Cardiac Contractility Modulation in Chagas Heart Disease
NCT ID: NCT05519046
Last Updated: 2025-04-04
Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
Recruitment Status
RECRUITING
Clinical Phase
NA
Total Enrollment
60 participants
Study Classification
INTERVENTIONAL
Study Start Date
2022-05-25
Study Completion Date
2026-12-31
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
Chagas disease is an endemic problem in Latin America, where millions of people are chronically infected with T. cruzi. Recently, it was assumed to have clinical and epidemiological relevance in several other countries due to migratory and globalizing social factors. CCC occurs in 30-50% of infected individuals, causing considerable morbidity/mortality rates. Heart failure is the most prevalent morbidity. While CRT and drug treatment have been advocated and implemented without much success to improve the clinical condition of patients with CCC, there is no consistent scientific evidence on the role of cardiac contractility modulation (CCM) as a form of adjuvant treatment for heart failure in patients with CCC.
The hypothesis of this study is that patients with CCC, advanced heart failure, severe systolic dysfunction, and non-LBB have better clinical and functional responses when undergoing implantation of a CCM device than when undergoing cardiac resynchronization therapy.
The hypothesis of this study is that patients with CCC, advanced heart failure, severe systolic dysfunction, and non-LBB have better clinical and functional responses when undergoing implantation of a CCM device than when undergoing cardiac resynchronization therapy.
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
Reveal Chagas: Clinical Evidence of the Implantable Cardiac Monitor in Patients With Chagas Disease
NCT01539161
Chagas Disease
Heart Diseases
TERMINATED
PHASE4
Cardiac Contractility Modulation Therapy in Amyloid Cardiomyopathy Patients With Heart Failure
NCT05167799
Amyloidosis Cardiac
Heart Failure
UNKNOWN
Coronary Heart Disease Complicated With Ischemic Mitral Regurgitation in China
NCT07230756
Ischemic Mitral Regurgitation
Coronary Heart Disease (CHD)
NOT_YET_RECRUITING
Percutaneous Mitral Valve Repair in Cardiogenic Shock: Mitra-Shock Study
NCT04399499
Mitral Regurgitation Functional
UNKNOWN
Transapical Beating-heart Septal Myectomy in Patient With Hypertrophic Obstructive Cardiomyopathy
NCT05332691
Hypertrophic Obstructive Cardiomyopathy
RECRUITING
NA
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
Chagas Disease:
Chagas disease (Trypanosomiasis Americana) is caused by the protozoan parasite Trypanosoma cruzi, which is transmitted to humans through the feces of a hematophagous insect (family Triatominae) in most cases. The infection usually occurs in childhood, and the acute phase has an incubation period of 1 to 2 weeks and can last up to 3 months. Then follows the chronic phase, in which for a long time - 2-4 decades most of the time - patients have only positive serology for Chagas disease (CD), without symptoms or other signs of clinically apparent disease.
Therefore, such patients present the so-called indeterminate form of Chagas disease, whose prognosis is essentially benign.
While due to pathogenic mechanisms still incompletely understood, many patients remain with this form of the disease for life around 30 to 50% of infected individuals evolve to certain forms like cardiac, digestive, or mixed. Chronic Chagas cardiomyopathy (CCC) has a hemodynamic pattern like dilated idiopathic cardiomyopathy but has marked pathophysiological peculiarities. The most common and most serious clinical form of CD is responsible for significant morbidity and mortality in many Latin countries -Americans (and with epidemiological relevance also contemporarily recognized in countries with immigration by individuals from those countries).
It is estimated that 8-10 million people are infected with Trypanosoma cruzi in Latin America and other countries. Considering the worst-case scenario, we can deduce that 3-5 million infected individuals will manifest clinical forms of the disease in its chronic phase.
The disease severity:
In addition to the criteria used in the risk stratification shown in Tables 1 and 2, several markers of worse prognosis have been identified by several authors, especially concerning sudden cardiac death in different clinical contexts.
