Yogatherapy in Ischemic Heart Disease

1. Ischemic heart disease: definition and relevance

A pathological condition characterized by a relative or complete disruption of the blood supply to the myocardium, the muscular layer of the heart, because of damage to the coronary arteries.

“From the Greek ischo, to restrain or stop, and haima, blood; synonym: coronary disease—a form of cardiac pathology comprising a group of diseases and pathological states whose principal causal factor is atherosclerosis of the coronary arteries. Under certain conditions this creates a mismatch between the myocardium’s need for blood and the amount of blood that can flow through the affected artery. Some researchers also include rare cases of ischemia and necrosis of a section of myocardium that arise for still unknown reasons while the coronary arteries remain unchanged.” — Great Medical Encyclopedia

Ischemia is a mismatch between a tissue’s need for oxygen and the oxygen actually delivered to it.

At present ischemic heart disease is one of the main causes of death worldwide, although the course of this disease and circulatory disease more generally varies between countries. World Health Organization data cited by the author showed a substantial decline in mortality in China and Korea, no change in Austria, Germany, and Sweden, and a substantial increase in post-Soviet countries and Russia compared with 1970. Climate alone would not explain the great differences between neighbouring countries such as Austria and Hungary, or Finland and Estonia.

Between 1979 and 1995, cardiovascular mortality in the United States fell by 26 percent; the paper notes that an opposite tendency was later being observed. A particularly marked difference appeared between Japan and Hungary. Before 1965 mortality in Hungary was lower than in Japan; later male mortality in Hungary rose, while women were affected less because of biological differences. At the time of writing Japan showed a negative cardiovascular trend while Hungary was a “leader” in mortality. In Israel mortality was approximately equal between men and women; France had the lowest mortality among women.

Ischemic heart disease is more frequent in developed countries. The paper associates this with technological progress, sedentary life, and a diet dominated by refined convenience foods. It argues that the domestic health system did not fully match the scale of the problem because a person with cardiovascular disease could not receive all needed care from one specialist. Heart diseases remained severe, while timely recognition and treatment reduced risk to life. These comments draw on Anatoly Vishnevsky, Evgeny Andreev, and Sergey Timonin, “Mortality from Diseases of the Circulatory System and Life Expectancy in Russia.”

Disability also raises acute questions of social adaptation. Comorbidities may worsen the underlying disease, and in the author’s view a disabled person in Russian society had fewer opportunities for self-realization, with psychological consequences. The author considered the problem’s relevance obvious and saw its complexity not only in disease but in human factors, state and commercial support for unhealthy lifestyles, and irresponsible conduct by local medical workers.

2. Etiology

Among the causes of ischemia, several “main” ones can be traced. The main triggering mechanisms, with a brief description, are presented below.

1. Disturbance of central hemodynamics (changes in arterial pressure and heart rhythm). The circulatory system is a collection of organs interacting precisely with one another. Changes in pressure or rhythm make negative adjustments to blood circulation and provoke ischemia, because stable and effective circulation is essential to sustaining life in every part of the body.
2. Blood loss. Both stroke volume and total circulating blood volume can fall, which also lowers arterial pressure and leads to ischemia.
3. Local arterial spasm. This can be a symptom of vegetative-vascular dystonia, which is an exclusively systemic disease and has an unquestionable influence on the quality of blood circulation.
4. Atherosclerosis. At the time of writing this is the most widespread cause of IHD. Dyslipidemia is the main factor in atherosclerosis and begins when the ratio of blood lipids—animal and vegetable fats—is disturbed. Lipids are deposited between the inner and muscular layers of the vessel wall; over time a plaque forms, the lumen narrows, and blood circulation becomes difficult or impossible.
5. Thrombosis and embolism. In one pathway an atherosclerotic artery suffers an endothelial rupture. The body uses platelets and fibrin—a fibrous protein substance that binds platelets—to form a blood clot and stop the “blood loss.” When a thrombus closes more than 75 percent of the arterial lumen, blood flow to tissue falls enough for hypoxia symptoms to appear. At more than 90 percent “obstruction,” ischemia and tissue necrosis may follow. Embolism is a typical pathological process in which particles not normally found in blood or lymph circulate and block a vessel. Types listed are: solid particles (tissue, microbes, parasites, foreign bodies); tissue and fat embolism, mainly after extensive severe trauma and long-bone fractures; liquids such as amniotic fluid or fat; gas or air during open-heart surgery, injury to large veins of the neck and chest, or decompression illness; bacterial embolism by accumulations of microbes; foreign bodies, mainly small fragments from gunshot wounds; thromboembolic disease, in which a detached thrombus or part of it lodges in the pulmonary artery or, in the systemic circulation, comes from deposits on valves or walls of the left heart; and medication embolism when an oily solution injected under the skin or into muscle accidentally enters a vessel, blocks an artery, impairs surrounding tissue nutrition, and causes necrosis.
6. External compression of an artery. This can occur with a neoplasm such as a tumour: the vessel is mechanically compressed and the capacity of a section of it is reduced.
7. Blood diseases. These are also an extremely significant factor in ischemia, because any pathological change in blood composition negatively affects the operation of the system as a whole.

