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Thermal Vasodilation Using a Portable Infrared Thermal Blanket in Decompensated Heart Failure

Marcelo Villaça Lima,1 MD, Marcelo E. Ochiai,1 MD, Kelly N. Vieira1, Airton Scipioni 1, Juliano N. Cardoso,1 MD, Robinson T. Munhoz,1 MD,

Paulo C. Morgado,1 MD, and Antonio C.P. Barretto,1 MD

Summary

Adjunctive and non-pharmacological therapies, such as heat, for the treatment of heart failure patients have been proposed. Positive results have been obtained in clinically stable patients, but no studies of the use of thermal therapy in patients with decompensated heart failure (DHF) have been reported. An open randomized clinical trial was designed in patients with DHF and controls. We studied 38 patients with a mean age of 56.9 years. A total of 86.8% were men, and 71% had nonischemic myocardiopathy. All participants were using dobutamine, and the median brain natriuretic peptide (BNP) level was 1396 pg/mL. An infrared thermal blanket heated the patients, who were divided into 2 groups: group T (thermal therapy) and group C (control). Group T underwent vasodilation using the thermal blanket at 50°C for 40 min-utes in addition to drug treatment. The cardiac index increased by 24.1% (P = 0.009), and systemic vascular resistance decreased by 16.0% in group T (P < 0.024) after thermal therapy. Heat as a vasodilator increased the cardiac index and lowered systemic vascular resistance in DHF patients. These data suggest thermal therapy as a therapeutic approach for the adjuvant treatment of DHF patients. (Int Heart J 2014; 55: 433-439)

Key words: Thermal therapy, Hyperthermia, Hemodynamics, Catheterization, Swan-Ganz

H eart failure (HF) is the final pathway of most heart dis-eases, and these patients exhibit high rates of hospi-talization and mortality.1) Patients in advanced stages

of the disease require hospitalization at some point. Hospitali-zation for decompensated heart failure (DHF) is urgent and re-quires immediate medical treatment.

Activation of the neurohormonal system occurs during decompensation with increased systemic vascular resistance, increased pulmonary capillary pressure, and reduced cardiac output.2) Patients at this stage present symptoms such as low cardiac output and systemic and pulmonary vasoconstriction, which may lead to hypotension, poor peripheral perfusion, de-creased levels of consciousness, generalized edema, and dysp-nea.

Most patients respond properly to treatment when the clinical and hemodynamic profile of decompensation is used.3) However, a subgroup of patients depends on inotropic drugs despite medication adjustment. The assessment of perfusion and congestion through clinical observation is impaired. There-fore, hemodynamic data using objective measures must be ob-tained. This subgroup is refractory to treatment.4,5)

The use of a pulmonary artery catheter (eg, Swan-Ganz) may be indicated for the treatment of hospitalized DHF pa-tients in select and difficult cases.5-8) This intervention may aid objective and timely treatment measures and guide medication

management using the hemodynamic data obtained. Adjuvant and non-pharmacological measures, such as heat, have been proposed for HF patients.9-17) Heat increases blood flow via ni-tric oxide production, which increases endothelial nitric oxide synthase (eNOS) activity. Heat activates CD34+ progenitor en-dothelial cells, which promote angiogenesis, improving cardiac perfusion and decreasing the systemic vascular resistance.18)

Thermal vasodilation, or thermotherapy, was used initial-ly to treat patients with functional class III or IV HF. The first studies were performed using hot immersion baths,12) but this method was improved using sauna sessions with infrared radi-ation. However, no studies of heat treatment have been per-formed in decompensated patients in advanced HF using intra-venous drugs. Patients at this stage require inotropes, are confined to bed, and cannot undergo sauna sessions or immer-sion baths. These patients require rest and may easily get worse with changes in decubitus or the need for transfer to per-form exams or complementary therapies. However, a method to warm the patient at the bedside could be developed, such as a handheld device that emits heat waves without the need for patient mobilization. Therefore, this study proposes the use of a thermal blanket to generate heat using direct infrared radia-tion.

