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CTRI Number  CTRI/2012/06/002734 [Registered on: 19/06/2012] Trial Registered Retrospectively
Last Modified On: 22/07/2013
Post Graduate Thesis  Yes 
Type of Trial  Interventional 
Type of Study   Yoga & Naturopathy 
Study Design  Randomized, Parallel Group Trial 
Public Title of Study   Benefits of yoga therapy for heart problem patients. 
Scientific Title of Study   Effect of yoga therapy on cardiac function, response to exercise, oxidative stress and quality of life in heart failure patients: a randomized controlled trial. 
Trial Acronym   
Secondary IDs if Any  
Secondary ID  Identifier 
NIL  NIL 
 
Details of Principal Investigator or overall Trial Coordinator (multi-center study)  
Name  Bandi Hari Krishna 
Designation  Ph D scholar ( DST-INSPIRE-JRF) 
Affiliation  JIPMER 
Address  Department of Physiology JIPMER Pondicherry

Pondicherry
PONDICHERRY
605006
India 
Phone  9751114541  
Fax    
Email  hariphd.jipmer@gmail.com  
 
Details of Contact Person
Scientific Query
 
Name  B Hari Krishna 
Designation  JUnior Research Fellow (PhD scholar) 
Affiliation  JIPMER 
Address  Department of Physiology JIPMER Pondicherry

Pondicherry
PONDICHERRY
605006
India 
Phone  9751114541  
Fax    
Email  hariphd.jipmer@gmail.com  
 
Details of Contact Person
Public Query
 
Name  Bandi Hari Krishna 
Designation  Ph D scholar ( DST-INSPIRE-JRF) 
Affiliation  JIPMER 
Address  Department of Physiology JIPMER Pondicherry


PONDICHERRY
605006
India 
Phone  9751114541  
Fax    
Email  hariphd.jipmer@gmail.com  
 
Source of Monetary or Material Support  
JIPMER, Puducherry. 
 
Primary Sponsor  
Name  JIPMER 
Address  Dhanvathari Nagar Pondhicherry. 
Type of Sponsor  Government medical college 
 
Details of Secondary Sponsor  
Name  Address 
NIL  NIL 
 
Countries of Recruitment     India  
Sites of Study  
No of Sites = 2  
Name of Principal Investigator  Name of Site  Site Address  Phone/Fax/Email 
Dr Balachander J  Dept of Cardiology  JIPMER Puducherry
Pondicherry
PONDICHERRY 
9842320952

jbc6@vsnl.com 
Bandi Hari Krishna  Dpt of Physiology  JIPMER Puducherry
Pondicherry
PONDICHERRY 
9751114541

hariphd.jipmer@gmail.com 
 
Details of Ethics Committee  
No of Ethics Committees= 1  
Name of Committee  Approval Status 
JIPMER, Institute Ethics Committee (Human Studies)  Approved 
 
Regulatory Clearance Status from DCGI  
Status 
Not Applicable 
 
Health Condition / Problems Studied  
Health Type  Condition 
Patients  Heart failure (NYHA I & II),  
 
