Sophie Lalande

Pulmonary vascular distensibility predicts aerobic capacity in healthy individuals

Pulmonary transit of agitated contrast (PTAC) occurs during exercise in healthy individuals. It has been suggested that positive PTAC reflects a greater pulmonary vascular reserve, allowing for the right ventricle to operate at a decreased afterload at high levels of exercise. In this study, we determined whether individuals with highest maximal aerobic capacity have the greatest pulmonary vascular distensibility, highest PTAC and greatest increase in the capillary blood component of lung diffusing capacity during exercise. We observed that individuals with highest maximal aerobic capacity have a more distensible pulmonary circulation as observed through greater pulmonary vascular distensibility, greater pulmonary capillary blood volume, and lowest pulmonary vascular resistance at maximal exercise. Pulmonary vascular distensibility predicts aerobic capacity in healthy individuals.

Reduced leg blood flow during submaximal exercise in type 2 diabetes.

UNLABELLED It is unclear whether impaired cardiac and/or vascular function contribute to exercise intolerance in patients with type 2 diabetes. PURPOSE Magnetic resonance imaging (MRI) was used to determine whether reductions in cardiac output and/or femoral arterial blood flow contribute to reduced aerobic capacity in patients with type 2 diabetes. METHODS Cardiac and femoral arterial blood flow MRI scans were performed at rest and during low-intensity leg exercise in eight patients with type 2 diabetes and 11 healthy individuals. Maximal aerobic capacity VO(2 max) and maximal oxygen pulse were also determined in all participants. RESULTS V O(2 max) was 20% lower and maximal oxygen pulse was 16% lower in patients with type 2 diabetes (P < 0.05), whereas maximal heart rate was the same between groups. Low-intensity exercise induced a 20% increase in heart rate and cardiac output as well as a 60-70% increase in femoral blood flow in both groups (P < 0.05). Femoral arterial blood flow indexed to thigh lean mass was reduced during exercise in patients with type 2 diabetes compared with healthy individuals. Stroke volume indexed to fat-free mass was lower in patients with type 2 diabetes, but greater heart rate allowed cardiac output to be maintained during submaximal exercise. CONCLUSIONS These findings suggest that impaired femoral arterial blood flow, an indirect marker of muscle perfusion, affects low-intensity exercise performance in patients with type 2 diabetes. However, because of lower exercising stroke volume, we propose that femoral arterial blood flow and, possibly, cardiac output, limit V O(2 max) in patients with type 2 diabetes.

Effect of reduced total blood volume on left ventricular volumes and kinetics in type 2 diabetes.

Aim:  Although impaired left ventricular (LV) diastolic function is commonly observed in patients with type 2 diabetes, it remains unclear whether the impairment is caused by altered LV relaxation or changes in LV preload. The purpose of this study was to examine the influence of LV function and LV loading conditions on stroke volume in men with type 2 diabetes.

Diastolic dysfunction: a link between hypertension and heart failure.

Diastolic heart failure is characterized by the symptoms and signs of heart failure, a preserved ejection fraction and abnormal left ventricular (LV) diastolic function caused by a decreased LV compliance and relaxation. The signs and symptoms of diastolic heart failure are indistinguishable from those of heart failure related to systolic dysfunction; therefore, the diagnosis of diastolic heart failure is often one of exclusion. The majority of patients with heart failure and preserved ejection fraction have a history of hypertension. Hypertension induces a compensatory thickening of the ventricular wall in an attempt to normalize wall stress, which results in LV concentric hypertrophy, which in turn decreases LV compliance and LV diastolic filling. There is an abnormal accumulation of fibrillar collagen accompanying the hypertension-induced LV hypertrophy, which is also associated with decreased compliance and LV diastolic dysfunction. There are no specific guidelines for treating diastolic heart failure, but pharmacological treatment should be directed at normalizing blood pressure, promoting regression of LV hypertrophy, preventing tachycardia and treating symptoms of congestion. Preventive strategies directed toward an early and aggressive blood pressure control are likely to offer the greatest promise for reducing the incidence of diastolic heart failure.

