Heart Failure (HF) is a growing and challenging public health concern in the United States. Current data suggest that there are about 5 million heart failure patients in this country with an additional 550,000 patients being diagnosed with this syndrome each year for the first time. Despite the significant advances in the management strategy of heart failure patients in the last 1-2 decades, there are about 1 million hospital admissions each year for Acute Decompensated Heart Failure (ADHF), almost double the number seen 15 years ago. The readmission rate for these patients at 6-month following discharge approaches about 50% with estimated 5-year mortality of 50%. Approximately, $23 billion are spent for the inpatient management of HF patients with another $40 billion for outpatient care. This prevailing situation mandates further exploration of novel therapeutic targets to treat this complex disease.
Chronic HF is accompanied by a sustained elevation in sympathetic nervous system activity, which is thought to be an important component in the pathophysiology and progression of the disease. HF patients also show abnormal breathing pattern with an increased respiratory rate and a lower tidal volume. Faster respiratory rate is associated with higher levels of sympathetic activity and potentiation of the chemoreflex response to hypoxia and hypercapnia. The relationship between sympathetic activity and spontaneous breathing rate is independent of age, body mass index, physical activity levels, percentage of body fat, or blood pressure. The arterial baroreflex sensitivity is also reduced in patients with heart failure. All these factors contribute to the distressing symptoms of fatigue, dyspnea and exercise intolerance in these patients.
Yoga trainees learn to breathe slowly, at a rate of about six breaths per minute, mobilizing in sequence the diaphragm and the upper and the lower chest. A handful of studies in normal subjects undergoing intensive training in yogic breathing techniques have demonstrated a marked improvement in cardiac hemodynamic parameters (cardiac output, cardiac index, stroke volume etc.), but such studies have not been conducted in patients with heart failure.
The purpose of our study is to evaluate the changes in cardiac hemodynamic parameters (cardiac output, cardiac index and thoracic fluid content) in patients with acute heart failure, chronic ambulatory heart failure and normal healthy subjects after a trial of controlled slow breathing. Subjects would undergo non-invasive measurement of cardiac hemodynamics while spontaneously breathing. They would then be given instructions in slow breathing at a rate of 6 to 10 breaths per minute and asked to practice it for some time using heart rate variability as biofeedback mechanism. Hemodynamic measurements would be repeated during and after the trial of slow breathing. The difference between these measurements would then be statistically analyzed. We hypothesize that even a short trial of controlled slow breathing using a biofeedback mechanism in patients with HF would produce significant favorable improvement in cardiac hemodynamics.