Intervention / Comparator Agent  
Type  Name  Details 
Comparator Agent  Standard medical therapy for heart failure  In our study we are recruiting the patients belongs to functional class NYHA I and II, we are administering the following therapy. Functional class ACE I ARB Diuretics β Blockers NYHA – I Yes Yes No In Post MI NYHA – II Yes Yes Yes – If fluid retention present In Post MI We are using the following: Name of Drug Initiating Dose Maximal Dose ACE – I Ramipril 1.25 – 2.5 mg bid 2.5 – 5.0 mg bid ARB Losartan 12.5 mg qd 50 mg qd β Blockers Carvediol 3.125 mg bid 25 – 50 mg bid Additional therapy Digoxin 0.125 mg qd less than 0.375 mg/d Route of administration: Oral Dietary salt restriction 2 – 3 g/day Activity: In euvolemic patients, regular isotonic exercise such as walking or riding stationary bicycle as tolerated is encouraged. (Some trials of exercise training have led to encouraging results with reduced symptoms increase exercise capacity and improvement in quality of life) The duration of the medical therapy should not be limited time period to all patients. Interim assessment of clinical symptoms and cardiac function will be done; accordingly the dosage of drug will be modified. (For this study we will do follow-up for 3 months, further the therapy continue based on the improvement of patient)  
Intervention  Yoga Therapy  The yoga therapy group patients also receive the STANDARD MEDICAL THERAPY and Yoga therapy as Add – On therapy. The patients will undergo yoga therapy in Dept. of Cardiology, JIPMER. Under our direct supervision for 3 days per week, the practices will be instructed by qualified, experienced yoga expert. Apart from the sessions of direct supervision, the patients are instructed to do these practices at home. The attendance will be maintained for Yoga therapy sessions, regularity of home practice will be monitored by regular phone contact. (The schedule of Yoga therapy, Handouts, Video CD which contains the instructions of procedures will be given to the patients.) Yoga therapy schedule for HF (3 months) [All procedures can be modified according to ability of patient] Loosening procedures : 5 min Suryanamaskar : 5 min [Repetitions based on ability of patient] Makarasana (for Relaxation) : 2 min Trikonasana : 2 min [Repetitions based on ability of patient] Ardhahalasana : 2 min [Repetitions based on ability of patient] Vakrasana : 2 min [Repetitions based on ability of patient] Makarasnsana (for Relaxation) : 3 min Savitri pranayama : 2 min [Repetitions based on ability of patient] Chandranadi pranayama : 3 min [Repetitions based on ability of patient] Bhramari pranayama : 2 min [Repetitions based on ability of patient] Nadishuddi pranayama : 2 min [Repetitions based on ability of patient] Shavasana : 20 min Total duration (approx) : 50 min  
 
Inclusion Criteria  
Age From  30.00 Year(s)
Age To  65.00 Year(s)
Gender  Both 
Details  Patients with systolic and / or diastolic heart failure
New York Heart Association (NYHA) class I & II
EjectionFraction: 30-50%
Able to walk without assistance
On stable medical therapy for heart failure.
 
 
ExclusionCriteria 
Details  Valvular heart disease
Pregnant or breast-feeding
Currently addicted to alcohol or drugs.
Patients having COPD
 
 
Method of Generating Random Sequence   Coin toss, Lottery, toss of dice, shuffling cards etc 
Method of Concealment   Sequentially numbered, sealed, opaque envelopes 
Blinding/Masking   Outcome Assessor Blinded 
Primary Outcome  
Outcome  TimePoints 
1. Cardiac function assessed by Echocardiography.
2. Functional capacity assessed by 6 min walk test.
3.Oxidative stress: Total antioxidant status, Plasma MDA.
4.Biomarkers:
Neurohormones – N terminal pro BNP.
Inflammation – hs CRP,TNFα
Oxidative stress marker – Plasma MDA, Uric acid
Hormonal and other markers of cachexia – Cholesterol
Comorbidities – Hb%, Creatinine
 
0 days, After 12 weeks of Yoga Therapy 
 
Secondary Outcome  
Outcome  TimePoints 
Cardiac autonomic function assessed by short term Heart Rate Variability.
QoL, Depression, Dyspnoea grading.
 
0 days, after 12 weeks of Yoga Therapy 
 
Target Sample Size   Total Sample Size="96"
Sample Size from India="96" 
Final Enrollment numbers achieved (Total)= ""
Final Enrollment numbers achieved (India)="" 
Phase of Trial   N/A 
Date of First Enrollment (India)   22/09/2011 
Date of Study Completion (India) Date Missing 
Date of First Enrollment (Global)  Date Missing 
Date of Study Completion (Global) Date Missing 
Estimated Duration of Trial   Years="2"
Months="0"
Days="0" 
Recruitment Status of Trial (Global)
Modification(s)  
Not Applicable 
Recruitment Status of Trial (India)  Completed 
Publication Details    
Individual Participant Data (IPD) Sharing Statement

Will individual participant data (IPD) be shared publicly (including data dictionaries)?  

