Repeated sauna treatment, known as Waon therapy, has been shown to improve cardiac function as well as exercise tolerance in patients with chronic heart failure. However, the underlying mechanisms of this therapy regarding these improvements remain to be elucidated. Forty-one patients with chronic heart failure (mean age 68.3 ± 13.5 years old) underwent Waon therapy 5 times a week for 3 weeks. Before and after treatment, a number of assessments were performed in all subjects: 6-minute walk test, echocardiography, determination of neurohumoral factors and number of circulating CD34 + cells, and a flow-mediated dilation (FMD) test of endothelial function. Cardiopulmonary exercise testing was also performed in 20 patients. Waon therapy increased the left ventricular ejection fraction (from 30.4 ± 12.6% to 32.5% ± 12.8%, p = 0.023) and reduced plasma levels of norepinephrine (from 400 ± 258 to 300 ± 187 pg/ml, p = 0.015) and brain natriuretic peptide (from 550 ± 510 to 416 ± 431 pg/ml, p = 0.035). Waon therapy increased the 6-minute walk distance (from 337 ± 120 to 379 ± 126 m, p <0.001) in association with an improvement in FMD (from 3.5 ± 2.3% to 5.5% ± 2.7%, p <0.001) and an increase in the number of circulating CD34 + cells (p = 0.025). Changes in 6-minute walk distance were correlated positively with those in the left ventricular ejection fraction and FMD and negatively with those in plasma levels of norepinephrine and brain natriuretic peptide levels. A multivariate analysis revealed that an increase in FMD was the only independent determinant of 6-minute walk distance improvement. Finally, Waon therapy significantly increased peak V o 2 , and this increase was also correlated with changes in FMD. In conclusion, repeated sauna therapy in patients with chronic heart failure improves exercise tolerance in association with improvement in endothelial function.
Repeated sauna treatment, known as Waon therapy, has favorable effects in patients with chronic heart failure (CHF) and also those with peripheral artery disease, including improvements in cardiac and autonomic nerve function and inhibition of neurohumoral activation. These effects might be mediated by an increase in endothelial nitric oxide synthase activity and subsequent improvement of endothelial dysfunction. Endothelial dysfunction has been documented in patients with CHF and might play an important role in exercise capacity in these patients. The purpose of the present study was to investigate whether Waon therapy could improve exercise tolerance in patients with CHF and, if so, to elucidate the underlying mechanisms involved.
Methods
All patients included in the present study had to satisfy ≥1 of the following criteria: CHF-associated symptoms of New York Heart Association functional class ≥II and/or previous hospitalization for worsening of heart failure. All patients were in compensated, stable conditions at the time of enrollment. The protocol of the present study was approved by the ethics committee of University of Toyama. Written informed consent was obtained from all study patients before the enrollment.
According to methods described previously, the study patients underwent Waon therapy with a far-infrared dry sauna, which was uniformly maintained at 60°C. Patients were placed in the sitting position in the dry sauna for 15 minutes and then kept on bed rest with a blanket to keep warm for an additional 30 minutes, resulting in an increase in the core temperature by 1.0°C to 1.2°C. Patients were weighed before and after the therapy and drank water to compensate for the weight loss. All patients underwent daily Waon therapy Monday through Friday for 3 weeks. Regular treatment for heart failure was continued during the study period.
The number of CD34 + cells in the peripheral blood, a putative precursor of endothelial progenitor cells (EPCs), was quantified using flow cytometry (EPICS-MCL; Beckman Coulter, Brea, California). White blood cells were dually stained with fluorescein isothiocyanate–conjugated CD45 and phycoerythrin-conjugated CD34 (StemONE System; Beckman Coulter). Cells expressing CD34 were determined by gating the progenitor population and expressed as the number of cells per microliter.
Exercise tolerance was evaluated by 6-minute walk distance (6MWD) in all study patients and by cardiopulmonary exercise testing in patients who were able to pump the pedals of an ergometer (n = 20). In the upright position, symptom-limited cardiopulmonary exercise testing was performed using expired gas analysis (Aeromonitor AE-300S; Minato Medical Science Co. Ltd., Osaka, Japan) and an ergometer (75XL III; Combiwelness, Tokyo, Japan). Peak oxygen uptake (peak V o 2 ) and ventilatory efficiency as assessed by the relation of minute ventilation (VE) to carbon dioxide production (V co 2 ; VE/V co 2 slope) were determined.
Vascular endothelial function was evaluated by flow-mediated dilation (FMD) of the brachial artery. Patients were instructed to fast overnight and to abstain from smoking and taking caffeine, vitamins, and medications for ≥12 hours before FMD testing. Vasodilatation responses of the brachial artery were determined via ultrasound technique using a semiautomatic device (EF18G; Unex, Nagoya, Japan). Briefly, the diameter of the brachial artery was measured from B-mode ultrasound images using a 10-MHz linear-array transducer. A blood pressure cuff placed over the proximal portion of the right forearm was inflated to 50 mm Hg above the systolic blood pressure for a period of 5 minutes. FMD was determined as the maximum change in diameter after cuff release normalized to the baseline diameter (percentage of baseline diameter).