3. Pathogenesis of the disease

Pathogenesis is “the mechanism by which a disease and its individual manifestations originate and develop.” When speaking about this mechanism, it must again be noted that an actual state of ischemia is reached when the balance between the myocardium’s real blood supply and its real need for blood supply is disturbed. As described above, many causes can start this pathological process.

Myocardial oxygen demand depends on the hemodynamic load on the cardiovascular system, the size of the heart, and the intensity of metabolism in cardiomyocytes (heart-muscle cells). The quality of oxygen delivery is determined by coronary blood flow, which can decline through both organic and functional disturbances in the coronary arteries.

The following pathogenetic mechanisms contribute to coronary insufficiency:

1. Organic obstruction of coronary arteries by an atherosclerotic process: infiltration of the wall by atherogenic lipoproteins and narrowing by plaques or a thrombus.
2. Dynamic obstruction of coronary arteries through coronary spasm caused by stimulation of alpha-adrenoreceptors.
3. Reduced adequacy of coronary dilation under local vasodilating metabolic factors—adenosine in particular—when myocardial oxygen demand increases.
4. Increased endothelial formation of procoagulant substances and factors that constrict arteries and increase platelet aggregation, including endothelin-1, together with inadequate production of prostacyclin and endothelium-derived relaxing factor, which dilate arteries and reduce platelet aggregation.
5. Increased platelet production of thromboxane, which increases aggregation and causes coronary spasm.
6. Increased platelet aggregation and formation of microaggregates in the microcirculatory bed.
7. Increased myocardial oxygen demand under intense physical exertion and emotional stress, which produce a high catecholamine release; excessive levels have a cardiotoxic effect.
8. “Intercoronary steal.” In people with stenosing atherosclerosis and developed collaterals, exercise-induced vasodilation increases flow in unaffected myocardium while reducing flow in areas supplied by affected coronary arteries.
9. Insufficient collateral circulation, especially when IHD develops at a young age.
10. Increased lipid peroxidation, modifying atherogenic lipoproteins and damaging endothelial function, including NO synthesis.

Endothelium-produced nitric oxide is involved in numerous physiological processes. In the cardiovascular system it regulates vascular tone; myocardial contractility; integrity and permeability of the endothelial layer; proliferation of smooth-muscle cells; adhesion and aggregation of platelets and leukocytes (monocytes) to endothelium; oxidation of plasma lipids; immune response through expression of chemotaxis and adhesion molecules on cell membranes; and degradation of circulating catecholamines and kinins. According to I. V. Zotova’s research as of 2002, a disturbance of nitric-oxide synthesis and metabolism plays the leading role in the pathogenesis of IHD.

Two further mechanisms are listed: development of immunological mechanisms—antibodies to myocardium, vascular-wall components, and atherogenic pre-beta and beta lipoproteins; sensitized T-lymphocytes to autoantigens from myocardium and vessel wall and to atherogenic lipoproteins; and increased cholesterol-containing immune complexes in the blood—and disturbed formation of endogenous opioid compounds, enkephalins and endorphins, as well as cytokines (interleukins) by immunocompetent cells.

On this basis, the main mechanisms of IHD are concluded to be coronary atherosclerosis, coronary spasm, microcirculatory disturbances, and coronary thrombosis.

Organic obstruction by atherosclerosis is then considered as the most common phenomenon. Practically the whole population of the planet is said to be susceptible to some degree. Besides initiating causes, risk factors stimulate and accelerate the process. Non-modifiable factors are heredity (cardiovascular disease in close relatives), age (men over 50 and women over 70), male sex, and physiological or surgical menopause. Modifiable factors are smoking, poor diet and disturbed lipid metabolism, diabetes mellitus, excessive alcohol intake, sedentary life, excess weight, high arterial pressure, and stress.

The paper repeats Zotova’s position that disturbed nitric-oxide synthesis and metabolism leads the vessel’s endothelial layer to structural change and partial loss of adaptation to external influences. Its integrity is lost, allowing monocytes—mature leukocytes with an unsegmented nucleus capable of engulfing large foreign particles—to penetrate and absorb accumulated lipoproteins. After absorbing lipids, the short-lived monocyte (three to four days) cannot return to the bloodstream, becomes a macrophage, and forms “colonies,” beginning an atherosclerotic plaque as a lipid spot. Plaque formation has many stages and takes years. The lumen does not change substantially at first, and pronounced symptoms do not appear until vessels narrow to a critical 70 percent of their original size. Symptoms depend on the degree of narrowing and on complete blockage of flow through the affected vessel.

4. Clinical presentation

Clinical presentation is “a conventional designation for the totality of a disease’s manifestations and the features of its course as the basis for diagnosis, prognosis, and treatment.”

The classical manifestations of ischemic heart disease are: pain behind the sternum, often radiating to the lower jaw, neck, left shoulder, forearm, hand, or back; pain that is pressing, compressing, burning, or suffocating and varies in intensity; provocation by physical or emotional factors and spontaneous cessation at rest; duration from 30 seconds to 5–15 minutes; and a rapid effect from nitroglycerin.

The symptom forms listed are stable exertional angina; unstable angina; primary myocardial infarction; recurrent myocardial infarction; repeat myocardial infarction; old, previously sustained myocardial infarction (post-infarction cardiosclerosis); sudden cardiac (arrhythmic) death; and heart failure resulting from myocardial damage due to IHD.