Characteristics such: as presyncope and syncope; left ventricular dysfunction; heart failure; sustained ventricular tachycardia (VT) or non-sustained ventricular tachycardia; severe bradyarrhythmia (sinus node disease and advanced atrioventricular block); and previous cardiac arrest were identified as markers of risk of sudden cardiac death (SCD). On the other hand, isolated ventricular extrasystoles on Holter monitoring and right bundle-branch block do not significantly interfere with the prognosis of CCC. SCD is often associated with manifestations of heart failure (HF), but it can also occur in patients with asymptomatic left ventricular dysfunction. It accounts for approximately 55 to 65% of all causes of death, whereas refractory HF is a cause of death in about 25 to 30% of patients and systemic or pulmonary thromboembolism in about 10 to 15%. Indicador não definido. Very rarely, aneurysm rupture can be the mechanism of sudden death in CCC.
Recently, the correlation between CCC stages and causes of mortality has been schematically described. SCD usually affects patients from stage II of the disease onwards, being more relevant in stage III and a little less in stage IV, in which refractory heart failure as a cause of death becomes quite frequent.
Therapeutic Options for Heart Failure. As in other heart diseases, the treatment of HF in CCC is based on the routine use of a combination of three types of drugs: diuretics, angiotensin-converting enzyme (ACE) inhibitors, or angiotensin receptor blockers (ARB) and adrenergic beta-blockers (BB). However, despite CD representing an important cause of HF in Latin America, patients with CD and HF were not included in the large studies that validated those drugs to treat HF. Therefore, the real efficacy and tolerability of these drugs in patients with CCC have not been scientifically established, and their use is empirically extrapolated from the support obtained in HF of other etiologies.
In the same sense, the scientific evidence regarding the role of CRT in CCC is not supported by randomized studies. Furthermore, the low prevalence of left bundle block, an independent marker of CRT response, in CCC is a limiting factor for its indication of this therapeutic option. Some observational studies have been carried out to recognize other candidates for CRT in CCC, but the evidence is still poor.
Heart transplantation is a good option for severe cases, but its application is very limited by the low availability of donors.
Recently, an excellent adjunctive option was introduced, and tested in several heart diseases but not in patients with CCC. It is an implantable device capable of modulating myocardial contractility: Cardiac Contractility Modulation (CCM).
Cardiac Contractility Modulation:
CCM consists of high-tension stimulation of the right ventricular septum during the absolute refractory period, 30-40ms after cardiomyocyte activation. This stimulation acts on calcium currents and increases ventricular contractility and, as a consequence, improves functional capacity.
In a 2019 meta-analytic study, Mando R et al. evaluated four randomized studies that applied the CCM technique compared to optimized drug therapy. The authors concluded that, in short-term follow-up, there is health-related quality of life gains (as measured by the Minnesota questionnaire) and that these were significantly greater in patients treated with CCM. However, they did not observe significantly better results in the functional test evaluated by the 6-minute walk test, nor regarding mortality and hospitalization from any causes.
Abraham WT et al. performed an open-label randomized trial to evaluate the adjunctive effect of CCM therapy to optimized therapy in 160 patients with symptoms of HF functional class III or IV by NYHA classification, sinus rhythm, QRS duration \<130ms, and LVEF ≥25%, and ≤45%. Of these, 74 patients underwent CCM therapy for 24 weeks. The results indicated that CCM therapy is safe and improves exercise tolerance and quality of life. The composite endpoint of cardiovascular death and HF hospitalizations was also reduced and clinical effects were observed for the entire LVEF range studied. More specifically, superior clinical efficacy was observed in patients with LVEF between 35% and 45%. These data point in the direction that CCM may be an interesting adjuvant option in HF therapy.
Hypothesis:
The hypothesis of this study is that patients with CCC, advanced heart failure, severe systolic dysfunction, and non-LBB have better clinical and functional responses when undergoing implantation of a CCM device than when undergoing cardiac resynchronization therapy.
Objectives:
Primary objective - To assess the short-term impact on quality of life and myocardial contractility of an implantable electronic cardiac device for cardiac contractility modulation compared to CRT in patients with CCC, non-LBBB, and advanced HF.
Secondary objectives - To record the clinical evolution, including the need for hospitalization, the functional class according to the New York Heart Association, and the functional capacity of an implantable electronic cardiac device for cardiac contractility modulation compared to CRT, in patients with CCC, non-LBBB, and advanced HF.
