Scientific Basis for Ayurvedic Therapies -35

Scientific Basis for

Ayurvedic Therapies 

edited by

Brahmasree Lakshmi Chandra Mishra

The major causes mentioned are unhealthy lifestyle, lack of physical exercise, excessive

indulgence in sleep, and sedentary habits.

In conventional medicine, the etiopathogenesis of IHD includes hyperlipidemia,

increased waist-hip ratio, hypertension, insulin resistance, stress, smoking, alcoholism,

and environmental pollution. Risk factors are causally related to the development of IHD

but do not imply that they are causal to all IHD; they merely indicate that they are the

determinants of the disease in a sufficiently large number of individuals in the population

studied.

30.5.1 Risk Factors for Ischemic Heart Disease

The differences in the incidence and prevalence of coronary artery disease among countries

have stimulated the search for factors that might predict the development of the

disease. These are now referred to as risk factors. They include not only the physiochemical

characteristics of the individuals, but also certain aspects of lifestyle such as

diet, smoking, and behavior patterns. It is hoped that the discovery of such risk factors

might help in the effort to prevent coronary heart disease. According to the World Health

Organization (WHO) (1985), the major modifiable risk factors associated with IHD are

serum cholesterol, cigarette smoking, high blood pressure, obesity, lack of physical

activity, and diabetes.

It is recognized that the association of these variables with the disease did not establish

any etiological relationship. Unfortunately, a high proportion of patients who develop

CVD do not have any treatable risk factors. Furthermore, a large proportion of patients

with risk factors do not develop the disease. Most of the reversible risk factors are predictive

of coronary artery disease only in relatively young people; this suggests that in

older people the disease process is principally related to aging rather than one of the

avoidable risk factors.

30.6 Pathogenesis and Pathology

In Ayurvedic texts, the causes of IHD are the intake of excessively hot, heavy, sour,

astringent, and bitter food; physical exhaustion; injury; habitually taking food before the

previous meal is digested; worry; and suppression of natural urges. When vitiated dosas

located in the heart afflict blood (rasa dhatu) to cause pain in cardiac region, the condition

is called heart disease. It is caused by the obstruction to the coronary arteries (dhamanis)

of the heart muscles. Because the heart muscles consume a huge amount of energy, they

need ceaseless nourishment, meaning they demand a good supply of blood. Any impairment

of these blood vessels interferes with adequate blood flow to the heart muscles. If

its blood flow is significantly diminished, then the heart signals its difficulties by registering

pain or discomfort in the chest. The vata located in the heart being obstructed by

kapha and pitta interacts with blood nutrients (rasa), causing pain, fainting, and (cardiac)

obstruction.

In conventional medicine, IHD implies structural and functional abnormalities of the

heart as a consequence of an inadequate supply of blood to its tissue. The heart suffers

from ischemia when the blood supply to the heart is decreased, either due to increased

demand or decreased supply or more commonly due to a combination of both these

factors. Ischemia is caused by the insufficiency of oxygen and reduced availability of

nutrient substrates and inadequate removal of metabolites.4 Once IHD develops, the cells

of the cardiac muscles suffer from a lack of O2 and nutrition, which may be critically low.

The condition is manifested as angina pain. This critical reduction of blood supply is

corrected either spontaneously, by resting, or by drugs. In conditions like unstable angina

and acute myocardial infarction, more aggressive intervention procedures like thrombolytic

drugs and surgical procedures are required to restore coronary blood flow.6

IHD is composed of four clinical syndromes caused by myocardial ischemia: angina

pectoris, acute myocardial infarction, chronic postischemic cardiac failure, and sudden

ischemic cardiac death.4 The four major pathogenic components of IHD are based primarily

on the consideration that the chronic atherosclerotic background determines manifestation

and outcomes of IHD. In addition, the components are also based on multiple acute

stimuli that cause transient or persistent myocardial ischemia and the heart’s response to

ischemia. The pathogenic components of IHD, with their individual etiologic and pathogenic

components, collectively cause the four major ischemic syndromes and determine

their outcomes. The most common cause of IHD is atherosclerotic, the narrowing of the

coronary arteries.

30.6.1 Atherosclerosis

This is a pathological condition that underlines several important disorders, including

coronary artery disease, cerebrovascular disease, and disease of aorta and peripheral

arterial circulation. It involves lesions of the intimal layer of the wall of epicardial coronary

arteries regardless of its nature or pathogenetic and etiologic mechanism. Serum lipids

play a significant role in the genesis and progression of atherosclerosis; low-density lipoprotein

(LDL) cholesterol is an especially strong atherogen. Recently, it has been documented

that oxidation of LDL molecules is needed for its atherogenic action.7,8

The variable severity of coronary atherosclerosis may result from various types of intimal

injury, a variable combination of smooth muscle cell proliferation and lipid ground substance

deposition, fibrinogen and fibrin deposition, and from thrombus organization.

Stimuli may suddenly reduce regional coronary blood flow, transiently or persistently

causing coronary constriction, thrombosis, or both. Weaker stimuli may be sufficient to

cause ischemia in the presence of a severe atherosclerotic background. Flow limiting

stenosis can reduce the coronary flow reserves and cause ischemia when the increase in

myocardial demand is excessive. The responses of the heart to ischemic insult in terms of

the development of collateral blood flow are angina, ischemia, necrosis, heart failure, and

fatal arrhythmias. Of these components of IHD, undoubtedly the most important is the

development of ischemic stimuli. The chronic atherosclerotic background and the response

of the heart predispose or modulate the effects of ischemic stimuli.