Angina pectoris

In 1772 the English physician William Heberden first offered the following description:

“...pain in the chest arising during walking and forcing the sufferer to stop, especially when walking soon after eating. It seems that if this pain were to continue or intensify, it could deprive a person of life; at the moment of stopping, all unpleasant sensations disappear. After the pain has continued to arise for several months, it no longer passes immediately upon stopping; and later it will continue to arise not only when the person walks, but when he lies down...”

Stable angina is a clinical syndrome characterized by episodic compressing or pressing retrosternal pain in response to a particular level of exertion. Unstable angina is the most severe period of exacerbation of IHD, threatening myocardial infarction or sudden death. In clinical manifestations it occupies an intermediate position between stable angina and acute myocardial infarction.

Myocardial infarction

By frequency of occurrence, the paper distinguishes primary, recurrent, and repeat infarction. A primary myocardial infarction is a focus of ischemic necrosis of the heart muscle. A recurrent infarction develops within eight weeks after the primary one. A repeat infarction develops within eight weeks after the previous one.

Post-infarction cardiosclerosis

This form of IHD manifests as replacement of part of the myocardial muscle tissue by connective tissue. It always develops as an outcome of myocardial infarction. Full healing of a necrotic area with scar formation takes about three weeks, and the diagnosis is therefore assigned automatically after this period.

Sudden cardiac (arrhythmic) death

Stable work of the heart muscle is provided by coordinated generation and conduction of electrical impulses through cardiomyocytes forming the cardiac conduction system, which provides the optimal rhythm of contractions. Disturbance of rhythm can cause sudden arrhythmic death.

Heart failure

Heart failure is described as a disease with a complex of characteristic symptoms associated with insufficient blood supply to organs at rest or during exertion and often accompanied by fluid retention. Chronic heart failure is based on a reduced ability of the heart to fill or empty, caused by damage to the heart muscle and by imbalance in systems that influence the cardiovascular system. These manifestations make up the clinical picture of IHD.

5. Review of diagnostic methods

The stated aims are to identify additional risk factors—high arterial pressure, blood cholesterol, signs of diabetes, and kidney damage; assess the state of the heart muscle; assess the coronary arteries; select treatment tactics; and predict whether heart surgery will be needed.

Additional risk factors can potentially be found at a cardiologist’s appointment by interviewing the patient or from an existing medical history. If that history contains no relevant information, the following tests are proposed.

Blood tests

1. Complete blood count. A universal laboratory diagnostic tool. Blood contains erythrocytes, leukocytes, and platelets performing different functions; their number is constant in a healthy person, and changes may indicate pathology.
2. Blood sugar (glucose). A laboratory method for detecting carbohydrate-metabolism disorders and diabetes by measuring glucose concentration in a fasting sample after at least eight hours without food.
3. Lipid profile. A set of specific blood tests that reveals disturbances in fat metabolism important for diagnosing atherosclerosis. Total cholesterol is the principal blood lipid, coming from food and liver synthesis; the stated normal range is 3.2–5.6 mmol/L. Low-density lipoproteins are described as an atherogenic, “harmful” cholesterol-rich fraction that can be retained in vessel cells and form plaques; stated normal LDL is 1.71–3.5 mmol/L. High-density lipoproteins are described as the one fraction preventing plaque formation by transporting cholesterol to the liver for disposal; stated normal HDL is above 0.9 mmol/L. Triglycerides are neutral fats in plasma; stated normal values are 0.41–1.8 mmol/L. The atherogenic coefficient expresses the ratio of atherogenic to anti-atherogenic fractions; its stated normal value is below 3.5.
4. Creatinine and urea. These reflect kidney function; evaluation is considered necessary because the kidneys are one link in the development of hypertension.

Urine tests

Proteinuria—an increased urine protein level—shows whether kidney damage exists. Microalbuminuria is albumin at low concentration and is described as recommended by then-recent studies as an additional IHD risk factor.

Diagnostic procedures

1. Measurement of arterial pressure for every patient. If results are doubtful, 24-hour monitoring or an exercise test may be prescribed.
2. Chest radiography to assess the size and shape of the heart and congestion in the lungs.
3. Resting ECG to reflect myocardial electrical activity and detect arrhythmias, myocardial infarction, and indirect signs of cardiac hypertrophy.
4. Holter ECG monitoring, continuous recording for 24 hours with a belt-mounted device and chest sensors while the patient lives normally and records the times of pain. This can capture abnormalities absent on a resting ECG.
5. Exercise ECG, recording ECG and blood pressure while the patient pedals a bicycle ergometer or walks on a treadmill. It evaluates general cardiovascular working capacity and, above all, distinguishes exertional angina from similar diseases involving heart pain.
6. Echocardiography, visual ultrasound assessment of heart function, identifying infarct zones, tissue thickening, enlargement, and valve function.
7. Coronary angiography. A long probe carries contrast from the femoral artery into the heart’s vessels, after which an X-ray visualizes plaque locations and the degree of narrowing and determines whether surgery is needed.

