Exertional oscillatory ventilation in subjects without heart failure reporting chronic dyspnoea.

Oscillatory ventilation detected on incremental cardiopulmonary exercise testing might be found in subjects without heart failure reporting exertional dyspnoea despite the best available therapy for their underlying cardiopulmonary disease https://bit.ly/3Tyl7bE.

Rib cage distortion and dynamic hyperinflation during two exercise intensities in people with COPD.

BACKGROUND: The relationship between rib cage (RC) motion abnormalities, dynamic hyperinflation (DH), and exercise capacity in people with COPD is controversial. AIM: To investigate RC distortion and operational chest wall volumes during moderate and high constant-rate exercises in people with COPD. METHODS: Seven male participants [median(Q1-Q3) age: 63(60.0-66.0) years; FEV1: 39.0(38.0-63.0)% of predicted] performed a symptom-limited incremental exercise testing on cycle ergometer, followed by constant-rate tests (60 % and 80 % of peak work rate). Optoelectronic plethysmography was used to evaluate RC distortion: phase angle-PhAng, inspiratory phase ratio-PhRIB, expiratory phase ratio-PhREB; and chest wall volumes: end-inspiratory volume-Vei and end-expiratory volume-Vee. RESULTS: PhRIB and PhREB significantly increased during both constant-rate exercise tests, without difference between them. In general, Vei of the chest wall significantly increased in both exercise intensities while Vee did not change. CONCLUSIONS: The occurrence of RC distortion seemed not to limit the exercise capacity in people with COPD evaluated, and it was present even in the absence of DH.

Effects of bi-level positive airway pressure on ventilatory and perceptual responses to exercise in comorbid heart failure-COPD.

This study tested the hypothesis that, by increasing the volume available for tidal expansion (inspiratory capacity, IC), bi-level positive airway pressure (BiPAP™) would lead to greater beneficial effects on dyspnea and exercise intolerance in comorbid heart failure (HF)-chronic obstructive pulmonary disease (COPD) than HF alone. Ten patients with HF and 9 with HF-COPD (ejection fraction = 30 ± 6% and 35 ± 7%; FEV1 = 83 ± 12% and 65 ± 15% predicted, respectively) performed a discontinuous exercise protocol under sham ventilation or BiPAP™. Time to intolerance increased with BiPAP™ only in HF-COPD (p < 0.05). BiPAP™ led to higher tidal volume and lower duty cycle with longer expiratory time (p < 0.05). Of note, BiPAP™ improved IC (by ∼0.5 l) across exercise intensities only in HF-COPD. These beneficial consequences were associated with lower dyspnea scores at higher levels of ventilation (p < 0.05). By improving the qualitative" (breathing pattern and operational lung volumes) and sensory (dyspnea) features of exertional ventilation, BiPAP™ might allow higher exercise intensities to be sustained for longer during cardiopulmonary rehabilitation in HF-COPD.

Exercise intolerance in comorbid COPD and heart failure: the role of impaired aerobic function.

Impaired aerobic function is a potential mechanism of exercise intolerance in patients with combined cardiorespiratory disease. We investigated the pathophysiological and sensory consequences of a low change in oxygen uptake (ΔV'O2 )/change in work rate (ΔWR) relationship during incremental exercise in patients with coexisting chronic obstructive pulmonary disease (COPD) and systolic heart failure (HF).After clinical stabilisation, 51 COPD-HF patients performed an incremental cardiopulmonary exercise test to symptom limitation. Cardiac output was non-invasively measured (impedance cardiography) in a subset of patients (n=18).27 patients presented with ΔV'O2 /ΔWR below the lower limit of normal. Despite similar forced expiratory volume in 1 s and ejection fraction, the low ΔV'O2 /ΔWR group showed higher end-diastolic volume, lower inspiratory capacity and lower transfer factor compared to their counterparts (p<0.05). Peak WR and peak V'O2 were ∼15% and ∼30% lower, respectively, in the former group: those findings were associated with greater symptom burden in daily life and at a given exercise intensity (leg discomfort and dyspnoea). The low ΔV'O2 /ΔWR group presented with other evidences of impaired aerobic function (sluggish V'O2 kinetics, earlier anaerobic threshold) and cardiocirculatory performance (lower oxygen pulse, lower stroke volume and cardiac output) (p<0.05). Despite similar exertional hypoxaemia, they showed worse ventilatory inefficiency and higher operating lung volumes, which led to greater mechanical inspiratory constraints (p<0.05).Impaired aerobic function due to negative cardiopulmonary-muscular interactions is an important determinant of exercise intolerance in patients with COPD-HF. Treatment strategies to improve oxygen delivery to and/or utilisation by the peripheral muscles might prove particularly beneficial to these patients.