Chagas disease (Trypanosomiasis Americana) is caused by the protozoan parasite Trypanosoma cruzi, which is transmitted to humans through the feces of a hematophagous insect (family Triatominae) in most cases. The infection usually occurs in childhood, and the acute phase has an incubation period of 1 to 2 weeks and can last up to 3 months. Then follows the chronic phase, in which for a long time - 2-4 decades most of the time - patients have only positive serology for Chagas disease (CD), without symptoms or other signs of clinically apparent disease.
Therefore, such patients present the so-called indeterminate form of Chagas disease, whose prognosis is essentially benign.
While due to pathogenic mechanisms still incompletely understood, many patients remain with this form of the disease for life around 30 to 50% of infected individuals evolve to certain forms like cardiac, digestive, or mixed. Chronic Chagas cardiomyopathy (CCC) has a hemodynamic pattern like dilated idiopathic cardiomyopathy but has marked pathophysiological peculiarities. The most common and most serious clinical form of CD is responsible for significant morbidity and mortality in many Latin countries -Americans (and with epidemiological relevance also contemporarily recognized in countries with immigration by individuals from those countries).
It is estimated that 8-10 million people are infected with Trypanosoma cruzi in Latin America and other countries. Considering the worst-case scenario, we can deduce that 3-5 million infected individuals will manifest clinical forms of the disease in its chronic phase.
The disease severity:
In addition to the criteria used in the risk stratification shown in Tables 1 and 2, several markers of worse prognosis have been identified by several authors, especially concerning sudden cardiac death in different clinical contexts.
Characteristics such: as presyncope and syncope; left ventricular dysfunction; heart failure; sustained ventricular tachycardia (VT) or non-sustained ventricular tachycardia; severe bradyarrhythmia (sinus node disease and advanced atrioventricular block); and previous cardiac arrest were identified as markers of risk of sudden cardiac death (SCD). On the other hand, isolated ventricular extrasystoles on Holter monitoring and right bundle-branch block do not significantly interfere with the prognosis of CCC. SCD is often associated with manifestations of heart failure (HF), but it can also occur in patients with asymptomatic left ventricular dysfunction. It accounts for approximately 55 to 65% of all causes of death, whereas refractory HF is a cause of death in about 25 to 30% of patients and systemic or pulmonary thromboembolism in about 10 to 15%. Indicador não definido. Very rarely, aneurysm rupture can be the mechanism of sudden death in CCC.
Recently, the correlation between CCC stages and causes of mortality has been schematically described. SCD usually affects patients from stage II of the disease onwards, being more relevant in stage III and a little less in stage IV, in which refractory heart failure as a cause of death becomes quite frequent.
Therapeutic Options for Heart Failure. As in other heart diseases, the treatment of HF in CCC is based on the routine use of a combination of three types of drugs: diuretics, angiotensin-converting enzyme (ACE) inhibitors, or angiotensin receptor blockers (ARB) and adrenergic beta-blockers (BB). However, despite CD representing an important cause of HF in Latin America, patients with CD and HF were not included in the large studies that validated those drugs to treat HF. Therefore, the real efficacy and tolerability of these drugs in patients with CCC have not been scientifically established, and their use is empirically extrapolated from the support obtained in HF of other etiologies.
In the same sense, the scientific evidence regarding the role of CRT in CCC is not supported by randomized studies. Furthermore, the low prevalence of left bundle block, an independent marker of CRT response, in CCC is a limiting factor for its indication of this therapeutic option. Some observational studies have been carried out to recognize other candidates for CRT in CCC, but the evidence is still poor.
Heart transplantation is a good option for severe cases, but its application is very limited by the low availability of donors.
Recently, an excellent adjunctive option was introduced, and tested in several heart diseases but not in patients with CCC. It is an implantable device capable of modulating myocardial contractility: Cardiac Contractility Modulation (CCM).
Cardiac Contractility Modulation:
CCM consists of high-tension stimulation of the right ventricular septum during the absolute refractory period, 30-40ms after cardiomyocyte activation. This stimulation acts on calcium currents and increases ventricular contractility and, as a consequence, improves functional capacity.
