pulmonary veno-occlusive disease (PVOD)?

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Dec 19, 2019 · PVOD is a rare cause of pulmonary hypertension, and is currently classified as a subgroup of PAH. The exact prevalence of PVOD remains unknown, because many cases are probably misdiagnosed as IPAH due to similar clinical and hemodynamic features and lack of histological or genetic confirmation.

What does PVOD mean in medical terms?

Pulmonary veno-occlusive disease (PVOD) is characterized by the blockage (occlusion) of the blood vessels that carry oxygen-rich (oxygenated) blood from the lungs to the heart (the pulmonary veins).

How do you treat PVOD?

The best treatment option for the majority of patients with PVOD is lung transplantation. Oxygen should be prescribed in patients that meet standard criteria (low measured oxygen levels).

Is PVOD curable?

Pulmonary veno-occlusive disease (PVOD) is a rare condition with poor prognosis, and lung transplantation is recommended as the only curative therapy.Dec 19, 2019

How is PVOD diagnosed?

Ultimately, the diagnosis of PVOD can be made by the constellations of high clinical suspicion, severe hypoxia on ABG, severely decreased DLCO on PFTs, normal V/Q scan, severe pulmonary hypertension on right heart catheterization, and high-resolution chest CT findings of ground glass opacities, hilar and mediastinal ...Apr 22, 2019

What is a PVOD release?

Premium. Premium video on demand (PVOD) is a version of TVOD which allows customers to access video-on-demand content sooner than they would have been able to otherwise – often feature films made available alongside, or in place of, a traditional release in movie theaters – but at a much higher price point.

What PCOS means?

Polycystic ovary syndrome (PCOS) is a condition in which the ovaries produce an abnormal amount of androgens, male sex hormones that are usually present in women in small amounts. The name polycystic ovary syndrome describes the numerous small cysts (fluid-filled sacs) that form in the ovaries.

What is pulmonary capillary Hemangiomatosis?

Pulmonary capillary hemangiomatosis (PCH) is a rare disorder of alveolar capillary proliferation that clinically masquerades as idiopathic pulmonary arterial hypertension, or pulmonary venoocclusive disease (PVOD).Jul 28, 2009

What is PVOD streaming?

The term PVOD (Premium Video On Demand) refers to the Premium version of TVOD (Transactional Video On Demand) which refers to exclusive content, generally exclusive movies that are only accessed on one platform with an additional payment to the membership.

What are complications of vaso occlusive disease in the lung?

Summary: The pulmonary complications of sickle cell disease include airway hyperreactivity, acute chest syndrome, chronic sickle lung disease, pulmonary hypertension, and sleep disordered breathing.

What does VOD mean in movies?

video-on-demandvideo-on-demand (VOD), technology for delivering video content, such as movies and television shows, directly to individual customers for immediate viewing.

What is PVOD in lung?

As the name suggests Pulmonary veno-occlusive disease (PVOD) uniquely involves the small veins of the lung circulation more than the small arteries. The veins become blocked with scar tissue that is not normally present. Sometimes PVOD occurs in patients affected by connective tissue diseases like scleroderma, or patients infected with ...

How rare is PVOD?

Many scientists believe that PVOD occurs about 5-10 times less often than pulmonary arterial hypertension (PAH), which makes it an extremely rare disease.

What is a PCH?

Pulmonary capillary hemangiomatosis (PCH) is a disease which mainly affects the lung capillaries (tiny vessels found between arteries and veins of the lungs.) The capillaries overgrow (or “proliferate”) in the lung tissue. The diagnosis can be made when pathologists see capillary overgrowth in a lung biopsy specimen. However, just like PVOD, lung biopsy often poses too much risk for patients with advanced pulmonary hypertension; forcing the doctor to make a provisional diagnosis of PCH.

What is a PVOD?