Current challenges in managing comorbid heart failure and COPD.

INTRODUCTION: Heart failure (HF) with reduced ejection fraction and chronic obstructive pulmonary disease (COPD) frequently coexist, particularly in the elderly. Given their rising prevalence and the contemporary trend to longer life expectancy, overlapping HF-COPD will become a major cause of morbidity and mortality in the next decade. Areas covered: Drawing on current clinical and physiological constructs, the consequences of negative cardiopulmonary interactions on the interpretation of pulmonary function and cardiopulmonary exercise tests in HF-COPD are discussed. Although those interactions may create challenges for the diagnosis and assessment of disease stability, they provide a valuable conceptual framework to rationalize HF-COPD treatment. The impact of COPD or HF on the pharmacological treatment of HF or COPD, respectively, is then comprehensively discussed. Authors finalize by outlining how the non-pharmacological treatment (i.e. rehabilitation and exercise reconditioning) can be tailored to the specific needs of patients with HF-COPD. Expert commentary: Randomized clinical trials testing the efficacy and safety of new medications for HF or COPD should include a sizeable fraction of patients with these coexistent pathologies. Multidisciplinary clinics involving cardiologists and respirologists trained in both diseases (with access to unified cardiorespiratory rehabilitation programs) are paramount to decrease the humanitarian and social burden of HF-COPD.

Excess Ventilation in Chronic Obstructive Pulmonary Disease-Heart Failure Overlap. Implications for Dyspnea and Exercise Intolerance.

RATIONALE: An increased ventilatory response to exertional metabolic demand (high [Formula: see text]e/[Formula: see text]co2 relationship) is a common finding in patients with coexistent chronic obstructive pulmonary disease and heart failure. OBJECTIVES: We aimed to determine the mechanisms underlying high [Formula: see text]e/[Formula: see text]co2 and its impact on operating lung volumes, dyspnea, and exercise tolerance in these patients. METHODS: Twenty-two ex-smokers with combined chronic obstructive pulmonary disease and heart failure with reduced left ventricular ejection fraction undertook, after careful treatment optimization, a progressive cycle exercise test with capillary (c) blood gas collection. MEASUREMENTS AND MAIN RESULTS: Regardless of the chosen metric (increased [Formula: see text]e-[Formula: see text]co2 slope, [Formula: see text]e/[Formula: see text]co2 nadir, or end-exercise [Formula: see text]e/[Formula: see text]co2), ventilatory inefficiency was closely related to PcCO2 (r values from -0.80 to -0.84; P < 0.001) but not dead space/tidal volume ratio. Ten patients consistently maintained exercise PcCO2 less than or equal to 35 mm Hg (hypocapnia). These patients had particularly poor ventilatory efficiency compared with patients without hypocapnia (P < 0.05). Despite the lack of between-group differences in spirometry, lung volumes, and left ventricular ejection fraction, patients with hypocapnia had lower resting PaCO2 and lung diffusing capacity (P < 0.01). Excessive ventilatory response in this group was associated with higher exertional PcO2. The group with hypocapnia, however, had worse mechanical inspiratory constraints and higher dyspnea scores for a given work rate leading to poorer exercise tolerance compared with their counterparts (P < 0.05). CONCLUSIONS: Heightened neural drive promoting a ventilatory response beyond that required to overcome an increased "wasted" ventilation led to hypocapnia and poor exercise ventilatory efficiency in chronic obstructive pulmonary disease-heart failure overlap. Excessive ventilation led to better arterial oxygenation but at the expense of earlier critical mechanical constraints and intolerable dyspnea.