In a 2019 meta-analytic study, Mando R et al. evaluated four randomized studies that applied the CCM technique compared to optimized drug therapy. The authors concluded that, in short-term follow-up, there is health-related quality of life gains (as measured by the Minnesota questionnaire) and that these were significantly greater in patients treated with CCM. However, they did not observe significantly better results in the functional test evaluated by the 6-minute walk test, nor regarding mortality and hospitalization from any causes.
Abraham WT et al. performed an open-label randomized trial to evaluate the adjunctive effect of CCM therapy to optimized therapy in 160 patients with symptoms of HF functional class III or IV by NYHA classification, sinus rhythm, QRS duration \<130ms, and LVEF ≥25%, and ≤45%. Of these, 74 patients underwent CCM therapy for 24 weeks. The results indicated that CCM therapy is safe and improves exercise tolerance and quality of life. The composite endpoint of cardiovascular death and HF hospitalizations was also reduced and clinical effects were observed for the entire LVEF range studied. More specifically, superior clinical efficacy was observed in patients with LVEF between 35% and 45%. These data point in the direction that CCM may be an interesting adjuvant option in HF therapy.
Hypothesis:
The hypothesis of this study is that patients with CCC, advanced heart failure, severe systolic dysfunction, and non-LBB have better clinical and functional responses when undergoing implantation of a CCM device than when undergoing cardiac resynchronization therapy.
Objectives:
Primary objective - To assess the short-term impact on quality of life and myocardial contractility of an implantable electronic cardiac device for cardiac contractility modulation compared to CRT in patients with CCC, non-LBBB, and advanced HF.
Secondary objectives - To record the clinical evolution, including the need for hospitalization, the functional class according to the New York Heart Association, and the functional capacity of an implantable electronic cardiac device for cardiac contractility modulation compared to CRT, in patients with CCC, non-LBBB, and advanced HF.
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Chagas Cardiomyopathy
Heart Failure
Systolic Dysfunction
Right Bundle Branch Block and Left Anterior Fascicular Block
Right Bundle Branch Block and Left Posterior Fascicular Block
Study Design
Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.
Allocation Method
RANDOMIZED
Intervention Model
PARALLEL
Primary Study Purpose
TREATMENT
Blinding Strategy
SINGLE
Participants
Study Groups
Review each arm or cohort in the study, along with the interventions and objectives associated with them.
Cardiac Contractility Modulation Group - CCM Group
CCM implantation.
Group Type
EXPERIMENTAL
Cardiac Contractility Modulation (CCM)
Intervention Type
DEVICE
Cardiac Contractility Modulation (CCM) implantation
Cardiac Resynchronization Therapy Group - CRT Group
CRT implantation
Group Type
ACTIVE_COMPARATOR
CRT
Intervention Type
DEVICE
Cardiac Resynchronization Therapy
Interventions
Learn about the drugs, procedures, or behavioral strategies being tested and how they are applied within this trial.
Cardiac Contractility Modulation (CCM)
Cardiac Contractility Modulation (CCM) implantation
Intervention Type
DEVICE
CRT
Cardiac Resynchronization Therapy
Intervention Type
DEVICE
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
* Signing of an informed consent form (ICF) before randomization and any study procedure,
* Both genders, age \>18 years and \<75 years,
* Recent positive (last two years) and documented serology for Chagas disease, in at least two different tests (indirect hemagglutination, indirect immunofluorescence, or ELISA),
* NYHA II-III heart failure functional class,
* LVEF\< 35%,
* Non left bundle branch block
* Intraventricular desynchrony (Yu index)
* Global longitudinal strain \>11 %.
* Both genders, age \>18 years and \<75 years,
* Recent positive (last two years) and documented serology for Chagas disease, in at least two different tests (indirect hemagglutination, indirect immunofluorescence, or ELISA),
* NYHA II-III heart failure functional class,
* LVEF\< 35%,
* Non left bundle branch block
* Intraventricular desynchrony (Yu index)
* Global longitudinal strain \>11 %.