6. Brief review of modern treatment methods

Treatment of ischemic heart disease is directed toward restoring the balance between the heart’s need for oxygen and oxygen delivery by strengthening hemodynamics in the coronary arteries. The methods are divided into medication and surgery.

Medication methods consist of taking drugs every day. Frequency, quantity, and composition are prescribed according to the severity of the patient’s condition. The drugs are generally tablets taken orally.

Aspirin

When aspirin is taken daily or every other day, the risk of angina or a heart attack and the likelihood of blood clots are reduced. Aspirin reduces the possibility that a blood clot will form at the site of a platelet rupture in a coronary artery, described as the main cause of myocardial infarction. Side effects are ulcers and bleeding.

Beta-adrenoblockers

These reduce heart rate and blood pressure, thereby reducing the heart’s oxygen demand. The paper states that clinical studies proved that this could prevent heart attack and sudden death.

Nitroglycerin

This reduces chest pain, lowers the heart’s oxygen demand, and dilates the coronary arteries, increasing incoming oxygen. A spray or tablet under the tongue acts immediately when urgent help is needed during angina. Long-acting tablets or skin patches act slowly for several hours.

Calcium-channel blockers

These drugs dilate the coronary arteries and improve blood flow. They also reduce blood pressure and heart rate.

ACE inhibitors

The paper says angiotensin-converting enzyme dilates blood vessels and increases blood flow. It reports that recent studies showed ACE inhibitors reduced cardiac disease, attacks, and deaths among people with IHD independently of their blood-pressure-lowering property, perhaps by an additional favourable effect on vascular and heart-muscle tissue, especially in people with diabetes and a weakened heart muscle.

Statin

This reduces blood lipids—cholesterol and other fats. As a result, the vascular endothelium changes and formation or enlargement of “platelets” becomes less likely. Statins are said to slow or stop IHD and prevent repeat heart attacks. The paper states that clinical studies showed greater benefit immediately after a heart attack or threat of one, stabilizing “platelets” even before fat levels decline.

Surgical treatment

Coronary angioplasty. A strong guiding catheter is inserted into an artery in the groin or arm. A hair-thin wire is passed through it into a coronary artery, and an even thinner catheter follows the wire into the blocked artery. A tiny balloon at its end is inflated at the obstruction to widen the artery and improve flow. The “platelet” does not disappear; it is flattened and remains on the arterial wall, after which balloon and catheter are removed.

Brachytherapy. Radiation is applied to an obstructed section from a very small source placed inside or beside the artery. It is used when a patient has already had angioplasty or stent treatment.

Coronary artery bypass grafting. Obstructed sections are bypassed with vessels “borrowed” from the chest (internal thoracic artery), arm (radial artery), or leg (saphenous vein).

Minimally invasive coronary bypass. If only the anterior or right coronary artery needs bypass, a surgeon can replace the blocked artery with an artery from the chest through a small incision without fully opening the chest cavity.

Transmyocardial laser revascularization. An alternative for people for whom angioplasty or bypass is undesirable. Using a laser catheter, the surgeon makes several punctures in the heart muscle. These small holes permit new blood vessels to form. The procedure can be performed alone or with coronary bypass.

7. Review of contemporary scientific sources reflecting the effectiveness of yoga practice in this disease

Physical activity in ischemic heart disease — Scrutinio D., Bellotto F., Lagioia R., Passantino A.

A sedentary lifestyle is one of five main IHD risk factors alongside hypertension, abnormal blood lipids, smoking, and obesity. After acute myocardial infarction, risk factors continue to act synergistically on clinical progression and provocation of IHD. Regular exercise was observed to improve exercise capacity and quality of life, reduce symptoms, and lower the risk of new coronary complications in patients with IHD. Through favourable effects on coronary risk factors, endothelial dysfunction, inflammation, thrombotic tendency, autonomic tone, and myocardial ischemia, regular physical activity may help reduce new complications and death. Given the clinical benefits and documented cardioprotective mechanisms, the source says general practitioners and cardiologists should consider regular physical activity a genuine and effective form of therapy for patients with IHD. The text then carries the heading “Review of yoga-therapy methods in the main yogic traditions.” (Monaldi Arch Chest Dis., June 2005.)

Physical activity and the risk of ischemic heart disease and stroke in older adults: Cardiovascular Health Study

Basic principles suggest that older people practise physical activity to reduce cardiovascular disease, yet surprisingly few studies existed, especially for people over 75, whose capacity for some forms of exercise may decline with age. It was found particularly important for people over 75 to perform even simple exercise such as walking. The most positive effect was observed in the group walking at a particular stable speed for a defined distance. The studies offer empirical data supporting physical activity, especially walking, to reduce cardiovascular disease in older people. (Soares-Miranda, 12 January 2016.)

Physical activity levels and ischemic heart disease: analysis of epidemiological and supporting studies

IHD, a primary health problem in Western life, is caused by the interaction of several factors. Absolute proof of the contribution of physical inactivity is impossible because of the complexity of IHD and the impossibility of a definitive clinical trial under logistical and economic constraints. Despite these limits, existing epidemiological studies strongly suggest, but do not prove, that habitual exercise provides partial protection from primary or secondary IHD events and associated mortality. Experimental data support this hypothesis and point to possible mechanisms.

