The influence of pulmonary disease on ventricular diastolic disfunction in COPD and idiopathic pulmonary fibrosis (IPF)

K. M. Antoniou, A. Dermitzakis, G. Meletis, M. Ferdoutsis, G. Patsourakis, N. Tzanakis, N. Bachlitzanakis, D. Bouros (Heraklion, Greece)

Source: Annual Congress 2002 - High altitude and hypoxia
Session: High altitude and hypoxia
Session type: Thematic Poster Session
Number: 689
Disease area: Pulmonary vascular diseases

Congress or journal article abstract

Abstract

PURPOSE: The aim of this study was to ascertain the influence of COPD and IPF on ventricular diastolic dysfunction and to compare the two groups.
METHODS: We studied 13 COPD patients (median age, 67yr) and 13 IPF patients with histologically proven disease (median age, 72 yr) with echocardiography. Parameters measured included isovolumic relaxation time (IVRT= time from semilunar valve closure to atrioventricular (AV) valve opening), early and late AV flow velocities (E and A wave, respectively), E/A ratio in right (RV) and left (LV) ventricle. Pulmonary arterial hypertension (PH) was assessed by measuring the systolic pressure of pulmonary artery.
RESULTS: RV IVTR was found abnormal, i.e. >30±]10 ms, in COPD (mean±]SD, 52.7±]17.3) and in IPF patients (38.02±]15.6). This difference is statistically significant (p=0.019). LV IVTR was preserved in both groups (COPD 86.3±]18.4, IPF 80.7±]12.3, p=0.44). The E/A ratio (normal value >1) was found abnormal in both groups, without significant difference between them (p>0.05). Mean+SD PH was moderately increased (46±]14 mmHg) in COPD and mildly (38±]9 mmHg) in IPF (p=0.22).
CONCLUSION: Our results show that both COPD and IPF have a negative influence on ventricular diastolic function and is more prominent in COPD.


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K. M. Antoniou, A. Dermitzakis, G. Meletis, M. Ferdoutsis, G. Patsourakis, N. Tzanakis, N. Bachlitzanakis, D. Bouros (Heraklion, Greece). The influence of pulmonary disease on ventricular diastolic disfunction in COPD and idiopathic pulmonary fibrosis (IPF). Eur Respir J 2002; 20: Suppl. 38, 689

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