Exclusion Criteria
* Participation in another study, presently or terminated \<1 year ago, except for a totally unrelated observational study,
* Other concomitant cardiovascular diseases, including uncontrolled diabetes mellitus (systemic arterial hypertension without permitted target organ compromise),
* Kidney dysfunction (serum creatinine \>1.5mg/dL or eGFR \<30mL/min/1.73m2) or liver dysfunction, with diagnosis of cirrhosis or portal hypertension or elevated serum enzymes (AST or ALT) \> 3x the upper limit of normality,
* Moderate or severe chronic obstructive pulmonary disease,
* Peripheral polyneuropathy,
* Hyperthyroidism,
* Current alcoholism or not abandoned for \>2 years,
* Diagnosed with psychopathy or psychosis or addiction to illicit drugs,
* Life expectancy \<1 year, due to the disease itself or comorbidities (including NYHA class IV),
* Pregnancy or breastfeeding,
* Potential to become pregnant during the study (non-menopausal patients who have not undergone a radical and safe contraceptive process),
* Previously withdrawn from this study.
* Other concomitant cardiovascular diseases, including uncontrolled diabetes mellitus (systemic arterial hypertension without permitted target organ compromise),
* Kidney dysfunction (serum creatinine \>1.5mg/dL or eGFR \<30mL/min/1.73m2) or liver dysfunction, with diagnosis of cirrhosis or portal hypertension or elevated serum enzymes (AST or ALT) \> 3x the upper limit of normality,
* Moderate or severe chronic obstructive pulmonary disease,
* Peripheral polyneuropathy,
* Hyperthyroidism,
* Current alcoholism or not abandoned for \>2 years,
* Diagnosed with psychopathy or psychosis or addiction to illicit drugs,
* Life expectancy \<1 year, due to the disease itself or comorbidities (including NYHA class IV),
* Pregnancy or breastfeeding,
* Potential to become pregnant during the study (non-menopausal patients who have not undergone a radical and safe contraceptive process),
* Previously withdrawn from this study.
Minimum Eligible Age
18 Years
Maximum Eligible Age
75 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
Impulse Dynamics
INDUSTRY
Sponsor Role
collaborator
I2medi Comercial Medica LTDA
UNKNOWN
Sponsor Role
collaborator
InCor Heart Institute
OTHER
Sponsor Role
lead
Responsible Party
Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.
Martino Martinelli Filho
Principal Investigator
Responsibility Role
PRINCIPAL_INVESTIGATOR
Locations
Explore where the study is taking place and check the recruitment status at each participating site.
InCor - HCFMUSP
São Paulo, São Paulo, Brazil
Site Status
RECRUITING
Countries
Review the countries where the study has at least one active or historical site.
Brazil
Central Contacts
Reach out to these primary contacts for questions about participation or study logistics.
Facility Contacts
Find local site contact details for specific facilities participating in the trial.
References
Explore related publications, articles, or registry entries linked to this study.
Dias JC, Kloetzel K. The prognostic value of the electrocardiographic features of chronic Chagas' disease. Rev Inst Med Trop Sao Paulo. 1968 May-Jun;10(3):158-62. No abstract available.
Reference Type
BACKGROUND
Espinosa R, Carrasco HA, Belandria F, Fuenmayor AM, Molina C, Gonzalez R, Martinez O. Life expectancy analysis in patients with Chagas' disease: prognosis after one decade (1973-1983). Int J Cardiol. 1985 May;8(1):45-56. doi: 10.1016/0167-5273(85)90262-1.
Reference Type
BACKGROUND
Carrasco HA, Parada H, Guerrero L, Duque M, Duran D, Molina C. Prognostic implications of clinical, electrocardiographic and hemodynamic findings in chronic Chagas' disease. Int J Cardiol. 1994 Jan;43(1):27-38. doi: 10.1016/0167-5273(94)90087-6.
Reference Type
BACKGROUND
Martinelli Filho M, Sosa E, Nishioka S, Scanavacca M, Bellotti G, Pileggi F. Clinical and electrophysiologic features of syncope in chronic chagasic heart disease. J Cardiovasc Electrophysiol. 1994 Jul;5(7):563-70. doi: 10.1111/j.1540-8167.1994.tb01297.x.
