Maximal respiratory pressures: Measurements at functional residual capacity in individuals with different health conditions using a digital manometer.

BACKGROUND: Measuring maximal respiratory pressure is a widely used method of investigating the strength of inspiratory and expiratory muscles. OBJECTIVES: To compare inspiratory pressures obtained at functional residual capacity (FRC) with measures at residual volume (RV), and expiratory pressures obtained at FRC with measures at total lung capacity (TLC) in individuals with different health conditions: post-COVID-19, COPD, idiopathic pulmonary fibrosis (IPF), heart failure (CHF), and stroke; and to compare the mean differences between measurements at FRC and RV/TLC among the groups. METHODS: Inspiratory and expiratory pressures were obtained randomly at different lung volumes. Mixed factorial analysis of covariance with repeated measures was used to compare measurements at different lung volumes within and among groups. RESULTS: Seventy-five individuals were included in the final analyses (15 individuals with each health condition). Maximal inspiratory pressures at FRC were lower than RV [mean difference (95% CI): 11.3 (5.8, 16.8); 8.4 (2.3, 14.5); 11.1 (5.5, 16.7); 12.8 (7.1, 18.4); 8.0 (2.6, 13.4) for COVID-19, COPD, IPF, CHF, and stroke, respectively] and maximal expiratory pressures at FRC were lower than TLC [mean difference (95% CI): 51.9 (37.4, 55.5); 60.9 (44.2, 77.7); 62.9 (48.1, 77.8); 58.0 (43.9, 73.8); 57.2 (42.9, 71.6) for COVID-19, COPD, IPF, CHF, and stroke, respectively]. All mean differences were similar among groups. CONCLUSION: Although inspiratory and expiratory pressures at FRC were lower than measures obtained at RV/TLC for the five groups of health conditions, the mean differences between measurements at different lung volumes were similar among groups, which raises the discussion about the influence of the viscoelastic properties of the lungs on maximal respiratory pressure.

Prospective analysis of myocardial strain through the evolution of Chagas disease in the hamster animal model.

Speckle tracking echocardiography (STE) enables early diagnosis of myocardial damage by evaluating myocardial strain. We aimed to study sequential changes in structural and ventricular functional parameters during Chagas disease (CD) natural history in an animal model. 37 Syrian hamsters were inoculated intraperitoneally with Trypanosoma cruzi (Chagas) and 20 with saline (Control). Echocardiography was performed before the infection (baseline), at 1 month (acute phase), 4, 6, and 8 months (chronic phase) using Vevo 2100 (Fujifilm Inc.) ultrasound system. Left ventricular end-diastolic diameter, Left ventricular end-systolic diameter (LVESD), Left ventricular ejection fraction (LVEF), Global longitudinal (GLS), circumferential (GCS) and radial (GRS) strain were evaluated. Tricuspid annular plane systolic excursion (TAPSE) was used to assess right ventricular function. At 8 months, animals were euthanized and LV myocardial samples were analyzed for quantitation of inflammation and fibrosis. LVEF decreased over time in Chagas group and a difference from Control was detected at 6 months (p-value of groups#time interaction = 0.005). There was a pronounced decrease in GLS, GCS and TAPSE in Chagas group (p-value of groups#time interaction = 0.003 for GLS, < 0.001 for GCS and < 0.009 for TAPSE vs Control) since the first month. LVESD, LVEF and GLS were significantly correlated to the number of inflammatory cells (r = 0.41, p = 0.046; r = - 0.42, p = 0.042; r = 0.41, p = 0.047) but not to fibrosis. In the Syrian hamster model of CD STE parameters (GLS and GCS) showed an early decrease. Changes in LVEF, LVESD, and GLS were correlated to myocardial inflammation but not to fibrosis.

Exercise Limitation in Children and Adolescents With Severe Refractory Asthma: A Lack of Asthma Control?

