Explore: The Journal of Science and Healing
Volume 8, Issue 1 , Pages 12-15, January 2012

Effect of Pranayama (Breathing Exercise) on Arrhythmias in the Human Heart

Article Outline

Background

Cardiac arrhythmias, especially ventricular tachyarrhythmias are an important public health problem. QT dispersion (QTd), defined as the difference between maximal and minimal QT intervals, reflects the regional inhomogeneity of ventricular repolarization dispersion and may mark the presence of malignant ventricular arrhythmias.

Purpose

To determine the effects of Pranayama (breathing exercise) on QTd in patients with arrhythmia.

Patients

Fifteen patients with arrhythmia and ejection fractions <40% (mean = 28 ± 9%) who were on a stable medical regimen.

Design and Intervention

Standardized 12-lead surface ECGs were obtained at the beginning and end of the Pranayama session, and QT and JT intervals were measured manually and corrected for heart rate by using Bazett's formula. QTd, heart rate-corrected QTd (QTc-d), JT dispersion (JTd), and heart ratecorrected JTd (JTc-d) were measured in at least eight ECG leads in each patient.

Results

Following the Pranayama session, patients with arrhythmia had only slight improvements in exercise capacity (results were not significant). However, these patients had marked improvements in QTd (71 ± 11 to 59 ± 17 ms; P < .02), QTc-d (82 ± 28 to 63 ± 17 ms; P < .01), JTd (76 ± 19 to 57 ± 18 ms; P < .002), and JTc-d (84 ± 23 to 61 ± 18 ms; P < .001) following the Pranayama session.

Conclusion

These data indicate that Pranayama significantly reduces the indices of ventricular repolarization dispersion in patients with arrhythmia. Further studies are needed to evaluate how effectively this reduction in ventricular repolarization dispersion decreases the risk of malignant ventricular arrhythmias and sudden death in patients with arrhythmia.

 

Despite recent pharmacologic advances, ventricular arrhythmia remains a highly lethal disease, with annual mortality rates as high as 50%.1, 2 Approximately 50% of deaths in patients with mild arrhythmia and 25% of deaths in patients with severe arrhythmia are sudden and unexpected.3, 4 Sudden death in these patients is a massive problem with no definitive predictors.5

Studies have suggested that a standard 12-lead surface ECG can provide prognostic information, particularly when related to measurements of ventricular repolarization dispersion. The heterogeneity of ventricular repolarization dispersion, as measured by calculating the QT dispersion (QTd), which is the difference between maximum and minimum QT intervals on a 12-lead surface ECG, has been shown to be a marker of myocardial electrical instability and may predict sudden death.6 More recently, JT dispersion (JTd) has been shown to be a better predictor of sudden death in patients with myocardial infarction.7

The beneficial effects of pranayama in patients with arrhythmia are well recognized.8, 9 There is some evidence that physical training reduces QTd in patients following recent myocardial infarction.10, 11, 12, 13, 14, 15, 16 To our knowledge, however, there is no such data available for patients with arrhythmia.

The purpose of this study was to evaluate any beneficial effects that Pranayama (breathing exercise) has on the indices of ventricular repolarization dispersion by measuring QTd and JTd on a 12-lead surface ECG in patients with arrhythmia (ejection fraction, <40%).

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Materials and Methods 

Patient Population 

We retrospectively evaluated 27 patients enrolled in pranayama sessions at our institute. Entry criteria included the following: (1) the presence of arrhythmia as diagnosed by a clinical presentation along with echocardiographic evidence of depressed left ventricular function (ejection fraction, <40%); (2) the absence of active ischemia as revealed by a clinical examination or by the exercise testing at the time of enrollment; (3) a stable medical regimen for at least two weeks prior to starting session and during the entire session; (4) the absence of any recent coronary revascularization procedure (≤3 months); and (5) no history of myocardial infarction in the eight weeks prior to enrollment. Exclusion criteria included the following: (1) class IA or III antiarrhythmic medications; (2) the inability to complete the pranayama session; (3) the absence of sinus rhythm at entry or completion of session; and (4) a complete bundle-branch block of either kind.

Patient Demographics 

Twelve patients were excluded from the final analyses for various reasons, including a technically poor ECG (n = 7), the presence of ischemia on cardiopulmonary stress testing at the initiation of the study (n = 2), and the development of ischemia at the time of the follow-up ECG (n = 3). Fifteen patients (12 were male) were included in the final analysis (mean age = 68 ± 11 years; ejection fraction = 28 ± 9%). All patients were in the pranayama session and remained there until the end of the study. Twelve patients had arrhythmia secondary to ischemic cardiomyopathy, whereas the other three had arrhythmia secondary to nonischemic dilated cardiomyopathy. All patients were on a stable medical regimen of diuretics, angiotensin-converting enzyme inhibitors, and digoxin. The 12 patients with ischemic cardiomyopathy were also taking aspirin and nitrates. There were no changes made in the dosage of these medications during the training period. As a group, the patients with ischemic cardiomyopathy had a lower ejection fraction than did the patients with nonischemic dilated cardiomyopathy (mean = 26 ± 9% versus 37 ± 6%; P = .06).

