Effects of repeated sauna treatment on ventricular arrhythmias in patients with chronic heart failure
Circ J 2004; 68: 1146 – 1151 Effects of Repeated Sauna Treatment on Ventricular Arrhythmias in Patients With Chronic Heart Failure
Takashi Kihara, MD; Sadatoshi Biro, MD; Yoshiyuki Ikeda, MD; Tsuyoshi Fukudome, MD;
Takuro Shinsato, MD; Akinori Masuda, MD; Masaaki Miyata, MD; Shuichi Hamasaki, MD;
Yutaka Otsuji, MD; Shinichi Minagoe, MD; Suminori Akiba, MD*; Chuwa Tei, MD
The aim of the present study was to determine whether repeated 60°C sauna treatment improves
cardiac arrhythmias in chronic heart failure (CHF) patients, because ventricular arrhythmias are an important therapeutic target in CHF. Methods and Results
Thirty patients (59±3 years) with New York Heart Association functional class II or III
CHF and at least 200 premature ventricular contractions (PVCs)/24 h assessed by 24-h Holter recordings were studied. They were randomized into sauna-treated (n=20) or non-treated (n=10) groups. The sauna-treated group underwent a 2-week program of a daily 60°C far infrared-ray dry sauna for 15 min, followed by 30 min bed rest with blankets, for 5 days per week. Patients in the non-treated group had bed rest in a temperature-controlled room (24°C) for 45 min. The total numbers of PVCs/24 h in the sauna-treated group decreased compared with the non-treated group [848±415 vs 3,097±1,033/24 h, p<0.01]. Heart rate variability (SDNN, standard deviation of normal-to-normal beat interval) increased [142±10 (n=16) vs 112±11 ms (n=8), p<0.05] and plasma brain natriuretic peptide concentrations decreased [229±54 vs 419±110 pg/ml, p<0.05] in the sauna-treated group compared with the non-treated group. Conclusion
Repeated sauna treatment improves ventricular arrhythmias in patients with CHF. 68: 1146 – 1151) Key Words: Heart failure; Heart rate variability; Premature ventricular contractions; Sauna
atients with chronic heart failure (CHF) have a high
in many patients.19–21 Furthermore, we have demonstrated
prevalence of potentially serious arrhythmias and
that repeated sauna treatment improves the prognosis in
P consequently, a high incidence of sudden cardiac hamsters with CHF.22It is well recognized that alterations in
death.1–4 The presence of ventricular arrhythmias defines a
the neural control of the heart, characterized by decreased
higher-risk patient group with either ischemic or non-
vagal activity and relative sympathetic predominance, play
ischemic cardiomyopathy.5–9 Antiarrhythmic medications,
a key role in the occurrence of cardiac arrhythmias in pa-
such as class I drugs, have been tested in myocardial infarc-
tients with CHF.23 Several studies have shown that reduced
tion survivors with depressed ventricular function and in
heart rate variability (HRV), determined from 24-h ambu-
atrial fibrillation patients with a history of congestive heart
latory electrocardiographic (ECG) recordings, is associated
failure, and most were found not to be helpful and may
with a greater risk for ventricular fibrillation and poor prog-
even increase the occurrence of arrhythmias and cardiac
nosis in patients with CHF.24–27 Therefore, we prospective-
mortality.10–12 Some studies have shown that amiodarone
ly investigated the effects of thermal therapy on cardiac
improves ventricular arrhythmias and sudden cardiac death
arrhythmias and HRV in patients with CHF.
mortality in patients with CHF, yet the improvement intotal mortality remains controversial.13–15 Previous studies
have demonstrated that vasodilators, such as angiotensin-converting enzyme inhibitors and angiotensin receptor
blockers, improve the prognosis and ventricular arrhyth-
We studied 30 patients with CHF, aged 28–80 years
mias in patients with CHF,16–18 therefore arrhythmia is an
(mean age: 59±3 years): 24 patients (16 men, 8 women) had
important target for therapy in patients with CHF.