Physiological and sensory consequences of exercise oscillatory ventilation in heart failure-COPD.

BACKGROUND: Exercise oscillatory ventilation (EOV) is associated with poor ventilatory efficiency and higher operating lung volumes in heart failure. These abnormalities may be particularly deleterious to dyspnea and exercise tolerance in mechanically-limited patients, e.g. those with coexistent COPD. METHODS: Ventilatory, gas exchange and sensory responses to incremental exercise were contrasted in 68 heart failure-COPD patients (12 EOV+). EOV was established by standard criteria. RESULTS: Compared to EOV-, EOV+ had lower exercise capacity, worse ventilatory inefficiency and higher peak dyspnea scores (p<0.05). Peak capillary PCO2 (PcCO2) was higher and end-tidal CO2 (PETCO2) was lower in EOV+. Thus, greater (i.e., more positive) P(c-ET)CO2 and dead space/tidal volume values were found in these patients compared to EOV- (p<0.05). Ventilatory inefficiency was related to increased dead space/tidal volume in EOV+ (r=0.74; p<0.01). Owing to higher operating lung volumes, inspiratory reserve volume (IRV) decreased to a greater extent in EOV+. Tidal volume oscillations consistently ceased when a "critical" IRV was reached (~0.3-0.5L); thereafter, PcCO2 stabilized or increased and dyspnea scores rose sharply. Exercise capacity was closely related to IRV decrements and peak dyspnea in EOV+ (r=-0.78 and 0.84, respectively; p<0.01). CONCLUSIONS: Dyspnea and exercise tolerance are negatively influenced by EOV in heart failure patients presenting with COPD as co-morbidity. Pharmacological and non-pharmacological interventions known to decrease EOV might prove particularly valuable to mitigate symptom burden and exercise intolerance in this specific heart failure group.

Exercise Ventilatory Inefficiency Adds to Lung Function in Predicting Mortality in COPD.

Severity of resting functional impairment only partially predicts the increased risk of death in chronic obstructive pulmonary disease (COPD). Increased ventilation during exercise is associated with markers of disease progression and poor prognosis, including emphysema extension and pulmonary vascular impairment. Whether excess exercise ventilation would add to resting lung function in predicting mortality in COPD, however, is currently unknown. After an incremental cardiopulmonary exercise test, 288 patients (forced expiratory volume in one second ranging from 18% to 148% predicted) were followed for a median (interquartile range) of 57 (47) months. Increases in the lowest (nadir) ventilation to CO2 output (VCO2) ratio determined excess exercise ventilation. Seventy-seven patients (26.7%) died during follow-up: 30/77 (38.9%) deaths were due to respiratory causes. Deceased patients were older, leaner, had a greater co-morbidity burden (Charlson Index) and reported more daily life dyspnea. Moreover, they had poorer lung function and exercise tolerance (p < 0.05). A logistic regression analysis revealed that ventilation/VCO2 nadir was the only exercise variable that added to age, body mass index, Charlson Index and resting inspiratory capacity (IC)/total lung capacity (TLC) ratio to predict all-cause and respiratory mortality (p < 0.001). Kaplan-Meier analyses showed that survival time was particularly reduced when ventilation/VCO2 nadir > 34 was associated with IC/TLC ≤ 0.34 or IC/TLC ≤ 0.31 for all-cause and respiratory mortality, respectively (p < 0.001). Excess exercise ventilation is an independent prognostic marker across the spectrum of COPD severity. Physiological abnormalities beyond traditional airway dysfunction and lung mechanics are relevant in determining the course of the disease.

Exercise ventilatory inefficiency in mild to end-stage COPD.