Pranayama Session Protocol 

All patients completed the 12-week program (36 pranayama sessions). Each session consisted of various pranayama practices for 45 minutes. Names and duration of the pranayama practices included in the program are shown in Table 1. Exercise intensity was prescribed individually so that patients' heart rates were approximately 70 to 85% of the maximum heart rate.

Table 1. Name and Duration of Various Pranayama Included in Pranayama Session
Sr. No.Name of PranayamaDuration
1Bhastrika- pranayama10 minutes per day
2Kapalbhati pranayama10 minutes per day
3Anilom-vilom pranayama15 minutes per day
4Bhramari5 times a day
5Udgit pranayama5 times a day

Before entering the session, patients underwent symptom-limited exercise testing, which usually consisted of their using a ramping treadmill protocol. Breath-to-breath on-line gas analysis was performed by using a metabolic cart (MedGraphics CPX/d; Medical Graphics Corporation; St. Paul, MN), with incremental data collected every 15 seconds. Maximal oxygen consumption, anaerobic threshold, and metabolic equivalents were determined on the basis of established criteria.

ECG Measurements 

Standard 12-lead surface ECGs were recorded at the beginning of the study at a paper speed of 25 m/s and an amplifier gain of 10 mm/mV. All ECGs were examined by one observer blinded to the clinical status and the follow-up results. Measurements of QT, JT, and RR intervals were performed manually. The QT interval was measured from the beginning of the QRS complex to the end of the T wave at the level of the TP isoelectric baseline. Biphasic T waves were measured to the time of their final return to the TP isoelectric baseline. If U waves were present, the QT interval was measured from the beginning of the QRS complex to the nadir of the curve between the T and U waves. The JT interval was measured from the end of the QRS complex, which was defined as the point at which the QRS complex returns to the TP isoelectric baseline (J point), to the end of the T wave at the level of the TP isoelectric baseline. Extrasystolic and postextrasystolic cycles were excluded from the measurement. If the end of the T wave could not be reliably determined, or if the T waves were isoelectric or of very low amplitude, QT or JT interval measurements were not made, and these ECG leads were excluded from the analysis. In order to get reasonably standardized sets of ECG leads, a lower limit of eight or more technically adequate measurable leads per ECG was set for inclusion into the study. Heart rate-corrected QT (QTc) and JT intervals (JTc) were calculated by using Bazett's formula (QTc = QT/RR−1/2).17 The ventricular repolarization dispersions were determined by calculating the difference between maximum and minimum QT or JT intervals in each ECG, and they were termed QTd, heart rate-corrected QTd (QTc-d), JTd, and heart rate-corrected JTd (JTc-d). ECGs were recorded at the initiation and completion of the pranayama session.

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Results 

Changes in Metabolic Parameters 

Table 2 shows the changes in exercise capacity that occurred during the pranayama program in terms of the metabolic equivalents, maximum oxygen consumption, and anaerobic threshold. The exercise capacity increased from 4±1 MET to 5±2 MET after pranayama and peak oxygen consumption increased from 15±4 mL O2/kg/min to16±6 mL O2/kg/min after pranayama, which did not reach statistical significance, whereas the anaerobic threshold remained the same 12±4 mL O2/kg/min after pranayama.

Table 2. Changes in Metabolic Parameters and Exercise Capacity Associated with Pranayama Session in Patients with Arrhythmia
Exercise StatusExercise Capacity, METsAnaerobic Threshold, mL O2/kg/minV̇O2max, mL O2/kg/min
Before pranayama session4±112±215±4
After pranayama session5±212±416±6
P valueNSNSNS

n = 15. Values are expressed as mean ± SD.

METs = metabolic equivalents, V̇O2max = maximal oxygen consumption; NS = not significant.

ECG Analysis 

Table 3 shows paired t test results from the QTd, QTc-d, JTd, and JTc-d. Although parameters of exercise capacity showed no significant increases, there were statistically significant decreases in all intervals at the completion of the pranayama program At the completion of the pranayama training, QTd decreased from 71±11 ms to 59±17 ms, QTc-d decreased from 82±28 ms to 63±17 ms, JTd decreased from 76±19 ms to 57±18 ms, The greatest decrease was seen in JTc-d, which had an absolute average reduction of 23 ms from 84±23 ms to 61±18 ms.

Table 3. Paired t Tests Showing Changes in Repolarization Dispersion Associated with Pranayama Session in Patients with Arrhythmia
Exercise StatusQTdQTc-dJTdJTc-d
Before pranayama session, ms71±1182±2876±1984±23
After pranayama session, ms59±1763±1757±1861±18
P value<.02<.01<.002<.0007

n = 15. Values are expressed as mean ± SD.

Repolarization Dispersion and Etiology of Heart Failure 

As shown in Table 4, we analyzed the differences between the indices of ventricular repolarization dispersion before and after exercise training, and we divided the results according to the etiology of heart failure. At the TP isoelectric baseline, QTd, QTc-d, JTd, and JTc-d were higher in patients with nonischemic dilated cardiomyopathy (n = 3) than they were in patients with ischemic cardiomyopathy, but statistical significance was not reached. This difference persisted following pranayama training when the magnitude of change in patients with nonischemic dilated cardiomyopathy was much more pronounced (Figure 1); however, statistically significant improvements were noted in the 12 patients with ischemic cardiomyopathy.