30.6.2 Natural Course of Myocardial Ischemia

Inadequate oxygenation causes disturbances in the cardiac function. When ischemic events

are transient, they may cause angina pectoris. If prolonged, they can lead to irreversible

injury to the affected part (myocardial infarction). Reestablishment of blood flow or reperfusion,

either spontaneous or drug- or surgery-induced, constitutes the only rational

therapeutic option for IHD. But it is an established fact that reperfusion of the ischemic

myocardium carries with it some detrimental effects that contribute significantly to the

delayed or loss of functional recovery of the heart.9 The whole phenomenon has given

birth to a well-known entity called ischemic reperfusion injury.10,11

Ischemic reperfusion injury is responsible for delayed or loss of recovery of cardiac

function depending on the duration and extent of preceding ischemia. If the ischemic

period is brief and is not associated with any irreversible myocardial injury, reperfusion

can cause myocardial stunning or postischemic myocardial dysfunction of a relatively

short duration (weeks to months). On the other hand, reperfusion of irreversibly injured

myocardial cells causes permanent loss of cardiac function. It is now well established that

ischemic-reperfusion injury plays a major role in the natural course of almost all forms of

IHD, such as exercise-induced angina, variant angina, unstable angina, acute myocardial

infarction with early reperfusion, coronary angioplasty, coronary graft surgery, and cardiac

transplant.6

30.7 Diagnosis and Prognosis

Ayurvedic diagnosis of heart diseases is made by observing the clinical features, description,

history, location, and characteristics of the pain as described in Section 30.3. In modern

medicine, IHD is diagnosed by physical and laboratory examinations, ECG, stress testing

(treadmill testing), and coronary arteriography.

30.7.1 Physical Examination

The patient’s appearance may reveal signs of risk factors associated with atherosclerosis

or diabetic lesions along with signs of anemia, thyroid disease, and cigarette smoking.

Palpitation can reveal thickened or absent peripheral arterial pulse, which are signs of

cardiac enlargement and abnormal enlargement of cardiac impulse. Examination of the

eyes may reveal increased light reflexes and arteriovenous nicking as evidence of hypertension,

whereas auscultation can uncover arterial bruits; a third or fourth heart sound;

and, if acute ischemia or previous myocardial infarction has impaired papillary muscle

function, a late epical systolic murmur. These disorders may cause angina even in the

absence of coronary artery disease.

30.7.2 Laboratory Examination

Urine is examined for evidence of diabetes mellitus and renal disease. Blood is examined

for measurements of lipids (cholesterol, total HDL, and LDL), glucose, creatinine kinase,

and lactate. A chest x-ray is performed to find gross structural changes secondary to IHD

(i.e., cardiac enlargement, ventricular aneurysm, or signs of heart failure). Chest fluoroscopy

is done to identify the calcification of the coronary arteries.

30.7.3 Electrocardiogram

A 12-lead ECG recorded at rest is normal in about half of the patients with typical angina

pectoris, but there may be signs of an old myocardial infarction. Serial tracings are particularly

useful to look for past or evolving myocardial infarction. They show repolarization

abnormalities (i.e., T-wave and ST segment changes) and intraventricular conduction

disturbances at rest, which are suggestive of ischemic heart disease; they are nonspecific,

because they can also occur in pericardial, myocardial, and valvular heart disease. Typical

ST segment and T-wave changes that accompany episodes of angina pectoris and disappear

thereafter are more specific.

30.7.4 Stress Testing

The most widely used test in the diagnosis of IHD involves recording the 12-lead ECG

before, during, and after exercise on a treadmill or using a bicycle ergometer. The test

consists of a standardized incremental increase in external workload while the patient’s

ECG, symptoms, and arm blood pressure are continuously monitored. Performance is

usually symptom limited and the test is discontinued upon evidence of chest discomfort,

severe shortness of breath, dizziness, and fatigue.

30.7.5 Coronary Arteriography

This invasive diagnostic method outlines the coronary anatomy and can be used to detect

important evidence of coronary artherosclerosis to assess the severity of obstructive lesions

in the major arteries. Coronary arteriography is indicated for the following:

1. Patients with chronic stable or unstable angina pectoris who are severely symptomatic

despite medical therapy and being considered for revascularization (i.e.,

percutaneous transluminal coronary angioplasty or coronary artery bypass graft

surgery)

2. Patients with troublesome symptoms that present diagnostic difficulties in whom

there is need to confirm or rule out the diagnosis of coronary artery disease

3. Patients suspected of having left main stem or three-vessel coronary artery disease

based on signs of severe ischemia on noninvasive testing, regardless of the presence

or severity of symptoms

30.7.6 Echocardiography

A two-dimensional echocardiography records the image of the left ventricle (LV), which

can identify regional wall motion abnormalities due to myocardial infarction or persistent

ischemia. This test can also be used as an aid in the diagnosis of IHD.

30.8 Therapy

In Ayurvedic texts, the treatment for all heart diseases is offered to promote biofire (agni)

and to purify the channels by panchakarma in addition to using natural palliative herbs

that have hypolipdemic and antistress activity. For heart diseases with a specific vitiated

dosa, herbs known to mitigate that dosa are given in the form of a decoction or medicated

A few examples of decoctions, medicated ghee, paste, and powders for each type of

heart disease as given in Ashtanghradaya Samhita text are cited here just to show the historic

use of the formulas. Some of these formulas are still used.

