Reduced systemic arterial compliance and subclinical LV systolic dysfunction in COPD

Abstract

Background: We hypothesized that COPD leads to alterations in systemic vascular structure and that systemic arterial compliance (SAC) would have impact on the LV function even in a population free of clinical cardiovascular disease. Methods: Patients with COPD (GOLD stage I-IV) and matched healthy controls were included. Those with LV disease were excluded. Coronary heart disease was excluded by exercise ECG. The following TDI based indices for LV function were performed: LV acceleration during isovolumic contraction (LVIVA), myocardial performance-index (LVMPI) and peak systolic velocity (LVSm). SAC was calculated as stroke volume (ml)/systemic pulse pressure (mmHg). Inflammatory markers (Table) were measured. Results: Consistent with reduced SAC, a significant increase in systolic blood pressure was observed in the patient group (Table). Stroke volume did not differ between the groups. Significantly higher levels of the biomarkers were found (all p<0.01) (Table). There were significant associations at p<0.01 between SAC and CRP and IL-6 in patients with COPD, but not in controls. Pulse pressure correlated with metalloproteinase (MMP-9), r=0.44 (p<0.01). LVEF was preserved; TDI measures for LV function were all significantly impaired in COPD (Table). SAC correlated significantly with LVIVA, LV Sm and LVMPI, r=-0.3, 0.4 and -0.3 (p<0.01), respectively. View this table: Table 1 Conclusions: COPD patients showed subclinical LV dysfunction by TDI along with systemic inflammation, increased elastolytic activity and reduced arterial compliance, compared to controls. The reduction in SAC provides one mechanism for the observed LV dysfunction in these patients.