All data are presented as mean ± SD. Paired Student’s t tests were performed for comparisons of pre– and post–Waon therapy data. Categorical variables were compared using chi-square tests. The relation between Waon therapy–induced changes in 6MWD and other variables was determined using Pearson’s product-moment correlation coefficients. A multiple regression analysis was performed to identify the independent determinants of Waon therapy–induced changes in 6MWD. A p value <0.05 was considered statistically significant.
Results
Baseline characteristics of the study patients are listed in Table 1 , and the effects of 3-week Waon therapy are summarized in Table 2 . In response to therapy, 6MWD increased, and peak V o 2 and VE/V co 2 slope by cardiopulmonary exercise testing improved. The left ventricular ejection fraction increased modestly but significantly, while neurohumoral activations were inhibited. The number of circulating CD34 + cells and FMD increased, a finding indicative of improvement of endothelial function. There were no differences in improvements in exercise tolerance and FMD according to age or the severity or cause of heart failure (i.e., ischemic vs nonischemic; data not shown).
| Variable | Value |
|---|---|
| Age (years) | 68.3 ± 13.5 |
| Men | 21 (51%) |
| Body mass index (kg/m 2 ) | 21.5 ± 4.2 |
| New York Heart Association functional class | |
| I | 4 |
| II | 15 |
| III | 22 |
| IV | 0 |
| Cause of heart failure | |
| Dilated cardiomyopathy | 20 (49%) |
| Ischemic heart disease | 14 (34%) |
| Hypertrophic cardiomyopathy | 3 (7%) |
| Valvular heart disease | 2 (5%) |
| Hypertensive heart disease | 2 (5%) |
| Co-morbidities | |
| Diabetes mellitus ⁎ | 10 (24%) |
| Hypertension † | 10 (24%) |
| Dyslipidemia ‡ | 13 (32%) |
| Atrial fibrillation or flutter | 12 (29%) |
| Medications | |
| Digoxin | 13 (32%) |
| β blockers | 28 (68%) |
| Angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers | 34 (83%) |
| Diuretics | 38 (93%) |
| Nonpharmacologic therapy | |
| Pacemaker | 4 (10%) |
| Implantable cardioverter-defibrillator/cardiac resynchronization therapy | 5 (12%) |
| Oxygen/noninvasive positive-pressure ventilation | 6 (15%) |
⁎ Fasting plasma glucose ≥126 mg/dl or plasma glucose ≥200 mg/dl under 75-g oral glucose tolerance test or long-term treatment with oral hypoglycemic agents or insulin.
† Blood pressure >140/90 mm Hg on repeated observations or long-term antihypertensive therapy.
‡ Plasma low-density lipoprotein cholesterol ≥140 mg/dl or plasma triglyceride ≥150 mg/dl or long-term lipid-lowering therapy.
| Variable | Baseline | After 3-Week Waon Therapy | p Value |
|---|---|---|---|
| Heart rate (beats/min) | 70 ± 11 | 66 ± 11 | 0.021 |
| Systolic blood pressure (mm Hg) | 101 ± 13 | 99 ± 14 | 0.099 |
| Diastolic blood pressure (mm Hg) | 64 ± 11 | 61 ± 9 | 0.109 |
| Body weight (kg) | 55 ± 16 | 54 ± 16 | 0.021 |
| New York Heart Association functional class | 0.535 | ||
| I | 4 | 7 | |
| II | 15 | 16 | |
| III | 22 | 18 | |
| IV | 0 | 0 | |
| Specific activity scale (METs) | 4.2 ± 1.6 | 4.7 ± 1.5 | <0.001 |
| Left ventricular end-diastolic dimension (mm) | 66 ± 11 | 64 ± 11 | <0.001 |
| Left ventricular ejection fraction (%) | 30 ± 13 | 33 ± 13 | 0.023 |
| Left atrial dimension (mm) | 47 ± 8 | 45 ± 9 | 0.010 |
| 6MWD (m) | 337 ± 120 | 379 ± 126 | <0.001 |
| Peak V o 2 (ml/min) | 804 ± 385 | 871 ± 362 | <0.001 |
| VE/V co 2 slope | 38 ± 10 | 33 ± 7 | 0.018 |
| Hematocrit (%) | 37 ± 6 | 36 ± 6 | 0.011 |
| Brain natriuretic peptide (pg/ml) | 550 ± 510 | 416 ± 431 | 0.035 |
| Plasma norepinephrine (pg/ml) | 400 ± 258 | 300 ± 187 | 0.015 |
| Circulating CD34 + cells (per mm 3 ) | 1.1 ± 1.0 | 1.3 ± 1.3 | 0.025 |
| FMD (%) | 3.5 ± 2.3 | 5.5 ± 2.7 | <0.001 |
Waon therapy–induced change in 6MWD was not correlated with age. However, significant correlations were found between change in 6MWD and changes in the left ventricular ejection fraction, plasma levels of norepinephrine and brain natriuretic peptide, and FMD ( Figure 1 ) . A multivariate analysis revealed that change in FMD was the only independent determinant of change in 6MWD ( Table 3 ). Waon therapy–induced change in peak V o 2 was significantly correlated with change in FMD ( Figure 2 ) .
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