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R Belardinelli

Publications and source records attributed to R Belardinelli.

At least 37 records · Page 2Linked to original sources

Low dose dobutamine echocardiography predicts improvement in functional capacity after exercise training in patients with ischemic cardiomyopathy: prognostic implication.

OBJECTIVES: This study sought to investigate whether the identification of hibernating myocardium by low dose dobutamine stress echocardiography (LDSE) may predict an improvement in functional capacity after moderate exercise training in patients with ischemic cardiomyopathy. Another objective was to assess whether exercise training may affect the outcome. BACKGROUND: There is evidence that exercise training improves left ventricular (LV) function as well as functional capacity in patients with a previous myocardial infarction and LV dysfunction. We hypothesized that the magnitude of these improvements might be related to the extent of hibernating myocardium. METHODS: We studied 71 consecutive patients 56+/-9 years old (mean +/- SD) with chronic heart failure secondary to ischemic cardiomyopathy (LV ejection fraction [LVEF] <40%). All patients were in sinus rhythm and were clinically stable during the previous 3 months. Patients were randomized into two matched groups. Group T (n = 36) underwent exercise training at 60% of peak oxygen uptake (Vo2) three times a week for 10 weeks. Group C (n = 35) did not exercise. At study entry and end, all patients underwent an exercise test with gas exchange analysis and LDSE (5 to 20 microg/kg body weight per min). RESULTS: At baseline, a positive contractile response (CS+) to LDSE was observed in 317 of 576 segments in group T and 291 of 560 segments in group C. After 10 weeks, peak Vo2 and peak work rate increased only in trained patients (peak Vo2: from 16.2+/-3 to 20.8+/-4 ml/kg per min; work capacity: from 108+/-20 to 131+/-25 W, p < 0.001 vs. group C for both). The presence of CS+ at baseline was associated with a sensitivity of 70% and a specificity of 77% for predicting an increase in the functional capacity after exercise training. Positive and negative predictive values of LDSE were 84% and 59%, respectively. Independent predictors of cardiac events were a pre-to-posttraining difference in LVEF at peak dobutamine infusion and the presence of a viable response at baseline (p = 0.004 and 0.008, respectively). The log-rank test demonstrated that trained patients had a significantly lower probability of cardiac events during follow-up than sedentary control patients (p < 0.001). CONCLUSIONS: The presence of hibernating myocardium as assessed by LDSE predicts the magnitude of improvement in functional capacity after moderate exercise training in patients with chronic heart failure. A significant increase in functional capacity after exercise training is associated with a lower incidence of cardiac events during follow-up.

Adult↗

Muscle oxygenation kinetics measured by near-infrared spectroscopy during recovery from exercise in chronic heart failure.

The aim of the present study was to determine the kinetics of recovery of muscle oxygenation (MO) from comparable levels of exercise in chronic heart failure (CHF) patients and normal subjects and to relate MO kinetics to the level of exercise intolerance. The rationale is based on the observation that the O2 debt is increased in patients with heart failure and repayment of the debt is relatively slow. Ten patients with stable CHF (mean age 47 +/- 10 years) and nine healthy control subjects (47 +/- 6 years) were studied. All patients had ischemic cardiomyopathy (ejection fraction 33 +/- 7%). On different days, all subjects performed an upright incremental cycle ergometer exercise test with gas-exchange analysis to determine peak VO2, and a 6-minute constant work-rate (CWR) protocol at 60% of peak VO2. Oxygenation of the vastus lateralis muscle was continuously monitored during exercise and recovery using near-infrared spectroscopy (NIRS). Both MO and VO2 responses to recovery were described by a monoexponential model with a time delay. The time constant and time delay were combined to calculate a mean response time (MRT). Recovery VO2 and MO MRTs for the incremental and constant work rate exercise test were longer in CHF patients than in control subjects (p < 0.05). Both VO2 and MO MRTs were inversely related to peak VO2 (r = -0.73 and -0.52, respectively; p < 0.05 for both). However, both kinetics were not significantly different within each group between the two exercise intensities. In conclusion, the greater the cardiac dysfunction, as assessed by peak VO2, the more the recovery of muscle and total body oxygenation from both maximal and submaximal exercise is delayed.