No data have demonstrated the efficacy of thermotherapy during the acute HF phase, and it is important to analyze the

From the 1 Heart Institute (Instituto do Coração - InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Sao Paulo, Brazil.This study was partially funded by the São Paulo Research Foundation (Fundação de Amparo à Pesquisa do Estado de São Paulo – FAPESP) (2010/06994-0).Address for correspondence: Marcelo Villaça Lima, MD, Av. Dr. Eneas Carvalho de Aguiar, 44 - Cerqueira Cesar, CEP: 05403-000 - Sao Paulo, SP – Brazil. E-mail:

villaca.lima@gmail.comReceived for publication March 28, 2014. Revised and accepted May 2, 2013.Released in advance online on J-STAGE July 28, 2014.All rights reserved by the International Heart Journal Association.

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effects of thermotherapy on the hemodynamic conditions of these patients during decompensation. The present study evalu-ated the acute hemodynamic effects of heat using a thermal blanket in patients with refractory DHF using intravenous va-soactive drugs. The increased cardiac index and reduced sys-temic vascular resistance were evaluated as outcomes.

Methods

This study was a unicentric open randomized clinical study of DHF patients and controls conducted between Octo-ber 2007 and April 2013. Patients were studied in a single day, and the acute effect of heat before and after the intervention was evaluated. Heat was generated using a thermal blanket with infrared radiation. Hemodynamic measurements were as-sessed using the invasive Swan-Ganz catheter.Population: Patients with DHF from the Emergency Unit of the Heart Institute (Instituto do Coração - Incor), Clinics Hos-pital, Faculty of Medicine, University of São Paulo were se-lected to continue treatment according to the following inclu-sion and exclusion criteria. The patients were receiving continuous intravenous inotropic drugs and were refractory to conventional treatment after the attempted removal of vasoac-tive drugs without success. All patients were using at least one oral vasodilator at the maximum tolerated dose. The diuretic of choice for congestion was intravenous furosemide, which was present in 100% of the assessed patients (mean dose of 59.6 mg/day).Inclusion criteria• Age > 18 years;• Left ventricle ejection fraction (LVEF) < 40%, as confirmed

via echocardiography using the method of Simpson or Teich-holz;

• Use of intravenous positive inotropic drugs (dobutamine or milrinone) for at least 5 days;

• Use of one or more oral vasodilator drugs (captopril/enal-april/losartan/hydralazine/isosorbide mononitrate).

Exclusion criteria• Heat intolerance;• Decubitus intolerance < 45 degrees;• Fever, defined as a body temperature above 37.8°C;• Duration of antibiotic;• Allergy to the thermal blanket;• Presence of decubitus ulcer;• Large-caliber varices;• Marked edema of the lower limbs;• Cardiac pacemaker or implantable cardioverter defibrillator

(ICD);• Technical difficulty obtaining deep venous access.

The patients were divided into 2 groups: group T (ther-motherapy) and group C (control). The first 8 patients were al-located to group T for safety analysis and validation of the pro-posed method. Thereafter, patients were randomly allocated to the groups. The T group underwent thermal vasodilation using a handheld device at bedside (ie, the thermal blanket) at a tem-perature of 50°C for 40 minutes during drug clinical treatment. Patients in group C received drug treatment, and the thermal blanket was positioned in the same manner as in group T but without heat for 40 minutes.Cardiac catheterization: Measurements were obtained via the

Swan-Ganz catheter following established recommendations.19) A cardiac output module (DX-AJDEC-0) compatible with a Dixtal® DX 2023 monitor was used for Swan-Ganz catheter measurements using the thermodilution method. Patients were monitored continuously using an electrocardiogram, pulse oxi-metry and blood pressure, which was measured automatically every 5 minutes using an arm cuff during the invasive proce-dure. A heart monitor continuously recorded ambient and pa-tient temperatures via the catheter during the procedure. He-modynamic measurements were performed during the pre- and post-intervention periods, with a 40-minute interval based on the randomization. Mean arterial pressure, pulmonary capillary pressure, cardiac index, and systemic vascular resistance meas-urements were analyzed.Thermal blanket: An Aesthetics infrared (Bio Term Manufac-ture and Commerce of Thermal Products LTD) thermal blan-ket was used for heating (Figure 1). The thermal blanket gen-erates heat via 44 infrared pads that emit waves from 4 to 14 microns in a single zone of resistance and are coated with 100% waterproof nylon, which prevents the penetration of liq-uids and secretions to the inside. The blanket is inexpensive and easy to maintain and clean. A digital control regulated the temperature, which could reach 50°C. Physicians and a multi-disciplinary team performed the intervention, which was dis-continued at any time if hemodynamic instability was ob-served. The temperature was set 5 minutes before the start of the intervention to reach 50°C throughout the procedure. The thermal blanket includes a thermostat to automatically turn the equipment off if the temperature sensor of the digital controller stopped functioning. A digital thermometer was also placed in the blanket to ensure the proposed temperature. A cotton sheet was placed between the patient and the thermal blanket to pre-vent burns. The patients were asked about symptoms or dis-comfort during the procedure, and patients could discontinue the proceedings at any time.Intervention: Patients who met the inclusion criteria freely signed an informed consent. This study was registered under number 0653/08 and approved by the Research Ethics Com-mittee of the Heart Institute and the Research Grants Commit-tee of the Faculty of Medicine, University of São Paulo. The