Ventilatory inefficiency during exercise is a key pathophysiological feature of chronic obstructive pulmonary disease. Currently, it is unknown how this physiological marker relates to clinically relevant outcomes as resting ventilatory impairment progresses across disease stages. Slope and intercept of the linear region of the ventilation-carbon dioxide output relationship and the ratio between these variables, at the lowest point (nadir), were contrasted in 316 patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages 1-4 (forced expiratory volume in 1 s, ranging from 148% pred to 12% pred) and 69 aged- and gender-matched controls, Compared to controls, slope and intercept were higher in GOLD stages 1 and 2, leading to higher nadirs (p<0.05). Despite even larger intercepts in GOLD stages 3 and 4, slopes diminished as disease evolved (from mean±sd 35±6 in GOLD stage 1 to 24±5 in GOLD stage 3, p<0.05). As a result, there were no significant differences in nadirs among patient groups. Higher intercepts, across all stages (p<0.01), and to a lesser extent lower slopes in GOLD stages 2-4 (p<0.05), were related to greater mechanical constraints, worsening pulmonary gas exchange, higher dyspnoea scores, and poorer exercise capacity. Increases in the ventilation intercept best indicate the progression of exercise ventilatory inefficiency across the whole spectrum of chronic obstructive pulmonary disease severity.

Clinical usefulness of response profiles to rapidly incremental cardiopulmonary exercise testing.

The advent of microprocessed "metabolic carts" and rapidly incremental protocols greatly expanded the clinical applications of cardiopulmonary exercise testing (CPET). The response normalcy to CPET is more commonly appreciated at discrete time points, for example, at the estimated lactate threshold and at peak exercise. Analysis of the response profiles of cardiopulmonary responses at submaximal exercise and recovery, however, might show abnormal physiologic functioning which would not be otherwise unraveled. Although this approach has long been advocated as a key element of the investigational strategy, it remains largely neglected in practice. The purpose of this paper, therefore, is to highlight the usefulness of selected submaximal metabolic, ventilatory, and cardiovascular variables in different clinical scenarios and patient populations. Special care is taken to physiologically justify their use to answer pertinent clinical questions and to the technical aspects that should be observed to improve responses' reproducibility and reliability. The most recent evidence in favor of (and against) these variables for diagnosis, impairment evaluation, and prognosis in systemic diseases is also critically discussed.

Nível de NT-proBNP em pacientes com síndrome coronariana aguda sem supradesnivelamento do segmento ST / NT-proBNP levels in patients with non-ST-segment elevation acute coronary syndrome

FUNDAMENTO: A síndrome coronariana aguda (SCA) sem supradesnivelamento do segmento ST (SCASEST) está associada ao supradesnivelamento do peptídeo natriurético tipo B (BNP) e aos marcadores de necrose miocárdica, embora se desconheça a correlação dessa síndrome ao escore de trombólise no infarto do miocárdio (TIMI) e à função ventricular esquerda. OBJETIVO: Avaliar a correlação entre os níveis do fragmento N-terminal do peptídeo natriurético tipo B (NT-proBNP) e os marcadores de necrose miocárdica (creatinofosfoquinase fração músculo-cérebro CK-MB e troponina I), bem como entre o escore de risco TIMI e a fração de ejeção do ventrículo esquerdo (FEVE) nos pacientes com síndrome coronariana aguda sem supradesnivelamento do segmento ST. MÉTODOS: Oitenta e sete pacientes com síndrome coronariana aguda sem supradesnivelamento do segmento ST foram divididos em dois grupos: 37 (42,5 por cento) com angina instável e 50 (57,5 por cento) com infarto agudo do miocárdio sem supradesnivelamento do segmento ST (IAMSSST). RESULTADOS: A fração de ejeção do ventrículo esquerdo superior a 40 por cento foi encontrada em 86,2 por cento do total da amostra. Os níveis séricos de NT-proBNP foram maiores em pacientes com infarto do miocárdio sem supradesnivelamento do segmento ST, em comparação àqueles com angina instável (p<0,001). O aumento dos níveis de NT-proBNP foi associado ao aumento de troponina I (rs=0,425, p<0,001), pico de CK-MB (rs=0,458, p<0,001) e FEVE (rs=-0,345, p=0,002), não havendo correlação com o escore de risco TIMI (rs=0,082, p=0,44). Na análise multivariada, a fração de ejeção do ventrículo esquerdo e a troponina I correlacionaram-se de forma independente aos níveis de NT-proBNP (p=0,017 e p=0,002, respectivamente). CONCLUSÃO: O aumento dos níveis de NT-proBNP em pacientes com síndrome coronariana aguda sem supradesnivelamento do segmento ST não está relacionado exclusivamente à redução da fração de ejeção do ventrículo esquerdo, mas também pode ser provocado pela presença de isquemia miocárdica e necrose.