Adult↗

Skeletal muscle oxygenation and oxygen uptake kinetics following constant work rate exercise in chronic congestive heart failure.

The aim of the present study was to determine the kinetics of recovery of muscle oxygenation (MO) from comparable levels of exercise in patients with chronic congestive heart failure (CHF) and in normal subjects, and to relate MO kinetics to the level of exercise intolerance. Ten patients with stable CHF secondary to ischemic cardiomyopathy (ejection fraction 34 +/- 6%) (mean age 47 +/- 10 years) and 8 healthy matched control subjects underwent an upright incremental cycle ergometer exercise test with gas exchange analysis and a 6-minute constant work rate protocol at 60% of peak oxygen consumption (VO2). Oxygenation of the vastus lateralis muscle was continuously monitored during exercise and recovery using near infrared spectroscopy. Recovery VO2 and MO mean response times for the constant work rate exercise test were longer in patients with CHF than in control subjects (p <0.05). Both VO2 and MO mean response times were inversely related to peak VO2 (r = -0.73 and -0.52, respectively; p <0.05 for both). Thus recovery of muscle and total body oxygenation from submaximal exercise is more delayed the greater the cardiac dysfunction, as assessed by peak VO2. This suggests that regeneration of phosphocreatine and/or resaturation of venous oxyhemoglobin take place more slowly the worse the cardiac function.

Adult↗

Lung function and exercise gas exchange in chronic heart failure.

BACKGROUND: The ventilatory response to exercise in patients with chronic heart failure (HF) is greater than normal for a given metabolic rate. The objective of the present study was to determine the mechanism(s) for the high ventilatory output in patients with chronic HF. METHODS AND RESULTS: Centers in Germany, Italy, Japan, and the United States participated in this study. Each center contributed studies on patients and normal subjects of similar age and sex. One hundred thirty patients with chronic HF and 52 healthy subjects participated. Spirometric and breath-by-breath gas exchange measurements were made during rest and increasing cycle exercise. Arterial blood was sampled for measurement of pH, PaCO2, PaO2, and lactate during exercise in 85 patients. Resting forced expiratory volume in 1 second (FEV1) and vital capacity (VC) were proportionately reduced at all levels of impairment. Patients with more severe HF had greater tachypnea and a smaller tidal volume (VT) at a given exercise expired volume per unit time (VE). This was associated with an expiratory flow pattern characteristic of lung restriction. VE and VCO2 as a function of VO2 were increased during exercise in HF patients. The increases were greater the lower the peak VO2 per kilogram of body weight. The ratio of VD (physiological dead space) to VT and the difference between arterial and end tidal PCO2 at peak VO2 also increased inversely with peak VO2/kg. In contrast, the difference between alveolar and arterial PO2 and PaCO2 were both normal, on average, at peak VO2 regardless of the level of impairment. The more severe the exercise limitation, the higher the lactate and the lower the HCO3- at a given VO2, although pH was tightly regulated. CONCLUSIONS: The increase in VE in chronic HF patients is caused by an increase in VD/VT due to high ventilation/perfusion mismatching, an increase in VCO2 relative to VO2 resulting from HCO3- buffering of lactic acid, and a decrease in PaCO2 due to tight regulation of arterial pH. With regard to the excessive VE in HF patients, the increases in VD/VT and VCO2 relative to VO2 are more important as the patient becomes more exercise limited. Regional hypoperfusion but not hypoventilation typifies lung gas exchange in HF. This and other mechanisms might account for the restrictive changes leading to exercise tachypnea in HF patients.

Carbon Dioxide↗

Diagnostic criteria and management of subacute ventricular free wall rupture complicating acute myocardial infarction.