Influence of bronchial blood flow and conductance on pulmonary function in stable systolic heart failure

BACKGROUND The aim of this study was to determine the relationship between airway blood flow (Q(aw)), airway conductance (G(f-aw)) and pulmonary function in patients with stable HF. METHODS 12 controls (CTRL: age=63±9 years, FVC=98±15%pred, LVEF=61±6%) (all data presented as mean±SD), 16 patients with mild HF (HF-A, NYHA I-II: age=64±9 years, FVC=90±17%pred, LVEF=28±6%), and 14 patients with moderate/severe HF (HF-B, NYHA III-IV: age=65±6 years, FVC=84±12%pred, LVEF=26±6%) were studied. Q(aw) was assessed using soluble gas measurements; perfusion pressure across airway bed (ΔP(aw)) was estimated from systemic and pulmonary pressure measurements; G(f-aw) was calculated as Q(aw)/ΔP(aw); PF was assessed by spirometry. RESULTS While Q˙(aw) was not significantly different between CTRL (61.3±17.9 μL min(-1)mL(-1)), HF-A (70.1±26.9 μL min(-1)mL(-1)) and HF-B (56.2±14.9 μL min(-1)mL(-1)) groups, G(f-aw), was elevated in HF-A (1.1±0.4 μL min(-1)mL(-1)mm Hg(-1), p<0.03) and tended to be elevated in HF-B (1.2±0.6 μL min(-1)mL(-1)mm Hg(-1), p=0.07) when compared to CTRL (0.8±0.3 μL min(-1)mL(-1)mm Hg(-1)). Significant positive correlations were found between G(f-aw) and RV/TLC for HF-A (r=0.63, p<0.02) and HF-B (r=0.58, p<0.05). CONCLUSIONS These results support the hypothesis that increased bronchial conductance and bronchial congestion may be related to greater small airway obstruction and as such may play a role in the PF abnormalities and symptoms of congestion commonly observed in HF patients.

Ventilatory Expired Gas at Constant-Rate Low-Intensity Exercise Predicts Adverse Events and is Related to Neurohormonal Markers in Patients With Heart Failure

BACKGROUND Ventilatory efficiency (VE/VCO(2) ratio) and the partial pressure of end-tidal carbon dioxide (P(ET)CO(2)), obtained during moderate to high levels of physical exertion demonstrate prognostic value in heart failure (HF). The present investigation assesses the clinical utility of these variables during low-intensity exercise. METHODS AND RESULTS One hundred and thirty subjects diagnosed with HF underwent a 2-minute, constant-rate treadmill session at 2 miles per hour. Both the VE/VCO(2) ratio and P(ET)CO(2) were recorded during exercise (30-second average) and their change (Delta) from rest. B-type and atrial natriuretic peptide (BNP and ANP) were also determined. Only P(ET)CO(2) and DeltaP(ET)CO(2) emerged from the multivariate Cox regression. Receiver operating characteristic curve analysis revealed the prognostic classification schemes were significant with thresholds of < or >or=34 mm Hg (hazard ratio: 4.2, 95% CI: 2.2-8.0, P < .001) and < or >or=1 mm Hg (hazard ratio: 3.5, 95% CI: 1.9-6.6, P < .001) being optimal for P(ET)CO(2) and DeltaP(ET)CO(2), respectively. Moreover, subjects with a P(ET)CO(2)>or=34 mm Hg had a significantly lower BNP (214.1 +/- 431.9 vs. 1110.5 +/- 1854.0 pg/mL, P=.005) and ANP (108.2 +/- 103.6 vs. 246.2 +/- 200.4 pg/mL, P < .001). CONCLUSIONS The results of this pilot study indicate ventilatory expired gas analysis during a short bout of low-intensity exercise may provide insight into prognosis and cardiac stability.

In vivo estimates of NO and CO conductance for haemoglobin and for lung transfer in humans

Membrane conductance (Dm) and capillary lung volume (Vc) derived from NO and CO lung transfer measurements in humans depend on the blood conductance (θ) values of both gases. Many θ values have been proposed in the literature. In the present study, measurements of CO and NO transfer while breathing 15% or 21% O2 allowed the estimation of θNO and the calculation of the optimal equation relating 1/θCO to pulmonary capillary oxygen pressure (PcapO2). In 10 healthy subjects, the mean calculated θNO value was similar to the θNO value previously reported in the literature (4.5mmHgmin(-1)) provided that one among three θCO equations from the literature was chosen. Setting 1/θCO=a·PcapO2+b, optimal values of a and b could be chosen using two methods: 1) by minimizing the difference between Dm/Vc ratios for any PcapO2, 2) by establishing a linear equation relating a and b. Using these methods, we are proposing the equation 1/θCO=0.0062·PcapO2+1.16, which is similar to two equations previously reported in the literature. With this set of θ values, DmCO reached the morphometric range.