30.8.1 Vataja Heart Disease

1. Water decoction of punarnava (Boerhovia diffusa), devadaru, pancamula, rasna (Pluchea

lanceolata), barley grains, bilva (Aegle marmelos), kulattha (Dolichos biflorus), and kola

2. Medicated ghee prepared with the paste of haritaki (Terminalia chebula), sunthi,

(Zinziber officinale), puskaramula (Iris germanica), vayahstha, guduci (Tinospora cardifolia),

kayastha, amalaki (Tinospora cardifolia), salt, and asafetida

3. Powder of dadima (Punica grantum), black salt, sunthi, asafetida, and amlavetasa

4. Paste of puskarahva, sathi (Hedychium spicatum), sunthi, root of bijapura and haritaki

mixed with ksara (yavaksara), and ghee

5. Decoction of yavani, salt, ksara, vaca (Acorus calamus), ajaji (Cuminum cyminum),

ausadha, putidaru, bijahva, palasa, sathi, and pauskara

6. Powder of pancakola (pippali, pippalimula, cavya, citraka, nagra), sathi (Hedychium

spicatum), pathya, guda (jaggery, molasses), bijahva, and pauskara made into a paste

with varuni (a kind of liquor) fried in yamaka (mixture of oil and ghee) and added

with salt

7. Decoction of sunthi or varuni, thin liquor of dadhi (curds), or fermented water

boiled with corn and made into a drink

ghee. These herbs are listed in Appendix 2.

8. Bala taila or sukumara or satapaka yasti taila or mahasneha

9. Decoction or paste of rasna, jinaka, jivanti (Leptedenia reticulate), bala (Sida cordifolia),

vyaghri, punarnava, bharangi (Cleodendron serratum), sthira (Desmodium gangeticum),

vaca, and vyosa, one fourth part of dadhi, and sour liquids

10. Warm oil mixed with sauviraka, curd water, buttermilk, and salt

11. Paste of puskaramula, sunthi, and sati mixed with alkali, water, dehydrated butter,

and salt

12. The paste of haritaki, sathi, puskaramula, pancakola, and matulunga fried in yamaka

and with jaggery, clear wine, and salt

13. Pippalyadi curna is given along with the decoction of triphala, dhanyamla (a sour

drink), decoction of kulattha, curd, madya (alcoholic drink), asava (a type of fermented

drink). The constituents are powders of pippali, ela, vaca, asafetida, yavaksara,

saindhava, sauvarcala, sunthi, and ajmoda (Carium roxburghiana).

30.8.2 Pittaja Heart Disease

1. The treatment is directed to mitigate pitta. Purgation is given with the juice of

draksa (Vitis vinifera), Iksu (Saccharum officinarum), sita (Santalum album), ksaudra,

and parusaka. Along with this emetic therapy is given with sriparni, madhuka

(Glycyrrhiza glabra), honey, sugar, and jaggery and is mixed with water.

2. Medicated ghee is prepared with the decoction or paste of sreyasi, sugar, draksa,

jivaka, rsabhaka, utpala, balam kharjura, kakoli and meda yugma with milk, and ghee.

3. Medicated ghee is prepared with the decoction or paste of prapaundarika, madhuka,

bisagranthi, kaseruka, sunthi, saivala, and milk.

4. Milk is boiled with the decoction of the bark of T. arjuna along with the sugar and

decoction of Pancamula, or Madhuka.

5. Powder of the bark of Terminalia arjuna along with ghee, milk, or jaggery.

30.8.3 Kaphaja Heart Disease

The patient suffering from kaphaja hridroga is given emetic therapy with the help of the

decoction of vaca and nimba and pippalyadi curna. A decoction of T. arjuna, as well as other

treatment given for kaphaja heart disease, is given as a palliative treatment.

30.8.4 Tridosaja Heart Disease

The patient is given a fasting therapy followed by a diet that is suitable for all three dosas.

After ascertaining less aggravated, more aggravated, and moderately aggravated dosas,

the patient is given the following therapies that will balance all dosas:

1. Wheat flour and T. arjuna bark powder boiled with oil, ghee, and jaggery and a

diet of milk as well as rice

2. A mixture of equal parts of fine powder of asafetida, ugragandha (Acorus calamus),

vida, visva, krsna, kustha (Soussera lappa), citraka (Plumbago zeylanica), and yav ksara

mixed with sufficient quantity of sauvarcala and puskaramula along with barley

3. Decoction of dasamula mixed with salt and ksara (alkali preparation)

4. A mixture of equal parts of fine powder of patha, vaca, yava, haritiki, amlaki (Phyllanthus

emblica), vetasa, duralabha (Fagonia arabica), citraka, tryusana, triphala, sathi,

puskaramula, tintidi, dadima (Punica grantum), and root of motulunga

30.8.5 Parasitic (Kramija) Heart Disease

The patients are given rice cooked with meat and ghee along with curd and patala. After

3 days, purgation therapy is given. Dhanyamla mixed with herbs, salt, ajaji, sugar, and

vidanga is also prescribed.

1. Vallabha ghrta — Ghee should be cooked with 50 matured fruits of haritaki and

two palas of sauvarcala (a kind of salt).

2. Baladya ghrta — Ghee is cooked with the decoction of bala, nagabala, and T. arjuna

and one fourth in quantity of the paste of yastimadhu (Glycyrrhiza glabra). (It is

good in rakta-pitta condition.)

3. Arjuna Ghrta — Ghee is cooked with the paste and juice (or decoction) of T. arjuna.

Most of the Ayurvedic formulations contain the bark of T. arjuna. It is one of the most

popular Ayurvedic herbs being used by the Ayurvedic practitioners for the prevention

and management of various CVDs. The stem bark of this plant is used for medicinal

purposes. This herb has been scientifically evaluated and has sufficient data to support

its use in IHD. The other herbs found useful in IHD are Aloe vera, Coleus forskohlli, Inula

recemosa, Andrographis panicilata, Centella asiatica, Piper longum, Picrorhiza kurrora, and Commiphora

mukul. These herbs have also been scientifically evaluated and found to be useful

in the management of IHD. Patent herbal formulas such as Abna, Hartone, and Lipistat

that contain several herbs are also commercially available.