In this prospective study we evaluated the value of the main diagnostic criteria for postinfarction subacute rupture of the ventricular free wall. Two-dimensional echocardiograms and recordings of right atrial pressure and waveform were immediately obtained in every patient exhibiting rapid clinical and/or hemodynamic compromise in the acute infarction setting. The same protocol was applied to patients referred from other hospitals for suspected myocardial rupture. In 28 cases a subacute free wall rupture was identified. In most of the patients the diagnosis was based on the demonstration of hemopericardium and cardiac tamponade by echocardiography, cardiac catheterization and, occasionally, by pericardiocentesis. In 2 instances, the identification of intrapericardial echo densities suggesting clots, in the absence of cardiac tamponade, allowed a diagnosis of subacute rupture. Direct, but indistinct visualization of myocardial rupture was obtained in 4 cases. Among the 28 patients with this complication, 4 died while awaiting surgery and 24 underwent surgical repair (mortality rate 33%). Long-term outcome of survivors was favorable. Various myocardial lesions underlie postinfarction subacute free wall rupture. Clinical presentation varied widely. The diagnosis was based, usually but not always, on the association of hemopericardium and signs of cardiac tamponade. An organized approach to management of this complication of acute myocardial infarction was suggested.

Aged↗

Nitric oxide production during exercise in chronic heart failure.

In chronic heart failure (CHF), the ventilatory response is increased compared with normal. This response is, in part, caused by reduced perfusion to ventilated lung. Nitric oxide (NO) is a potent vasodilator and may have an important role in pulmonary vasodilatation during exercise. NO is present in exhaled air. The amount of NO in exhaled air, when breathing NO-free compressed air, is known to increase in normal subjects during exercise. In this study, we quantified NO output in exhaled air in patients with CHF during exercise. Six patients with CHF (New York Heart Association Class II and III; two with dilated cardiomyopathy, three with ischemic heart disease, and one with hypertensive heart disease) and six normal subjects were studied with a symptom-limited incremental exercise test on a cycle ergometer. Oxygen uptake (VO2), carbon dioxide output (VCO2), and minute ventilation (VE) were measured breath by breath with a mass spectrometer, flow meter, and computer. The NO concentration was continuously measured in mixed expired air by chemiluminescence. Peak exercise work rate was lower in patients with CHF than in normal subjects (71.3 +/- 41.6 W vs 257.0 +/- 49.7 W; p < 0.01). Patients with CHF showed a higher VE/VCO2 level at peak exercise than normal subjects (CHF, 47.0 +/- 10.7; normal subjects, 35.6 +/- 5.2; p < 0.01). NO concentration of exhaled air at rest was lower in CHF patients than in normal subjects (4.0 +/- 2.2 ppb vs 10.5 +/- 6.2 ppb, respectively; p < 0.05). NO output from the respiratory tract (VNO) was significantly lower in patients with CHF compared with normal subjects at rest (45.3 +/- 24.3 nl/min, 117.5 +/- 60.1 nl/min, respectively, p < 0.05), and although it increased during exercise, it did not increase in patients with CHF as much as in normal subjects (75.3 +/- 43.4 nl/min vs 512.9 +/- 253.6 nl/min, respectively; p < 0.01). The increase above rest (exercise/rest) was smaller in patients with CHF than in normal subjects (2.10 +/- 1.92 vs 4.81 +/- 2.67, p < 0.05). These data support the concept that the smaller increase in NO production (VNO) during exercise may be responsible for a blunted vasodilation in patients with CHF, resulting in a smaller reduction in dead space/tidal volume and VE/VCO2 at the lactic acidosis threshold than normal. This finding may play a role in the abnormally high ventilatory response to exercise in patients with CHF.

Adult↗

Comparison of impedance cardiography with thermodilution and direct Fick methods for noninvasive measurement of stroke volume and cardiac output during incremental exercise in patients with ischemic cardiomyopathy.

