There is a growing prevalence of chronic obstructive pulmonary disease (COPD) globally and 15.2% of Americans suffer from this disease.1 The lungs and cardiovascular systems are intimately linked and it is well known that smoke inhalation is a major risk factor for vascular disease. In addition, the lungs and heart compete for intrathoracic space and alterations in lung mechanics associated with lung disease – hyperinflation – and shifts in intrathoracic pressure due to lung disease likely also impact central hemodynamics.2–4 Furthermore, pulmonary vascular remodeling occurs in COPD, which consequently influences pulmonary vascular pressures.5,6 Therefore, the present study investigated the relationship between lung function and central aortic hemodynamics in COPD, and the response of central aortic hemodynamics to acute exercise.

The present study was reviewed and approved by Mayo Clinic Institutional Review Board. Twenty-five patients with COPD provided written informed consent and underwent pulmonary function testing (PFT), quality of life questionnaire assessment, as well as quantification of blood pressure (BP) and heart rate (HR). Subsequently, subjects were divided into either a more moderate disease group (MOD) or a mild group (MLD) based on scoring of COPD severity using lung function. Severity score was determined by quantifying lung diffusing capacity for carbon dioxide (DLCO), forced vital capacity (FVC), forced expiratory flow between 25 and 75% of FVC (FEF25−75), forced expiatory volume-one second (FEV1), maximum voluntary ventilation (MVV), and then ranking subjects from 1st (the most severe) to 24th (the least severe) based on percent predicted value for each parameter. The rankings for each of the 5 parameters were then averaged for each subject, and severity status determined by the average rank such that the 1st to 12th ranked subjects were defined as severe (MOD, n = 12) and the 13th to 24th ranked subjects were defined as moderate (MLD, n = 12). Table 1 demonstrates the subjects’ characteristics.

Peripheral systolic blood pressure (pSBP) and diastolic blood pressure (pDBP) was measured manually, while central systolic pressure (cSBP), central diastolic pressure (cDBP), central pulse pressure (cPP), pressure of the incident wave (P1), augmentation pressure (AP), pulse wave velocity (PWV), augmentation index (AIx) were assessed via central arterial pressure waveform analysis (Sphygmocor, AtCor Medical, Australia). All subjects underwent a symptom-limited incremental exercise test on a cycle ergometer and the wattage was increased by 10−15 watts every minute to exertional exhaustion. During exercise, respiratory gas exchange, heart rate (HR), pSBP, pDBP, oxygen saturation (SaO2), rate of perceived exertion (RPE) and dyspnea were assessed. After exercise, subjects were at rest for 20 min before a repeat central hemodynamic assessment was obtained.

To examine the relationships between central aortic hemodynamics and pulmonary function measures in all subjects (n = 24), correlation coefficient analysis was conducted. To compare group differences (MOD vs MLD) at pre-exercise, independent t-test and the Mann-Whitney U non-parametric t-test were conducted. To examine an exercise effect, a repeated-measures analysis of variance (ANOVA) was conducted to observe alterations in central hemodynamic parameters from pre- to post-exercise.

Central diastolic blood pressure is elevated in COPD patients, linked to disease severity, and remains elevated after exercise-induced reductions in peripheral diastolic blood pressure. However, these observations occurred similarly between mild and more moderate disease.

The authors have no conflicts of interest to declare.