Figure 1. Patient at rest on a bed. Use of heat through the handheld infra-red device (thermal blanket) at the bedside under continuous non-invasive hemodynamic monitoring.

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bed was prepared, and the thermal blanket was properly posi-tioned with the patient lying at rest. The Swan-Ganz catheter was introduced under patient monitoring, and the following hemodynamic measurements were obtained: right atrial pres-sure or central venous pressure (CVP), right ventricular pres-sure, pulmonary artery pressure, pulmonary artery or pulmo-nary capillary occlusion pressure, cardiac output, and, indirectly, systemic vascular resistance and cardiac index. Sev-en consecutive measurements were performed on each ap-proach to calculate the mean cardiac output for statistical anal-ysis and to avoid variability in results and differences in value greater than 10% between measurements. The central body temperature was measured continuously during invasive moni-toring. The first 8 patients were allocated to the intervention group, and allocation occurred randomly beginning with the 9th patient. Patients were subjected or not to thermotherapy for 40 minutes after randomization, and all previously performed measurements were repeated for comparison. The thermal blanket was turned on for patients in group T. The thermal blanket remained off for patients in group C. The Swan-Ganz catheter was removed after completion of the procedure, and the patient remained on the bed covered with a synthetic wool blanket for 30 minutes to maintain the heat.Statistical analysis: The classification variables are presented in the Table as absolute (n) and relative (%) frequencies. The association between variables was evaluated using Fisher’s ex-act test or the likelihood ratio. The normality of the quantitative

variables was evaluated using the Kolmogorov-Smirnov test. The quantitative variables are presented descriptively in tables and graphs as the mean and standard deviation (SD). The means of the variables were evaluated using analysis of vari-ance for repeated measures (ANOVA). The measured values were compared using Student’s t test. A P < 0.05 was consid-ered statistically significant.20)

Sample and randomization: The sample was calculated 21) in 25 patients with an 80% power based on data presented in 2008.22) Twenty one and 23 patients were required to detect an increase in the cardiac index from 2.18 ± 0.81 to 3.29 ± 1.57 L/minute/m2 and a reduction in systemic vascular resistance from 2151 ± 578 to 1631 ± 699 dynes/second/cm-5, respective-ly. This subject number was determined because the present study was an initial project with this type of intervention. No parameters were reported in the literature to allow calculations for the evaluation of clinically relevant outcomes in the decom-pensated stage of HF. Patients were randomized in exchangea-ble blocks of 4 into 2 groups: the thermotherapy (group T) and control (group C). The sequence of randomization was built using random distribution in blocks through tables of numbers with the aid of a computerized system. The sequence was closed in individually numbered and sealed opaque enve-lopes.23) A person who did not participate in the study per-formed the assembly process and sealed the envelopes. These envelopes were opened at bedside minutes before the interven-tion.