In the last decade, an inexpensive and simple noninvasive method (i.e., transthoracic electrical bioimpedance cardiography, has been tested in healthy subjects and patients with various heart disease for measuring stroke volume and cardiac output at rest and/or during exercise. However, the results are still controversial, especially when measurements are obtained during exercise and data on reproducibility during exercise are lacking. Twenty-five consecutive patients (20 men and 5 women, mean age 48 +/- 9 years) in sinus rhythm with documented coronary artery disease and a previous myocardial infarct were studied. Patients were divided into 2 groups. Group A had ischemic cardiomyopathy, characterized by left ventricular (LV) enlargement and LV ejection fraction depression (35 +/- 8%). Group B had normal LV dimensions and ejection fraction (62 +/- 9%). After a familiarization study, all patients underwent an exercise test with gas exchange analysis and hemodynamic measurements. Stroke volume and cardiac output were simultaneously obtained at rest and at the end of each work rate stage with 3 methods: impedance, thermodilution, and direct Fick. Group A reached a lower peak oxygen uptake (56%), peak work load (60%), and peak systolic blood pressure (69%) than group B. Cardiac output and stroke volume were significantly greater at submaximal and peak exercise in group B than in group A (p < 0.0001). There were no significant differences in stroke volume and cardiac output in the 3 techniques at any matched work rate. There was no significant difference between measurements obtained by 2 experienced observers or between those obtained on 2 exercise tests performed on 2 different days. These results demonstrate that impedance cardiography is a noninvasive, simple, accurate, and reproducible method of measurement of cardiac output and stroke volume over a wide range of workloads.

Cardiac Catheterization↗

Effects of exercise training on left ventricular filling at rest and during exercise in patients with ischemic cardiomyopathy and severe left ventricular systolic dysfunction.

The aim of our study was to determine whether exercise training can augment left ventricular diastolic filling at rest and during exercise in patients with ischemic cardiomyopathy and whether any correlation exists between changes in diastolic filling and changes in exercise tolerance. Forty-three consecutive patients (mean age, 54 +/- 8 years) with ischemic cardiomyopathy and severe left ventricular systolic dysfunction (election fraction <30%) were studied. Group T (29 patients) was exercised on a cycle ergometer 3 times a week for 8 weeks at 60% of peak oxygen uptake. Group C (14 patients) was not exercised. All patients underwent an exercise test and a radionuclide ventriculography at baseline and after 8 weeks. At the end, no changes were found in group C. In group T, exercise training increased peak oxygen uptake (1 5%; p < 0.0001), work rate (1 5%; p < 0.005), peak early filling rate (10%; p < 0.02), and peak filling rate (1 1%; p < 0.03). At submaximal exercise, peak filling rate increased at all matched heart rates. The increase in peak filling rate was correlated with the increase in cardiac index (r= 0.72; p < 0.0001) at peak exercise. The independent predictors of the increase in peak oxygen uptake were changes in work capacity and peak early filling rate. The data demonstrate that exercise training can improve the exercise capacity of patients with ischemic cardiomyopathy and severe systolic-dysfunction. The increase in early diastolic filling at rest and during exercise may contribute to the improvement in peak oxygen uptake.

Cardiac Output↗

Comparison of electron beam computed tomography scanning and magnetic resonance imaging quantification of right ventricular mass: validation with autopsy weights.