Brief Summary  

 Heart failure is the end stage of all diseases of heart and is a major cause of morbidity and mortality. The overall prevalence of the heart failure is 3-20 per 1000 population, although this exceeds 100 per 1000 in those aged 65 years and over. The overall incidence of heart failure is likely to increase in future, because of both increase in ageing population and therapeutic advances in the management of acute myocardial infarction leading to improved survival in patients with impaired cardiac function 15. Heart failure is one of the most prevalent chronic illnesses of the modern times with a profound clinical economic impact on society. The symptoms of the disease significantly reduce the quality of life among those live with HF1. HF ranks among the top chronic illnesses with a profound clinical and socioeconomic impact. The manifestation of this may lead to a significant reduction in quality of life. In patients with both systolic and diastolic HF, these symptoms often limit functional capacity3. The epidemic of heart failure is a leading cause of morbidity and mortality worldwide. The hallmark of this pathology is maladaptive ventricular remodelling that precipitates contractile dysfunction and ultimately leads to the overt syndrome of congestive heart failure. The central feature in this malignant cascade is typically the injury to cardiac myocytes, followed by replacement fibrosis, negative ventricular remodelling that ultimately leads to organ failure further accelerated by hemodynamic overload, inflammatory, oxidative stress and/or impaired vascularisation9. Autonomic system imbalance is associated with mortality in patients with cardiocascular diseases12. Autonomic system imbalance and weakened central haemodynamics forms the pathophysiological basis of the impaired cardiovascular function and decreased physical capacity of HF patients14. HF is a multisystem syndrome with the autonomic, neurohumoral abnormalities of increasing sympathetic and decreasing parasympathetic activity. Evidence of ANS dysfunction includes decreased HRV2. Heart failure is associated with severe impairment of exercise capacity, functional ability and health related quality of life 10. Original observations suggest that endothelial dysfunction may be evident in CHF patient, possibly due to enhanced ROS activity. Increased MDA and decreased concentrations of glutathione, Vitamin C & E  were correlated with NYHA functional class14. Progressive increase in free radical injury and encorchment on antioxidant reserves with the evolution of HF, they also suggest that oxidative stress may be an important determinant of prognosis. There was significant relation between the patients MDA levels and functional class 4. Recent experimental and clinical studies have suggested that generation of ROS to increase in chronic HF. ROS can cause contractile failure and structural damage to the myocardium. The importance of oxidative stress is increasingly emerging with respect to pathophysiological mechanism of LV remodelling and failure responsible for HF progression. Oxidative stress could be the mechanistic basis also for muscle fatigue and reduced exercise tolerance in HF patients. ROS play an important role in the muscle atrophy commonly seen in HF patients through the induction of apoptosis. Oxidative stress is now proved to play an important role in the development and progression of myocardial remodelling and failure 5. Multiple lines of evidence support the “cytokine hypothesis” which suggests that inflammation plays an important role in the development and progression of heart failure. Circulating markers of inflammation, such as C reactive protein may be useful in the diagnosis, gauging, prognosis and evaluating the response to therapy in patients with heart failure 6. HF is associated with increased oxidative stress, and many of our therapies proven to be of clinical benefit may have mechanisms of action related to reducing this stress in vivo. Increased oxidative stress is recognized to be important in the pathogenesis of cardiovascular disease including HF 7.