BACKGROUND: Patients with severe refractory asthma (SRA), even when using high doses of multiple controller medications in a regular and appropriate way, can have persistent complaints of exercise limitation. METHODS: This was a cross-sectional study involving patients with SRA (treated with ≥ 800 µg of budesonide or equivalent, with ≥ 80% adherence, appropriate inhaler technique, and comorbidities treated), who presented no signs of a lack of asthma control other than exercise limitation. We also evaluated healthy controls, matched to the patients for sex, age, and body mass index. All participants underwent cardiopulmonary exercise testing (CPET) on a cycle ergometer, maximum exertion being defined as ≥ 85% of the predicted heart rate, with a respiratory exchange ratio ≥ 1.0 for children and ≥ 1.1 for adolescents. Physical deconditioning was defined as oxygen uptake (VO2) < 80% of predicted at peak exercise, without cardiac impairment or ventilatory limitation. Exercise-induced bronchoconstriction (EIB) was defined as a forced expiratory volume in one second ≥ 10% lower than the baseline value at 5, 10, 20, and 30 minutes after CPET. RESULTS: We evaluated 20 patients with SRA and 19 controls. In the sample as a whole, the mean age was 12.9 ± 0.4 years. The CPET was considered maximal in all participants. In terms of the peak VO2 (VO2 peak), there was no significant difference between the patients and controls, (P = 0.10). Among the patients, we observed isolated EIB in 30%, isolated physical deconditioning in 25%, physical deconditioning accompanied by EIB in 25%, and exercise-induced symptoms not supported by the CPET data in 15%. CONCLUSION AND CLINICAL RELEVANCE: Physical deconditioning, alone or accompanied by EIB, was the determining factor in reducing exercise tolerance in patients with SRA and was not therefore found to be associated with a lack of asthma control.

Physical training improves myocardial perfusion but not left ventricular function response to exercise in patients with microvascular angina.

BACKGROUND: Patients with primary microvascular angina (PMA) commonly exhibit abnormal left ventricular function (LVF) during exercise, potentially owing to myocardial ischemia. Herein, we investigated in PMA patients the effect of the reduction of myocardial perfusion disorders, by using aerobic physical training, upon LVF response to exercise. METHODS: Overall, 15 patients (mean age, 53.7±8.9 years) with PMA and 15 healthy controls (mean age, 51.0±9.4 years) were studied. All subjects were subjected to baseline resting and exercise ventriculography, myocardial perfusion scintigraphy (MPS), and cardiopulmonary testing. PMA group members then participated in a 4-month physical training program and were reevaluated via the same methods applied at baseline. RESULTS: Baseline left ventricular ejection fraction (LVEF) determinations by ventriculography were similar for both groups (PMA, 67.7±10.2%; controls, 66.5±5.4%; P=0.67). However, a significant rise in LVEF seen in control subjects during exercise (75.3±6.2%; P=0.0001) did not materialize during peak exercise in patients with PMA (67.7±10.2%; P=0.47). Of the 12 patients in the PMA group who completed the training program, 10 showed a significant reduction in reversible perfusion defects during MPS. Nevertheless, LVEF at rest (63.5±8.7%) and at peak exercise (67.3±15.9%) did not differ significantly (P=0.30) in this subset. CONCLUSIONS: In patients with PMA, reduced left ventricular inotropic reserve observed during exercise did not normalize after improving myocardial perfusion through aerobic physical training.

Chronic cholinergic stimulation promotes changes in cardiovascular autonomic control in spontaneously hypertensive rats.

Hypertension is often accompanied by autonomic dysfunction, which is detrimental to cardiac regulation. On the other hand, cholinergic stimulation through inhibition of acetylcholinesterase appears to have beneficial effects on cardiac autonomic control. Thus, our objective was to investigate the effects of chronic cholinergic stimulation on hemodynamic and cardiovascular autonomic control parameters in spontaneously hypertensive rats (SHR). For this, 26-week-old SHR (N = 32) and Wistar Kyoto rats (WK; N = 32) were divided into two groups: one treated with vehicle (H2O; N = 16) and the other treated with pyridostigmine bromide (PYR; N = 16) in drinking water (25 mg/kg/day) for 2 weeks. All groups were subjected to recording of arterial pressure (AP) and heart rate (HR), quantification of ejection fraction (EF), evaluation of cardiac tonic autonomic balance by means of double autonomic blockade with methylatropine and propranolol, analysis of systolic AP (SAP) and HR variability (HRV), and evaluation of baroreflex sensitivity (BRS). AP, HR, and EF were reduced in the SHR-PYR group compared with the SHR-H2O group. Evaluation of autonomic parameters revealed an increase in vagal tone participation in cardiac tonic autonomic balance and reduced SAP variability; however, no changes were observed in HRV or BRS. These results suggest that chronic cholinergic stimulation with pyridostigmine bromide promotes reduction in the hemodynamic parameters AP, HR, and EF. Additionally, tonic autonomic balance was improved and a reduction in LF oscillations of SAP variability was observed that could not be attributed to BRS, as the latter did not change. Further studies should be conducted to identify the mechanisms involved in the observed responses.