RATIONALE AND OBJECTIVES: We compared, in the same human hearts, the ability of magnetic resonance (MR) imaging and electron beam computed tomography (CT) scanning to accurately quantify the free wall and septal components of right ventricular (RV) mass. METHODS: Eleven hearts extracted at autopsy were subjected to MR imaging and electron beam CT scanning in short-axis projections. Regression analyses of mass determinations obtained by manual planimetry MR imaging and electron beam CT scanning and autopsy weights were performed. RESULTS: RV free wall mass by both MR imaging (53.4 +/- 19.1 g) and electron beam CT scanning (53.9 +/- 20.4 g) correlated well with autopsy weight (57.7 +/- 20.2 g). Regression analysis showed a strong correlation for MR imaging (r = .88, slope = .88, standard error the estimate [SEE] = 7.2 g, p < .001) and electron beam CT scanning (r = .95, slope = .95, SEE = 6.6 g, p < .001). RV septal mass by MR imaging (10.8 +/- 3.5 g) and electron beam CT scanning (7.1 +/- 2.4 g) correlated less well with the autopsy weight (12.5 +/- 6.5 g). Regression analysis showed a fair correlation for MR imaging (r = .45, slope = .83, SEE = 2.05 g, p = .001) and a poor correlation for electron beam CT scanning (r = .46, slope = .17, SEE = 2.25 g, p = .57). CONCLUSION: Both MR imaging and electron beam CT scanning accurately predict RV free wall mass but have difficulty predicting the septal component. Because the septal component constitutes only a small proportion of the total RV mass, determinations of RV mass should be based solely on the free wall component.

Autopsy↗

Exercise training improves left ventricular diastolic filling in patients with dilated cardiomyopathy. Clinical and prognostic implications.

BACKGROUND: Patients with dilated cardiomyopathy (DCM) often have left ventricular (LV) diastolic dysfunction that can precede the development of systolic dysfunction. Recent reports showed that exercise training (ET) improves the exercise capacity of these patients. Although this improvement is primarily due to peripheral adaptations, the contribution of LV diastolic filling has not been well defined. The purpose of this study was to determine whether ET can induce changes in LV diastolic filling that can account for an increase in exercise capacity and whether these changes can influence prognosis. METHODS AND RESULTS: We prospectively studied 55 consecutive patients (mean age, 55 +/- 7 years) with DCM. Patients were randomized into a training group (36 patients) or a control untrained group (19 patients) and matched for clinical and functional characteristics. All patients underwent a pulsed Doppler echocardiographic study, a radionuclide angiographic study, and a cardiopulmonary exercise test before and after a 2-month ET program. On the basis of the Doppler LV diastolic filling pattern at the beginning of the study, patients were prospectively divided into three subgroups: A (restrictive pattern), B ("normal" pattern), and C (abnormal relaxation pattern). In the trained group, peak VO2 (+12%; P < .0001), peak workload (+8.5%; P < .005), and lactic acidosis threshold (+12%; P < .0001) were significantly increased after training without changes in LV ejection fraction. However, only subgroup C demonstrated significant improvement in peak VO2 (+15%; P < .005). No changes were observed in the untrained group. In the trained subgroups a significant increase in rapid filling fraction (RFF), peak filling rate (PFR), peak early filling velocity (E), and E/A ratio was noted. A significant decrease in atrial filling fraction (AFF), peak atrial filling velocity (A), deceleration time of early filling velocity (EDT), and isovolumic relaxation time (IVRT) was observed only in subgroup C. No changes were found in untrained subgroups. A good correlation was found between Doppler and radionuclide LV diastolic filling parameters before and after training (P < .0001). Multiple stepwise regression analysis demonstrated that pretraining E/A ratio (P < .0001) and peak heart rate (P < .0002) were positive predictors of pretraining peak VO2. Posttraining increase in exercise tolerance (P < .0001) and increase in E/A ratio (P < .0001) were the strongest predictors of an increase in peak VO2. The independent predictors of cardiac events were a greater RFF and a shorter IVRT and EDT. Stepwise logistic regression showed that Doppler LV diastolic filling patterns are independent predictors of overall cardiac events (P = .02), and restrictive pattern has a worse prognosis compared with B (P = .04) and C (P = .007). However, ET did not reach statistical significance (P = .54) as a predictor of cardiac events. CONCLUSIONS: These data demonstrate that ET induces significant improvement in exercise capacity only in patients with DCM and a pattern of abnormal LV relaxation. The improvement in peak VO2 is significantly correlated with an increase in peak early filling rate and peak filling rate as well as a decrease in atrial filling rate. Doppler echocardiography may be a valuable tool in the prognostic assessment of patients with DCM who will benefit from exercise training.