Reference Type
BACKGROUND
Mady C, Cardoso RH, Barretto AC, da Luz PL, Bellotti G, Pileggi F. Survival and predictors of survival in patients with congestive heart failure due to Chagas' cardiomyopathy. Circulation. 1994 Dec;90(6):3098-102. doi: 10.1161/01.cir.90.6.3098.
Reference Type
BACKGROUND
Bestetti RB, Dalbo CM, Freitas OC, Teno LA, Castilho OT, Oliveira JS. Noninvasive predictors of mortality for patients with Chagas' heart disease: a multivariate stepwise logistic regression study. Cardiology. 1994;84(4-5):261-7. doi: 10.1159/000176409.
Reference Type
BACKGROUND
de Paola AA, Gomes JA, Terzian AB, Miyamoto MH, Martinez Fo EE. Ventricular tachycardia during exercise testing as a predictor of sudden death in patients with chronic chagasic cardiomyopathy and ventricular arrhythmias. Br Heart J. 1995 Sep;74(3):293-5. doi: 10.1136/hrt.74.3.293.
Reference Type
BACKGROUND
Bestetti RB, Dalbo CM, Arruda CA, Correia Filho D, Freitas OC. Predictors of sudden cardiac death for patients with Chagas' disease: a hospital-derived cohort study. Cardiology. 1996 Nov-Dec;87(6):481-7. doi: 10.1159/000177142.
Reference Type
BACKGROUND
Carrasco HA, Guerrero L, Parada H, Molina C, Vegas E, Chuecos R. Ventricular arrhythmias and left ventricular myocardial function in chronic chagasic patients. Int J Cardiol. 1990 Jul;28(1):35-41. doi: 10.1016/0167-5273(90)90006-q.
Reference Type
BACKGROUND
Lopes ER. Sudden death in patients with Chagas disease. Mem Inst Oswaldo Cruz. 1999;94 Suppl 1:321-4. doi: 10.1590/s0074-02761999000700061. No abstract available.
Reference Type
BACKGROUND
Rassi A Jr, Rassi SG, Rassi A. Sudden death in Chagas' disease. Arq Bras Cardiol. 2001 Jan;76(1):75-96. doi: 10.1590/s0066-782x2001000100008. No abstract available. English, Portuguese.
Reference Type
BACKGROUND
Bestetti R. Stroke in a hospital-derived cohort of patients with chronic Chagas' disease. Acta Cardiol. 2000 Feb;55(1):33-8. doi: 10.2143/AC.55.1.2005715.
Reference Type
BACKGROUND
Carod-Artal FJ, Vargas AP, Horan TA, Nunes LG. Chagasic cardiomyopathy is independently associated with ischemic stroke in Chagas disease. Stroke. 2005 May;36(5):965-70. doi: 10.1161/01.STR.0000163104.92943.50. Epub 2005 Apr 21.
Reference Type
BACKGROUND
Sousa AS, Xavier SS, Freitas GR, Hasslocher-Moreno A. Prevention strategies of cardioembolic ischemic stroke in Chagas' disease. Arq Bras Cardiol. 2008 Nov;91(5):306-10. doi: 10.1590/s0066-782x2008001700004. English, Portuguese.
Reference Type
BACKGROUND
Oliveira JS, Barbieri Neto J. [Chagasic cardiopathy. Rupture of the apical aneurysm]. Arq Bras Cardiol. 1970 Oct;23(5):335-8. No abstract available. Portuguese.
Reference Type
BACKGROUND
Pinto Dias JC. [Natural history of Chagas disease]. Arq Bras Cardiol. 1995 Oct;65(4):359-66. No abstract available. Portuguese.
Reference Type
BACKGROUND
Rassi A Jr, Rassi A, Marin-Neto JA. Chagas disease. Lancet. 2010 Apr 17;375(9723):1388-402. doi: 10.1016/S0140-6736(10)60061-X.
Reference Type
BACKGROUND
Dias JC. The indeterminate form of human chronic Chagas' disease A clinical epidemiological review. Rev Soc Bras Med Trop. 1989 Jul-Sep;22(3):147-56. doi: 10.1590/s0037-86821989000300007.
Reference Type
BACKGROUND
Barretto AC, Ianni BM. The undetermined form of Chagas' heart disease: concept and forensic implications. Sao Paulo Med J. 1995 Mar-Apr;113(2):797-801. doi: 10.1590/s1516-31801995000200010.