30.9 Scientific Basis

Pharmacological and clinical investigations are reviewed to explore the scientific basis for

the use of Ayurvedic therapies. Clinical and biological studies on several botanicals, including

Crataegus oxycantha, T. arjuna, Inula racemosa, and Astragalus membranaceus, have been

reviewed and found to have therapeutic benefit for the treatment of CVD.12 The studies are

primarily focused on cardioprotective effects against chemical or biological injuries of the

heart. The effects studied include anticoagulant, angiogenic, antiatherosclerotic, anti-infarction,

blood vessel endothelium protection, and anticholesterol. All these effects are, directly

or indirectly, cardioprotective. They can be useful in the management of IHD.

30.9.1 Terminalia arjuna

30.9.1.1 Animal Studies

T. arjuna has been a major treatment for IHD in Ayurveda. Because anticoagulants have

been found useful in IHD, T. arjuna was investigated for a possible anticoagulant activity.

An emulsion of T. arjuna bark powder (10 g/kg) was given to rabbits orally for 7 days at

the dosage of 10 g/kg body weight. The treatment caused a significant increase in prothrombin

time (20 sec vs. 10.01 sec) and decrease in platelet count (44 vs. 473/thousand).

In a similar study13–15 with the alcoholic extract, there was no change in prothrombin time.

A water-soluble portion of the total alcoholic extract of T. arjuna was found to cause an

increase in the force of contraction of a frog heart.16 In later studies,17,18 both negative and

positive ionotropic effects were observed in isolated perfused frog and rabbit hearts and

isolated frog and rat atria. It was suggested that the extract consists of a mixture of

subsatances capable of exerting both positive and negative ionotropic effects.19 The aqueous

extract of T. arjuna was also found to produce dose-dependent sustained hypotension

and bradycardia in dogs.20 Intracerebroventricular and intravertebral injection of the

extract in chloralose anesthetized dogs caused hypotension and bradycardia in doses as

small as 1/10th and 1/20th, respectively, of the intravenous dose. Prior bilateral vagotomy

blocked the bradycardia, associated hypotension, and the ability of the intravertebral dose

of T. arjuna to produce these effects in a lower dose. These observations led the authors

to propose that the active constituent in the extract acts centrally.20 The hypotensive effect

of the alcoholic extract in dogs is abolished by pretreatment with atropine.17

Subsequently, a study19 on the isolated rat thoracic aorta showed that the aqueous extract

caused contraction of the aorta followed by relaxation. The initial contraction was blocked

by propranolol, whereas the vaso relaxant effect was unaffected. Similarly, in another

study,21 both the aqueous extract as well as the fraction of the extract containing tanninrelated

compounds (F2), produced hypotensive effects. The hypotensive effect of F2 was

not affected by pretreatment of rats with propranolol but was attenuated by pretreatment

with atropine. The authors suggested that the hypotensive effect of F2 may be mediated

by cholinergic mechanisms. In another study,22 it was observed that aortic prostaglandin

E2–like (PGE2) activity was enhanced in ischemic rabbit aorta pretreated with T. arjuna.

This finding is significant because PGE2 causes coronary vasodilatation, and this may

explain the beneficial effect of T. arjuna in patients with cornary artery disease (CAD). In

a subsequent study,23 myocardial ischemia in rabbits was produced by isoproternol infusion

and confirmed by ECG and later by histopathological examination. In this study, the

onset of ischemia and its severity were both reduced by T. arjuna. Abana, an herbal formula

containing T. arjuna, significantly increased creatinine phosphokinase (CPK), glutamate

oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), and gammaglutamyltranspeptidase

(g-GT) in serum following myocardial necrosis.24 The study also

showed that 90% of the protection against reduction in glycogen levels in ischemic rats

was provided by T. arjuna. The beneficial effect of abana was further evident from the

reduction in mitochondrial enzymes, such as g-GT and sorbitol dehydrogenase (SDH), by

44 and 48%, respectively.

T. arjuna has also been reported to possess significant hypolipidemic effect in rabbits

fed T. arjuna bark for 3 months.23 In another study,25,26 it was shown that rabbits fed T.

arjuna along with a high-cholesterol diet showed a lesser increase in total cholesterol and

triglycerides and no change in high-density lipoprotein (HDL) cholesterol as compared

with control rabbits. In addition, treating hypercholesterolemic rabbits with T. arjuna led

to a marked reduction in total cholesterol and triglycerides as well as elevation in HDLcholesterol

as compared with hypercholesterolemic control rabbits. The chronic oral

administration of T. arjuna was found to augment the endogenous antioxidant compounds

of rat heart and also prevented oxidative stress associated with myocardial ischemic

reperfusion injury.27 In a recent study,28 pre- and posttreatment of rats with arjunolic acid,

a new triterpene and a potent active principle from the bark of T. arjuna, provided significant

cardiac protection in isoproterenol induced myocardial necrosis in the rats.