The epidemiological evidence also suggests that physical inactivity is probably not as strong an individual risk factor as high serum cholesterol, hypertension, and cigarette smoking, and that exercise’s protective effects can be overwhelmed by high levels of these major factors. Some evidence indicates that exercise can attenuate other risk factors directly and through associated weight loss. Epidemiological studies also suggest a relationship between activity and IHD indicators. The source says optimal effects on the ischemic heart require about 2,000 kcal per week of moderate-intensity dynamic exercise—for example, walking or jogging about 20 miles per week—or at least one hour of intermittent physical labour. Experimental studies suggest this amount provides enough stimulus for favourable change in HDL cholesterol and perhaps other risk factors, especially with weight loss. (Leon A. S., January 1985.)

8. Review of yoga-therapy methods in the main yogic traditions

In my view, the optimal rehabilitation method at the initial stage of recovery is to perform uncomplicated “vinyasas” at a calm, relaxed pace, guided by the patient’s well-being, with or without connected Ujjayi.

Static standing asanas

Long holds will oppose venous return. The wave-like contraction of the calf muscle, as in walking, strongly supports venous return, while holding the calf contracted for a long time will oppose it and increase pressure in the venous bed. This complicates the circulation and adds load to the heart. Although the heart is not the principal instrument maintaining circulation throughout the system, it participates sufficiently through left-ventricular systole, which pushes, and right-atrial diastole, which draws in. With short holds, standing asanas may have a beneficial effect on venous return and make the heart’s work easier.

Seated asanas and vinyasas

Because the body is seated—partly relieving the heart since it need not oppose gravity to pump circulating blood—it makes sense to avoid long holds. More attention should be given to opening the chest. The maximum tolerable physical load depends directly on maximum lung ventilation, and thus on respiratory-muscle development and mobility of the chest joints.

According to Sri Krishna Pattabhi Jois, vinyasas should also be performed between asanas. After an asana, a vinyasa releases tension from muscles and joints; forward and backward bends alternately activate the sympathetic and parasympathetic nervous systems. Increased muscle tone creates extra oxygen demand and resistance to blood circulation and therefore extra strain on the heart. Alternating contraction and relaxation of all muscle groups and pressure changes in joints, including spinal joints, bring complete or partial balance to circulation and the organism. Omitting vinyasas can produce ever higher tone in individual muscles or groups. Correct Upward-Facing and Downward-Facing Dog intensely open chest joints; Downward-Facing Dog, as a partial inversion, increases venous return from the pelvis while the heart is not overloaded because most venous blood remains in the legs. Omitting vinyasas will increase strain on the heart through elevated muscle tone and oxygen demand.

Backbends

Backbends make sense once the patient’s adaptation to physical load is obvious, because the exercise and its modifications have a sympathicotonic effect. At first they are better performed with equipment—a ball or bench—very calmly and in relaxation like Savasana. Despite mechanical action on the adrenal glands, the muscles can relax and cease obstructing circulation while the chest-opening effect remains.

Artem, this rehabilitation exercise was described by Dhirendra Brahmachari. I am not as experienced as you in cardiology, but I am not trying to fantasize either; I am simply developing the logic. If you consider backbends categorically contraindicated during rehabilitation, I will rewrite this point, since you are accepting the paper...

Smooth standing backbends with the arms stretching upward and backward, soft prolonged Ujjayi, and instructor support would also, in my view, be useful. The exercise would help open chest joints, while the chest’s suction effect during inhalation would benefit venous return. Mechanical action on the kidney area could also potentially have a positive effect and produce renin, raising arterial pressure—which is not recommended in IHD—but an increase in circulating blood volume would also increase kidney activity and then reduce circulating volume, relieving intense cardiac load. The instructor sets the intensity and depth.

Inverted asanas

At the initial recovery stage they should be performed only in modified form, if at all. In inversion, venous blood from the legs and pelvis—areas especially prone to stagnation and varicose nodes—returns to the heart under gravity. When varicosity causes one-way venous valves to atrophy, reverse outflow is intensified and blood rises only through the pressure of arterial blood. This also produces an oxygen deficit in the affected area and ultimately makes the heart work harder to deliver arterial blood where it is needed. There is more blood than necessary in the venous bed and correspondingly less in the arterial bed. Heart work intensifies because of lower stroke volume and reverse venous outflow; myocardial oxygen demand rises and ischemia becomes more likely.

With modified inversions, gravity returns venous blood to the heart without requiring it to expend substantial effort supporting venous return. Although large volumes arrive, the heart has a certain throughput capacity. Potential chamber dilation is not expected in this situation because the heart only temporarily restores lost throughput. Quality venous return relieves at least the left ventricle and right atrium. The left-ventricular muscle layer is stretched to some degree by the increased arrival of blood; the greatest stretch in diastole ensures the most effective contraction in systole, which the author calls training of the heart muscle in the literal sense.

Inversions can have sympathicotonic or parasympathetic effects. They are not allowed at the initial stage, but during rehabilitation the heart should experience load—not overload. Aerobic loads are optimal; inversions are not aerobic. If breathing is controlled, as practice requires, this exercise will not increase oxygen demand, or, if it does, only insignificantly, which the author considers useful and even necessary during rehabilitation.