Table. Patient Characteristics Divided Per Group

Variable Control (n = 15) Thermotherapy (n = 23) P

Sex 0.979 Male, n (%) 13 (86.7) 20 (86.9) Female, n (%) 2 (13.3) 3 (13.1)Age (years) 54.4 ± 11.2 59.4 ± 9.3 0.150Ethnicity 0.399 White, n (%) 9 (60.0) 12 (52.2) Other, n (%) 6 (40.0) 11 (47.8)Etiology 0.692 Ischemic, n (%) 5 (33.3) 6 (26.1) Non-ischemic, n (%) 10 (66.7) 17 (73.9) VAD (days) 14 ± 10.6 18.6 ± 13.5 0.418Dobutamine, n (mcg/kg/minute) 15 (7.75 ± 4.22) 23 (10.79 ± 3.85) 1.000Milrinone, n (mcg/kg/minute) 0 1 (0.375) -Echocardiogram Aorta (mm) 32.1 ± 3.8 31.6 ± 1.9 0.821 Left atrium (mm) 48.9 ± 4.9 52.7 ± 7.4 0.123 LVD (mm) 68.4 ± 8.4 69.3 ± 8.0 0.872 LVS (mm) 58.7 ± 8.0 60.6 ± 9.5 0.872 LVEF (%) 24.0 ± 6.9 22.8 ± 7.2 0.551Atrial fibrillation, n (%) 4 (26.7) 7 (30.4) 0.441BNP (pg/mL) 1235.9 ± 1181.8 1556.6 ± 1079.3 0.568Hemodynamic variables HR (bpm) 82.5 ± 17.2 85.7 ± 16.0 0.441 SBP (mmHg) 93.1 ± 13.8 97.4 ± 10.3 0.507 MAP (mmHg) 73.4 ± 11.1 76.3 ± 9.2 0.390 DBP (mmHg) 63.1 ± 10.8 65.6 ± 9.3 0.805 PCP (mmHg) 25.4 ± 8.7 31.2 ± 8.2 0.074 CI (L/minute/m2) 3.18 ± 0.68 2.94 ± 0.75 0.638 SVR (dynes/second/cm-5) 1479.1 ± 444.5 1707.0 ± 573.6 0.675

VAD indicates vasoactive drug; LVD, diastolic diameter of the left ventricle; LVS, systolic diameter of the left ventricle; LVEF, ejection fraction of the left ventricle; BNP, brain natriuretic peptide; HR, heart rate; SBP, systolic blood pressure; MAP, mean ar-terial pressure; DBP, diastolic blood pressure; PCP, mean pulmonary capillary pressure; CI, cardiac index; and SVR, systemic vascular resistance.

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Results

A total of 165 patients were evaluated for eligibility. Twelve of these patients refused the study, and 105 were ex-cluded by the exclusion criteria. Forty-eight patients were in-cluded, but 10 patients were excluded before randomization. Two patients had hypovolemia, and the cardiac output could not be measured through the Swan-Ganz catheter due to tech-nical difficulties in 2 patients. Two patients had severe dyspnea during the procedure, which prevented continuation of the in-tervention, and deep venous access was not possible in 4 pa-tients. One patient in the thermotherapy group died (Appen-dix).

Eight patients who underwent heat sessions for safety and method validation were evaluated initially, and 30 patients were randomized to the end of the study. A total of 38 patients were studied. The study profile is shown above (Figure 2). No differences in baseline characteristics were observed between the groups (Table).

A total of 38 patients with DHF were evaluated. Most pa-tients were male (86.8%) with a mean age of 56.9 years, no-nischemic etiology (71%), and a left ventricular ejection frac-tion (LVEF) of 23.4%. All patients were using dobutamine at a mean dose of 9.27 mcg/kg/minute with a mean use time of 16.3 days. An association of milrinone was observed in one patient in the thermotherapy group. The mean initial BNP was 1396 pg/mL. Atrial fibrillation was present in 28.5% of the pa-tients. Patients exhibited an initial MAP of 74.8 mmHg, PCP of 28.3 mmHg, CI of 3.06 L/minute/m2, and SVR of 1.593 dynes/second/cm-5. Hemodynamic measurements were ob-tained during dobutamine administration, when they were transferred from the emergency room for adjustment and con-tinuity of treatment.

The results of the hemodynamic variable measurements are presented in Figures 3-6.Mean arterial pressure (MAP): No significant differences were found in the behavior of the two groups post-intervention (P = 0.968). (Figure 3)Pulmonary capillary pressure (PCP): No significant differ-ences were found in the behavior of the two groups post-inter-vention (P = 0.521). (Figure 4)Cardiac index (CI): The CI increased in group T post-inter-vention (P = 0.009). (Figure 5)Systemic vascular resistance (SVR): The SVR decreased in group T post-intervention (P = 0.024). (Figure 6)

Discussion

This report is the first study to include thermotherapy as a non-pharmacological method for DHF treatment in hospital-ized patients at an advanced stage of the disease who were de-pendent on vasoactive drugs and refractory to conventional treatment. The patients exhibited low cardiac output, vasocon-striction, and prolonged use of a vasoactive drug. This type of patient does not often fit into the guidelines or published pa-pers on HF treatment because this population is severe with high in-hospital mortality. Therefore, this work is novel due to the profile of the population studied and the use of heat as an adjuvant measure for the treatment of cardiac decompensation.