Blood Flow Velocity↗

Changes in skeletal muscle oxygenation during incremental exercise measured with near infrared spectroscopy.

To determine the change in muscle oxygenation in response to progressively increasing work rate exercise, muscle oxyhemoglobin + oxymyoglobin saturation was measured transcutaneously with near infrared spectroscopy in the vastus lateralis muscle during cycle ergometry. Studies were done in 11 subjects while gas exchange was measured breath-by-breath. As work rate was increased, tissue oxygenation initially either remained constant near resting levels or, more usually, decreased. Near the work rate and metabolic rate where significant lactic acidosis was detected by excess CO2 production (lactic acidosis threshold, LAT), muscle oxygenation decreased more steeply. As maximum oxygen uptake (VO2max) was approached, the rate of desaturation slowed. In 8 of the 11 subjects, tissue O2 saturation reached a minimum which was sustained for 1-3 min before VO2max was reached. The LAT correlated with both the VO2 (r = 0.95, P < 0.0001) and the work rate (r = 0.94, P < 0.0001) at which the rate of tissue O2 desaturation accelerated. These results describe a consistent pattern in the rate of decrease in muscle oxygenation, slowly decreasing over the lower work rate range, decreasing more rapidly in the work rate range of the LAT and then slowing at about 80% of VO2max, approaching or reaching a minimum saturation at VO2max.

Acidosis, Lactic↗

Low intensity exercise training in patients with chronic heart failure.

OBJECTIVES: The present study was designed to evaluate whether a specific program of low intensity exercise training may be sufficient to improve the exercise tolerance of patients with chronic heart failure. BACKGROUND: Recent studies have shown that exercise training can improve exercise tolerance in patients with stable chronic heart failure, mainly through peripheral adaptations. These changes have been observed with exercise regimens at intensities of 70% to 80% of peak oxygen uptake and > 8 weeks. METHODS: We studied 27 patients (23 men, 4 women; mean [+/- SD] age 57 +/- 6 years) with mild chronic heart failure. We classified patients into two groups: trained group and untrained group. The trained group underwent a low intensity (40% of peak oxygen uptake) training program three times/week for 8 weeks. The untrained group performed no exercise. RESULTS: An increase in peak oxygen uptake (17%, p < 0.0001), lactic acidosis threshold (20%, p < 0.0002) and peak work load (21%, p < 0.0002) were obtained in the trained group only. Cardiac output and stroke volume were unchanged. A high correlation was found between the increases in peak oxygen uptake and volume density of mitochondria of vastus lateralis muscle (r = 0.77, p < 0.0002). CONCLUSIONS: Patients with stable chronic heart failure can achieve significant improvement in functional capacity from a low intensity exercise training regimen. The mechanism responsible for this favorable effect involves an increase in mitochondrial density, which reflects an improvement in oxidative capacity of trained skeletal muscles.

Anaerobic Threshold↗

Near infrared spectroscopy and changes in skeletal muscle oxygenation during incremental exercise in chronic heart failure: a comparison with healthy subjects.