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension (PH) characterised by preferential remodelling of the pulmonary venules. In the current PH classification, PVOD and pulmonary capillary haemangiomatosis (PCH) are considered to be a common entity and represent varied expressions of the same disease. The recent discovery of biallelic mutations in the EIF2AK4 gene as the cause of heritable PVOD/PCH represents a major milestone in our understanding of the molecular pathogenesis of PVOD. Although PVOD and pulmonary arterial hypertension (PAH) share a similar clinical presentation, with features of severe precapillary PH, it is important to differentiate these two conditions as PVOD carries a worse prognosis and life-threatening pulmonary oedema may occur following the initiation of PAH therapy. An accurate diagnosis of PVOD based on noninvasive investigations is possible utilising oxygen parameters, low diffusing capacity for carbon monoxide and characteristic signs on high-resolution computed tomography of the chest. No evidence-based medical therapy exists for PVOD at present and lung transplantation remains the preferred definitive therapy for eligible patients.

What is a group 1 PH?

Group 1 PH consists of PAH and its various subtypes such as idiopathic, heritable and drug-induced PAH as well as those associated with connective tissue disease, HIV infection, portal hypertension, congenital heart disease and schistosomiasis. Although PVOD is classified as belonging to group 1 PH, it has been given a special subgroup designation of group 1′ under the unified entity of PVOD/pulmonary capillary haemangiomatosis (PCH). Previously regarded by some as different entities, current evidence supports the concept that PVOD and PCH are in fact varied expressions of the same disorder. Indeed, clinico-pathological studies indicate marked overlap in the histological findings of PVOD and PCH [ 10 ], and their clinical and radiographic findings are virtually indistinguishable [ 11 – 13 ]. The notion of a common disorder is further emphasised by the recent discovery that mutations in the EIF2AK4 gene are responsible for heritable cases of both PVOD and PCH [ 8, 14 ].

Is PVOD a PH?

PVOD is an uncommon form of PH, but clinical recognition is crucial due to its dismal prognosis and nonresponsiveness to PAH therapy. Diagnosis remains challenging in clinical practice, but a high degree of diagnostic confidence is possible based on a battery of noninvasive investigations. The discovery of biallelic mutations of the EIF2AK4 gene in heritable disease will pave the way to allow a better understanding of the molecular pathogenesis of PVOD, akin to the manner in which the discovery of BMPR2 mutation in PAH has led to a major advancement of knowledge. Animal models of PVOD will enable novel therapeutic targets to be tested with eventual translation to human studies. Lung transplantation remains the current therapy of choice for eligible patients with PVOD.

What is the most widely used technique for the detection of PH?

Transthoracic echocardiography remains the most widely used technique for the detection of PH [ 75 ]. No specific features of PVOD are found on echocardiographic examination, and findings reflect the presence of precapillary PH with elevated tricuspid regurgitation velocity with or without right-sided chamber dysfunction depending on disease severity. Echocardiography may be useful to exclude left-sided cardiac disease as a cause of pulmonary oedema.

Is occupational exposure a risk factor for PVOD?

Occupational exposure is emerging to be a potentially relevant and frequently encountered risk factor for PVOD. In a recent case–control study comparing PVOD patients with PAH [ 41 ], PVOD was linked to occupational exposure to organic solvents, with trichloroethylene (a chlorinated solvent) being the main agent implicated in this association. A history of significant trichloroethylene exposure was found in 42% of PVOD patients versus only 3% of PAH (adjusted OR 8.2, 95% CI 1.4–49.4). PVOD patients with a positive exposure history were characterised by older age of disease onset and the absence of mutations for the EIF2AK4 gene, whereas those without an exposure history were typically younger and a significant proportion harboured biallelic EIF2AK4 mutations [ 41 ].

What is a PVOD?

Pulmonary veno-occlusive disease (PVOD), a subgroup of pulmonary arterial hypertension (PAH), is a rare and devastating condition histologically characterized by occlusion of pulmonary veins and venules with widespread fibrous intimal thickening and patchy capillary proliferation. Although PVOD shares similar clinical features with idiopathic PAH (IPAH), it progresses more rapidly even while on therapy and carries a worse prognosis with a dismal 1-year mortality rate of 72% [ 1 ].

Is PVOD a pulmonary hypertension?

