Methods

The study subjects were 34 patients with chronic CHF, of whom 26 (19 men and 7 women) had idiopathic dilated cardiomyopathy and 8 (7 men and 1 woman) had coronary artery disease. The patients’ ages ranged from 17 to 83 years (mean, 58±14 years). Symptoms at hospitalization were New York Heart Association (NYHA) functional class II in 2, class III in 19, and class IV in 13 patients. The mean left ventricular ejection fraction was 25±9% (range, 9% to 44%). Table 1⇓ lists the patients’ symptoms and radiographic and echocardiographic findings at hospitalization.

Of the 34 patients, 24 had a warm-water bath first so we could monitor hemodynamic changes. After a 1- to 2-day interval, they had a sauna with hemodynamic monitoring. Of the remaining 10 patients, 2 had a warm-water bath only and 8 had a sauna only. Thus, the acute hemodynamic effects of warm-water bathing were investigated in 26 patients and of sauna in 32 patients. The study was conducted without alterations in current medications. Informed consent was obtained from each patient after they fully understood the purpose and methodology of the study.

Changes in blood pressure, heart rate, and rhythm were monitored with an automatic sphygmomanometer and ECG monitor, and changes in core body temperature (pulmonary arterial blood temperature), pulmonary arterial pressure, pulmonary capillary wedge pressure, and right atrial pressure were monitored with a Swan-Ganz catheter. Cardiac output was measured by the thermodilution method. Determination of peripheral resistance was calculated using the following formulas: total systemic vascular resistance=[mean systemic arterial pressure (mm Hg)−mean systemic venous pressure (mm Hg)]/cardiac output (L/min) and pulmonary vascular resistance=[mean pulmonary arterial pressure (mm Hg)−mean pulmonary artery wedge pressure (mm Hg)]/cardiac output (L/min). We also recorded two-dimensional and M-mode echocardiograms using an ultrasound diagnostic system (SSD 870, Aloka Co, Ltd). The left ventricular and left atrial dimensions were measured on the M-mode echocardiograms, and the ejection fraction was calculated by the method of Teichholz et al¹⁷ before and after each bath. In patients with mitral regurgitation, regurgitant volume changes were monitored by the color Doppler method during and after the bath. Semiquantitative assessment of mitral regurgitation was performed using the area of the maximum regurgitant jet.¹⁸ Changes in oxygen consumption were monitored with an expiratory gas meter (MG-390, Minato Co).

In an additional study, 13 healthy control subjects (mean age, 52±13 years) and 13 patients with dilated cardiomyopathy (mean age, 56±15 years; 9 idiopathic and 4 ischemic; NYHA functional class II in 7, III in 5, and IV in 1 patient; mean left ventricular ejection fraction, 29±10%) were studied to measure changes in circulating catecholamines before, during, and 30 minutes after sauna bathing.

Before applying thermal vasodilation to patients with CHF, we conducted studies using healthy volunteers to determine the most appropriate temperature and duration of warm-water and sauna bathing. Based on these trials, we developed the methods used in the present study.

Results

No patients experienced dyspnea, angina pectoris, or arrhythmia during the warm-water or sauna bathing; examination was safely completed in all patients. Table 2⇓ is a summary of the measurements of oxygen consumption, core body temperature, heart rate, blood pressure, cardiac index, stroke index, peripheral vascular resistance, and intracardiac pressures before, during, and 30 minutes after the warm-water bath or sauna. Table 3⇓ shows the changes in cardiac dimensions and ejection fraction before and 30 minutes after the warm-water bath or sauna. Table 4⇓ shows the fluctuations in catecholamine levels before, during, and after sauna bathing.

Cardiac Index and Stroke Index

Cardiac index increased markedly from the control level during the warm-water bath and sauna; it remained significantly higher than the control level even 30 minutes after the bath or sauna (Fig 1⇓). Stroke index also increased significantly during and after the bath and sauna (Fig 2⇓).

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Figure 1.

Bar graphs of changes in cardiac index during warm-water and sauna bathing. Note that the cardiac index increased significantly both during and 30 minutes after warm-water bath and sauna.

 

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Figure 2.

Bar graphs of changes in stroke index during warm-water and sauna bathing. Note that the stroke index increased significantly both during and 30 minutes after warm-water bath and sauna.

 

Peripheral Vascular Resistance

Both systemic and pulmonary vascular resistances decreased significantly from the control level during the warm-water and sauna bath; this significant change persisted 30 minutes after bathing (Figs 3⇓ and 4⇓).

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Figure 3.

Bar graphs of changes in systemic vascular resistance during and after warm-water bath and sauna. Note the significant decrease in systemic vascular resistance during warm-water bath and sauna compared with control and the persistent decrease 30 minutes after each bath.