Kapalabhati

It may be used traditionally—two exhalations per second for three minutes, three rounds—or much more slowly—one exhalation every two seconds for 30–60 seconds, two or three rounds. Minute respiratory volume will rise, leading to hyperventilation, then hypoxia, then ischemia; the risk of hyperventilation objectively exists. Kapalabhati can place the organism in hyperventilation under a certain performance regime.

A high-frequency version at 120 exhalations per minute is described as practically safe from hyperventilation because of functional dead space: the parts of the respiratory system without alveoli and therefore without gas exchange—the nasopharynx, trachea, and large bronchi. Lower in the bronchial tree there are alveoli; above them air returns unchanged. Part of inhaled volume therefore takes no part in exchange. Average functional dead-space volume is about 150 ml. Dead space explains why one cannot breathe through a long tube deep under water: lengthening the tube increases dead volume and removes a substantial part of respiratory capacity from exchange.

The shallower the breath in Kapalabhati, the smaller the tidal volume, the smaller total lung ventilation, and the farther from hyperventilation. At some point breathing operates only in dead space: air enters and leaves only passages without gas exchange. Hyperventilation then apparently cannot occur and “inhaled air will almost not reach the alveoli” (R. Schmidt and G. Thews). — A. Frolov

Other breathing techniques and bandhas

Uddiyana: performed intensely, its effect may be negative because wave-like abdominal pressure change also changes chest pressure and could damage an atherosclerotic plaque, reduce vessel capacity, and cause ischemia. Because it is performed with retention after exhalation, lack of oxygen may also provoke ischemia while muscles continue working and consuming oxygen. A soft Uddiyana partly supports venous return and makes the heart’s work easier; its gentle intestinal massage is also considered beneficial.

Agni Sara Dhauti is called contraindicated because its retained, wave-like chest-pressure changes could provoke another plaque rupture, thrombus, reduced or lost vessel capacity, and recurrent infarction. Ujjayi is permitted when unforced, prolonged, comfortable, soft, and quiet because it is assigned a parasympathetic calming effect. Bhastrika and Surya Bhedana are called contraindicated sympathicotonic techniques. Chandra Bhedana is said to activate the parasympathetic system. Nadi Shodhana without retentions is assigned a parasympathetic effect and called indicated. All breath retentions and locks are called contraindicated except Mula Bandha, which the paper calls a parasympathetic tool through action on the sacral “underwater” nerve plexus.

Relaxation and shatkarmas

Relaxation techniques are said to have reliably beneficial effects and are included in rehabilitation: meditation; Yoga Nidra for muscular and mental relaxation; Trataka as calming to the brain; Savasana for deep muscular relaxation; and chanting Om as calming to the frontal lobe involved in thought.

Trataka is also treated as a cleansing, parasympathetic shatkarma. Sutra and Jala Neti have no directed effect here but are not contraindicated and are considered useful for general tone. Basti could accelerate evacuation of faeces and “free” bodily energy for other needs. Vamana Dhauti is called contraindicated because it is sympathicotonic and entails oscillating chest-pressure changes. The author would not use Nauli for the same reasons. Varisara Dhauti is called contraindicated as a long-term sympathicotonic stress.

From the techniques offered by the yoga schools discussed, the author concludes that parasympathetic techniques are the basic component of rehabilitation. The schools do not offer fundamentally different approaches; the number and severity of cases, results, and accumulated experience shape the method.

The author returns separately to Sirsasana. It has many performance variations; while the classical form can unquestionably harm, a modified form may have a positive effect. “Since I must criticize, although criticism is not necessarily disagreement,” he disagrees with the great B. K. S. Iyengar for proposing Sirsasana in rehabilitation. Depending on the case, however, he would also base yoga-therapy principles on the methods of these teachers.

“I can only say that I have not lost faith in a miracle, and personal experience helps me maintain that faith. The health of a patient who trusts me is unquestionably above everything, and one unquestionably should not experiment by trying something new or merely following one’s feeling. But when one arrives at something through experience, that is the miracle. What worked for one may not work for another because of Ayurvedic constitution, age, and so on. It seems to me that the Teachers were not afraid to experiment, while of course relying on basic knowledge.”

9. Presentation of the proposed yoga-therapy methodology with rationale for its mechanisms

Initial work

First, a meeting must be held to establish every possible detail directly related to the disease and to the patient’s condition as a whole. All available test results should be requested. If they do not exist, the patient should be offered an exercise test, allowing the rehabilitation program to keep the patient within a safe heart-rate range by monitoring it.

Quality-of-life questionnaires such as SF-36 should also be completed. Initially this gives the fullest view of the patient’s condition; later it makes it possible to see and compare changes in condition and subjective well-being. To build the most effective program, the medical history must be studied in as much detail as possible because comorbid diseases can substantially affect program design. In other words, contraindications must be identified; otherwise the probability of harming the patient is extremely high.

In my view it also makes sense to determine the patient’s constitution according to Ayurvedic values. At minimum this permits more effective influence through an optimal diet and sleep regime. Although not primary, this is not unimportant in rehabilitation from any disease. After selecting the diet, body mass index should be calculated and considered when selecting physical load. BMI, age, state of the spine, exercise-test indicators, and medical history will reveal contraindications and inform a particular sequence of exercises and breathing practices.

