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)
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