PVOD is a rare cause of pulmonary hypertension, and is currently classified as a subgroup of PAH. The exact prevalence of PVOD remains unknown, because many cases are probably misdiagnosed as IPAH due to similar clinical and hemodynamic features and lack of histological or genetic confirmation. It was estimated PVOD accounted for around 10% cases of IPAH [ 4 ]. Unlike IPAH which has a female predominance, PVOD seems to affect men and women equally [ 27 ]. Its molecular pathogenesis remains unclear, risk factors such as genetic factors, chemicals and chemotherapies, autoimmunity and inflammation, and cigarette smoking exposure have been reported to be associated with the development of PVOD [ 1, 5 ], and three of our patients got tobacco exposure which caused endothelial dysfunction and induced vascular remodeling in animal models of pulmonary hypertension.

What is a PVOD?

Pulmonary veno-occlusive disease (PVOD) is defined by specific pathologic changes of the pulmonary veins. A definite diagnosis of PVOD thus requires a lung biopsy or pathologic examination of pulmonary explants or postmortem lung samples. However, lung biopsy is hazardous in patients with severe pulmonary hypertension, and there is a need for noninvasive diagnostic tools in this patient population. Patients with PVOD may be refractory to pulmonary arterial hypertension (PAH)-specific therapy and may even deteriorate with it. It is important to identify such patients as soon as possible, because they should be treated cautiously and considered for lung transplantation if eligible. High-resolution computed tomography of the chest can suggest PVOD in the setting of pulmonary hypertension when it shows nodular ground-glass opacities, septal lines, lymph node enlargement, and pleural effusion. Similarly, occult alveolar hemorrhage found on bronchoalveolar lavage in patients with pulmonary hypertension is associated with PVOD. We conducted the current study to identify additional clinical, functional, and hemodynamic characteristics of PVOD.

What is PAH in cardiac?

PAH was defined as mPAP >25 mm Hg with a normal PCWP <15 mm Hg. Hemodynamic evaluation by right heart catheterization was performed at baseline in all subjects according to our previously described protocol 45. Cardiac output was measured by the standard thermodilution technique. The cardiac index (CI) was calculated as the cardiac output divided by the body surface area, and systolic index as the CI divided by cardiac frequency. The mean systolic arterial pressure (mSAP), mPAP, PCWP, right atrial pressure, and mixed venous oxygen saturation were recorded during right heart catheterization. The indexed total pulmonary resistance (TPRi) and indexed pulmonary vascular resistance (PVRi) were calculated as (mPAP)/CI and (mPAP-PCWP)/CI, respectively, and results were expressed as Wood units/m 2. Baseline hemodynamic data and response to short-term vasodilator nitric oxide (NO) obtained through right heart catheterization were obtained for all subjects. A NO challenge (10 ppm for 5-10 min) was used; a positive acute response was defined as a decrease in mPAP >10 mm Hg compared to the baseline mPAP reaching a mPAP <40 mm Hg and a normal or increased cardiac output, as previously described 24,46.

What is a pulmonary arterial hypertension?

Pulmonary arterial hypertension (PAH) is a severe condition, characterized by elevated pulmonary artery pressure leading to right heart failure and death 39,44. Although pulmonary hypertension can be screened by Doppler echocardiography, a definite diagnosis of PAH requires right heart catheterization showing a mean pulmonary artery pressure (mPAP) >25 mm Hg at rest or >30 mm Hg during exercise and normal pulmonary capillary wedge pressure (PCWP) 39,44. PAH is divided into several subcategories according to the 2003 World Symposium clinical classification of pulmonary hypertension: idiopathic PAH, familial PAH, PAH associated with different conditions (connective tissue diseases, congenital heart diseases, human immunodeficiency virus [HIV], portal hypertension, and exposure to drugs and/or toxins), and PAH associated with significant venous or capillary involvement 21,44. This latter group mainly corresponds to pulmonary veno-occlusive disease (PVOD), an uncommon cause of PAH 18,26,28,34,44. While pulmonary vascular pathology of idiopathic or familial PAH is characterized by a major remodeling of small precapillary pulmonary arteries (<200 μm) with typical plexiform and/or thrombotic lesions, PVOD preferentially affects the postcapillary venous pulmonary vessels and may include significant pulmonary capillary dilatation and/or proliferation 26,34. The pathologic hallmark of PVOD is the extensive and diffuse occlusion of pulmonary veins by fibrous tissue 18,26,28,34. Intimal thickening involves venules and small veins in lobular septa and, rarely, larger veins 18,26,28,34. It is well accepted that a definite diagnosis of PVOD requires histologic analysis of a lung sample 18,28. However, surgical lung biopsy is too invasive for these frail patients, emphasizing the importance of developing less invasive tools to obtain the diagnosis 36,38.

