Jinelle Gelinas

Aerobic exercise training does not alter vascular structure and function in chronic obstructive pulmonary disease

What is the central question of this study? Chronic obstructive pulmonary disease (COPD) is associated with endothelial dysfunction, arterial stiffness and systemic inflammation, which are linked to increased cardiovascular disease risk. We asked whether periodized aerobic exercise training could improve vascular structure and function in patients with COPD. What is the main finding and its importance? Eight weeks of periodized aerobic training did not improve endothelial function, arterial stiffness or systemic inflammation in COPD, despite improvements in aerobic capacity, blood pressure and dyspnoea. Short‐term training programmes may not be long enough to improve vascular‐related cardiovascular risk in COPD.

Ventricular-Arterial Coupling in Breast Cancer Patients After Treatment With Anthracycline-Containing Adjuvant Chemotherapy

BACKGROUND Anthracycline-containing chemotherapy (Anth-C) is associated with long-term cardiovascular mortality. Although cardiovascular risk assessment has traditionally focused on the heart, evidence has demonstrated that vascular dysfunction also occurs during and up to 1 year following Anth-C. Whether vascular dysfunction persists long-term or negatively influences cardiac function remains unknown. Hence, the present study evaluated ventricular-arterial coupling, in concert with measures of vascular structure and function, in the years following Anth-C. METHODS Arterial elastance (Ea), end-systolic elastance (Ees), and ventricular-arterial coupling (Ea/Ees) were measured during rest and exercise using echocardiography. Resting vascular function (flow-mediated dilation) and structure (carotid intima-media thickness, arterial stiffness) were also measured. RESULTS Thirty breast cancer survivors (6.5 ± 3.6 years after Anth-C) with normal left ventricular ejection fraction (LVEF) (60% ± 6%) and 30 matched controls were studied. At rest, no differences were found in Ea, Ees, Ea/Ees, or LVEF between groups. The normal exercise-induced increase in Ees was attenuated in survivors at 50% and 75% of maximal workload (p < .01). Ea/Ees was also higher at all workloads in the survivors compared with the controls (p < .01). No differences in vascular structure and function were observed between the two groups (p > .05). CONCLUSION In the years after Anth-C, ventricular-arterial coupling was significantly attenuated during exercise, primarily owing to decreased LV contractility (indicated by a reduced Ees). This subclinical dysfunction appears to be isolated to the heart, as no differences in Ea were observed. The previously reported adverse effects of Anth-C on the vasculature appear to not persist in the years after treatment, as vascular structure and function were comparable to controls. IMPLICATIONS FOR PRACTICE Anthracycline-induced cardiotoxicity results in significantly impaired ventricular-arterial coupling in the years following chemotherapy, owing specifically to decreased left ventricular contractility. This subclinical dysfunction was identified only under exercise stress. A comprehensive evaluation of vascular structure and function yielded no differences between those treated with anthracyclines and controls. Combined with a stress stimulus, ventricular-arterial coupling might hold significant value beyond characterization of integrative cardiovascular function, in particular as a part of a risk-stratification strategy after anthracycline-containing chemotherapy. Although vascular function and structure were not different in this cohort, this does not undermine the importance of identifying vascular (dys)function in this population, because increases in net arterial load during exercise might amplify the effect of reductions in contractility on cardiovascular function after anthracycline-containing chemotherapy.

The haemodynamic response to incremental increases in negative intrathoracic pressure in healthy humans

What is the central question of this study? The haemodynamic response to incremental increases in negative intrathoracic pressure (nITP) during spontaneous breathing and the mechanisms of cardiac impairment at these levels of nITP remain unclear. What is the main finding and its importance? nITP of −20 cmH2O or greater reduces stroke volume in healthy, spontaneously breathing supine humans due to direct ventricular interaction and increased left ventricular afterload.