Breathing strategy to preserve exercising cardiac function in patients with heart failure

The heart and lungs are closely linked as they lie in series, share a common surface area and compete for space within the thoracic cavity. The heart and lungs are exposed to the similar changes in intrathoracic pressure, and reflexes within one organ can influence the other (i.e. vagal influence of lung inflation on heart rate). In patients with heart failure, these cardiopulmonary interactions may be altered due to decreased lung and left ventricular compliance, increased cardiac size, high cardiac filling pressure and altered receptor sensitivity to neural activation. Exercise further affects the cardiopulmonary interactions by stimulating an increase in the depth and frequency of breathing which accentuates the fluctuations in intrathoracic pressure, and by requiring large increases in stroke volume and heart rate in order to respond to the increased metabolic demand. Previous work from our laboratory suggested that patients with heart failure avoid high lung volumes during exercise, often at the expense of unnecessary large positive expiratory intrathoracic pressures resulting in significant wasted effort. Moreover, we also observed that voluntarily increases in lung volume in patients with heart failure induced a mild relative bradycardia, a response not observed in similar aged healthy individuals. Thus, we hypothesized that the rapid shallow low lung volume breathing, in combination with positive expiratory intrathoracic pressure, often adopted by patients with heart failure during exercise is an attempt to preserve, or even enhance, the cardiac response to exercise.

Determination of blood volume by pulse CO-oximetry.

The objective of this study was to determine whether changes in carboxyhaemoglobin (COHb) saturation following carbon monoxide (CO) rebreathing can be accurately detected by pulse CO-oximetry in order to determine blood volume. Noninvasive measurements of carboxyhaemoglobin saturation (SpCO) were continuously monitored by pulse CO-oximetry before, during and following 2 min of CO rebreathing. Reproducibility and accuracy of noninvasive blood volume measurements were determined in 16 healthy non-smoking individuals (15 males, age: 28 ± 2 years, body mass index: 25.4 ± 0.6 kg m(-2)) through comparison with blood volume measurements calculated from invasive measurements of COHb saturation. The coefficient of variation for noninvasive blood volume measurements performed on separate days was 15.1% which decreases to 9.1% when measurements were performed on the same day. Changes in COHb saturation and SpCO following CO rebreathing were strongly correlated (r = 0.90, p < 0.01), resulting in a significant correlation between invasive and noninvasive blood volume measurements (r = 0.83, p = 0.02). Changes in SpCO following CO rebreathing can be accurately detected by pulse CO-oximetry, which could potentially provide a simplified, convenient and reproducible method to rapidly determine blood volume in healthy individuals.

Effect of exercise training on diastolic function in metabolic syndrome.

It has been reported that metabolic syndrome (MetS) impairs left ventricular (LV) diastolic function. The objective of this study was to determine whether exercise training can improve LV diastolic function in individuals with MetS. Twenty-eight individuals with MetS (9 males, aged 60 ± 5 years) underwent a 1-year combined endurance and resistance exercise training program; maximal aerobic capacity (V̇O2max), blood pressure, blood markers, and LV diastolic function were measured at weeks 0, 12, 24, and 52 throughout the training. Pulsed wave Doppler echocardiography across the mitral valve was used to assess peak early flow velocity (E) and peak atrial flow velocity (A) to determine the E/A ratio. Individuals with MetS had a reversed E/A ratio, suggesting impaired LV relaxation, the first stage of LV diastolic dysfunction. Exercise training reduced systolic blood pressure (SBP) (129 ± 14 to 120 ± 12 mm Hg; p < 0.01) and increased V̇O2max (29.2 ± 6.3 to 33.4 ± 6.5 mL·kg(-1)·min(-1); p < 0.01) and high-density lipoprotein cholesterol (1.04 ± 0.21 to 1.12 ± 0.25 mmol·L(-1); p = 0.02), but did not improve LV diastolic function. Individuals with an E/A ratio <1 at the start of training had a tendency toward an increased E/A ratio (p = 0.12) accompanied by significant decreases in SBP and increases in V̇O2max with exercise training. Combined resistance and aerobic exercise training improved cardiometabolic health but did not improve the impaired LV diastolic function of individuals with MetS.