Can pulmonary function test be used for PVOD?

Pulmonary function tests may help in the diagnostic approach to PVOD. We have confirmed a lower baseline PaO2 at rest in PVOD patients, which could indicate a possible PVOD in conjunction with radiographic findings. Pulmonary function tests analyzed during spirometry and plethysmography were similar in both groups. Reports of low DLCO in patients with PVOD and PAH have been published 11,18. We documented a significantly more severe reduction in DLCO/VA in most of the patients with PVOD compared with the PAH group. In the current study, more than 80% of PVOD patients had a DLCO/VA lower than 55%, compared with 21% in PAH patients. Even though PVOD patients had lower PaO2 and DLCO/VA, their 6-minute walk distance was similar to that of the PAH patients. However, PVOD patients had a lower nadir SpO2 during the test. These findings suggest that noninvasive pulmonary function tests could be helpful to suggest PVOD in patients with low PaO2 at rest, low SpO2 during the 6-minute walk test, and a DLCO/VA <55%.

What is hematoxylin eosin saffron staining?

Hematoxylin-eosin-saffron staining was used in all histologic specimens to characterize pulmonary vascular abnormalities. The pathologic hallmark of pulmonary arteriopathy observed in PAH was defined as medial hypertrophy, intimal thickening, and plexiform lesions 34. The pathologic hallmark of PVOD was defined as an extensive and diffuse obstruction of pulmonary veins and venules by intimal thickening, with either fibrosis, cellular proliferation, or muscularization 6,9,34. Figure 1 shows characteristic pathologic findings found in patients with idiopathic, familial, or anorexigen-associated PAH (A, B, C) and PVOD (D, E, F), respectively. In the PVOD group, the histologic specimens were obtained by autopsy in 14 patients (58%), surgical biopsy in 3 patients (13%), and from explanted lung in 7 patients (29%). In the PAH group, histologic confirmation was obtained by autopsy in 9 patients (38%), surgical biopsy in 1 patient (4%), and from explanted lung in 14 patients (58%).

Is PVOD worse than PAH?

Some studies have reported a worse prognosis for PVOD compared with PAH, and have suggested that PVOD patients presented with worse baseline conditions. In the current study focusing on 2 severe populations of PVOD and PAH patients in whom a lung sample was available, prognostic factors of PAH, such as NYHA functional class, clinical signs of right heart failure at diagnosis, 6-minute walk distance, and baseline hemodynamics, were broadly similar in both groups, suggesting similar disease severity at diagnosis. Nevertheless, survival from diagnosis of this small PVOD population was significantly worse than that of PAH patients.

Is PVOD a rare disease?

PVOD is a rare form of PAH that remains a poorly understood entity. It is critically important to diagnose this condition rapidly for many reasons. Indeed, PVOD has been reported to have a worse prognosis than idiopathic, familial, or anorexigen-associated PAH, and death usually occurs within 2 years of the diagnosis 18. Therefore, listing on a lung transplantation program is often necessary for eligible PVOD patients. In addition, these patients are at high risk of developing acute severe pulmonary edema with vasodilator therapy 18,33, warranting precautions when using these agents in a patient with suspected PVOD. A diagnosis of PVOD is usually suspected when radiologic abnormalities are present in a patient with PAH (including ground-glass opacities with a centrilobular distribution, septal lines, and lymph node enlargement) 38. However, these findings are not present in all cases, and they may be difficult to identify in the early stages of the disease 10,38. We have recently shown that evidence of occult alveolar hemorrhage pleads in favor of PVOD 36. However, this is not a specific sign of the disease, and, furthermore, fiberoptic bronchoscopy and bronchoalveolar lavage may be hazardous in these frail patients. The occurrence of pulmonary edema with PAH-specific therapy such as intravenous epoprostenol is highly suggestive of PVOD, but all patients do not develop pulmonary edema with these agents, and such a complication may be life-threatening and cannot be regarded as a diagnostic tool. In theory, confirmation of a PVOD diagnosis requires histologic analysis of a lung sample. However, lung biopsy should not be recommended in the management of PAH because of the risk of severe complications in these patients after surgery 30. Therefore, it is of major importance to better describe the clinical, functional, and hemodynamic characteristics of PVOD patients, in order to propose the best management (including lung transplantation in eligible patients) and close monitoring when PAH therapy is initiated.