 The management of patients with chronic congestive heart failure has changed considerably during the last decade until recently, restriction of physical activity was recommended for patients with chronic heart failure patients. However, the knowledge that training influences largely the peripheral rather than the heart itself has led to a dramatic change in the approach toward training in patients with chronic HF 11. India has a rich tradition of yogic practices. Now-a-days yoga, the ancient practice of postures, breathing and meditation is gaining a lot of attention from health care professionals with increasing scientific research in yoga, its therapeutic aspects are also being explored 16. Yoga is known for its beneficial effects on physiologic and psychological functions. During the last 3 decades, extensive physiologic research   has been done on yogic practices. It has been reported that yoga can increase muscular efficiency, endurance time and aerobic capacity and can reduce perceived exertion after exercise. Yoga is widely used as a stress reliever. Additionally yoga has a profound effect on ANS and may reduce stress level in individuals via this effect. Regarding oxidative stress reports have suggested that yoga can decrease oxidative stress reduce the malandialdehyde level and increase superoxide dismutase activity and catalase activity 8. Slowing respiratory rates reduces dyspnoea and improves both pulmonary gas exchange and exercise performance in patients with CHF 17. In addition to allowing for a predominance of the parasympathetic state, yoga may also promote effective extraction of oxygen by peripheral tissues. When muscle is stretched, the O2 composition increases 1. Yoga may upregulate the antioxidant capacity of cells to combat oxidative stress. Regular yoga practice can maintain or improve antioxidant level of the body 8. Yoga may improve functional capacity and quality of life by lowering sympathetic response to physical activity, leading to a reduction in cytokines and oxidative stress 1. Despite yoga’s wide spread appeal, there is no data on whether the addition of yoga therapy improves symptoms of health related QOL in patients with compensated HF 3.

Relevant References:     

  1. Paula R.Pullen,Walter R.Thompson et.al., “Benefits of Yoga for African American Heart Failure Patients”. Medicine & science in sports & exercise  2010 ; 0195-9131/10/4204-0651/0.

2.    Jill Howie-Equivel , Jiyeon lee et.al., “Yoga in Heart failure : A Pilot study” , J Cardiac failure 2010 ; 16 : 742 – 749.

  1. Pullen PR, Nagamia SH, Mehta PK, et al. “Effects of yoga on inflammation and exercise capacity in patients with chronic heart failure”. J Cardiac Fail 2008;14:407e13.
  2. M ketih, A Germanmayegan et.al., “Increased oxidative stress in patients with congestive heart failure” J Am coll Cardiology 1998; 31; 1352-1356.
  3. Hiroyuki Tsutsu., “Mitochondrial oxidative stress and heartfailure novel pathological insight and treatment strategies” Currnt Cardiology Reviews, 2005,1 37-44.
  4. John W Petersen, Michael Felker et.al., “ Inflammatory Biomarkers in Heart failure” CHF 2006 ; 12 : 324-328
  5. Lenong L. Ng, “Targetting oxidative stress in heart failure” Heart Metab. 2009; 42:21-24.
  6. Snchari sinha, Som nath singh et.al., “Improvement of glutathione and total antioxidant status with yoga” The Journal Of Alternative and Complimentary Medicine” 2007, 13;10: 1085-1090
  7. Jozef bartunek “Biomarkers: old-new, cardiac-noncardiac, all paving the way for better stratification in heart failure” Biomarkers Med 2009;3(5):435-437
  8.  Miles D. Withmam, Ishabel S. Argo et.al., “Predictors of exercise capacity and everyday activity in older heart failure patients” The European Journal ofHeart Failure 8 2006; 203-207
  9.  Paul Dubach, Sebastian sixt et.al., “ Exercise training in chronic heart failure:Why,When,How” SWISS MED WKLY 2001;131 ; 510-514
  10.  Andrea Radzewitz,Eckart Miche et.al., “Exercise and muscle strength training and their effect on quality of life in patients with chronic heart failure” The Europen Journal of Heart failure 2002; 2 : 627-634
  11.  George Papathanasiou, Nikolaos Tsamis et.ai., “Beneficial Effects of Physical Training and Methodology of Exercise Prescription in Patients with Heart Failure” Hellinic J Cardiol 2008;49:267-277.
  12.  Carlene A. AHMILTON, William H. MILLER et.al., “Strategies to reduce oxidative stress in cardiovascular disease” Clinical Science 2004; 106: 219-234
  13.  R C Davis, F D R Hobbs et.al., “ABC of heart failure History and epidemiology” BMJ 2000; 320: 39-42
  14.  Kanwaljeet singh, Baljinder singh bal et.al., “The effect of suryanamskar yogasana on muscular endurance and flexidility among intercollege yoginis”  Journal of Physical Education and Sport” 2010;2:61-67
  15.  Luciano Bernardi, Giammario spadancini, “Effect of breathing rate on oxygen saturation and exercise performance in chronic heart failure” Lancet 1998; 351: 1308-11.

 

 
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