No abstract

Right ventricular (RV) wall tension in pulmonary arterial hypertension (PAH) is determined not only by pressure, but also by RV volume. A larger volume at a given pressure generates more wall tension. Return of reflected waves early after the onset of contraction, when RV volume is larger, may augment RV load. We aimed to elucidate: (1) the distribution of arrival times of peak reflected waves in treatment-naïve PAH patients; (2) the relationship between time of arrival of reflected waves and RV morphology; and (3) the effect of PAH treatment on the arrival time of reflected waves. Wave separation analysis was conducted in 68 treatment-naïve PAH patients. In the treatment-naïve condition, 54% of patients had mid-systolic return of reflected waves (defined as 34-66% of systole). Despite similar pulmonary vascular resistance (PVR), patients with mid-systolic return had more pronounced RV hypertrophy compared to those with late-systolic or diastolic return (RV mass/body surface area; mid-systolic return 54.6 ± 12.6 g m -2 , late-systolic return 44.4 ± 10.1 g m -2 , diastolic return 42.8 ± 13.1 g m -2 ). Out of 68 patients, 43 patients were further examined after initial treatment. At follow-up, the stiffness of the proximal arteries, given as characteristic impedance, decreased from 0.12 to 0.08 mmHg s mL -1 . Wave speed was attenuated from 13.3 to 9.1 m s -1 , and the return of reflected waves was delayed from 64% to 71% of systole. In conclusion, reflected waves arrive at variable times in PAH. Early return of reflected waves was associated with more RV hypertrophy. PAH treatment not only decreased PVR, but also delayed the timing of reflected waves.

This study aimed to determine the differences in haemodynamic responses to a standard incremental exercise test between outpatients with chronic obstructive pulmonary disease (COPD) and age-matched controls and to discover the relationship between severity of airflow obstruction and exercise haemodynamics in COPD. Twenty-two male patients with COPD (forced expiratory volume in one second (FEV1)/vital capacity (VC))<80% predicted) and 20 age-matched male controls performed an incremental exercise test (10 W x min(-1)) with ventilatory function and changes in stroke volume (deltaSV) and cardiac output (deltaCO) measured by means of electrical impedance cardiography (EIC). Submaximal deltaSV and deltaCO were lower in COPD patients. Peak exercise deltaSV were equal in patients and controls (128+/-33 versus 129+/-29%, p=0.98), whereas peak deltaCO was lower in patients (COPD versus controls: 232+/-71 versus 289+/-54%, p<0.005). In COPD patients, FEV1 (% pred) was significantly correlated to deltaSV at all submaximal exercise intensities, to peak exercise deltaSV and to peak exercise deltaCO. FEV1/VC (% pred) was significantly correlated to deltaSV at 30 and 60 W. In conclusion, in chronic obstructive pulmonary disease an aberrant haemodynamic response to exercise was found, especially in patients with severe airflow obstruction. This aberrant response is related to the degree of airflow obstruction and may limit exercise performance in patients with severe chronic obstructive pulmonary disease.