30.9.1.2 Clinical Studies

The usefulness of T. arjuna in IHD has been confirmed in many clinical studies.29–31 In one

study,32 T. arjuna was found to be a mild diuretic without any cardiotonic action, but in

another study it was reported to be beneficial.33 A decoction prepared from the bark of T.

arjuna was administered to patients of chronic heart failure (CHF), essential hypertension,

and cirrhosis of the liver. The decoction showed clinical improvement in 42, 62, and 40%

of patients, respectively.33 Improvement in CHF substantiated earlier claims of its cardiotonic

property. On the basis of the description in Chakradutta Samhita (an Ayurvedic text)

that T. arjuna bark powder with milk, water, or ghee causes relief in heart pain,34,35 a clinical

trial in 12 patients with angina pectoris and hemiplegia following cerebral thrombosis

was conducted.17 A total dose of 20 g of crude bark powder of T. arjuna was administered

to the patients in divided doses for 1 month. At the end of this period, approximately 80%

of the patients showed increase in prothrombin time (24.3 ± 2.65 sec vs. 13.4 ± 1.22 sec; p

< 0.001) along with some degree of functional improvement. T. arjuna was also reported

to provide marked improvement in a case of Stokes-Adam’s attack following chest pain

after 3 months of therapy.17

T. arjuna was further tested in 30 patients with stable angina pectoris.35 These patients

were administered 25 mg/kg body weight dose of T. arjuna bark powder divided into

three doses per day. The mean anginal frequency by the end of 3 months had declined

(1.57 ± 1.28 vs. 3.47 ± 1.04/day). By the end of 1 month, 10% of patients did not require

sublingual nitrate. There was concurrent reduction in systolic blood pressure (p < 0.001)

without much change in the diastolic blood pressure. Electrocardiographic improvement

in terms of reduction in the depth of Q- and T-waves and changes in ST segment configuration,

decrease in heart rate, and correction of rhythm disturbance (particularly ventricular

premature contraction) was also noted. Biochemical parameters, such as plasma

catecholamines, plasma cortisol, blood sugar, and serum cholesterol had declined. A

significant reduction in body weight was also evident.35

In a double-blind study36 in 30 patients of decompensated rheumatic valvular heart

disease, treatment with 200 mg of T. arjuna improved LV fraction significantly (54.41 ±

11.62 vs. 41.47 ± 8.62%; p < 0.001). The exercise duration, as obtained on bike ergometry,

improved from 98.5 ± 44.2 sec to 178.7 ± 6.1 sec. Heart size also decreased significantly.

In a subsequent study,37 500 mg of T. arjuna extract was administered twice daily in 25

patients with CAD. After 3 months of therapy, reduction in grade of positivity of a

treadmill test response was observed in 6 patients. Also, improvement in exercise tolerance

was evident with concurrent reduction in frequency of anginal attacks and use of sublingual

nitrates.

In another similar study,38 500 mg T. arjuna was administered twice daily to 20 patients;

15 had stable angina pectoris (Group A) and 5 had unstable angina pectoris (Group B).

In both these groups, patients experienced a reduction in anginal frequency and increase

in LV ejection fraction (39.7 ± 9.93 vs. 36.2 ± 10.08%). Group A cases also exhibited a decline

in mean systolic blood pressure and body mass index. Treadmill testing on 10 patients of

stable angina pectoris showed reversion from moderate to mild changes after 3 months

of therapy. The target heart rate during exercise could be achieved without significant

chest pain.

In a double-blind, crossover design, placebo-controlled study,39 500 mg of aqueous and

alcoholic extract of the bark of T. arjuna was administered every 8 h to 12 patients of

refractory chronic CHF (New York Heart Association [NYHA] class IV). It was given in

addition to maximal tolerable doses of conventional therapy (i.e., digitalis, diuretics, and

vasodilators). In this study, T. arjuna therapy as compared with placebo was associated

with the following improvements:

1. Symptoms and signs of heart failure

2. Improvement in NYHA classes (class III vs. class IV)

3. Decrease in echo-LV end diastolic (125.28 ± 27.91 vs. 134.56 ± 29.71 ml/

m2; p < 0.005) and end systolic volume (81.06 ± 24.6 vs. 94.1 ± 24.62 ml/

m2; p < 0.005) indices

4. Increase in left ventricular stroke volume index (44.21 ± 11.92 vs. 40.45 ± 11.56

ml/m2; p < 0.005)

5. Increase in left ventricular ejection fractions (35.33 ± 7.85 vs. 30.24 ± 7.13%;

p < 0.005)

These patients were followed up with T. arjuna therapy for another 20 to 28 months

(mean 24 months) during phase II of the study. There was further improvement in symptoms,

signs, effort tolerance, and NYHA class.39

The adjuvant T. arjuna therapy has been found to reduce LV mass (140.62 ± 55.65 vs.

159.18 ± 51.11 g/m2) and frequency of angina pectoris (1.08 ± 1.08 vs. 3.5 ± 1.98) per day.

Besides these findings, it also improved LV ejection fraction (52.67 ± 12.32 vs. 42.25 ±

9.96%).40 Similar observations have been reported in a recent open study41 conducted on

20 patients of hypertension. Oral administration of Abana, a compound formulation

containing T. arjuna (30 mg/tablet), resulted in significant reduction of the systolic blood

pressure, ECG LV internal diameter, posterior wall thickness, and interventricular septum

thickness.41 The reduction in LV mass was seen from 18 weeks onward and lasted through

42 weeks. Compared with these observations, the decrease in LV mass was found at 12

weeks and maintained up to 36 weeks in those patients who were kept on propranolol.