idiopathic dilated cardiomyopathy and 6 (5 men, 1 woman)
We have used thermal therapy with a 60°C dry sauna in
had ischemic cardiomyopathy. Inclusion criteria included
patients with CHF, and found that it improves hemodynam-
the presence of symptomatic CHF, left ventricular ejection
ic parameters, endothelial function, and clinical symptoms
fraction (LVEF) <50% by echocardiography, New YorkHeart Association (NYHA) functional class II–III, and
(Received April 5, 2004; revised manuscript received September 21,
>200 premature ventricular contractions (PVCs) per day on
2004; accepted September 28, 2004)
24-h Holter monitoring. Seven patients were in NYHA
Departments of Cardiovascular, Respiratory and Metabolic Medicine,
functional class II, and the other 23 were in class III. They
*Epidemiology and Preventive Medicine, Graduate School of Medi-
were randomized into a sauna-treated group (n=20) or a
cine, Kagoshima University, Kagoshima, Japan
non-treated group (n=10). The mean number of PVCs/24 h
Mailing address: Chuwa Tei, MD, Department of Cardiovascular,
was 3,123±819; the mean cardiothoracic ratio (CTR) on
Respiratory and Metabolic Medicine, Graduate School of Medicine,Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520,
chest radiography was 58.5±1.0% (range: 49–75%); and
the mean LVEF on echocardiography was 29±2% (range:
Circulation Journal Vol.68, December 2004
Sauna Improves Ventricular Arrhythmias in CHF
Baseline Clinical Characteristics of the 2 Groups Antiarrhythmic drugs (%) MexiletineDCM, idiopathic dilated cardiomyopathy; ICM, ischemic cardiomyopathy; NYHA, New York Heart Association; SBP, systolic blood pressure; DBP, diastolic blood pressure; ACE, angiotensin-converting enzyme; NS, not significant. All values are given as the mean ± SE.
10–48%). All patients were receiving maintenance doses of
graphy, and both plasma ANP and BNP concentrations were
medications for heart failure and arrhythmias, including
measured by radioimmunoassay. Chest radiography (CTR)
angiotensin-converting enzyme inhibitors, diuretics,
and echocardiography (LVEDD, left ventricular end dias-
blockers, digitalis and antiarrhythmic drugs (mexiletine),
tolic dimension; LAD, left atrial dimension; LVEF) also
and they were in a stable clinical condition for 1 month be-
fore entering the study. They also did not have symptomaticarrhythmias. Their medications were unchanged for at least
1 month before or during this study. Written informed con-
Ambulatory ECG monitoring was by 2-lead 24-h Holter
sent was obtained from all patients prior to participation,
monitoring (DMC-4502, Nihon Koden, Tokyo, Japan). The
and the protocol was approved by the Ethics Committee of
Holter tape recordings were analyzed on a full disclosure
the Faculty of Medicine, Kagoshima University.
unit that printed out each individual QRS complex forsubsequent visual examination. Complete determination of
PVC frequency with a description and quantification of
Thermal therapy with a far infrared-ray 60°C dry sauna
complex forms (multiform PVCs, couplets, and ventricular
was performed as previously reported.19 Patients remained
tachycardia) was undertaken by manual analysis of the full
supine on a bed during the sauna for 15 min, followed by
disclosure data. For the purpose of this study, PVCs were
30 min of bed rest with a blanket to keep them warm. Pa-
defined as any beat of ventricular origin faster than the sinus
tients were weighed before and after the sauna treatment.
rate, including the premature beats in couplets and ventricu-
Oral hydration with water was used to compensate for lost
lar tachycardia. Ventricular tachycardia was defined as ≥3
weight. Patients in the non-treated group remained supine
consecutive premature beats at a rate of ≥100 beats/min.
