The distorted, damaged lung airways thus have impaired mucociliary clearance; leading to mucous stasis and bacterial colonization leading to further neutrophil activation and thus fueling a self-perpetuating "vicious cycle" of inflammation in bronchiectasis. This "vicious cycle" theory is the generally accepted explanation for the pathogenesis of bronchiectasis.Endobronchial tuberculosis commonly leads to bronchiectasis, either from bronchial stenosis or secondary traction from fibrosis. Traction bronchiectasis characteristically affects peripheral bronchi (which lack cartilage support) in areas of end-stage fibrosis. Diagnosis
The goals of a diagnostic evaluation for bronchiectasis are radiographic confirmation of the diagnosis, identification of potential treatable causes, and functional assessment of the patient. A comprehensive evaluation consists of radiographic imaging, laboratory testing, and lung function testing.Laboratory tests that are commonly part of the initial evaluation include a complete blood count, sputum cultures for bacteria, mycobacteria, and fungi, testing for cystic fibrosis, and immunoglobulin levels. Additional tests that are sometimes indicated include testing for specific genetic disorders.Lung function testing is used for the assessment and monitoring of functional impairment due to bronchiectasis. These tests may include spirometry and walking tests. Obstructive lung impairment is the most common finding but restrictive lung impairment can be seen in advanced disease. Flexible bronchoscopy may be performed when sputum studies are negative and a focal obstructing lesion is suspected.A chest x-ray is abnormal in most patients with bronchiectasis. Computed tomography is recommended to confirm the diagnosis and is also used to describe the distribution and grade the severity of the disease. Radiographic findings include airway dilation, bronchial wall thickening, and atelectasis.
In cardiology, hibernating myocardium is a state when some segments
of the myocardium exhibit abnormalities of contractile function. These
abnormalities can be visualised with echocardiography,  cardiac magnetic resonance imaging (CMR), nuclear medicine (PET) or ventriculography. Echocardiography: A wall motion abnormality at rest which improves during a low-dose dobutamine stress test is classified as "hibernating myocardium." Low dose dobutamine stimulates contractile function and thus helps to predict functional recovery after revascularization. Cardiac magnetic resonance: The most frequently used MR contrast agents based on Gd-chelates accumulate in the extracellular space which is increased in scarred myocardium. This leads to a signal increase which can be visualised with the "late gadolinium enhancement technique." This is probably the most accurate way to visualise scarred myocardium. An alternative (or additional) technique with CMR is the use of low dose dobutamine similar to echocardiography. PET: The finding of a perfusion or metabolic mismatch between PET-FDG and PET-NH3 is indicative of decreased metabolism. The wall of the affected segments is hypo-, a-, or dyskinetic.The phenomenon is highly significant clinically because it usually manifests itself in the setting of chronic ischemia, that is potentially reversible by revascularisation via cardiac catheterization. The regions of myocardium are still viable and can return to normal function. There develops a new steady state between myocardial blood flow (MBF) and myocardial function, MBF reduced and in consequence function is reduced too. The clinical situations where one can expect hibernating myocardium are:
chronic stable angina
unstable angina
silent ischemia
after AMI

See also
Stunned myocardium
Myocardial scarring


== References ==