Abstract

We aimed to assess prevalence of left ventricular (LV) systolic and diastolic function in stable cohort of COPD patients, where LV disease had been thoroughly excluded in advance. 100 COPD outpatients in GOLD II-IV and 34 controls were included. Patients were divided by invasive mean pulmonary artery pressure (mPAP) in COPD-PH (≥25 mmHg) and COPD-non-PH (<25 mmHg), which was subdivided in mPAP ≤20 mmHg and 21-24 mmHg. LV myocardial performance index (LV MPI) and strain by tissue Doppler imaging (TDI) were used for evaluation of LV global and systolic function, respectively. LV MPI ≥0.51 and strain ≤-15.8% were considered abnormal. LV diastolic function was assessed by the ratio between peak early (E) and late (A) velocity, early TDI E´, E/E´, isovolumic relaxation time, and left atrium volume. LV MPI ≥0.51 was found in 64.9% and 88.5% and LV strain ≤-15.8% in 62.2.% and 76.9% in the COPD-non-PH and COPD-PH patients, respectively. Similarly, LV MPI and LV strain were impaired even in patients with mPAP <20 mmHg. In multiple regression analyses, residual volume and stroke volume were best associated to LV MPI and LV strain, respectively. Except for isovolumic relaxation time, standard diastolic echo indices as E/A, E´, E/E´ and left atrium volume did not change from normal individuals to COPD-non-PH. Subclinical LV systolic dysfunction was a frequent finding in this cohort of COPD patients, even in those with normal pulmonary artery pressure. Evidence of LV diastolic dysfunction was hardly present as measured by conventional echo indices.

Highlights

  • In patients with chronic obstructive pulmonary disease (COPD), and in particular in those with severe emphysema, pulmonary hypertension and right ventricular (RV) enlargement, the left ventricle is compressed

  • Subclinical left ventricular (LV) systolic dysfunction was a frequent finding in this cohort of COPD patients, even in those with normal pulmonary artery pressure

  • Because of this and the symptom similarity between heart failure and COPD, there is a need for more sensitive diagnostic tools to unmask if LV systolic subclinical impairment is present in COPD patients

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Summary

Introduction

In patients with chronic obstructive pulmonary disease (COPD), and in particular in those with severe emphysema, pulmonary hypertension and right ventricular (RV) enlargement, the left ventricle is compressed. The majority of COPD patients with such findings shows a leftward ventricular septum deviation, most marked at end systole and early diastole, associated with a distortion of LV geometry and reduction of early diastolic filling [1, 2]. This mechanism is thought to be the most likely cause for the decreased LV size, stroke volume and under filling of the left ventricle [1,2,3]. There is only a few existing studies on COPD and LV function recruiting mostly severe COPD, having small number of participants, and they are deficient with respect to invasive pressure data [6,7,8]

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