In an open comparative trial42 of safety and efficacy of Hartone (herbal product containing

TA) in stable angina pectoris patients, 10 patients were given Hartone 2 capsules twice

daily for 6 weeks and 1 capsule twice daily for the next 6 weeks. Hematological and

biochemical investigations to assess safety were carried out on days 0, 42, and 84. A serum

lipid profile was done before and after therapy. Efficacy was based on the reduction in

the number of angina episodes and improvement in stress test. These results were compared

with 10 patients of stable angina pectoris on isosorbide mononitrate (ISMN) (20 mg

twice/day). In this study, Hartone afforded symptomatic relief in 80% of patients and

ISMN in 70%. The number of angina attacks was reduced from 79 to 24/week by Hartone

and from 26 to 7/week by ISMN. Although patients of both groups showed improvement

in several stress test parameters compared with baseline, the difference was not statistically

significant. Hartone improved blood pressure response to stress test in two patients and

ejection fraction in one. Hartone was better tolerated than ISMN and showed no evidence

of hepatic or renal impairment. Its effects on lipid profile were not consistent. The authors

of the study suggested that Hartone is a safe and effective antianginal agent comparable

with ISMN and is better tolerated.42

In a double-blind, placebo-controlled crossover study43 comparing T. arjuna with ISMN

in chronic stable angina patients, 58 male patients with chronic stable angina (NYHA

class II-III) with evidence of provocable ischemia on the treadmill exercise test received

T. arjuna (500 mg), isosorbide mononitrate (40 mg/day), or a matching placebo for 1

week each, separated by a wash-out period of at least 3 days. The patients underwent

clinical, biochemical, and treadmill exercise evaluation at the end of each therapy; the

scores were compared during the three therapy periods. T. arjuna therapy was associated

with a significant decrease in the frequency of angina and need for isosorbide dinitrate

(5.69 ± 6.91 mg/week in the treated group vs. 18.22 ± 9.29 mg/week in the placebo

therapy; p < 0.005). The treadmill exercise test parameters improved significantly during

therapy with T. arjuna compared with those with placebo. The total duration of exercise

increased (6.14 ± 2.51 vs. 4.76 ± 2.38 min; p < 0.005), maximal ST depression during the

longest equivalent stages of submaximal exercise decreased (1.41 ± 0.55 vs. 2.21 ± 0.56

mm; p < 0.005), time to recovery decreased (6.49 ± 2.37 vs. 9.27 ± 3.39 min; p < 0.005),

and higher double products were achieved (25.75 ± 4.81 vs. 23.11 ± 4.83 ¥ 103; p < 0.005)

during the T. arjuna therapy. Similar improvements in clinical and treadmill exercise test

parameters were observed with ISMN compared with placebo therapy. No significant

differences were observed in clinical or treadmill exercise test parameters when T. arjuna

and ISMN therapies were compared. No significant untoward effects were reported

during T. arjuna therapy. T. arjuna bark extract (500 mg) given every 8 h to patients with

stable angina with provocable ischemia on treadmill exercise. The treatment led to an

improvement in clinical and treadmill exercise parameters as compared with placebo

therapy. These benefits were similar to those observed with ISMN (40 mg/day) therapy

and the extract was well tolerated.43

The antioxidant and hypocholesterolaemic effects of T. arjuna bark powder was

compared with a known antioxidant, vitamin E, in a randomized controlled trial.44

One hundred five patients with coronary heart disease were recruited and separated

into 3 groups of 35 each using a Latin-square design.44 The groups were matched for

age, lifestyle and dietary variables, clinical diagnosis, and drug treatment status. None

of the patients took lipid-lowering drugs. Supplemental vitamins were stopped for 1

month before the study began, and American Heart Association Step II dietary advice

was given to all. At baseline, total cholesterol, triglycerides, HDL and LDL cholesterol,

and lipid peroxide estimated as thiobarbituric acid reactive substances were determined.

Group I received placebo capsules, Group II received vitamin E capsules (400

units/day), and Group III received fine powder of T. arjuna tree bark (500 mg/day)

in capsules. Lipids and lipid peroxide levels were determined at 30 days follow-up.

The response rate in various groups varied from 86 to 91%. No significant changes in

total HDL, LDL cholesterol, and triglycerides levels were seen in Groups I and II

(paired t-test p < 0.05). In Group III (T. arjuna-treated group) there was a significant

decrease in total cholesterol (9.7 ± 12.7%) and LDL cholesterol (15.8 ± 25.6%) (paired

t-test p < 0.01). Lipid peroxide levels decreased significantly in both treatment groups

(p < 0.01). This decrease was more in the vitamin E group (36.4 ± 17.7%) as compared

with the T. arjuna-treated group (29.3 ± 18.9%). In this study, T. arjuna exhibited a

significant antioxidant effect that was comparable with vitamin E. In addition, it also

had a significant hypocholesterolemic effect.44

In toxicological studies13 conducted in rats and rabbits, no histopathological changes in

the heart, liver, and kidney of these animals were evident even after they had been

administered 10 g/kg body weight of T. arjuna orally for 40 days. The LD50 of T. arjuna

extract was 2.5 g/kg by intraperitoneally in albino mice.20 It appears that mice are more

sensitive to T. arjuna than are rats and rabbits.

In various clinical studies,38 T. arjuna has been used in the dose of 1 to 2 g/day, and this

dose was found to be the optimum in patients with CAD. At this dose, it is well tolerated.37

However, some patients complained of mild gastritis, headache, and constipation.39 No

metabolic, renal, and hepatic toxicity has been reported even when patients were administered

T. arjuna for more than 24 months.39

30.9.2 Aloe vera

In an in vitro study,45 angiogenic activity of Aloe vera gel was investigated by using the

most active fraction (F3) from dichloromethane extract of Aloe vera gel. The F3 increased

the proliferation of calf pulmonary artery endothelial (CPAE) cells. In addition, it induced

CPAE cells to invade type 1 collagen gel and form a capillary-like tube in an in vitro

angiogenesis assay; it also increased the invasion of CPAE cells into matrigel through an

in vitro invasion assay. F3 also increased the effect on the messenger ribonucleic acid

expression of proteolytic enzymes, which are the key participants in regulation of extracellular

matrix degradation.

