Journal of Bronchology & Interventional Pulmonology:
*D.N. Sharma Hospital, Sonipat, Haryana
†Lung Care & Sleep Centre, Fortis Hiranandani Hospital, Vashi, Navi Mumbai, India
‡Respiratory Institute, Cleveland Clinic, Cleveland, OH
Disclosure: There is no conflict of interest or other disclosures.
Reprints: Atul C. Mehta, MD, FACP, FCCP, Respiratory Institute, Cleveland Clinic, 9500 Euclid Avenue, A-90, Cleveland, OH 44195 (e-mail: firstname.lastname@example.org).
Received August 30, 2013
Accepted February 28, 2014
Chronic pulmonary venous hypertension causes dilatation and engorgement of bronchial veins because of a close communication between bronchial and pulmonary veins. We report a case of severe left ventricular systolic dysfunction with chronically elevated pulmonary venous pressure leading to characteristic bronchoscopic findings of engorgement of bronchial veins.
Pulmonary venous hypertension, also referred as type II pulmonary hypertension, is associated with left heart diseases such as ventricular systolic and valvular dysfunctions, constrictive pericardial diseases, and restrictive cardiomyopathy.1 There is a study documenting a close communication between the pulmonary and bronchial venous systems. Whenever pulmonary venous pressure increases, a reverse flow takes place from the pulmonary veins to the bronchial veins. This leads to dilatation of submucosal bronchial veins in the endobronchial tree.2 With the increasing use of flexible bronchoscopy in the diagnosis and management of respiratory diseases, we are encountering various endobronchial findings related to systemic diseases with increasing frequency. Here we present characteristic bronchoscopic findings of dilated and tortuous submucosal bronchial veins in a 48-year-old male with nonischemic cardiomyopathy, leading to chronically elevated pulmonary venous pressure.
A 48-year-old male with a history of nonischemic dilated cardiomyopathy presented for the evaluation of possible heart transplantation. He was symptomatic with dry cough, dyspnea on exertion—NYHA grade II, weight loss of 8 pounds in last 6 months, and intermittent bilateral leg swelling. The patient denied history of fever, chest pain, or night sweats and had no prior history of tuberculosis. On physical examination, the patient had increased jugular venous distension, bilateral pedal edema, bibasal crepitations, systolic murmur, and abdominal distension with shifting dullness. Echocardiography revealed left ventricular ejection fraction of 15%, 4 chambers dilatation, estimated right ventricular systolic pressure of 44 mm Hg, mild mitral valve regurgitation with annular calcification, and moderate to severe tricuspid regurgitation. Right heart catheterization revealed pulmonary venous hypertension (mean pulmonary artery pressure: 53 mm Hg, pulmonary capillary wedge pressure: 36 mm Hg, pulmonary vascular resistance: 3 woods units) with marked elevated filling pressures and moderately reduced cardiac index of 2.26 L/min/m2. His serum Quantiferon test was positive for latent tuberculosis. On further evaluation, plain and contrast computed tomography (CT) of thorax revealed subcarinal and right paratracheal noncalcified lymphadenopathy and nonspecific ground-glass opacities in both lungs. Considering above findings, bronchoscopy and endobronchial ultrasound–guided transbronchial needle aspiration was performed to rule out active tuberculosis before considering the heart transplantation. Flexible bronchoscopy revealed increased vascularity with engorged tortuous submucosal vessels without any other bronchial abnormality (Figs. 1, 2). On the basis of the patient’s hemodynamic parameters, these vessels were identified as bronchial veins.
Incidentally, all bronchoscopy specimens were negative for active mycobacterial infection.
The pulmonary and bronchial venous circulation systems are connected to each other through bronchial venous plexuses. Auld and colleagues documented that when pulmonary venous pressure increases, the amount of blood flow originating in the bronchial arteries and returning to pulmonary veins through bronchial veins decreases. They also observed an increase in the amount of blood flow into azygos and hemiazygos veins with establishment of reverse flow from pulmonary veins to the bronchial veins. This reverse flow functions as an escape pathway to decrease the pulmonary venous pressure.3,4 The above phenomenon leads to dilatation and engorgement of bronchial venous plexus as seen in our patient. Such patients are more prone to hemoptysis on minimal stimuli such as cough or sudden elevation of the left atrial load.5 Our patient has not experienced hemoptysis, yet.
Similar bronchoscopic findings are also observed in fibrosing mediastinitis and superior vena cava (SVC) obstruction syndrome.4,6 In fibrosing mediastinitis, the distal fibrotic masses could cause partial obliteration of bronchial arteries and veins, leading to high intravascular pressures.6 It can be differentiated from the above by a CT scan of the chest. Findings suggestive of the latter on CT are obliteration of fat planes of the mediastinum and the presence of discrete masses or/and extensive calcified mediastinal lymphadenopathy causing circumferential encasement of the mediastinal structures.6 In SVC syndrome, dilatation of bronchial veins occurs because of obstruction to the blood flow into the hemiazygos veins. The other mechanism is a reverse flow from azygos or hemiazygos vein into pulmonary veins.4 The SVC syndrome can also be ruled out easily by the CT scan findings.
In conclusion, chronic left ventricular systolic dysfunction leads to pulmonary venous hypertension, which can present with characteristic bronchoscopic findings of engorged bronchial veins.
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