 

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Figure 4.

Bar graphs of changes in pulmonary vascular resistance during and after warm-water bath and sauna. Note the significant decrease in pulmonary vascular resistance both during and 30 minutes after warm-water bath and sauna compared with control.

 

Intracardiac Pressures

Mean pulmonary arterial, pulmonary capillary wedge, and right atrial pressures increased significantly during the warm-water bath. After the bath, these parameters decreased significantly compared with baseline values. During sauna bathing, however, all of these parameters decreased significantly, with even lower values at 30 minutes after the sauna (Fig 5⇓).

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Figure 5.

Plots of changes in intracardiac pressures during and after warm-water bath and sauna. Mean pulmonary artery pressure (mPAP), mean pulmonary capillary wedge pressure (mPCWP), and mean right atrial pressure (mRAP) increased significantly during warm-water bath but decreased significantly 30 minutes after the bath compared with control. In the case of sauna, these pressures decreased significantly even during the bath, with the maximum effect observed 30 minutes after the sauna.

 

Mitral Regurgitation

Mitral regurgitation was detected in 26 of the 34 patients at baseline. It decreased significantly in 20 of 26 patients, although to varying degrees, during the bath. No patients showed an increase in mitral regurgitation. Although the degree of regurgitation tended to return to the control level after the bath, mitral regurgitation remained significantly less than at baseline, even 30 minutes after the bath. Fig 6⇓ is an example during warm-water bathing and sauna of when mitral regurgitation was noted to almost disappear.

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Figure 6.

Color Doppler echocardiographs of the same patient with dilated cardiomyopathy showing change in functional mitral regurgitation during warm-water bath and sauna. Note that mitral regurgitation is significantly decreased during warm-water bath and sauna compared with control.

 

Ejection Fraction

Ejection fraction increased significantly after warm-water and sauna bathing compared with control values (Fig 7⇓).

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Figure 7.

Bar graphs of change in ejection fraction after warm-water bath and sauna. Note the significant increase in ejection fraction after warm-water bath and sauna.

 

Discussion

The present study represents the first investigation into the hemodynamic effects of thermal vasodilation in patients with CHF. We confirmed that a warm-water bath or sauna decreases systemic and pulmonary vascular resistances and increases cardiac and stroke indexes after transient thermal exposure as indicated by the rise in pulmonary arterial blood temperature. In addition, right atrial, pulmonary arterial, and pulmonary capillary wedge pressures decrease with improvement in ejection fraction after bathing. The key findings appear to be improvement in left and right ventricular functions associated with reduction in afterload (total peripheral vascular resistance for the left ventricle and pulmonary vascular resistance for the right ventricle) on thermal vasodilation. Warming is also expected to dilate the venous system.^{6 9 13} The redistribution of blood from the intrathoracic compartment toward the peripheral venous system with thermal venous dilatation results in a decrease in pulmonary congestion. The increase in venous capacity is important in preload reduction as indicated by the decrease in right atrial pressure and left atrial and left ventricular dimensions. The increase in heart rate may be associated with a vasodilation-related reflex and the direct cardiac effect of warming or stimulation of the sympathetic nervous system; however, the increase in stroke volume suggests improved cardiac function by afterload reduction.

A major reason why warm-water or sauna bathing has been considered inappropriate for patients with CHF is the concern that cardiac work increases. Therefore, in the present study, the effects of thermally induced sympathetic hypertonia and various bath-related activities were minimized; the warm-water bath temperature was set at a comfortable 41°C, and a bathtub with automatic motion was used. None of our patients complained of excessive heat stimulation. In the sauna experiment, a far infrared-ray sauna was used at a room temperature of 60°C to prevent thermal stimulation due to high-temperature air inhalation. This temperature is lower than that of a conventional sauna. Physical activity was minimized by providing aid to the patients when entering or leaving the sauna. As a result, both warm-water and sauna bathing were safely accomplished without arrhythmias, dyspnea, or angina occurring, and there was an increase in oxygen consumption of only 0.3 METs.