Reference Type
BACKGROUND
Marin-Neto JA, Cunha-Neto E, Maciel BC, Simoes MV. Pathogenesis of chronic Chagas heart disease. Circulation. 2007 Mar 6;115(9):1109-23. doi: 10.1161/CIRCULATIONAHA.106.624296.
Reference Type
BACKGROUND
Schmunis GA. Epidemiology of Chagas disease in non-endemic countries: the role of international migration. Mem Inst Oswaldo Cruz. 2007 Oct 30;102 Suppl 1:75-85. doi: 10.1590/s0074-02762007005000093.
Reference Type
BACKGROUND
Dias JC, Prata A, Correia D. Problems and perspectives for Chagas disease control: in search of a realistic analysis. Rev Soc Bras Med Trop. 2008 Mar-Apr;41(2):193-6. doi: 10.1590/s0037-86822008000200012.
Reference Type
BACKGROUND
Moncayo A, Silveira AC. Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy. Mem Inst Oswaldo Cruz. 2009 Jul;104 Suppl 1:17-30. doi: 10.1590/s0074-02762009000900005.
Reference Type
BACKGROUND
Rassi A Jr, Dias JC, Marin-Neto JA, Rassi A. Challenges and opportunities for primary, secondary, and tertiary prevention of Chagas' disease. Heart. 2009 Apr;95(7):524-34. doi: 10.1136/hrt.2008.159624. Epub 2009 Jan 8.
Reference Type
BACKGROUND
Rassi A Jr, Rassi A, Little WC, Xavier SS, Rassi SG, Rassi AG, Rassi GG, Hasslocher-Moreno A, Sousa AS, Scanavacca MI. Development and validation of a risk score for predicting death in Chagas' heart disease. N Engl J Med. 2006 Aug 24;355(8):799-808. doi: 10.1056/NEJMoa053241.
Reference Type
BACKGROUND
Brunckhorst CB, Shemer I, Mika Y, Ben-Haim SA, Burkhoff D. Cardiac contractility modulation by non-excitatory currents: studies in isolated cardiac muscle. Eur J Heart Fail. 2006 Jan;8(1):7-15. doi: 10.1016/j.ejheart.2005.05.011. Epub 2005 Oct 3.
Reference Type
BACKGROUND
Kahwash R, Burkhoff D, Abraham WT. Cardiac contractility modulation in patients with advanced heart failure. Expert Rev Cardiovasc Ther. 2013 May;11(5):635-45. doi: 10.1586/erc.13.48.
Reference Type
BACKGROUND
Abi-Samra F, Gutterman D. Cardiac contractility modulation: a novel approach for the treatment of heart failure. Heart Fail Rev. 2016 Nov;21(6):645-660. doi: 10.1007/s10741-016-9571-6.
Reference Type
BACKGROUND
Mando R, Goel A, Habash F, Saad M, Ayoub K, Vallurupalli S, Maskoun W. Outcomes of Cardiac Contractility Modulation: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. Cardiovasc Ther. 2019 Jun 17;2019:9769724. doi: 10.1155/2019/9769724. eCollection 2019.
Reference Type
BACKGROUND
Abraham WT, Kuck KH, Goldsmith RL, Lindenfeld J, Reddy VY, Carson PE, Mann DL, Saville B, Parise H, Chan R, Wiegn P, Hastings JL, Kaplan AJ, Edelmann F, Luthje L, Kahwash R, Tomassoni GF, Gutterman DD, Stagg A, Burkhoff D, Hasenfuss G. A Randomized Controlled Trial to Evaluate the Safety and Efficacy of Cardiac Contractility Modulation. JACC Heart Fail. 2018 Oct;6(10):874-883. doi: 10.1016/j.jchf.2018.04.010. Epub 2018 May 10.
Reference Type
BACKGROUND
Hinkle LE Jr, Thaler HT. Clinical classification of cardiac deaths. Circulation. 1982 Mar;65(3):457-64. doi: 10.1161/01.cir.65.3.457.
