Examples include collapsed lungs which have formed bullae, chronic obstructive lung disease, lung cancer, and fibrocavitary sarcoidosis. Another risk factor is immunosuppression; most commonly, this includes allogeneic stem cell transplantation, prolonged neutropaenia, immunosuppressive drug therapy, chronic granulomatous disease and haematological malignancies. Certain demographics are also at higher risk, including the elderly, male gender and those with a low body mass index.There appears to be increasing evidence for complex genetic factors increasing the risk of developing chronic pulmonary aspergillosis, such as defects to toll-like receptor (TLR) 4, IL1 and IL15, TLR3, TLR10, TREM1, VEGFA, DENND1B, and PLAT. Mechanism
The full underlying pathogenesis is not completely understood. Most people with chronic pulmonary aspergillosis have functional immune status, but usually have underlying structural damage to the lungs from an underlying process or disease. Most commonly, pre-existing pulmonary cavities from other diseases such as tuberculosis become colonised with Aspergillus conidia which have been inhaled—humans inhale between 1,000 and 10 billion spores per day, of which A. fumigatus is the most common.Aspergillomas themselves usually form in existing cavities but the cavities may form directly from chronic pulmonary aspergillosis. People with pulmonary tuberculosis with a cavity larger than 2 cm appear to have a 20% increased risk of developing chronic pulmonary aspergillosis.It is postulated that conidia, once inhaled, are attacked by the host immune defences—specifically phagocytes and alveolar macrophage resident in the small airways. It is unknown whether these defences are sufficient to clear conidia or whether they are directly responsible for the inflammation leading to chronic pulmonary aspergillosis.
During diastole, less blood flow in left ventricle allows for more room for filling in right ventricle and therefore a septal shift occurs.During expiration, the amount of blood entering the left ventricle will increase, allowing the interventricular septum to bulge towards the right ventricle, decreasing the right heart ventricular filing. Diagnosis
The diagnosis of constrictive pericarditis is often difficult to make. In particular, restrictive cardiomyopathy has many similar clinical features to constrictive pericarditis, and differentiating them in a particular individual is often a diagnostic dilemma. Chest X-Ray - pericardial calcification (common but not specific), pleural effusions are common findings. Echocardiography - the principal echographic finding is changes in cardiac chamber volume. CT and MRI - CT scan is useful in assessing the thickness of pericardium, calcification, and ventricular contour. Cardiac MRI may find pericardial thickening and pericardial-myocardial adherence. Ventricular septum shift during breathing can also be found using cardiac MRI. Late gadolinium enhancement can show enhancement of the pericardium due to fibroblast proliferation and neovascularization. BNP blood test -  tests for the existence of the cardiac hormone brain natriuretic peptide, which is only present in restrictive cardiomyopathy but not in constrictive pericarditis
Conventional cardiac catheterization
Physical examination - can reveal clinical features including Kussmauls sign and a pericardial knock. Treatment
The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart.