Relationship of maximum walking speed with peak oxygen uptake and anaerobic threshold in male patients with heart failure.

This retrospective observational study aimed to examine the relationships of maximum walking speed (MWS) with peak oxygen uptake (peak VO2) and anaerobic threshold (AT) obtained by cardiopulmonary exercise testing (CPX) in patients with heart failure. The study participants were 104 consecutive men aged ≥ 20 years who had been hospitalized or had undergone outpatient care at our hospital for heart failure between February 2019 and January 2023. MWS was measured in a 5-m section with a 1-m run-up before and after the course. Multivariable analysis was used to examine the association between MWS and peak VO2 and AT by CPX. The Pearson correlation coefficient showed that MWS was positively correlated with percent-predicted peak VO2 and percent-predicted AT (r = 0.463, p < 0.001; and r = 0.485, p < 0.001, respectively). In the multiple linear regression analysis employing percent-predicted peak VO2 and percent-predicted AT as the objective variables, only MWS demonstrated a significant positive correlation (standardized ß: 0.471, p < 0.001 and 0.362, p < 0.001, respectively). Multiple logistic regression analyses, using an 80% cutoff in percent-predicted peak VO2 and AT, revealed that only MWS was identified as a significant factor in both cases (odds ratio [OR]: 1.239, 95% confidence interval [CI]: 1.071-1.432, p = 0.004 and OR: 1.469, 95% CI: 1.194-1.807, p < 0.001, respectively). MWS was correlated with peak VO2 and AT in male patients with heart failure. The MWS measurement as a screening test for exercise tolerance may provide a simple means of estimating peak VO2 and AT in heart failure patients.

Solutions for retention of female cardiologists: from the survey of gender differences in the work and life of cardiologists.

BACKGROUND: To prevent a future shortage of cardiologists, it is important for female cardiologists to continue working. Gender differences in the professional and private lives of cardiologists, as well as the barriers to work for female cardiologists, were surveyed. METHODS AND RESULTS: In August 2007, a questionnaire was mailed to all 195 faculty members/fellows and 155 alumni of the Department of Cardiovascular Medicine at Nippon Medical School. More female cardiologists were dissatisfied with their job than male cardiologists (34% vs 17%, P<0.005). Women reported greater career limitation by family responsibilities and housework. Men and women both reported that long working hours was the most problematic issue, but significantly more women reported this than men (76% vs 94%, P<0.05). Female cardiologists were more concerned about occupational radiation exposure (88% vs 59%, P<0.01) and wanted opportunities for retraining after childcare leave (100% vs 76%, P<0.01). CONCLUSIONS: The following measures should be taken: (1)establishment of more family-friendly working conditions in hospitals, (2)provision of various work positions that allow more flexibility and predictability for women, (3)establishment of a retraining system, and (4)development of work and research opportunities that are attractive to women. The Japanese Circulation Society is expected to establish a retraining system at certified institutions.

Relationship between plasma norepinephrine at peak exercise and 123I-MIBG imaging of the heart and lower limbs in heart failure.

BACKGROUND: Past studies suggested that plasma norepinephrine during exercise originates in sympathetic nerve endings and that the main origin differs among pathophysiological conditions. AIMS: This study investigated the most important site of sympathetic terminals as an origin of plasma norepinephrine during exercise in patients with heart failure using (123)I- metaiodobenzylguanidine (MIBG) scintigraphy. METHODS AND RESULTS: Twenty patients with organic heart disease underwent exercise testing and (123)I-MIBG scintigraphy. Systemic (123)I-MIBG uptake was measured 4 hours after (123)I-MIBG injection, and the heart-to-brain (H/B) and lower limb-to-brain ratios (L/B) were calculated. Plasma norepinephrine concentration was measured at rest and at peak exercise. Subjects were divided into two groups: those with preserved left ventricular ejection fraction (LVEF> or =45%, n=8) and those with reduced LVEF (<45%, n=12). Plasma norepinephrine at rest did not correlate with H/B or L/B. In the preserved LVEF group, plasma norepinephrine at peak exercise was correlated with H/B (r=0.722), but not with L/B. In the reduced LVEF group, the norepinephrine response to peak exercise correlated with L/B (r=0.642), but not with H/B. CONCLUSION: The present findings suggest that norepinephrine concentration is regulated by sympathetic terminal function of working muscles in patients with impaired LVEF and by that of the heart in patients with preserved LVEF.