Cerebrovascular Function in Patients with Chronic Obstructive Pulmonary Disease: The Impact of Exercise Training

This study examined cerebral blood flow (CBF) and its regulation before and after a short-term periodized aerobic exercise training intervention in patients with chronic obstructive pulmonary disease (COPD). Twenty-eight patients with COPD (forced expiratory volume in 1 s/forced vital capacity < 0.7 and <lower limit of normal) and 24 healthy control subjects participated in the study. Extracranial CBF (duplex ultrasound), middle cerebral artery velocity (MCAv; transcranial Doppler), cerebrovascular reactivity to hypocapnia and hypercapnia, and dynamic cerebral autoregulation (transfer function analysis) were quantified. These tests were repeated in both patients with COPD ( n = 23) and control subjects ( n = 20) after 8 wk of periodized upper and lower body aerobic exercise training (3 sessions/wk). At baseline, global extracranial CBF was comparable between the COPD and control groups (791 ± 290 vs. 658 ± 143 ml/min, P = 0.25); however, MCAv was lower in patients with COPD compared with control subjects (46 ± 9 vs. 53 ± 10 cm/s, P = 0.05). Although there were no group differences in dynamic cerebral autoregulation or the MCAv response to hypercapnia, patients with COPD had a lower MCAv response to hypocapnia compared with control subjects (-1.1 ± 1.5 vs. -1.6 ± 1.3 cm·s-1·mmHg-1, P = 0.02). After aerobic training, absolute peak O2 consumption increased in both groups, with a greater improvement in control subjects (1.7 ± 0.4 vs. 4.1 ± 0.2 ml·kg-1·min-1, respectively, P = 0.001). Despite these improvements in peak O2 consumption, there were no significant alterations in CBF or any measures of cerebrovascular function after exercise training in either group. In conclusion, patients with COPD have a blunted cerebrovascular response to hypocapnia, and 8 wk of aerobic exercise training did not alter cerebrovascular function despite significant improvements in cardiorespiratory fitness. NEW & NOTEWORTHY No study to date has investigated whether exercise training can alter resting cerebral blood flow (CBF) regulation in patients with chronic obstructive pulmonary disease (COPD). This study is the first to assess CBF regulation at rest, before, and after aerobic exercise training in patients with COPD and healthy control subjects. This study demonstrated that while exercise training improved aerobic fitness, it had little effect on CBF regulation in patients with COPD or control subjects.

Hemodynamic effects of incremental lung hyperinflation

Dynamic hyperinflation (DH) is common in chronic obstructive pulmonary disease and is associated with dyspnea and exercise intolerance. DH also has adverse cardiac effects, although the magnitude of DH and the mechanisms responsible for the hemodynamic impairment remain unclear. We hypothesized that incrementally increasing DH would systematically reduce left ventricular (LV) end-diastolic volume (LVEDV) and LV stroke volume (LVSV) because of direct ventricular interaction. Twenty-three healthy subjects (22 ± 2 yr) were exposed to varying degrees of expiratory loading to induce DH such that inspiratory capacity was decreased by 25%, 50%, 75%, and 100% (100% DH =  inspiratory capacity of resting tidal volume plus inspiratory reserve volume ≈ 0.5 l). LV volumes, LV geometry, inferior vena cava collapsibility, and LV end-systolic wall stress were assessed by triplane echocardiography. 25% DH reduced LVEDV (-6 ± 5%) and LVSV (-9 ± 8%). 50% DH elicited a similar response in LVEDV (-6 ± 7%) and LVSV (-11 ± 10%) and was associated with significant septal flattening [31 ± 32% increase in the radius of septal curvature at end diastole (RSC-ED)]. 75% DH caused a larger reduction in LVEDV and LVSV (-9 ± 7% and -16 ± 10%, respectively) and RSC-ED (49 ± 70%). 100% DH caused the largest reduction in LVEDV and LVSV (-13 ± 9% and -18 ± 9%) and an increase in RSC-ED (56 ± 63%). Inferior vena cava collapsibility and LV afterload (LV end-systolic wall stress) were unchanged at all levels of DH. Modest DH (-0.6 ± 0.2 l inspiratory reserve volume) reduced LVSV because of reduced LVEDV, likely because of increased pulmonary vascular resistance. At higher levels of DH, direct ventricular interaction may be the primary cause of attenuated LVSV, as indicated by septal flattening because of a greater relative increase in right ventricular pressure and/or mediastinal constraint. NEW & NOTEWORTHY By systematically reducing inspiratory capacity during spontaneous breathing, we demonstrate that dynamic hyperinflation (DH) progressively reduces left ventricular (LV) end diastolic volume and LV stroke volume. Evidence of significant septal flattening suggests that direct ventricular interaction may be primarily responsible for the reduced LV stroke volume during DH. Hemodynamic impairment appears to occur at relatively lower levels of DH and may have important clinical implications for patients with chronic obstructive pulmonary disease.