Reference Type
BACKGROUND
Parissis JT, Nikolaou M, Farmakis D, Paraskevaidis IA, Bistola V, Venetsanou K, Katsaras D, Filippatos G, Kremastinos DT. Self-assessment of health status is associated with inflammatory activation and predicts long-term outcomes in chronic heart failure. Eur J Heart Fail. 2009 Feb;11(2):163-9. doi: 10.1093/eurjhf/hfn032.
Reference Type
BACKGROUND
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
57563722.3.0000.0068
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.
Late Clinical Outcomes of Percutaneous Mitral Commissurotomy in Patients With Mitral Stenosis
NCT04112108
COMPLETED
Haemodynamics of Mitral Regurgitation Reduction
NCT05403840
UNKNOWN
Safety and Feasibility of the Transcatheter Tricuspid Valve Repair System (Trialign)
NCT04936802
UNKNOWN
NA
Transapical Beating-Heart Septal Myectomy in Patients With Symptomatic Nonobstructive Hypertrophic Cardiomyopathy
NCT05952154
UNKNOWN
NA
Safety and Efficacy Study of Intramyocardial Stem Cell Therapy in Patients With Dilated Cardiomyopathy
NCT01350310
COMPLETED
PHASE2
Feasibility Study of Dragonfly System for Severe Tricuspid Regurgitation
NCT04921605
UNKNOWN
NA
ATTR Amyloid Cardiomyopathy: Characterization of Extracellular Vesicles as Potential Disease Stratifiers and Prognostic Biomarkers
NCT07314268
RECRUITING
Remote Ischemic Preconditioning With Postconditioning in Heart Transplantation Surgery
NCT02149316
COMPLETED
NA
Patients' Long-Term Survival of Obstructive Hypertrophic Cardiomyopathy (HCM)
NCT04603521
COMPLETED
Feasibility Study of the DragonFly-T System for Severe Tricuspid Regurgitation
NCT05671640
UNKNOWN
NA
Prosthetic Valve and Graft Endocarditis With Mycobacterium Chimaera
NCT04429256
COMPLETED
Transcatheter Closure Versus Surgery of Perimembranous Ventricular Septal Defects
NCT00890799
COMPLETED
NA
Bioabsorbable Occluder for Outlet VSD: Safety and Aortic Valve Effects
NCT07040579
NOT_YET_RECRUITING
Mitral Valve in Hypertrophic Cardiomyopathy
NCT03877731
COMPLETED
NA
A Prospective Multicenter Cohort Study on Surgical Treatment Strategies for Pediatric Mitral Regurgitation
NCT07284212
COMPLETED
Functional Capacity and Quality of Life Following Septal Myectomy in Patients With HCM
NCT03092843
COMPLETED
The Effectiveness of Surgical Treatment of Patients With Ischemic Cardiomyopathy
NCT04489355
COMPLETED
To Evaluate Safety and Effectiveness of Transcatheter Aortic Valve System in Patients With Severe Aortic Insufficiency
NCT05424653
UNKNOWN
NA
Surgery in Secondary Tricuspid Regurgitation
NCT03953755
SUSPENDED
NA
Risk Stratification, Early Prevention and Treatment Strategies for Arrhythmogenic Cardiomyopathy
NCT06352307
RECRUITING
Safety and Efficacy Continued Access Study of the Medtronic CoreValve® System in the Treatment of Symptomatic Severe Aortic Stenosis in Very High Risk Subjects and High Risk Subjects Who Need Aortic Valve Replacement
NCT01531374
COMPLETED
NA
Treatment of Concomitant Mitral Regurgitation by Mitral Valve Clipping in Patients With Successful Transcatheter Aortic Valve Implantation.
NCT04009434
UNKNOWN
NA
Prediction of Reverse Remodeling and Outcome in Patients With Severe Secondary Mitral Valve Regurgitation Undergoing Transcatheter Edge-to-edge Mitral Valve Repair
NCT04913727
RECRUITING
NA
Transcatheter Mitral Valve Repair for Inotrope Dependent Cardiogenic Shock
NCT05298124
RECRUITING
NA
Induced Angiogenesis by Genic Therapy in Advanced Ischemic Cardiomyopathy
NCT00744315
UNKNOWN
PHASE2