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Circulation. 1999;100:1808-1815

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(Circulation. 1999;100:1808-1815.)
© 1999 American Heart Association, Inc.


Clinical Investigation and Reports

Central Pulmonary Artery Lesions in Chronic Obstructive Pulmonary Disease

A Transesophageal Echocardiography Study

Aldo Russo, MD; Massimo De Luca, MD; Carlo Vigna, MD; Vincenzo De Rito, MD; Michele Pacilli, MD; Antonella Lombardo, MD; Michele Armillotta, MD; Raffaele Fanelli, MD; Francesco Loperfido, MD

From the Departments of Cardiology (A.R., C.V., V.D., M.P., R.F.) and Radiology (M.A.), Ospedale Casa Sollievo della Sofferenza, IRCCS, San Giovanni Rotondo, and the Institute of Cardiology, Catholic University Sacro Cuore (M.D., A.L., F.L.), Rome, Italy.

Correspondence to Prof Francesco Loperfido, Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Complesso Integrato Columbus, Via G. Moscati, 31/33, 00168 Roma, Italy. E-mail columbus.cardio{at}linet.it

Background—In patients with acute pulmonary embolism, transesophageal echocardiography (TEE) often reveals presumably thrombotic lesions within the central pulmonary arteries (CPAs). These CPA lesions, when found in patients with primary pulmonary hypertension, have been attributed to in situ thrombosis or atherosclerosis. We hypothesized that similar CPA lesions may also develop in patients with chronic obstructive pulmonary disease (COPD) in the absence of pulmonary embolism.

Methods and Results—We examined by TEE 25 patients with COPD and 27 control patients with left heart disease. None of the patients had previous pulmonary embolism or ileofemoral and popliteal vein thrombosis. By use of TEE, CPA lesions were found in 12 COPD patients (48%) and 2 control patients (7.4%) (P<0.01). When CPA lesions were subdivided into types 1 (protruding and mobile) and 2 (wall-adherent), type 1 lesions proved to be uncommon, being found within the pulmonary trunk in 12% and 3.7% of COPD and control patients, respectively (P=NS). Conversely, type 2 lesions, which were always localized in the right pulmonary artery, were frequent in COPD patients (36%) and rare in control patients (3.7%) (P<0.01). When available, helical CT and MR angiography confirmed TEE findings, supporting an atherosclerotic origin of type 2 lesions, which were different from typical thrombotic lesions. FEV1/FVC ratio, RV/TLC ratio, PaO2, hematocrit value, and pulmonary artery systolic pressure were not significantly different in COPD patients with and without CPA lesions. At TEE, however, COPD patients with CPA lesions showed a larger size of the main and right pulmonary arteries.

Conclusions—TEE often reveals CPA lesions in stable patients with COPD even in the absence of significant pulmonary hypertension and not in close relation with the severity of pulmonary dysfunction.


Key Words: echocardiography • thrombus • pulmonary heart disease




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