on a bed in a temperature-controlled room (24°C) for
There was an excellent correlation between the 2 observers
with respect to determining the total number of PVCs(r=0.99), and the number of episodes of ventricular tachy-
cardia (r=0.99). The technician and physician were
Clinical symptoms, such as dyspnea, fatigue, sleepless-
unaware of the clinical information associated with the
ness, edema, appetite-loss and constipation, were evaluated
recording. Reproducibilities of the results of 24-h Holter
by a self-assessment quality of life (QOL) questionnaire.20
monitoring performed twice were assessed in 13 patients
Each item had 4 grades: remarkably improved, improved,
with CHF: total beats, r=0.99, p<0.0001; PVCs, r=0.91,
no change, or worsened. Patients were classified into 3
p<0.0001; couplets, r=0.95, p<0.0001; ventricular tachy-
groups based on the results of the questionnaire. Patients
who answered ‘improved’ to more than 3 items weredefined as the improved group, those who answered ‘wors-
ened’ for at least 1 item were defined as the worsened
Time-domain parameters of HRV were analyzed on a
group, and the others were defined as the unchanged group.
MARS8000 analysis system (GE Medical SystemsInformation Technologies, Milwaukee, WI, USA) from
2-lead 24-h Holter recordings. All tapes were manually
A fasting blood sample was obtained in the morning to
edited for exclusion of artifacts and premature beats. A
measure plasma concentrations of neurohormonal factors,
minimum of 18 h of analyzable data and a minimum of
including catecholamines, atrial natriuretic peptide (ANP),
85% successive RR intervals were required for a tape to be
and brain natriuretic peptide (BNP). Plasma catecholamine
accepted as valid. The time interval between 2 consecutive
(norepinephrine, epinephrine, and dopamine) concentrations
QRS complexes was calculated as the normal-to-normal
were measured with high-performance liquid chomato-
(NN) interval. Abnormal QRS complexes and RR intervals
Circulation Journal Vol.68, December 2004Frequency of Ventricular Arrhythmias and Heart Rate Variability at Baseline and After 2 Weeks in the 2 Groups PVCs, premature ventricular contractions; VT, ventricular tachycardia; SDNN, standard deviation of NN interval; NS, not significant. All values are given as the mean ± SE; **p<0.01 vs baseline.Various Parameters at Baseline and After 2 Weeks in the 2 Groups NYHA, New York Heart Association; SBP, systolic blood pressure; DBP, diastolic blood pressure; CTR, cardiothoracic ratio; LVEDD, left ventricular end diastolic dimension; LAD, left atrial dimension; LVEF, left ventricular ejection frac tion; NE, norepi-nephrine; EP, epinephrine; DOPA, dopamine; ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; NS, not significant. All values are given as the mean ± SE; *p<0.05 vs baseline, **p<0.01 vs baseline.
were replaced by a linear interpolation algorithm. The stan-
inhibitor, -blockers, diuretics, nitrates, and antiarrhythmic
dard deviation (SD) of all normal beat intervals and the
drugs, at baseline between the 2 groups. All patients
mean length of the NN intervals (SDNN) were used for
enrolled completed the study. In the sauna-treated group,
time-domain measures from the entire recording period.
no patient experienced dyspnea, angina pectoris or palpita-
We analyzed 24 patients; 6 patients with atrial fibrillation
tions. Clinical symptoms related to dyspnea, fatigue,
edema, appetite-loss, constipation and insomnia wereimproved in 17 of 20 patients and unchanged in 3 patients
after the 2-week sauna treatment. However, no patients had
Sauna treatment was performed daily for 5 days each
worsening of clinical symptoms. In the non-treated group,
week, for a total of 2 weeks. All examinations were per-
clinical symptoms did not change after 2 weeks.
formed before the first treatment and on the day after thelast treatment.
At baseline, the total number of PVCs, couplets and
episodes of ventricular tachycardia per day were similar
All data are expressed as the mean ± SEM. Differences
between the 2 groups (Table 2). In the sauna-treated group,
in baseline characteristics were evaluated by the chi-square
the total number of PVCs decreased in all patients 2 weeks
test and unpaired t-test. Within-group changes between
after treatment. The total number of PVCs in the sauna-
baseline and after 2 weeks were evaluated by paired t-test
treated group was significantly decreased compared with
or Wilcoxon signed rank test for variables that were not
the non-treated group after 2 weeks (p<0.01, Table 2). The
normally distributed. Between-group comparisons were
total number of couplets and episodes of ventricular tachy-
evaluated by Mann-Whitney’s U test using differences
cardia per day also decreased significantly in the sauna-
between baseline and after 2 weeks. A value of p<0.05 was
treated group compared with the non-treated group
considered statistically significant.