Improvement of sympathetic response to exercise by oral administration of ascorbic acid in patients after myocardial infarction.

BACKGROUND: Recent studies indicated that excessive oxidative stress in an animal heart failure model injures both the sympathetic nerve endings and receptors, resulting in disturbance of norepinephrine release and sensitivity to norepinephrine. However, it has not been clarified whether this phenomenon is expressed clinically in patients with heart disease. Therefore, we examined the efficacy of ascorbic acid administration as an antioxidant vitamin in relation to the heart rate and norepinephrine response to exercise in patients after myocardial infarction. METHODS: In this randomized crossover trial, 21 male patients who had had myocardial infarction underwent symptom-limited ergometer cardiopulmonary exercise testing twice, that is, without and with ascorbic acid (2 g) administration. Plasma norepinephrine concentrations were assessed at rest and at peak exercise, and heart rate responsiveness to the norepinephrine increment from rest to peak exercise (DeltaHR/logDeltaNE) was calculated. RESULTS: In the exercise test after ascorbic acid administration, peak oxygen consumption (VO(2)) improved over baseline. Ascorbic acid administration significantly increased the change in heart rate and norepinephrine from rest to peak exercise and DeltaHR/logDeltaNE. The increment in heart rate was significantly correlated with peak VO(2) in each test. CONCLUSION: Ascorbic acid intake before exercise improved exercise capacity through enhancement of the heart rate and norepinephrine response to exercise in patients after myocardial infarction. These findings suggest that ascorbic acid intake improves sympathetic dysfunction resulting from injury by excessive oxidative stress after myocardial infarction.

Impaired baroreflex as a cause of chronotropic incompetence during exercise via autonomic mechanism in patients with heart disease.

PURPOSE: It is thought that the mechanisms responsible for impaired chronotropic response to exercise are related to disturbance of cardiovascular autonomic regulation such as the baroreflex. However, it is still unclear whether the baroreflex mechanisms modulate heart rate (HR) responses to exercise via vagal and/or sympathetic alteration. We therefore investigated the effects of baroreflex sensitivity (BRS) on the exercise HR response in the early phase of vagal deactivation and in the later phase of sympathetic excitation via metabolic stimulation. METHODS: Twenty-four patients (18 males and 6 females, age 59+/-9 years) with heart disease underwent symptom-limited treadmill exercise testing according to the Bruce protocol, and BRS was measured utilizing the phenylephrine method. Subjects were grouped by their resting BRS value: 12 with normal BRS (> or =6 ms/mmHg) and 12 with depressed BRS (<6 ms/mmHg). The HR response to exercise was assessed using two parameters: the increment in HR during exercise and the ratio of HR response to the metabolic reserve (chronotropic index). RESULTS: (1) In the patients with depressed BRS, the HR responses within 1 min after the start of exercise and from 1 min to peak exercise were attenuated compared with those having a normal BRS (15+/-8 vs. 24+/-8 bpm and 36+/-9 vs. 47+/-15 bpm, respectively). (2) The chronotropic index in the patients with depressed BRS was lower than in those with normal BRS (0.50+/-0.14 vs. 0.64+/-0.08). CONCLUSION: These findings suggest that impaired BRS modulates both the parasympathetic influence in early exercise and sympathetic effects in the later phase on HR response to exercise.

Clinical backgrounds and the time course of sleep-disordered breathing in patients after myocardial infarction.