Contraindications and physical practice

The main contraindication in this disease will be intensive use of sympathicotonic techniques. Parasympathetic techniques are the basic aspect of the rehabilitation program. At first practice is performed at a calm, comfortable pace with an accessible range of motion.

Begin with joint exercises accompanied by natural breathing. If the patient can perceive and follow, propose awareness of the pause between exhalation and inhalation and try to superimpose movement on the breath. A yoga-therapeutic Surya Namaskar is accompanied by natural breathing if awareness of the natural pause has not been learned. Allow 30 minutes if heart rate remains stable.

Every ten minutes the patient practices a five-minute Savasana, producing a calming effect and helping the circulatory system adapt. Heart rate is measured every three minutes to provide conditional control over the heart and avoid exceeding permitted indicators. Conclusions should not be based only on subjective feeling at the initial stage, because ischemia may occur without angina and in this context could have a fatal outcome.

As the organism adapts, the number of physical-exercise elements increases. Since aerobic load is optimal for this disease, which Yoga is not—unless it is Thailand and unless it is Ashtanga Vinyasa—it makes sense once or twice per week to increase practice intensity by increasing movement and breathing speed. Heart rate continues to be monitored to understand change or stability and adjust intensity during the session.

Modified inverted positions can begin: lying on the back with legs at 45 degrees on a wall bar, later increasing the angle to 90 degrees, and then placing a bolster under the sacrum. This is considered sufficient to ease venous outflow from the legs fully. Full inversion is contraindicated at the initial stage.

Backbends, despite their sympathicotonic effect, are allowed in certain forms: lying relaxed over a ball or standing with instructor support, raising and spreading the arms without reaching maximum range, easily and without tension. These move the chest joints and may eventually improve lung excursion and potentially relieve pressure around the heart. A spinal yoga-therapy sequence will be the basic practice.

Breathing practices

Breathing practices have an important place. Initially sympathicotonic techniques are not used. Begin with soft, prolonged Ujjayi for three to five minutes. After a brief two-minute Savasana, practise Bhramari for three to five minutes, Chandra Bhedana for about five minutes, and finally Nadi Shodhana without retentions or locks for five minutes. These are assigned a parasympathetic effect, which is the program’s main design principle.

Between every technique the patient remains in Savasana for two minutes. Daily practice therefore takes about half an hour and gently accustoms the respiratory, nervous, and circulatory systems to new states.

As adaptation develops, pranayama can be diversified. With stable monitored heart rate, a session can begin with Kapalabhati at one exhalation every two seconds for 40 cycles, gradually increasing from one to three rounds. The paper says this regime is not sympathicotonic while retaining positive effects: cleansing the upper airways, some influence on the brain through movement of exhaled air, and removal of stale air from the lungs. Full breathing performed calmly is assigned a parasympathetic effect and may be included. Soft Uddiyana at this stage is also considered useful for venous outflow. In my view, this is sufficient for breathing exercises during rehabilitation.

Relaxation techniques

Meditation is used throughout the program: initially 20 minutes in the morning observing inhalation and exhalation, and the same technique before sleep. Since meditation is intensive work with consciousness, short sessions help a person with no previous experience adapt mentally to longer practice. Over time the number of sessions is brought to the maximum and techniques are diversified. Laughter, crying, and gibberish meditations are not used because they most likely have a sympathicotonic effect.

Yoga Nidra is important because, despite mental activity, the practitioner can enter deep muscular relaxation. Savasana is also extremely important during and after physical load and during and after breathing exercises. It can sometimes be practised with a bolster under the thoracic spine, positively affecting chest-joint mobility.

Shatkarmas and load

Cleansing procedures can be used with contraindications taken into account. Sutra and Jala Neti have no targeted effect on this disease, but certainly will not harm general tone. Basti with lemon, apple vinegar, chamomile decoction, and other cleansing and calming compositions can be used for the same purpose. Trataka is a parasympathetic technique and will be used in daily 15-minute sessions.

The effect will depend on time and quality of technique. During rehabilitation it is important not to overdo intensity, with heart-rate monitoring as the indicator. It is also important not to “under-give” the load. Exercises will in any case have a positive effect, but an optimal result requires selecting the volume and intensity that keep the patient’s heart rate within the values found in the exercise test.

10. Practical case

This case occurred before the author completed the yoga-therapy course, so he could not apply knowledge acquired during the training. He states that Thai law did not permit this activity without documentation of qualification; the person undergoing rehabilitation was his brother.

The man was 43. Before his health crisis he drank alcohol excessively and smoked about one and a half packs of cigarettes daily. He stopped drinking and smoking after coronary bypass surgery. His work involved physical labour, but he had done no deliberate exercise for about 20 years. His Ayurvedic constitution was recorded as Kapha–Vata, 55–35 percent.

History: coronary bypass grafting after a pre-infarction state; left-ventricular hypertrophy; atherosclerosis; traumatic brain injury affecting the area associated with smell, scar formation, and complete loss of smell; low acidity; chronic pancreatitis; impotence; varicose veins; nephroptosis; osteochondrosis; “vegetative-vascular dystonia”; depression; and hypertension. An exercise test gave a heart-rate range of 115–125 beats per minute, monitored with a wrist device during exercise. He took many medications daily, including aspirin.