(Table 2). The prevalence of couplets and ventriculartachycardia in the sauna-treated group compared with the
non-treated group was 45% vs 90%, p<0.05, and 20% vs80%, p<0.01, respectively. The total number of PACs did
Baseline Clinical Characteristics and Assessment of
not significantly change between the 2 groups after 2 weeks
Baseline clinical characteristics are summarized in
Table 1. There were no differences in age, gender, NYHA
functional class, mean heart rate, blood pressure or use of
There was no difference in SDNN at the baseline
drugs, such as digoxin, angiotensin-converting enzyme
between the 2 groups, but after 2 weeks, SDNN was sig-
Circulation Journal Vol.68, December 2004
Sauna Improves Ventricular Arrhythmias in CHF
nificantly greater in the sauna-treated group compared with
with CHF.22 We suggest that improvement of ventricular
arrhythmias may be one of the mechanisms by which re-peated thermal therapy improves the prognosis in patients
At baseline, there were no differences in the plasma con-
Although the mechanisms of ventricular arrhythmias
centrations of ANP, BNP, or catecholamine between the 2
occurring in patients with CHF are still unclear, experimen-
groups. After 2 weeks, there were no differences in the
tal evidence suggests that the development of delayed and
plasma concentrations of ANP or catecholamine between
early afterdepolarization-induced triggered activity and
the 2 groups, but the plasma concentration of BNP in the
automaticity, in addition to conditions favoring reentry, are
sauna-treated group was significantly lower than in the non-
related to arrhythmias in the setting of heart failure. Modu-
treated group (229±54 pg/ml vs 419±110 pg/ml, p<0.05;
lating factors, such as sympathetic activation, electrolyte
disturbances and chronic left ventricular stretch, are alsopresent in the setting of heart failure.39,40 It is well-estab-
NYHA Functional Class, Chest Radiography, Echocardio-
lished that the sympathetic nervous system is activated in
patients with CHF41–43 and analysis of HRV provides im-
At baseline, there were no differences in NYHA func-
portant information about sympathetic nervous activity in
tional class, CTR or LVEDD between the 2 groups, but
these patients.25,44 Data from the recent United Kingdom-
after 2 weeks, there was a significant difference in NYHA
Heart failure Evaluation and Assessment of Risk Trial
functional class, body weight, and CTR in the sauna-treated
(UK-HEART) suggest that reduced HRV, analyzed by a
group; LVEDD did not change between the 2 groups.
traditional time-domain method (including SDNN), is
Laboratory parameters, including liver function tests
related to the risk of ventricular arrhythmias and sudden
(aspartate aminotransferase, alanine aminotransferase,
death in patients with CHF,24 and we suggest that one of the
mechanisms by which repeated sauna treatment significant-
creatinine, electrolytes (Na, Cl, K) and hematocrit, did not
ly improves ventricular arrhythmias is by increasing HRV,
change after 2 weeks in either group (data not shown).
although we have not clarified the underlying mechanismsof that effect of thermal therapy. On the other hand, the
self-assessment QOL questionnaire revealed 17 of 20 pa-tients who answered ‘improved’ to more than 3 of 6 clinical
In the present study, we found that repeated 60°C sauna
symptoms that comprised dyspnea, fatigue, sleeplessness,
treatment improved ventricular arrhythmias. Furthermore,
edema, appetite-loss and constipation, and furthermore,
we observed that thermal therapy increased HRV and
none of the patient answered ‘worsened’ for any symptom.