Table 4. Repolarization Dispersion in Ischemic Cardiomyopathy and Nonischemic Dilated Cardiomiopathy, Before and After Pranayama Session
CardiomyopathyQTdPreQTdPostQTc-dPreQTc-dPostJTdPreJTc-dPost
Ischemic (n = 12)69±1262±1581±3167±1675±2158±19
Nonischemic dilated (n = 3)77±647±2185±1346±1680±1053±15
P value.3.1.8.06.7.6

Values are expressed as mean ± SD.

Pre = before exercise training; post = after exercise training.

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Discussion 

The exercise capacity increased from 4±1 MET to 5±2 MET, or approximately 25% after pranayama training. Although the patients in this cohort had only modest improvements in exercise capacity following the pranayama session, our data demonstrate that their indices of ventricular repolarization dispersion were markedly reduced; hence, the patients' risk of having malignant ventricular dysrhythmias or experiencing sudden cardiac death could have been reduced as well.

The precise mechanism behind the increases in the homogeneity of ventricular repolarization dispersion remains elusive. The duration of the action potential is primarily responsible for the time span of the repolarization. Cells isolated from failing human and animal hearts reveal action potentials that have a significantly longer prolongation than the action potentials in normal hearts, an effect that is independent of the underlying cause of arrhythmia.18 If the prolongation of action potential were homogeneous, it would not necessarily produce an arrhythmogenic milieu.19 But variations in the duration of the action potential would create a ventricular repolarization dispersion that could be arrhythmogenic.20 Regional differences in the density of potassium currents have been demonstrated in human hearts.21 It is conceivable that the reductions in the densities of currents generated by repolarization in the failing heart are nonuniform, thus creating regional differences in repolarization.20

Influences of the autonomic nervous system on QT dispersion are well demonstrated.22 The heterogeneity of sympathetic innervation is well described in patients with heart failure and may contribute to the heterogeneity of repolarization.23, 24 Patchy myocardial fibrosis causing local disturbances in repolarization may also be a contributing factor in some cases.6

Pranayama practice restores the heart rate variability, increases the vagal tone, and reduces the sympathetic tone in patients after myocardial infarction.25 This beneficial effect of breathing exercise is also demonstrated in patients with chronic heart failure (CHF).8, 26 In addition, the favorable effect that exercise training has in reducing QT dispersion has been demonstrated in patients following myocardial infarction.10 This improvement in the autonomic profile may be one of the mechanisms responsible for reducing the ventricular repolarization dispersion, as measured by QTd and JTd in our study group of patients with arrhythmia.

In a study of 163 patients with CHF due to ischemic cardiomyopathy and nonischemic dilated cardiomyopathy, Fu et al.27 found that JTc-d is a powerful independent predictor of sudden cardiac death. A cutoff value of 85 ms for JTc-d had a 74% positive and a 98% negative predictive accuracy in identifying risk for sudden cardiac death. The mean value of JTc-d in our study group was 84 ms, which is quite similar to that of the cohort in the study by Fu et al.27

There were differences between patients with ischemic cardiomyopathy and patients with nonischemic dilated cardiomyopathy in that their indices of ventricular repolarization dipersion differed at the TP isoelectric baseline and following session. Patients with nonischemic dilated cardiomyopathy seemed to have more pronounced improvements following exercise in QTc-d and JTc-d than did patients with ischemic cardiomyopathy; however, the small number of patients with nonischemic dilated cardiomyopathy in our study group (n = 3) makes interpretation of these findings difficult.

Measurements of QTd may provide an advantage over those of heart rate variability in clinical settings. A limitation in using heart rate variability as an index of the effect of the autonomic nervous system on the ventricle is that it is indirect, reflecting changes in the RR interval by way of reflex mechanisms mediated by the sinus node. The QT interval is an index of ventricular repolarization dispersion that is directly influenced by myocardial health and autonomic nervous system activity. Therefore, variability of the QT interval should predict cardiac risk more directly and accurately than variability of the RR interval does.20

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Conclusion 

Following a Pranayama training program, JTc-d decreased by an average of 23 milliseconds, with other indices of ventricular repolarization dispersion significantly improving as well. These marked improvements may translate into substantial clinical benefits, but prospective data in a large patient population are needed to confirm this.

Our study adds to the evidence of the beneficial effects of pranayama training in patients with arrhythmia. Measurement of QTd and JTd on a surface ECG is a noninvasive technique that seems to reflect the risks of malignant ventricular dysrhythmias and sudden cardiac death. Although marked improvements were noted in indices of ventricular repolarization dipersion following exercise training in patients with CHF, large-scale prospective trials are needed to validate these findings and to determine whether these improvements translate into significant reductions in major cardiac events.

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References 

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PII: S1550-8307(11)00283-7

doi:10.1016/j.explore.2011.10.004

Explore: The Journal of Science and Healing
Volume 8, Issue 1 , Pages 12-15, January 2012

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