In a clinical study,46 5000 patients with atheromatous heart disease presented as angina

pectoris were studied over a period of 5 years with diet containing Aloe vera and husk of

isabgol. The dietary treatment increased HDL and produced a marked reduction in total

serum cholesterol, serum triglycerides, fasting and postprandial blood sugar levels in

diabetic patients, and total lipids. The clinical profile showed a reduction in the frequency

of anginal attacks; gradually, the doses of the drugs, such as verapamil, nifedipine, betablockers,

and nitrates, were reduced. Diabetic patients benefited the most. Although the

exact mechanism of the action of the above two herbs is not known, it appears that they

probably act through their high fiber contents. Both these herbs should be further studied.

No undesirable side effects were noted.

30.9.3 Coleus forskohlii

C. forskohlii (CF) has been used in Ayurvedic medicine for heart diseases, spasmodic pain,

painful micturition, and convulsions. Forskolin, an alkaloid isolated from CF, inhibits

adenosine di-phosphate (ADP)-induced and collagen-induced platelet aggregation in

human and rat platelet-rich plasma.47 These studies demonstrated an important role of

plasma adenosine, a natural antiplatelet and vasodilatory agent produced by vascular

endothelium, in the antiplatelet activity of forskolin. Findings also proved that the effect

can be greatly potentiated by the clinically used drugs dipyridamole and dilazep. The

anticoagulant effect of C. forskohlii may be helpful in IHD.

Coleonol, a diterpene isolated from C. forskohlii, has been shown to lower the blood

pressure of anesthetized cats and rats and of spontaneously hypertensive rats due to

relaxation of the vascular smooth muscle.48 In small doses it showed a positive inotropic

effect on isolated rabbit hearts as well as on cat hearts in vivo. Coleonol also exhibits

nonspecific spasmolytic activity on the smooth muscle of the gastrointestinal tract in various

species but not on the bronchial musculature of guinea pig. Large doses of coleonol have

a depressant action on the central nervous system. The positive ionotropic effect of C.

forskohlii provides the rationale for its use in IHD. In another study,49 forskolin activated a

membrane bound adenylatecyclase and a cytoplasmic cAMP-dependent protein kinase to

a much higher degree than does isoprenaline. The authors postulated that the adenylatecyclase

activation may be correlated with the positive inotropic effect via an enhanced

calcium uptake by the heart muscle cell.

30.9.4 Inula recemosa

The effects of I. recemosa on biochemical parameters in rats with myocardial infarction

induced by isoprenaline injection was investigated.50 The effects on circulating GOT, LDH,

CPK, cAMP, cortisol, pyruvate, lactate glucose, and cardiac cAMP adenyl cyclase levels

were gradually increased, and serum and cardiac cAMP-PDE levels were gradually

© 2004 by CRC Press LLC

Ischemic Heart Disease 529

decreased from 1 to 120 h after the first injection of isoprenaline. The rats pretreated with

ciplar (beta-blocker) or pushkarmula (indigenous drug) showed fewer changes as compared

with untreated infarcted rats. Posttreatment with I. recemosa also produced similar results.

I. recemosa was found to be more effective given before infarction induction rather than

given after infarction induction.

30.9.5 Andrographis paniculata (Kirata)

A. paniculata (AP) (Kirata) was investigated in seven infarction-induced dogs to study the

protective effect.51 One hour after the development of myocardial infarction by formation

of thrombus, aqueous extract of AP was injected intravenously. Six infarction-induced dogs

served as the control group. As compared with the control group, the treated group showed

increased levels of prostacyclin (PG12), inhibition of thromboxane A2 (TXA2), elevated

cAMP in platelets, lowered creatine kinase isoenzyme MB (CK-MB) peak, shortened

euglobulin lysis time (ELT), decreased release of platelet beta-(1-4)galactosyl transferase

(beta-GT) and inhibited platelet maximum aggregation rate, reduced size of the ischemic

area recorded by epicardial ECG, and a lowered amplitude of ST segment elevation; a Qwave

appeared in only one dog. Pathologically, the myocardial structure surrounding the

initial ischemic area became relatively normal, whereas the degree of myocardial degeneration

and necrosis in the central part of the ischemic area was mild. These data suggest

that AP may limit the expansion of ischemic focus, exert marked protective effect on

reversibly ischemic myocardium, and demonstrate a weak fibrinolytic action. These observations

support the use of AP in Ayurvedic therapies of IHD.

The effect of AP and fish oil was further studied on atherosclerotic stenosis and restenosis

after coronary angioplasty in dogs.52 Preliminary results showed that AP can significantly

relieve atherosclerotic iliac artery stenosis induced by both deendothelialization and high

cholesterol diet. The authors concluded that AP may play an important role in preventing

restenosis after coronary angioplasty, and fish oil may be useful in reducing the extent of

restenosis after coronary angioplasty. AP has also been shown to alleviate the ischemiareperfusion

injury in experimental dogs.53 As compared with a control ischemia group,

the AP-treated group showed reversal of the changes in the following parameters: superoxide

dismutase (SOD), malondialdehyde (MDA), Ca2+ in myocardial cells, and ultrastructural

changes of myocardial tissues. The observations were confirmed in additional

studies.54

A component (API0134) of AP was studied in an experimental atherosclerotic rabbit

model to determine the effects on on nitric oxide, endothelin, cyclic guanosine monophosphate,

lipid peroxide, and superoxide dismutase. The study showed that API0134 possesses

the effects of antioxidation, preserving endothelial function, and maintaining the

balance of NO/ET. A. paniculata crude extracts were further fractionated and studied for

various cardiovascular activities, mainly the hypotensive and the antithrombotic

effects.55,56

30.9.6 Lipistat

Lipistat is made up of equal proportions of extracts of T. arjuna, I. racemosa Hook, and

latex of C. mukul. The formula was given to rats at different doses (225, 350, 450 mg/kg)

orally daily for 6 days/week for 60 days.58 Thereafter, the rats were subjected to isoproterenol-(

ISO) induced (85 mg/kg, s.c. for 2 days) myocardial necrosis. Gross and microscopic

examinations (histopathology) were done along with estimations of myocardial

tissue high energy phosphates stores and lactate content. The study showed protective

effect of the formula. The authors suggested that the formula may be potentially useful

in the prevention of IHD.