reduced the plasma concentration of BNP in patients with
Therefore, the improvement may be related to better mood
as a result of repeated sauna treatment. Further study is
The incidence of ventricular arrhythmias is extremely
high in patients with CHF: approximately 80% or more of
The chronic stretch of cardiac myocytes contributes to
CHF patients have frequent ventricular premature beats
shortening of the action potential duration and mild de-
and approximately 50% of them have runs of nonsustained
creases in the action potential amplitude and resting mem-
ventricular tachycardia.3,28–30 Sudden death because of
brane potential.45 These changes may be arrhythmogenic by
ventricular arrhythmias accounts for approximately half of
increasing reentry and abnormal automaticity.46 In patients
all deaths in patients with CHF.4,31–33 Several studies have
with CHF, the ventricular wall is chronically stretched
shown an association between ventricular arrhythmias and
because of increases in ventricular volume and/or pressure
mortality in patients with CHF,5–9,34–36 but unfortunately,
overload. It is well-established that BNP is secreted pre-
current antiarrhythmic medications, such as class I drugs,
dominantly by the ventricle in response to ventricular wall
have only limited efficacy in these patients and may even
stretch.47 On the basis of our findings, including previous
be associated with worsening ectopic activity and hemo-
data,20 which showed significantly decreased plasma con-
dynamic deterioration.10–12 In large randomized trials with
centrations of BNP after 2 weeks of sauna treatment, we
amiodarone, a potent antiarrhythmic drug with additional
speculate that another mechanism responsible for decreased
sympatholytic and minor negative inotropic effects, the
ventricular arrhythmias may be reduction of ventricular
Group for the Study of Survival in Heart Failure in
Argentina (GESICA) demonstrated that low doses reduced
Electrolyte disturbances, such as hypokalemia and hypo-
ventricular arrhythmias and mortality in patients with
magnesemia, are prevalent in patients treated with diuretics
CHF;13 however, the Survival Trial of Antiarrhythmic
and are implicated as a cause of ventricular arrhythmias
Therapy in Congestive Heart Failure had conflicting results
associated with CHF. However, we did not observe signifi-
concerning mortality.14 Previous studies have demonstrated
cant changes in the electrolyte concentrations after 2 weeks
-blockers, which also have antiarrhythmic effects,
reduce mortality and the risk of sudden cardiac death, as
We have treated many CHF patients with sauna therapy
well as ventricular arrhythmias, in patients with CHF37 and
and so far none of the in-hospital patients has shown any
other studies have shown that ventricular arrhythmias in
deterioration in their condition. However, thermal therapy
patients with CHF are improved by treatment with non-
does not appear to be indicated for CHF patients with aortic
antiarrhythmic drugs, such as angiotensin-converting en-
stenosis or obstructive hypertrophic cardiomyopathy be-
zyme inhibitors16–18 and spironolactone.38 Our present
cause the pressure gradient is increased. In the present
results demonstrated that thermal therapy reduced the total
study, only CHF patients with NYHA functional class II or
number of PVCs, couplets, and episodes of ventricular
III underwent sauna treatment. It is well-known that the
tachycardia in patients with CHF and we have already
more severe the CHF, the more prevalent are ventricular
shown that thermal therapy reduced mortality in hamsters
arrhythmias. We evaluated the effects of sauna therapy on
Circulation Journal Vol.68, December 2004
ventricular arrhythmias at 2 weeks, but further studies of
325: 303 – 310.
the long-term effects and benefit in CHF patients with
19. Tei C, Horikiri Y, Park JC, Jeong JW, Chang KS, Toyama Y, et al.
Acute hemodynamic improvement by thermal vasodilation in conges-
NYHA functional class IV are needed.
tive heart failure. Circulation 1995; 91: 2582 – 2590.
In conclusion, repeated 60°C sauna treatment decreased
20. Kihara T, Biro S, Imamura M, Yoshifuku S, Takasaki K, Ikeda Y, et
ventricular arrhythmias in CHF patients with NYHA func-
al. Repeated sauna treatment improves vascular endothelial and car-
diac function in patients with chonic heart failure. J Am Coll Cardiol 2002; 39: 754 – 759.
21. Tei C, Tanaka N. Thermal vasodilation as a treatment of congestive
heart failure: A novel approach. J Cardiol 1996; 27: 29 – 30.