Near infrared spectroscopy (NIRS) is a noninvasive technique of monitoring tissue oxygen saturation by detecting changes in tissue absorbance of two wavelengths (850 and 760 nm) reflecting the relative oxygenation of hemoglobin and myoglobin. Aim of the present study was to determine whether changes in skeletal muscle oxygen saturation during incremental exercise detected by NIRS can reflect an impared oxygen delivery and an early onset of anaerobic metabolism in patients with chronic heart failure (CHF). We studied 19 subjects (mean age 43 +/- 16 years). Seven patients had a history of CHF with a diagnosis of ischemic cardiomyopathy (Group A) and 12 were healthy sedentary (Group B). All patients had a history of dyspnea on exertion (NY-HA II), peripheral edema, pulmonary rales and cardiac gallop sounds over the last 6 months. They were in sinus rhythm and stable clinical condition in the last 3 months. They were well matched regarding age, sex and body surface area. All subjects performed an incremental work rate test in a ramp pattern on a upright cycle ergometer until volitional fatigue. Gas exchange was measured breath by breath with a metabolic chart. Muscle oxygenation was determined, transcutaneously, during the exercise test over the vastus lateralis muscle with NIRS. At peak exercise, work rate, VO2, anaerobic threshold (LAT), heart rate and systolic blood pressure were significantly lower in Group A compared to Group B (92 +/- 28 vs 232 +/- 17 watts; 14 +/- 2 vs 21 +/- 2 ml/kg/min; 868 +/- 225 vs 1317 +/- 354 ml/min; 149 +/- 7 vs 172 +/- 18 b/min; 145 +/- 18 vs 195 +/- 21 mm Hg, respectively; p < 0.0001 for all). In both groups, as work rate increased, tissue oxygenation initially either remained constant near resting levels or decreased. In both groups, muscle oxygenation decreased more steeply near the work rate where lactic acidosis (LAT) was detected. However, patients with CHF had an earlier acceleration in muscle deoxygenation compared to the other group, indicating a premature onset of anaerobic metabolism. Moreover, Group A had a flatter increase in both heart rate and systolic blood pressure and a steeper slope of oxygenation profile at all matched workloads compared to normals (Group A: -0.13 +/- 0.03 ml/min; Group B: -0.06 +/- 0.015 ml/min; p < 0.0001). The LAT correlated with the work rate at which the rate of tissue O2 desaturation accelerated (r = 0.94; p < 0.0001).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Skeletal muscle oxygenation during constant work rate exercise.

We compared the slow rise in VO2 during heavy exercise (i.e., greater than lactic acidosis threshold (LAT)) with changes in muscle oxyhemoglobin+oxymyoglobin (O2Hb/O2Mb) saturation by reflectance near infrared spectroscopy. Ten subjects performed four 6-min cycle ergometer tests with two constant work rates less than and two greater than the LAT, equivalent to 20, 40, 65 and 75% peak VO2. During less than LAT exercise, O2Hb/O2Mb saturation decreased to a minimum by 2 min and then remained constant or rose slightly. For greater than LAT work rates, the initial fall in O2Hb/O2Mb saturation was greater the higher the work rate and continued to decrease with time after 3 min. Between minutes 3 and 6, the rate of decrease in O2Hb/O2Mb saturation correlated with the increase in VO2 (r = -0.69, P < 0.0001). These studies support the hypothesis that the slow rise in VO2 during heavy constant work rate exercise is associated with a progressive decline in O2Hb/O2Mb saturation in the contracting muscles themselves that may be facilitated by capillary oxyhemoglobin dissociation owing to tissue lactic acidosis (Bohr effect).

Adult↗

[Effects of aerobic training in patients with moderate chronic heart failure].