The safety and feasibility of the method was demonstrat-

ed initially in a group of critically ill patients because no data exist for this scenario. Preliminary results suggested hemody-namic improvement 22) through an increased cardiac index and

Figure 2. Study profile. ICD indicates implantable cardioverter defibrilla-tor.

Figure 3. MAP indicates arterial pressure pre- and post-intervention.

Figure 4. PCP indicates pulmonary capillary pressure pre- and post-inter-vention.

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decreased systemic vascular resistance with heat. However, the clinical behavior of patients admitted for DHF in the presence of thermotherapy was not certain.

A total of 38 patients were evaluated in this study pre- and post-intervention. The hemodynamic improvement report-ed by patients undergoing thermotherapy was apparent. Ther-mal vasodilation increased the CI by 24.1% (P = 0.009) and reduced systemic vascular resistance by 16% (P = 0.024) with-out affecting patient mean blood pressure (group C: 73.4 ± 13.3 to 73.8 ± 12.4 mmHg; group T: 76.3 ± 11.7 to 76.7 ± 13.3 mmHg; P = 0.968) or heart rate (group C: 83.3 ± 18.6 to 86.9 ± 19.8 bpm; group T: 89.5 ± 19.0 to 95.1 ± 21.8; P = 0.355). An immediate hemodynamic effect of heat is observed due to peripheral vasodilatation, especially through the type of radia-tion used in this study. The choice of infrared radiation in pre-vious studies was due to its higher heat transfer compared to other methods.24)

Tei, et al 12-15) first described thermotherapy at the end of the 1980s. Hot immersion baths were described initially and improved in 2007 with the use of saunas with infrared radia-tion (eg, Waon therapy). Waon therapy uses saunas with infra-red radiation unlike traditional saunas, which are heated by hot stones or electric elements. Only approximately 20% of the heat in these traditional saunas is transferred in the form of ra-diation. In contrast, the infrared heating elements transfer ap-proximately 90% of their energy through infrared radiation. Tadashi Ishikawa invented these “modern” infrared heaters in 1965. The infrared radiation penetrates deep into the body, which likely underlies the greater heat effect in these treat-ments.24)

Hot immersion baths or transfer for saunas during patient hospitalization in this study would not be possible because of

their hemodynamic conditions. Therefore, thermotherapy was applied using an infrared thermal blanket with the same fea-tures as infrared saunas with the benefits of portability and ease of use at bedside. This blanket generates heat directly on hospitalized patients via infrared radiation pads connected to the socket. The target temperature (50°C) was adjusted and maintained during the entire procedure using the thermostat.

The patients were monitored continuously throughout the procedure. The Swan-Ganz catheter and a digital thermometer monitored patient temperature during heat treatment. A differ-ence of at most 1°C was found in the central body temperature of patients undergoing thermotherapy. No statistically signifi-cant changes in body temperature were observed, which may be a risk predictor for the procedure (group C: 36.9 ± 0.52 to 37.01 ± 0.48°C; group T: 37.03 ± 0.50 to 37.3 ± 0.36°C; P = 0.359).

Most studies on the use of heat in HF patients involved symptomatic patients (NYHA Class III and IV) without the need for vasoactive drugs. Kihara, et al 25) studied 20 patients with congestive HF who received Waon therapy (15 minutes of sauna per day). Symptoms improved in 17 of 20 patients af-ter 2 weeks of treatment. Kihara, et al 26) subsequently followed a protocol similar to the first study and evaluated 30 patients with complex ventricular arrhythmias (> 200 ectopic ventricu-lar beats/day). After randomization, 20 patients received Waon therapy for 5 days per week for two weeks, and 10 patients in the control group remained at rest for 45 minutes in a room at 24°C. A statistically significant reduction in the number of ventricular ectopic beats was observed in the group that re-ceived thermotherapy, which is more important data to explain patient hemodynamic improvement.