Attention should be paid, however, to the effects of hydrostatic pressure during warm-water bathing. With the water level below the subclavicular region and patients in semirecumbency with the lower limbs extended, as in the present study, right atrial, pulmonary arterial, and pulmonary capillary wedge pressures increased significantly during the bath; these findings are consistent with those of previous studies.^{13 14 15} All pressure parameters decreased with abolition of hydrostatic pressure after the bath and as anticipated were not significantly increased during the sauna. Thus, the increase in intracardiac pressures during warm-water bathing is mainly attributable to the increase in venous return by hydrostatic pressure.^{11 12 13 14 15} Although none of our patients experienced dyspnea during warm-water bathing, deeper immersion and thermal stress with higher bath temperatures may further increase intracardiac pressures.¹⁵ In studies of healthy volunteers, right atrial pressures increased to approximately 15 to 20 mm Hg during immersion up to the neck.^{11 12} It has been suggested that water immersion to the neck causes a greater blood shift into the thorax.¹¹ In this regard, the sauna, where hydrostatic pressure is nonexistent, appears safer than warm-water bathing. Therefore, when warm-water bathing is performed for severe CHF, it may be important to ensure that the water depth is below subclavian level and to keep any exposed skin warm with a towel.

Concerning arrhythmias, Luurila¹⁹ has reported a 10% to 20% incidence of extrasystole induction or tachycardia during sauna bathing at 90°C in the post–myocardial infarction setting. The same report also states that extrasystoles disappeared from approximately 10% of the subjects. On the other hand, extrasystoles were sometimes observed in some healthy persons having a sauna and in healthy subjects during the first few minutes of warm-water immersion to the neck level.¹¹ It is speculated that an acute strain of the right heart may elicit extrasystoles. In the present study of patients with CHF, however, only 2 patients showed sporadic extrasystoles during warm-water bathing, whereas multiform or coupled extrasystoles disappeared in 2 patients after the 60°C sauna. It appears unlikely that warm-water and sauna bathing aggravate arrhythmias, provided that due care is paid to providing correct bath temperature, to limiting patient exertion, and to ensuring correct depth of water immersion.

A warm-water bath or sauna reportedly affects sympathetic nervous system activity and norepinephrine, renin, and thyroid hormone secretions in healthy subjects.^{20 21 22} According to the study by Kukkonen-Harjula et al²¹ of healthy men exposed for 19 to 32 minutes to a 80° to 100°C dry sauna until subjective discomfort was felt, plasma norepinephrine level increased approximately 100% to 160%. However, the increase in plasma norepinephrine level was considerably less during 15 minutes of dry sauna at 60°C in patients with dilated cardiomyopathy (25%) as well as in healthy subjects (32%). With higher temperatures and prolonged exposure until subjective discomfort, sympathetic nervous system stimulation was even more pronounced and resulted in a greater increase in plasma norepinephrine level. Thus, we believe that use of comfortable temperatures and optimization of the duration of sauna bathing results in less sympathetic nervous system stimulation by heat stress.

In the present study, the acute hemodynamic changes in CHF were examined for one warm-water bath or sauna. The long-term effect of repeated baths remains a subject of interest. A number of patients have since shown good responses to several months of daily warm-water or sauna bathing (unpublished data).We are impressed that repeated thermal vasodilation improves the quality of life of patients by permitting an increase in daily activities and improving appetite, sleep quality, and general well-being. However, further investigations are needed regarding the clinical applicability of warm-water and sauna bathing as a nonpharmacological, vasodilation therapy for patients with CHF.

In the present study, we did not demonstrate the effect on the myocardial circulation of thermal vasodilation. By placing a Webster multithermistor catheter into the coronary sinus during and after sauna in patients with idiopathic dilated as well as ischemic cardiomyopathy,²³ we have recently found in a limited number of patients that thermal vasodilation causes a decrease in coronary vascular resistance, an increase in coronary sinus flow, and improvement of myocardial metabolism. These data suggest that thermal vasodilation may be responsible for increased myocardial blood flow and clinical improvement in these patients.

The method of warm-water or sauna bathing we describe should be safe in patients with CHF. We have not observed patients with CHF to deteriorate symptomatically during and after the bath or sauna using this method; all patients in the present study remained comfortable during the procedure. However, a few caveats must be emphasized. First, although we have previously shown an improvement in myocardial blood flow with sauna bathing,²³ there remains the potential danger of an increase in heart rate in patients with ischemic cardiomyopathy during thermal exposure. Second, more exhaustive neurohumoral studies are required to establish the safety of thermal vasodilation therapy; although the transient rise in norepinephrine levels during bathing is of uncertain significance, other studies have demonstrated an association between high cathecholamine levels and a poorer prognosis in patients with CHF.^{24 25}

In conclusion, cardiovascular hemodynamics improve after a warm-water bath or sauna in patients with chronic CHF due to ischemic or idiopathic dilated cardiomyopathy. This is presumably due to a reduction in cardiac preload and afterload by thermal systemic arterial, pulmonary arterial, and venous vasodilation. The results of the present study suggest that thermal vasodilation has salutary effects even for patients with severe heart failure and may represent a novel nonpharmacological therapy for patients with CHF. The long-term benefits of these interventions warrant further investigation.