BACKGROUND: Non-ST-segment elevation acute coronary syndrome is associated with elevation of brain natriuretic peptide and markers of myocardial necrosis, although its relationship with the TIMI score and left ventricular function are largely unknown. OBJECTIVE: To evaluate the correlation between plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) and markers of myocardial necrosis [creatine phosphokinase muscle-brain fraction (CK-MB) and troponin I], TIMI risk score and left ventricular ejection fraction in patients with non-ST-segment elevation acute coronary syndrome. METHODS: Eighty-seven patients with non-ST-segment elevation acute coronary syndrome were divided into two groups: 37 (42.5 percent) with unstable angina and 50 (57.5 percent) with non-ST-segment elevation myocardial infarction. RESULTS: Left ventricular ejection fraction more than 40 percent was found in 86.2 percent of the total sample. Serum levels of NT-proBNP was higher in patients with non-ST elevation myocardial infarction than in those with unstable angina (p<0.001). Increased levels of NT-proBNP were associated with increases in troponin I (rs=0.425, p<0.001), peak CK-MB (rs=0.458, p<0.001) and low left ventricular ejection fraction (rs=-0.345, p=0.002); no correlation was found with the TIMI risk score (rs=0.082, p=0.44). Multivariate analysis revealed that left ventricular ejection fraction and troponin I levels were independently correlated with NT-proBNP levels (p=0.017 and p=0.002, respectively). CONCLUSION: Increased levels of NT-proBNP in patients with non-ST-segment elevation acute coronary syndrome are not related exclusively to low left ventricular ejection fraction, but can also be caused by the presence of myocardial ischemia and necrosis.

NT-proBNP levels in patients with non-ST-segment elevation acute coronary syndrome.

BACKGROUND: Non-ST-segment elevation acute coronary syndrome is associated with elevation of brain natriuretic peptide and markers of myocardial necrosis, although its relationship with the TIMI score and left ventricular function are largely unknown. OBJECTIVE: To evaluate the correlation between plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) and markers of myocardial necrosis [creatine phosphokinase muscle-brain fraction (CK-MB) and troponin I], TIMI risk score and left ventricular ejection fraction in patients with non-ST-segment elevation acute coronary syndrome. METHODS: Eighty-seven patients with non-ST-segment elevation acute coronary syndrome were divided into two groups: 37 (42.5%) with unstable angina and 50 (57.5%) with non-ST-segment elevation myocardial infarction. RESULTS: Left ventricular ejection fraction more than 40% was found in 86.2% of the total sample. Serum levels of NT-proBNP was higher in patients with non-ST elevation myocardial infarction than in those with unstable angina (p<0.001). Increased levels of NT-proBNP were associated with increases in troponin I (rs=0.425, p<0.001), peak CK-MB (rs=0.458, p<0.001) and low left ventricular ejection fraction (rs=-0.345, p=0.002); no correlation was found with the TIMI risk score (rs=0.082, p=0.44). Multivariate analysis revealed that left ventricular ejection fraction and troponin I levels were independently correlated with NT-proBNP levels (p=0.017 and p=0.002, respectively). CONCLUSION: Increased levels of NT-proBNP in patients with non-ST-segment elevation acute coronary syndrome are not related exclusively to low left ventricular ejection fraction, but can also be caused by the presence of myocardial ischemia and necrosis.