Program as reported

Mornings began with 40 minutes of breathing exercises: prolonged Ujjayi, Chandra Bhedana, and Nadi Shodhana, plus brief gentle Uddiyana while observing sensations around the heart and pancreas. After a 30-minute break came modified Surya Namaskar at an easy level, with periodic Savasana, for about 30 minutes in week one. Time and intensity increased with adaptation, subjective state, and heart rate.

After exercise he took a daily cold-water shower, which the author interpreted as a brief sympathetic stress mobilizing hidden resources. Because pancreatitis strongly influenced planning, he moved to small, tolerated vegetarian meals. He reported more energy after four days and regular morning defecation. Enemas with varying solutions were used every other night. He practiced 40 minutes of Yoga Nidra daily, interpreted as parasympathetic work that unloaded the heart and potentially affected hypertrophy. Every other day he practiced Vamana Dhauti, which the author linked to low acidity and digestive secretion.

Evening exercise included modified Surya Namaskar, backbends over a ball, long Savasana, and 20 minutes of Anapana meditation observing inhalation and exhalation. After ten days, with no pain around the kidneys, heart, or pancreas, Agni Sara Dhauti was added. As heart rate became stable and exercise tolerance improved, standing and seated postures and a Sarvangasana series were introduced gently with short holds and periodic Savasana. Blood pressure stabilized and the man stopped measuring it. He continued taking medication. Fresh cucumber and apple juices were added.

Wheatgrass juice was used once as an intestinal-transit indicator; green coloration reportedly took a week to pass, leading them to speculate about adhesions or obstruction. On day 14 lower abdominal pain appeared. They speculated that abdominal manipulation might have affected adhesions, so Uddiyana and Agni Sara were suspended. Pain resolved the next day. Other procedures continued, and supported Sirsasana on blocks for 10–30 breaths was added in the evening.

By day 20 he performed the full beginner Ashtanga Vinyasa sequence in 80 minutes, held Sirsasana for 2.5 minutes in the evening, and practiced morning pranayama for one hour. He began to smell acetone and reported the return of mild morning erections, then discomfort around the pancreas. Examination and palpation did not intensify the pain. Abdominal manipulations and inversions were stopped and the situation observed.

By the end of week four, the author recorded better general well-being, some ability to distinguish smells, full return of morning erections, stable blood pressure, disappearance of kidney-area pain, no observed depressive state, and new interest in philosophy and yoga history. Pancreatic-area pain persisted unchanged. Examination, palpation, and ultrasound found the pancreas normal; the source of pain remained unclear. A fasting rest day did not change it.

After a month the man left the centre and was examined in Russia. He reported an unspecified abnormality of the large intestine but gave no details.

Original summary

The flight from Thailand to Russia passed without blood-pressure measurement because no discomfort occurred. The author interpreted restored sexual function as a possible sign of circulatory stability, and considered exercise tolerance clearly improved. He attributed disappearance of kidney-area pain to strengthening of the renal bed and return of the kidneys to position, with a positive influence on circulating blood volume.

After returning to Russia the man stopped practice completely. At last contact blood pressure remained stable, the sense of smell had disappeared again, and no other information was available.

11. References

1. Iyengar, B. K. S. Light on Yoga: Clarification of Yoga. Moscow: Alpina Non-Fiction, 2017.
2. Iyengar, B. K. S. Yoga: The Path to Holistic Health. Moscow: Flinta, 2007.
3. Brahmachari, D. Yogasana Vijnana. Moscow: Prospekt, 2006.
4. Brahmachari, D. Yoga Sukshma Vyayama. Moscow: Sofia, 2000.
5. Lad, V. Ayurveda for Beginners. Moscow: FAIR Publishing, 2010.
6. Swami Swatmarama. Hatha Yoga Pradipika. Moscow: Aslan, 1994.
7. Solovyova, L. N. Ayurveda: Three Paths to Absolute Health. Bryansk, 2003.
8. Frolov, A. Yoga Therapy: A Practical Guide. Second expanded edition. Moscow: Orientalia, 2016.
9. Benito, D. P. Yoga for Prevention and Healing Myocardial Infarction. Mysore: Ananda Yoga India School of Bharat Shetty, 2014.
10. Desikachar, T. K. V. The Heart of Yoga: Developing a Personal Practice. India: Replika Press, 1995.
11. Feuerstein, G. The Encyclopedia of Yoga and Tantra. Boston and London: Shambhala, 2011.
12. Maharshi Gheranda, translated and commented by Swami Niranjanananda Saraswati. Munger: Yoga Publications Trust, 2012.
13. Jois, S. K. P. Yoga Mala. New York: North Point Press, 2010.
14. Khattab, K., Khattab, A., Ortak, J., Richardt, G., and Bonnemeier, H. “Iyengar Yoga Increases Cardiac Parasympathetic Nervous Modulation Among Healthy Yoga Practitioners.” Published online 27 October 2007. doi:10.1093/ecam/nem087.
15. Saraswati, S. N. Prana and Pranayama. Munger: Yoga Publications Trust, 2009.
16. Saraswati, S. S. Asana Pranayama Mudra Bandha. Munger: Yoga Publications Trust, 2013.