22. Ikeda Y, Biro S, Kamogawa Y, Yoshifuku S, Kihara T, Minagoe S,
This study was supported in part by a Grant-in-Aid from the Japan
et al. Effect of repeated sauna therapy on survival in TO-2 cardio-
Heart Foundation/Pfizer Grant for Cardiovascular Disease Research.
myopathic hamsters with heart failure. Am J Cardiol 2002; 90: 343 – 345. References
23. Meredith IT, Broughton A, Jennings GL, Esler MD. Evidence of a
selective increase in cardiac sympathetic activity in patients with
1. Wilson JR, Schwartz JS, Sutton MS, Ferraro N, Horowitz LN,
sustained ventricular arrhythmias. N Engl J Med 1991; 325: 618 –
Reichek N, et al. Prognosis in severe heart failure: Relation to hemo-
dynamic measurements and ventricular ectopic activity. J Am Coll
24. Nolan J, Batin PD, Andrews R, Lindsay SJ, Brooksby P, Mullen M,
Cardiol 1983; 2: 403 – 410.
et al. Prospective study of heart rate variability and mortality in
2. Meinertz T, Hofmann T, Kasper W, Treese N, Bechtold H, Stienen
chonic heart failure: Results of the United Kingdom heart failure
U, et al. Significance of ventricular arrhythmias in idiopathic dilated
evaluation and assessment of risk trial (UK-heart). Circulation 1998;
cardiomyopathy. Am J Cardiol 1984; 53: 902 – 907. 98: 1510 – 1516.
3. Maskin CS, Siskind SJ, LeJemtel TH. High prevalence of nonsus-
25. Fauchier L, Babuty D, Cosnay P, Fauchier JP. Prognostic value of
tained ventricular tachycardia in severe congestive heart failure. Am
heart rate variability for sudden death and major arrhythmic events in
Heart J 1984; 107: 896 – 901.
patients with dilated cardiomyopathy. J Am Coll Cardiol 1999; 33:
4. Koseki Y, Watanabe J, Shinozaki T, Sakuma M, Komaru T, Fukuchi
M, et al. Characteristics and 1-year prognosis of medically treated
26. Bilchick KC, Fetics B, Djoukeng R, Fisher SG, Fletcher RD, Singh
patients with chonic heart failure in Japan: Chonic Heart Failure
SN, et al. Prognostic value of heart rate variability in chonic conges-
Analysis Registry in Tohoku district (CHART). Circ J 2003; 67:
tive heart failure (Veterans affairs’ survival trail of antiarrhythmic
therapy in congestive heart failure). Am J Cardiol 2002; 90: 24 – 28.
5. Holmes J, Kubo SH, Cody RJ, Kligfield P. Arrhythmias in ischemic
27. Koyama J, Watanabe J, Yamada A, Koseki Y, Konno Y, Toda S, et
and nonischemic dilated cardiomyopathy: Prediction of mortality by
al. Evaluation of heart-rate turbulence as a new prognostic marker in
ambulatory electrocardiography. Am J Cardiol 1985; 55: 146 – 151.
patients with chonic heart failure. Circ J 2002; 66: 902 – 907.
6. Dargie HJ, Cleland JGF, Leckie BJ, Inglis CG, East BW, Ford I.
28. Meinertz T, Hofmann T, Kasper W, Treese N, Bechtold H, Stienen
Relation of arrhythmias and electrolyte abnormalities to survival in
U, et al. Significance of ventricular arrhythmias in idiopathic dilated
patients with severe chonic heart failure. Circulation 1987; 75(Suppl
cardiomyopathy. Am J Cardiol 1984; 53: 902 – 907.
IV): IV-98 – IV-107.
29. Gradman A, Deedwania P, Cody R, Massie B, Packer M, Pitt B, et
7. De Maria R, Gavazzi A, Caroli A, Ometto R, Biagini A, Camerini F.
al. Predictors of total mortality and sudden death in mild to moderate
Ventricular arrhythmias in dilated cardiomyopathy as an independent
heart failure. J Am Coll Cardiol 1989; 14: 564 – 570.
prognostic hallmark. Am J Cardiol 1992; 69: 1451 – 1457.