A randomized trial of the effects of exercise training in Chagas cardiomyopathy.

AIMS: The effects of exercise training in chronic heart failure are well established, however, they have not been evaluated in Chagas cardiomyopathy (ChC). We sought to determine the effects of exercise training on functional capacity, health-related quality of life (HQoL), and brain natriuretic peptide (BNP) levels in patients with ChC. METHODS AND RESULTS: This randomized, controlled, single-blind trial included 40 patients with ChC (age 49.5 +/- 7.8 years, 57.5% male) who did not practice regular exercise. All patients were assessed, at baseline and at the end of the study, by exercise test (VO(2) and exercise time), six-minute walk test (6MWT), Goldman Specific Activity Scale (SAS), HQoL, and BNP levels. Patients were randomized to inactive control group (ICG = 19) or exercise training group (ETG = 21). Exercise training group patients underwent 12 weeks of exercise training: walking for up to 30 min (intensity 50-70% HR reserve + HR at rest) and warm-up and cooling-down exercising, three times a week. The data were analysed for delta values (Delta= end - baseline). After intervention, compared with the ICG, the ETG had significant increases in functional parameters including, DeltaVO(2) (6.5 vs. 2.8 mL/kg/min, P = 0.001), Delta exercise time (2.9 vs.1.1 min, P < 0.001), Delta6MWT distance (83.5 vs. 2.0 m, P = 0.001) improved DeltaSAS (8 vs. 1 patient, P = 0.008), and HQoL: Delta domains vitality (7.5 vs. 0 points, P = 0.013), Delta emotional aspects (16.7 vs. 0 points, P = 0.012), and Delta mental health (16.1 vs. 0 points, P = 0.031). There was no difference in BNP levels. CONCLUSION: In patients with ChC, exercise training was associated with a major improvement in functional capacity and HQoL without any adverse effects.

Left ventricular diastolic function and exercise capacity in patients with Chagas cardiomyopathy.

UNLABELLED: Parameters of diastolic function have been shown to correlate with exercise capacity (EC) in individuals with impaired left ventricular (LV) systolic function. However, the role of LV diastolic function in predicting EC in Chagas cardiomyopathy has not been reported. OBJECTIVES: This study aimed to determine the relationship between LV diastolic parameters assessed by echocardiography and EC in patients with Chagas cardiomyopathy. METHODS: We studied 40 patients (23 men; 49 + or - 8 years), with diagnosis of Chagas disease and dilated cardiomyopathy. Medical therapy was individually adjusted according to standardized guidelines. Methods of acquiring two-dimensional Doppler, tissue Doppler imaging (TDI), and their measurements were described. Exercise testing was performed by a Bruce protocol. Brain natriuretic peptide (BNP) levels were also determined. RESULTS: Most patients (63%) were in NYHA functional class I. Mean peak oxygen consumption estimated (peakVO(2)) was 31.7 + or - 10.2 mL/kg per minute, and mean left ventricular ejection fraction (LVEF) was 36.3 + or - 7.8%. Univariate analysis showed that various echocardiographic parameters of diastolic function were correlated with peakVO(2). There was no correlation between BNP levels or LVEF and EC. Multivariate analysis, after adjustment for age and gender, revealed that E/E' ratio and left atrial volume (LAV), emerged as independent predictors of EC, as demonstrated in the model: peakVO(2)= 60.825 + (0.439 x LAV) - (1.620 x E/E' ratio) - (0.483 x age) - (4.821 x female gender). The R(2) of this model was 0.52. CONCLUSIONS: Functional capacity assessed by peakVO(2) was related to increase LV filling pressures, independently on systolic function in patients with Chagas cardiomyopathy. (Echocardiography 2010;27:519-524).