INTRODUCTION: Previous studies have suggested that sleep-disordered breathing (SDB) frequently develops after myocardial infarction (MI) and leads to a poor prognosis. However, the details remain unclear. Therefore, we examined the clinical backgrounds and the time course of SDB in patients after MI. METHODS: The subjects were 92 consecutive patients (mean age, 65 ± 12 years) who had MI without decompensated heart failure or uncontrolled myocardial ischemia. All subjects underwent overnight sleep studies, and we investigated baseline clinical characteristics. Among the patients with confirmed SDB, the 38 patients who agreed underwent nighttime multichannel respiratory monitoring at both 14 days and 2 months after the onset of MI, and we investigated their clinical features. RESULTS: The percentage of patients with SDB 14 days after MI was high (93.5%). Among all patients, 6.5% had no SDB, 39.1% had mild SDB, 29.3% had moderate SDB, and 25.0% had severe SDB. The clinical features of patients with moderate-to-severe SDB (apnea-hypopnea index [AHI] ≥15 times/hour) did not differ significantly from those of patients with mild SDB or patients without SDB (AHI <15 times/hour). In patients with central SDB and AHI ≥10 times/hour, there was a significant improvement in AHI from 14 days to 2 months after MI. Multiple regression analysis showed that central SDB and nighttime onset of MI were associated with a decrease in AHI. CONCLUSION: These findings suggest that SDB after MI should be managed on the basis of the type of SDB and the time of MI onset.

Baroreflex mechanisms and response to exercise in patients with heart disease.

BACKGROUND: Past reports showed that the baroreflex continuously regulates hemodynamics during exercise. However, it is still clinically unclear. If baroreflex mechanism is able to influence actually exercise cardiovascular control, baroreflex sympathetic and/or parasympathetic function relates to response to exercise. Therefore, we examined the relationship of heat rate changes to both blood pressure increment and decrement with tolerance and chronotropic response to peak exercise in patients with heart disease. METHODS: In 25 male heart disease patients (60 ± 9 years) without decompensated heart failure, baroreceptor reflex sensitivity (BRS ms mmHg(-1) ) was measured by reflex heart rate responses to changes in blood pressure after phenylephrine (P-BRS) and nitroglycerin (N-BRS) injection, respectively. Symptom-limited treadmill exercise test was performed according to Bruce's protocol. RESULTS: (i) The absolute values of blood pressure change after the administrations were similar between the agents because the dosages of nitroglycerin and phenylephrine were set to equalize absolute changes in blood pressure. (ii) In this study population, the ratio of N-BRS to P-BRS was not significantly correlated with hypertension and diabetes mellitus. (iii) Exercise capacity (METs) (r= -0.626) and heart rate response to exercise per METs (r=0.670) was significantly related to N-BRS but not to P-BRS. CONCLUSION: We found that the abnormality of baroreflex function in the presence of blood pressure decrements can lead to insufficient capacity and easy sympathetic activation during exercise.

Sleep-disordered breathing with nighttime hypocapnia relates to daytime enhanced ventilatory response to exercise in patients with heart disease.

BACKGROUND: Sleep-disordered breathing (SDB) induces nighttime disturbance of arterial gases, such as carbon dioxide. However, it is still unclear whether nighttime SDB-related gas abnormality is related to respiratory dysregulation in daytime. Therefore, we examined the relationship between the arterial partial pressure of carbon dioxide (PaCO(2)) at nighttime and the respiratory response to exercise in daytime. METHODS: Eighteen men (age, mean ± SD; 55 ± 11 years) with heart disease underwent multichannel respiratory monitoring through the night with transdermal measurement of PaCO(2) (PtcCO(2)) reflecting PaCO(2) and a cardiopulmonary exercise test in daytime. The ventilatory equivalent (VE)/carbon dioxide production (VCO(2)) slope as an index of ventilatory response to exercise and peak oxygen consumption (VO(2)) were obtained with a cardiopulmonary exercise test. RESULTS: Of the 18 patients, 10 patients had obstructive SDB, 5 had central SDB, and 3 patients did not have SDB. The mean apnea-hypopnea index was 21 ± 17. Minimum nighttime saturation of O(2) was positively correlated with peak VO(2), but not with VE/VCO(2). Nighttime PtcCO(2) was not correlated with peak VO(2) but was negatively correlated with the VE/VCO(2) slope of the daytime cardiopulmonary exercise test (r=-0.53). CONCLUSION: Nighttime lowering of PaCO(2) in SDB is related to an abnormal ventilatory response to exercise testing in the daytime. This finding suggests that nighttime hyperventilation in SDB alters both nighttime and daytime pathophysiological conditions in patients with heart disease.