Abstract
BackgroundBoth pulmonary arterial stiffening and systemic arterial stiffening have been described in COPD. The aim of the current study was to assess pulse wave velocity (PWV) within these two arterial beds to determine whether they are separate or linked processes.Materials and methodsIn total, 58 participants with COPD and 21 healthy volunteers (HVs) underwent cardiac magnetic resonance imaging (MRI) and were tested with a panel of relevant biomarkers. Cardiac MRI was used to quantify ventricular mass, volumes, and pulmonary (pulse wave velocity [pPWV] and systemic pulse wave velocity [sPWV]).ResultsThose with COPD had higher pPWV (COPD: 2.62 vs HV: 1.78 ms−1, p=0.006), higher right ventricular mass/volume ratio (RVMVR; COPD: 0.29 vs HV: 0.25 g/mL, p=0.012), higher left ventricular mass/volume ratio (LVMVR; COPD: 0.78 vs HV: 0.70 g/mL, p=0.009), and a trend toward a higher sPWV (COPD: 8.7 vs HV: 7.4 ms−1, p=0.06). Multiple biomarkers were elevated: interleukin-6 (COPD: 1.38 vs HV: 0.58 pg/mL, p=0.02), high-sensitivity C-reactive protein (COPD: 6.42 vs HV: 2.49 mg/L, p=0.002), surfactant protein D (COPD: 16.9 vs HV: 9.13 ng/mL, p=0.001), N-terminal pro-brain natriuretic peptide (COPD: 603 vs HV: 198 pg/mL, p=0.001), and high-sensitivity troponin I (COPD: 2.27 vs HV: 0.92 pg/mL, p<0.001). There was a significant relationship between sPWV and LVMVR (p=0.01) but not pPWV (p=0.97) nor between pPWV and RVMVR (p=0.27).ConclusionPulmonary arterial stiffening and systemic arterial stiffening appear to be disconnected and should therefore be considered independent processes in COPD. Further work is warranted to determine whether both these cause an increased morbidity and mortality and whether both can be targeted by similar pharmacological therapy or whether different strategies are required for each.
Highlights
The aim of the current study was to examine the association between aortic and pulmonary arterial stiffening using pulse wave velocity (PWV) and their effects on cardiac remodeling with the hypotheses that 1) aortic stiffening and pulmonary stiffening occur in parallel; 2) inflammatory markers would explain this interaction; and 3) elevated PWV would be associated with adaptive ventricular remodeling with an increased ventricular mass to end diastolic volume ratio
Despite approximate age and sex matching, those with COPD were significantly older (p,0.001) and had a higher body mass index (BMI; COPD: 26.8±5.3 kg/m2 vs healthy control (HC): 24.6±2.5 kg/m2, p=0.02). While those with COPD had a significantly higher prevalence of hypertension, there was no significant difference in blood pressure or pulse pressure due to a higher prevalence of antihypertensive medication prescription
We have seen that 1) both pulmonary and systemic arteries are stiffer in COPD compared with controls; 2) aortic PWV and pulmonary PWV are associated with different clinical parameters and biomarkers from one another; and 3) aortic but not pulmonary PWV is associated with ventricular hypertrophy
Summary
Despite being a disease of the pulmonary parenchyma, COPD is associated with significant cardiac morbidity and mortality, with up to 43% of mortality in COPD secondary to cardiovascular causes.[1,2,3] Even in the absence of pulmonary hypertension, those with COPD demonstrate right ventricular (RV) dysfunction,[4,5] and diastolic and systolic left heart failures are present in .20% of those with moderate-to-severe COPD.[6,7]. Both pulmonary arterial stiffening and systemic arterial stiffening have been described in COPD. Cardiac MRI was used to quantify ventricular mass, volumes, and pulmonary (pulse wave velocity [pPWV] and systemic pulse wave velocity [sPWV]).
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