30. Podrid PJ, Fogel RI, Fuchs TT. Ventricular arrhythmias in conges-
8. Doval HC, Nul DR, Grancelli HO, Varini SD, Soifer S, Corrado G,
tive heart failure. Am J Cardiol 1992; 69: 82G – 96G.
et al. Nonsustained ventricular tachycardia in severe heart failure: In-
31. Brandenburg RO. Cardiomyopathies and their role in sudden death.
dependent marker of increased mortality due to sudden death. J Am Coll Cardiol 1985; 5: 185B – 189B. Circulation 1996; 94: 3198 – 3203.
32. Packer M. Sudden unexpected death in patients with congestive heart
9. Stevenson WG, Sweeney MO. Arrhythmias and sudden death in
failure: A second frontier. Circulation 1985; 72: 681 – 685.
heart failure. Jpn Circ J 1997; 61: 727 – 740.
33. Olshausen KV, Witt T, Pop T, Treese N, Bethge KP, Meyer J. Sudden
10. The Cardiac Arrhythmias Suppression Trial (CAST) Investigators.
cardiac death while wearing a Holter monitor. Am J Cardiol 1991;
CAST mortality and morbidity: Treatment versus placebo. N Engl J67: 381 – 386. Med 1991; 324: 781 – 788.
34. Romeo F, Pelliccia F, Cianfrocca C, Cristofani R, Reale A. Predictors
11. Pratt CM, Eaton T, Francis M. The inverse relationship between
of sudden death in idiopathic dilated cardiomyopathy. Am J Cardiol
baseline left ventricular ejection fraction and outcome of antiarrhyth-
1989; 63: 138 – 140.
mic therapy: A dangerous imbalance in the risk-benefit ratio. Am
35. Singh SN, Fisher SG, Carson PE, Fletcher RD. Prevalence and
Heart J 1989; 118: 433 – 440.
significance of nonsustained ventricular tachycardia in patients with
12. Flaker GC, Blackshear JL, McBride R, Kronmal RA, Halperin JL,
premature ventricular contractions and heart failure treated with
Hart RG. Antiarrhythmic drug therapy and cardiac mortality in atrial
vasodilator therapy. J Am Coll Cardiol 1998; 32: 942 – 947.
fibrillation: The Stroke Prevention in Atrial Fibrillation Investigators.
36. Singh BN. Significance and control of cardiac arrhythmias in patients
J Am Coll Cardiol 1992; 20: 527 – 532.
with congestive heart failure. Heart Fail Rev 2002; 7: 285 – 300.
13. Doval HC, Nul DR, Grancelli HO, Perrone SV, Bortman GR, Curiel
37. Cice G, Tagliamonte L, Ferrara L, Lacono A. Efficacy of carvedilol
R. Randomized trial of low-dose amiodarone in severe congestive
on complex ventricular arrhythmias in dilated cardiomyopathy:
heart failure. Lancet 1994; 344: 493 – 498.
Double-blind, randomized, placebo-controlled study. Eur Heart J
14. Singh SN, Fletcher RD, Fisher SG, Singh BN, Lewis HD, Deedwania
2000; 21: 1259 – 1264.
PC, et al. Amiodarone in patients with congestive heart failure and
38. Ramires FJ, Mansur A, Coelho O, Maranhao M, Gruppi CJ, Mady C,
asymptomatic ventricular tachycardia. N Engl J Med 1995; 333: 77 –
et al. Effect of spironolactone on ventricular arrhythmias in conges-
tive heart failure secondary to idiopathic dilated or to ischemic car-
15. Julian DG, Camm AJ, Frangin G, Janse MJ, Munoz A, Schwartz PJ,
diomyopathy. Am J Cardiol 2000; 85: 1207 – 1211.
et al. Randomised trial of effect of amiodarone on mortality in pa-
39. Vermeulen JT. Mechanisms of arrhythmias in heart failure. J Car-
tients with left-ventricular dysfunction after recent myocardial infarc-
diovasc Electrophysiol 1998; 9: 208 – 221.
tion: EMIAT. Lancet 1997; 349: 667 – 674.
