Exercise testing is increasingly utilized to evaluate the level of exercise intolerance in patients with lung and heart diseases. Cardiopulmonary exercise testing (CPET) is considered the gold standard to study a patient’s level of exercise limitation and its causes. The 2 CPET protocols most frequently used in the clinical setting are the maximal incremental and the constant work rate tests. The aim of this review is to focus on the main respiratory diseases for which exercise tolerance is indicated; for example, chronic obstructive pulmonary disease, interstitial lung disease, primary pulmonary hypertension and cystic fibrosis. This review also focuses on the variables/indices that are utilized in the functional and prognostic evaluation. The recognition of abnormal response patterns of ventilatory, cardiac and metabolic limitation to exercise may help in the diagnostic evaluation. In addition, CPET indexes can provide important functional and prognostic information regarding patients with pulmonary disease. Exercise indices, such as peak oxygen uptake (V’O2 peak), ventilatory equivalents for carbon dioxide production (V’E-/V’CO2) and arterial oxygen saturation (SpO2), have in fact proven to be better predictors of prognosis than lung function measurements obtained at rest. Moreover, useful information on the effects of therapeutic interventions may be obtained by CPET by studying the changes in endurance capacity during high-intensity constant work rate protocols.
Respiratory mechanical abnormalities in patients with chronic obstructive pulmonary disease (COPD) may impair cardiodynamic responses and slow down heart rate (HR) kinetics compared with normal resulting in reduced convective oxygen delivery during exercise. We reasoned that heliox breathing (79% helium-21% oxygen) and the attendant reduction of operating lung volumes should accelerate HR kinetics in the transition from rest to high-intensity exercise. Eleven male ambulatory patients with clinically stable COPD undertook constant work-rate cycle testing at 80% of each individuals' maximum work capacity while breathing room air (RA) or heliox (HX), randomly. Mean response time (MRT) for HR and dynamic end-expiratory lung volume (EELV) were measured. Resting EELV was not affected by HX breathing, while exercise EELV decreased significantly by 0.23 L at isotime during HX breathing compared with RA. During HX breathing, MRT for HR significantly accelerated (p = 0.002) by an average of 20 s (i.e., 17%). Speeded MRT for HR correlated with indices of reduced lung hyperinflation, such as EELV at isotime (r = 0.88, p = 0.03), and with improved exercise endurance time (r = -0.64, p = 0.03). The results confirm that HX-induced reduction of dynamic lung hyperinflation is associated with consistent improvement in indices of cardio-circulatory function such as HR kinetics in the rest-to-exercise transition in COPD patients.
BackgroundThe independent prognostic impact of diabetes mellitus (DM) and prediabetes mellitus (pre‐DM) on survival outcomes in patients with chronic heart failure has been investigated in observational registries and randomized, clinical trials, but the results have been often inconclusive or conflicting. We examined the independent prognostic impact of DM and pre‐DM on survival outcomes in the GISSI‐HF (Gruppo Italiano per lo Studio della Sopravvivenza nella Insufficienza Cardiaca‐Heart Failure) trial.Methods and ResultsWe assessed the risk of all‐cause death and the composite of all‐cause death or cardiovascular hospitalization over a median follow‐up period of 3.9 years among the 6935 chronic heart failure participants of the GISSI‐HF trial, who were stratified by presence of DM (n=2852), pre‐DM (n=2013), and non‐DM (n=2070) at baseline. Compared with non‐DM patients, those with DM had remarkably higher incidence rates of all‐cause death (34.5% versus 24.6%) and the composite end point (63.6% versus 54.7%). Conversely, both event rates were similar between non‐DM patients and those with pre‐DM. Cox regression analysis showed that DM, but not pre‐DM, was associated with an increased risk of all‐cause death (adjusted hazard ratio, 1.43; 95% CI, 1.28–1.60) and of the composite end point (adjusted hazard ratio, 1.23; 95% CI, 1.13–1.32), independently of established risk factors. In the DM subgroup, higher hemoglobin A1c was also independently associated with increased risk of both study outcomes (all‐cause death: adjusted hazard ratio, 1.21; 95% CI, 1.02–1.43; and composite end point: adjusted hazard ratio, 1.14; 95% CI, 1.01–1.29, respectively).ConclusionsPresence of DM was independently associated with poor long‐term survival outcomes in patients with chronic heart failure.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00336336.
The Liou model did not adequately predict 5-year survival in our CF population that, compared to the one in which it was originally tested, could benefit from 10 years of improvement in treatments and practice patterns. A new generated model, based on only four variables, was more accurate in predicting 5-year survival in Italian CF patients.
a b s t r a c tThe relationship between work rate (WR) and its tolerable duration (t LIM ) has not been investigated at high altitude (HA). At HA (5050 m) and at sea level (SL), six subjects therefore performed symptomlimited cycle-ergometry: an incremental test (IET) and three constant-WR tests (% of IET WR max , HA and SL respectively: WR 1 70 ± 8%, 74 ± 7%; WR 2 86 ± 14%, 88 ± 10%; WR 3 105 ± 13%, 104 ± 9%). The power asymptote (CP) and curvature constant (W ) of the hyperbolic WR-t LIM relationship were reduced at HA compared to SL (CP: 81 ± 21 vs. 123 ± 38 W; W : 7.2 ± 2.9 vs. 13.1 ± 4.3 kJ). HA breathing reserve (estimated maximum voluntary ventilation minus end-exercise ventilation) was also compromised (WR 1 : 25 ± 25 vs. 50 ± 18 l min −1 ; WR 2 : 4 ± 23 vs. 38 ± 23 l min −1 ; WR 3 : −3 ± 18 vs. 32 ± 24 l min −1 ) with nearmaximal dyspnea levels (Borg) (WR 1 : 7.2 ± 1.2 vs. 4.8 ± 1.3; WR 2 : 8.8 ± 0.8 vs. 5.3 ± 1.2; WR 3 : 9.3 ± 1.0 vs. 5.3 ± 1.5). The CP reduction is consistent with a reduced O 2 availability; that of W with reduced muscle-venous O 2 storage, exacerbated by ventilatory limitation and dyspnea.
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