What is a PVOD?

Pulmonary veno-occlusive disease (PVOD) is a rare cause of PH where there is involvement of the post-capillary vasculature. It is difficult to make this diagnosis in vivo and a histopathological diagnosis using open surgical biopsy is usually contraindicated in these patients due to general frailty of this patient group. Two studies that retrospectively identified 15 and 8 patients with PVOD, studied the radiological features that would assist non-invasive CT assessment in these patients ( Swensen et al., 1996; Resten et al., 2004 ). The most common CT findings were septal lines, ground glass opacities particularly with a centrilobular distribution and lymphadenopathy. In the absence of other causes of PH; e.g., CTEPH and left sided heart disease, adenopathy was highly specific for PVOD. Normal left sided cardiac chambers and normal pulmonary capillary wedge pressure allows distinction of PVOD from pulmonary venous hypertension.

What is PVOD in medical terms?

Pulmonary veno-occlusive disease (PVOD) is a rare form of PAH that shares many features with other types of PAH but retains a unique histopathological pattern . As such, it is classified under a distinct subgroup category termed Group 1’ PAH, alongside pulmonary capillary hemangiomatosis (PCH).

What is PVOD in pulmonary hypertension?

PVOD should be suspected in patients with rapidly progressive and profound hypoxia, radiographic evidence of ground glass opacities interlobular septal thickening, pleural effusions and lymphadenopathy in the setting of pulmonary hypertension.

Is PVOD a PAH?

Though classified as PAH, with characteristic pathologic and clinical findings, including small arteriolar involvement, PVOD and PCH are felt to share a distinct pathophysiologic and clinical spectrum with varying degrees of septal vein and venule (PVOD) and capillary (PCH) involvement ( Lantuejoul et al., 2006 ). PVOD/PCH can complicate many other forms of PAH, including CTD (SSc, SLE, MCTD, and RA have been reported), HIV, and sarcoid, among others, but has also been associated with exposure to anorexigens, mitomycin, and post- bone marrow transplant ( Dorfmuller et al., 2007; Montani et al., 2009a; Simonneau et al., 2019 ).

What is PVOD and PAH?

PVOD and PAH share a common clinical presentation and are characterised by insidious onset of fatigueand breathlessness progressing to symptoms of right heart failure in end-stage disease. Similar to PAH,diagnosis is often delayed and most patients are in New York Heart Association functional class III or IVby the time of formal diagnosis [25, 73, 74]. Typical clinical signs of PH are found with right ventricularheave, a loud pulmonary component of the second heart sound and a systolic murmur of tricuspidregurgitation together with signs of overt right heart failure in decompensated disease. Auscultatorycrackles over the lung fields and pleural effusions may be present but these features are rare apart from thesituation of pulmonary oedema complicating pulmonary vasodilator therapy. The development ofpulmonary oedema following vasodilator therapy strongly supports the diagnosis of PVOD. Despite thepresence of alveolar haemorrhage on histological examination and bronchoalveolar lavage (BAL), clinicallyapparent haemoptysis is not more common than what is observed in PAH [25]. Clubbing and Raynaud’sphenomenon are reported to occur in both PVOD and PAH in a comparable proportion [25].

What is PVOD in avasculopathy?

The defining pathological feature of PVOD is the diffuse involvement of venules and septal veins in avasculopathy character ised by intimal fibrosis resulting in luminal narrowing or obliteration (figure 1) [4, 17].The massive involvement of small pre-septal venules with occlusive or near occlusive fibrous thickening of theintima is usually considered necessary for the diagnosis of PVOD, since moderate fibrous changes and“arterialisation” of pulmonary veins can be seen in other forms of long standing pulmonary venoushypertension such as mitral stenosis [17]. In PVOD, intimal remodelling of veins and venules may rangefrom loose fibrous tissue with variable cellularity to dense, paucicellular, sclerotic lesions. It is conceivable thatsuch variations reflect different stages in the evolution of vascular lesions. Elastic fibres within the venous wallmay display calcium incrustations, which appear as black pigment-like deposits. Small granulomas containinggiant cells that show phagocytosis of degraded elastic fibres are regularly encountered in the vicinity of smallveins and sometimes arteries.