30.9.7 Centella asiatica

The effects of the total triterpenic fraction of C. asiatica on serum levels of the uronic acids

and lysosomal enzymes involved in mucopolysaccharide metabolism (beta-glycuronidase,

beta-N-acetylglucosaminidase, arylsulfatase) in patients with varicose veins were studied.

58 The results of this trial provide an indirect confirmation of regulatory effects of the

extract of C. asiatica on metabolism in the connective tissue of the vascular wall and thus

may prove useful in treatment of IHD. Total triterpenic fraction of C. asiatica has been

found effective in improving venous wall alterations in chronic venous hypertension and

in protecting the venous endothelium.59

30.9.8 Piper longum

An amide, dehydropipernonaline, isolated from P. longum has been shown to have coronary

vasorelaxant activity.60

30.9.9 Picrorhiza kurrora

The ethanol extract of P. kurrora rhizomes and roots was found to exhibit a cardioprotective

effect on ISO-induced myocardial infarction in rats as measured by lipid metabolism in

serum and heart tissue.61

30.9.10 Commiphora mukul

Hypercholesterolemia is a known risk factor for IHD. In a clinical trial62 with 61 hypercholesterolemia

patients, 31 patients were given guggulipid, representing 50 mg of guggul

sterones, and 30 patients were given placebo capsules twice daily for 24 weeks. The

compliance of patients was greater than 96%. In the treated group, total cholesterol level

decreased by 11.7%, the LDL by 12.5%, triglycerides by 12.0%, and the total cholesterol/

HDL cholesterol ratio by 11.1% as compared with baseline levels; the levels were

unchanged in the placebo group. The lipid peroxides, indicating oxidative stress, declined

33.3% in the guggulipid group without any decrease in the placebo group. The combined

effect of diet and guggulipid at 36 weeks was as great as the reported lipid-lowering effect

of modern drugs. After a wash-out period of another 12 weeks, changes in blood lipoproteins

were reversed in the guggulipid group without any changes in the placebo group.

Side effects of guggulipid were headache, mild nausea, eructation, and hiccups in a few

patients. In another similar study,63 guggulipid also showed similar results.

30.10 Summary and Discussion

In recent years, considerable attention has been paid to the utilization of traditional

systems of medicine including Ayurveda in the management of IHD. WHO has recom-

mended utilization of alternative forms of medicine for total health care. T. arjuna is one

of several popular Ayurvedic herbs already being utilized by the Ayurvedic practitioners

for the prevention and management of IHD. Other herbs with great potential to improve

quality of life of individuals with IHD and that are commonly used are Aloe vera, Cole

forskohlii, Inula recemosa, Andrographis paniculata, Centella asiatica, Piper longum, Picrorhiza

kurrora, and Commiphora mukul. The experimental data available supports their use in IHD.

According to Ayurveda, IHD is the outcome of faulty diet and stressful lifestyle which

leads to an ama state (i.e., hyperlipidemia) leading further to dhamani praticaya (thickening

of arteries) and dhamani kathinya (hardening of arteries), resulting into angio-obstruction

and aggravation of vata dosa showing chest pain and angina. The principle treatment is

to promote agni (biofire) and to purify the channels by panchakarma in addition to the use

of natural palliative drugs that have cardiotonic, hypotensive, hypolipidemic, and anticoagulant

properties. The recent studies show that T. arjuna has shown varying degrees of

cardioprotective effect as evaluated in terms of being cardio tonic, hypotensive, hypolipidemic,

and anticoagulant. Toxicity studies show that T. arjuna is a safe and effective herb

in the treatment of IHD without any harmful side effects.

In modern medicine, the treatment of IHD involves expensive and chronic drug therapy

or equally expensive interventional procedures, such as thrombolytic therapy and surgical

recanalization. Reperfusion injuries and undesired side effects of drugs are the major

drawbacks of the conventional therapies. There is a vast and untapped source of medicinal

plants with cardioprotective effects used in Ayurvedic therapies. The recent research on

T. arjuna and other Ayurvedic herbs suggests a better cost-effective and socially acceptable

therapeutic option for IHD.

The drugs mentioned in this chapter have been used in the treatment of heart disease

for thousands of years. The current research data show that they can be utilized effectively

in deadly heart diseases, including IHD. The relief provided by T. arjuna in angina

and its effect on ST segment changes and T-wave depression in IHD are quite impressive.

The Ayurvedic herbs discussed in this chapter have the potential of improving quality

of life, while avoiding the side effects of conventional treatment. LV function improvement

by T. arjuna in IHD cannot be overlooked, especially in view of the fact that IHD

has an annual mortality rate of 40% under conventional treatment. The widespread use

of T. arjuna and the other herbs can improve the quality of life in individuals with IHD

and potentially save millions of lives.

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Om Tat Sat

                                                        

(Continued...) 

(My humble salutations to H H Maharshi ji,  Brahmasri Sreeman Lakshmi Chandra Mishra ji and other eminent medical scholars and doctors   for the collection)