Kihara, et al 27) published the results of a third trial in April 2009. This study assessed 129 patients with HF (NYHA functional class III or IV), and 64 patients were treated with Waon therapy for 5 days during hospitalization and at least twice per week after discharge. The data were compiled after 5 years and analyzed. Twelve patients in the control group died, and 8 patients in the Waon group died. Over the 5 years, 31% of patients who received Waon therapy were re-hospitalized for HF or died from heart disease compared to 69% in the un-treated group (P < 0.01).

Clinical, hemodynamic and laboratory parameters in pa-tients with prolonged hospitalization lost diagnostic value in the present study from the moment the patients become refrac-tory to conventional treatment. The BNP dose during hospitali-zation for prognosis assessment would be significant with a longer follow-up,28) which was not evaluated in this work.

Miyata, et al 29) conducted a prospective multicenter study to confirm the results of thermotherapy using laboratory mark-ers. A total of 188 patients received conventional treatment for HF for 1 week, and 112 patients received Waon therapy. A to-tal of 76 patients were in the control group. The Waon group received the same protocol (ie, 15 minutes of sauna per day at 60°C followed by 30 minutes of rest with a blanket, 5 days per week for 2 weeks). Echocardiography and BNP dose were as-sessed before and after treatment and again two weeks later. A statistically significant improvement was observed in all meas-ures in the Waon group patients after treatment.

Fujita, et al 16) demonstrated a decrease in oxidative stress in patients undergoing Waon therapy. Forty patients were di-vided into a control group (n = 20) and a Waon therapy group

Figure 5. CI indicates cardiac index pre- and post-intervention.

Figure 6. SVR indicates systemic vascular resistance pre- and post-inter-vention.

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(n = 20). Hydrogen peroxide and BNP concentrations de-creased significantly in the Waon group after 4 weeks of daily sessions, but nitric oxide metabolites increased. No changes were observed in the control group.

The advanced stage of heart failure, especially the de-pendence on vasoactive drugs and treatment resistance, is a time when small hemodynamic changes may occur frequently and result in disease evolution in patients, which hampers treatment. The functional loss of baroreceptors that suppress sympathetic activity and inhibit vasopressin secretion prolongs decompensation even in the presence of circulatory compensa-tion.30) Vasodilators, such as prostaglandins and nitric oxide, are released to compensate for the vasoconstriction. Therefore, heat would act as another vasodilator in the hemodynamic ad-aptation process.

Heat can be used acutely as an important adjunct therapy for clinical improvement in DHF patients. Intermittent, and not daily, sessions of heat with pharmacological treatment may be necessary to promote the expected clinical improvement at this stage. Ochiai, et al 31) demonstrated that DHF in patients who received more than 2 oral vasodilators during hospitalization (multiple vasodilations) exhibited higher cardiac indexes and lower systemic vascular resistance compared to patients treated with only one vasodilator. These data support the use of ther-motherapy as another option for vasodilation in decompensa-tion. Therefore, the addition of other vasodilators may effec-tively change the prognosis in decompensation in the presence of oral vasodilators when the usual treatments are ineffective.

In conclusion, the use of heat (ie, thermotherapy) as a va-sodilator increased the cardiac index and reduced systemic vascular resistance in decompensated HF.

The data from this sample suggest that thermotherapy is a therapeutic adjuvant for the treatment of DHF patients. How-ever, a randomized clinical trial using a larger patient sample is required to explore the potential clinical efficacy.Limitations of the study: Some variables in this initial explo-ration were not analyzed. The echocardiographic variables that were not repeated after the use of heat were considered impor-tant. The BNP dose would be important in long-term follow-up studies during hospitalization for clinical outcomes.

Only a long-term randomized clinical trial with a larger sample and more clinically relevant outcomes would provide evidence of thermotherapy efficacy in DHF.

Appendix

Male patient, 60 years-old, admitted with a diagnosis of idiopathic decompensated heart failure, hospitalized at 37 days since then with dob-utamine at a mean dose of 15 mcg/kg/minute and milrinone associated with a mean dose of 0.375 mcg/kg/minute. Already using oral vasodilators and diuretics without clinical improvement. Attempted withdrawal of va-soactive drugs 3 times without success, presenting hemodynamic instabil-ity. The left ventricle ejection fraction was 21%, with important diffuse hypokinesia and without thrombi. He was randomized to the thermothera-py group. On the sixth day, he suffered cardiorespiratory arrest in PEA readily assisted, and died. No necropsy was performed due to the severity of the case.

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