UNLABELLED: To evaluate the effects of a program of moderate intensity in patients (pts) with clinically stable chronic heart failure (CHF), we studied 20 pts (18M, 2F, mean age 61 years) with dilated cardiomyopathy, Weber Class B, ejection fraction (EF) < 40% and aerobic capacity of 16 +/- 2 ml/kg/min on cardiopulmonary exercise testing. We randomly assigned pts to 2 groups, a training group (T, 10 pts) and a control group (C, 10 pts), similar for anatomical and clinical characteristics, group T underwent a thrice weekly, 8 week-long ambulatory program of aerobic activity, beginning at 40% of maximal oxygen uptake. At the end, in Group T we observed a significant increase of exercise tolerance (+45%; p < 0.005), peak oxygen uptake (VO2 max) (+20%; p < 0.001), anaerobic ventilatory threshold (AT) (+37%; p < 0.005), lactate threshold (+36%; p < 0.005), peak heart rate (< 10%; p < 0.01) and of peak systolic pressure (+12%; p < 0.007); and a significant reduction in resting heart rate (-17%; p < 0.005), resting diastolic pressure (-11%; p < 0.005), plasma lactate (LA) at rest (-26%; p < 0.01), at peak (-21%; p < 0.005) and at recovery (-22%; p < 0.005), plasma norepinephrine (NE) both at rest (-38%; p < 0.005) and at peak (-13%; p < 0.005) and of plasma epinephrine (E) (-38%; p < 0.005; -32%, p < 0.001, respectively). We observed no change in EF at the end in both groups nor any untoward cardiac effects during training. We didn't note any correlation between AT and venous oxygen saturation (r = 0.15; p = 0.65) changes at the end. The increase in peak VO2 after training was not correlated to any AT increase (r = 0.12; p = 0.72). We observed, however, a significant correlation between lactate threshold and AT changes after training (r = 0.81; p = 0.005) and between LA and resting, submaximal and peak NE (r = 0.89; p = 0.005) and E (r = 0.78; p = 0.007) changes at the end of training. CONCLUSIONS: a) in pts with clinically stable CHF a program of aerobic activity well tolerated in terms of frequency, intensity and duration may determine a significant increase in exercise tolerance, aerobic capacity, AT and LA threshold, and a significant decrease in plasma LA, NE and E at rest, submaximal and peak levels; b) in our opinion, such modifications are partly determined by a delay in lactate accumulation and partly by sympathetic tone lowering, and permit us to underline the concept that physical inactivity may provoke important peripheral changes that, in turn, may reduce exercise tolerance and aerobic capacity, by creating a vicious circle difficult to break by medical therapy alone.

Anaerobic Threshold↗

beta-N-acetylhexosaminidase isoenzymes during chick embryo development.

1. Two forms (I and II) with acidic pH optima and a neutral form of beta-hexosaminidase has been separated by DEAE-cellulose chromatography and characterized in skin and lung of 7, 9, 11, 14 day chick embryos and 1 day old chicken. 2. Forms I and II are similar to hexosaminidase A and B for their behaviour on DEAE-cellulose chromatography, Concanavalin A-Sepharose column and thermal stability. 3. Neutral form has a neutral pH optimum and higher molecular weight and a more acidic I. P. than forms I and II, a low beta-N-acetylgalactosaminidase activity and it is not bound by a Concanavalin A-Sepharose column and in that resemble hexosaminidase C and/or other neutral hexosaminidases. 4. We have found differences in the percentage of neutral form and in the specific activities of the extracts in the skin in different stages of development. 5. No significant differences were observed in the lung.

Animals↗

[Echocardiographic and clinical correlations in infectious endocarditis of the left heart].

UNLABELLED: The echocardiographic features were correlated with the clinical findings and outcome in 35 patients with aortic and/or mitral valve endocarditis. There were 26 males and 9 females with a mean age of 38 years. The infection involved native valves in 27 patients and prosthetic valves in 8 patients. Echocardiographically, fourteen patients had involvement of native aortic valve. All patients in this group required surgical intervention, nine patients during antimicrobial therapy. Congestive heart failure was the clinical indication for valvular replacement. A patient died immediately after surgery from low cardiac output syndrome. Six patients had echocardiographic evidence of aortic and mitral valves involvement. A patient in this group expired before surgery, five underwent surgery because of progressive heart failure (aortic or aortic and mitral valves replacement). Seven patients showed lesions on native mitral valve (6 in this group had prolapse syndrome). A patient died from cerebrovascular embolus, two underwent surgery because of persistent infection and embolic events, four were successfully treated with medical therapy. Among patients with prosthetic valve endocarditis, four showed signs of valvular dehiscence and required surgical intervention, during antimicrobial therapy, from congestive heart failure; one patient expired from recurrent infection. The pathological findings correlated well with echocardiographic findings. CONCLUSIONS: in IE the localization of lesions by echo has prognostic significance: most patients with aortic valve or aortic and mitral valves endocarditis require early surgical intervention because of congestive heart failure. On the contrary, mitral valve involvement carries a better prognosis, requiring less frequently valvular replacement; the patients with echocardiographic signs of prosthetic valve dehiscence require urgent intervention.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