What is a rare form of pulmonary hypertension?

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension (PH)characterised by preferential remodelling of the pulmonary venules. In the current PH classification, PVODand pulmonary capillary haemangiomatosis (PCH) are considered to be a common entity and representvaried expressions of the same disease. The recent discovery of biallelic mutations in theEIF2AK4gene asthe cause of heritable PVOD/PCH represents a major milestone in our understanding of the molecularpathogenesis of PVOD. Although PVOD and pulmonary arterial hypertension (PAH) share a similarclinical presentation, with features of severe precapillary PH, it is important to differentiate these twoconditions as PVOD carries a worse prognosis and life-threatening pulmonary oedema may occur followingthe initiation of PAH therapy. An accurate diagnosis of PVOD based on noninvasive investigations ispossible utilising oxygen parameters, low diffusing capacity for carbon monoxide and characteristic signson high-resolution computed tomography of the chest. No evidence-based medical therapy exists forPVOD at present and lung transplantation remains the preferred definitive therapy for eligible patients.

What is a group 1 PH?

Group 1 PH consists of PAH and its varioussubtypes such as idiopathic, heritable and drug-induced PAH as well as those associated with connectivetissue disease, HIV infection, portal hypertension, congenital heart disease and schistosomiasis. AlthoughPVOD is classified as belonging to group 1 PH, it has been given a special subgroup designation of group1′ under the unified entity of PVOD/pulmonary capillary haemangiomatosis (PCH). Previously regardedby some as different entities, current evidence supports the concept that PVOD and PCH are in factvaried expressions of the same disorder. Indeed, clinico-pathological studies indicate marked overlap in thehistological findings of PVOD and PCH [10], and their clinical and radiographic findings are virtuallyindistinguishable [11–13]. The notion of a common disorder is further emphasised by the recent discoverythat mutations in theEIF2AK4gene are responsible for heritable cases of both PVOD and PCH [8, 14].

Can hypoxaemia be corrected with oxygen?

Hypoxaemia should be corrected by oxygen administration to prevent further aggravation of PH fromhypoxic pulmonary vasoconstriction. No outcome data on anticoagulation in PVOD exists and its use hasbeen extrapolated from recommendations made for PAH [92]. Similar to PAH,in situthromboses of thepulmonary microcirculation are observed in PVOD [4], supporting the biological rationale ofanticoagulation. However, occult pulmonary haemorrhage is also a common finding in PVOD andanticoagulation should not be given to patients with a history of haemoptysis. Recent ESC/ERS guidelinesconcluded that evidence of oral anticoagulation is confined to patients with idiopathic PAH, heritable PAHand PAH due to anorexigens. No recommendation of anticoagulation has been proposed for PVOD [1].

Is venular involvement associated with PAH?

It is increasingly recognised that significant venular involvement may be a relatively common occurrencein connective tissue disease-associated PAH, particularly systemic sclerosis [21, 46, 47]. PVOD has alsobeen reported to be associated with other inflammatory disorders such as sarcoidosis [48], Langerhans’cell granulomatosis [49] and Hashimoto’s thyroiditis [50], although these associations are restricted toisolated case reports or small series. The true prevalence of PVOD in connective tissue disease-associatedPAH is unknown, as sufficiently large histological series are unavailable for systematic evaluation.However, a recent study suggested that as many as two-thirds of patients with precapillary PH due tosystemic sclerosis may display radiological signs of PVOD on high-resolution computed tomography(HRCT) of the chest [51], consistent with the estimation of proportion of significant venous involvementin histological series of connective tissue disease-associated PAH [21].

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Pathophysiology

• As the name suggests Pulmonary veno-occlusive disease (PVOD) uniquely involves the small veins of the lung circulation more than the small arteries. The veins become blocked with scar tissue that is not normally present.

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