40. Wit AL, Rosen MR. Pathophysiologic mechanisms of cardiac
16. The SOLVD Investigators. Effect of enalapril on survival in patients
arrhythmias. Am Heart J 1983; 106: 798 – 811.
with reduced left ventricular ejection fractions and congestive heart
41. Leimbach WN Jr, Wallin BG, Victor RG, Aylward PE, Sundlof G,
failure. N Engl J Med 1991; 325: 293 – 302.
Mark AL. Direct evidence from intraneural recordings for increased
17. Fletcher RD, Cintron GB, Johnson G, Orndorff J, Carson P, Cohn
central sympathetic outflow in patients with heart failure. Circulation
JN, for the V-HeFT II VA Cooperative Studies Group. Enalapril
1986; 73: 913 – 919.
decreases prevalence of ventricular tachycardia in patients with
42. Swedberg K, Eneroth P, Kjekshus J, Wilhelmsen L. Hormones regu-
chonic congestive heart failure. Circulation 1993; 87(Suppl VI): VI-
lating cardiovascular function in patients with severe congestive
heart failure and their relation to mortality. Circulation 1990; 82:
18. Cohn JN, Johnson G, Ziesche S, Cobb F, Francis G, Tristani F, et al.
A comparison of enalapril with hydralazine-isosorbide dinitrate in
43. Meredith IT, Eisenhofer G, Lambert GW, Dewar EM, Jennings GL,
the treatment of chonic congestive heart failure. N Engl J Med 1991;
Esler MD. Cardiac sympathetic nervous activity in congestive heart
Circulation Journal Vol.68, December 2004
Sauna Improves Ventricular Arrhythmias in CHF
failure: Evidence for increased neuronal norepinephine release and
46. Hansen DE, Craig S, Hondeghem LM. Stretch-induced arrhythmias
preserved neuronal uptake. Circulation 1993; 88: 136 – 145.
in the isolated canine ventricle: Evidence for the importance of
44. Task Force of the European Society of Cardiology and the North
mechanoelectrical feedback. Circulation 1990; 81: 1094 – 1105.
American Society of Pacing and Electrophysiology, 1996. Heart rate
47. Yasue H, Yoshimura M, Sumida H, Kikuta K, Kugiyama K,
variability: Standards of measurement, physiological interpretation,
Jougasaki M, et al. Localization and mechanism of secretion of B-
and clinical use. Circulation 1996; 93: 1043 – 1065.
type natriuretic peptide in comparison with those of A-type natriuretic
45. Franz MR, Cima R, Wang D, Profitt D, Kurz R. Electrophysiological
peptide in normal subjects and patients with heart failure. Circula-
effects of myocardial stretch and mechanical determinants of stretch-
tion 1994; 90: 195 – 203.
activated arrhythmias. Circulation 1992; 86: 968 – 978. Circulation Journal Vol.68, December 2004
Spezial Kontaktlinsen Abbildung 2 Beispielfragen zu Symptomen (CLDEQ, Indiana University ) 5 Fragen zu TROCKENHEITSSYMPTOMEN AM AUGE: a) Wie oft fühlten sich Ihre Augen beim Kontaktlinsentragen in der vergangenen Woche an einem typischen Tag trocken an? Wenn sich Ihre Augen trocken anfühlten, wie intensiv war das Trockenheitsgefühl beim Dr. Robin Chalmers und Dr. Carolyn Beg
EIS Clinical Pre-Study of Stress-Related Erectile Dysfunction Clinical Investigator Professor Giuseppe Tritto Andrology Department St. Louis Hospital Paris, France Sponsor and Monitor Mr. Albert Maarek Site of Investigation St. Louis Hospital Paris, France Final Report May 15, 2005 Summary A test group of 37 male patients with erectile dysfunction (ED) undergoing consultation i