“HRIDROGA SAMPRAPTI AND MODERN

PATHOLOGY OF IHD”
Heart is regarded as one of the vital organ of the human body, cessation of
which leads to death. According to Ayurved, it is one among the fifteen
Koshtangas and it is derived from mother i.e. it is regarded as “MmaatRja
Avayava”. The word “HRIDAYA” is composed of HRU+DAA+YA, meaning,
Hru- hrit – to receive i.e. it deoxygenated blood from the various parts of the
body, Daa-yacCit- to distribute i.e to distribute oxygenated blood to all parts of
the body, Ya-yamyait- to move i.e. moving the blood, oxygen, etc all over the
body and thus keeping the wheel of life in motion. The importance of heart is also
stated by Charaka and Sushruta. Charaka stated that heart is one of that beats i.e.
spMdto. He has regarded it as the seat of consciousness. Sushruta has regarded it
as a SIRA marma, it is one in number and one among the TRIMARMAS i.e.
Hridaya, Shira, and Basti. He further regards it as sad\yap`aNahr mama-
which means injury to which leads to death.
Thus understanding the impotence of Hridaya it is important to know any
disease of Hridaya i.e. “Hridroga”
)id baaQaaM p`kuva-int )d`aogaM tM p`caxato l

The above definition of Hridroga tells that ‘Impairment of functions of heart

is Hridroga’. It is Madhyama Margashrtita (Marmashti-Sandhi) Vyadhi. For
understanding the various diseases of heart it is important to know the normal
structure and functioning of Hridaya.
According to Sushruta, it is the base of Pranavaha Dhamanya. Pleeha is to
the below and left to it, Yakruta is right to it. Ashtang Sangraha states the size of
heart to be two Anguli breadths. Sushruta and Vagbhata states that big vessels i.e.
Dhamani originate from heart through which Rasa, Rakta outflows and is supplied
to all over the body while all Siras terminate in the heart as all river terminate in
the ocean. Thus the idea of arterial and venous blood flow is completely found in
Ayurvedic literature. Commentator of Ashtang Hridaya, Arunadatta stated that
purified bloodfrom lungs returns back to heart and then ‘Vyana Vayu’ presses it to
flow in the whole the body. According to Charaka, Hridaya is the seat of
circulatory system (rsavah s~aotsa) as well as respiratory system (p`aNavah
s~aotsa ). Thus it is important organ of cardio respiratory system.
Of all the various types of Tridoshas, Prana Vayu, Vyana Vayu, Sadhaka
Pitta, Avalambaka Kapha resides in the Hridaya. Hence their normal function
maintains the normal health of the heart and their vitiation leads to various
hridrogas. The main function of Prana Vayu is )d\QaRk, . The circulation and
other activities of cells, Bhutangas, Shadangas i.e. Indriya and Atma depends upon

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the Hridaya. Prana Vayu is mainly responsible for rhythemicity and contractility of
heart. Vyana Vayu promotes the movements of Rasa and Kapha all over the body.
In Hridaya Kapha and Tama Gunas are present in Hridaya. With the help of power
of essence of food present in Hridaya, the Avalambaka Kapha supports the body.
Hridaya is also regarded as the seat of Pranavaha and Rasavaha Strotas.
According to modern Rasa is the nourishing part of the blood and Prana is the
oxygen part of the blood, both of which are circulated by heart to various parts of
the body for normal functioning of the respected parts. There is another concept of
Oja in Ayurved. Out of the two types of Oja, Para Oja which is Ashtabindu in
quantity is located in the heart, decrease of which in heart shows emaciating effect
on the body. Hridaya is further regarded by Vagbhata as a site of mind and hence
an abnormality of mind will show negative effect of heart. This is concluded by
observing instability of mind leading to heart diseases.
Before describing the actual pathogenesis of Hridroga let us go through
causative factors of Hridroga.
A%yauYNagauvaa-
nnakYaayait>EamaaiBaGaataQyaSanap`saMgaO: l l
saMicantnnaO: vaogaivaQaarNaOXca )damaya: pMcaivaQa:
p`ivaYT: l l
(maaQava inadana)
Hridroga hetu can be classified under headings Sharirika, Manasika and Aghataj.
Sharirika can be classified into Aharaja and Viharaja. Let s first consider Aharaja
Hetu. They are as follows Atirukshanna sevana, Atishushkanna sevan, Atiushna,
Atiguru, Atisnigdha, AjirnaBhojan Atikatu, Lavana, Amla Rasatmaka, Ati
Kshariya, Madhyatireka, Atyalpa Bhojan. After knowing Aharaja factors, the
Viharaja factors are as follows Ativyayama, Alpacheshtana, Aatapsevana,
Nidradhikya. Lastly the Manasika causes are as follows shoka, Achintana, Krodha
and Bhaya.
Among these factors some which will be responsible for manifestation of
different types of heart diseases e.g.- Doshaja Hridroga,
rsar>ivaxaopjanyaivakRit i.e. abnormal circulation Qvaina ivakRit i.e.
heart murmur and other heart diseases like )dd`va i.e. pericardial effusion )
%SaUla i.e. angina pectoris )d\vyaasa i.e. hypertrophy of chamber or
cardiomegaly and )dyaaiBaGaat i.e. heart attack, etc. according to Modern
science for the purpose of pathological discussion of heart diseases they are
categorized as anatomical and functional impairment e.g.-Heart failure, Congenital
Heart Disease (CHD), Ischemic Heart Disease(IHD), Hypertensive Heart Disease,
Rheumatic Heart Disease(RHD), and Valvular Deformities, etc.
In children’s CHD and Valvular Diseases are common all over the world. On
the other hand IHD and Hypertensive Cardiomyopathy is the major in adults. IHD

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is caused by various diseases affecting the coronary arteries which is accounting
for more than 90% cases of atherosclerosis and other causes are responsible for
less than 10%.
Now let us explain the Samprapti of Hridroga under the following topics-
according to causes (Hetu), According to Shatkriyakala, Samanya Samprapti
and According to modern science pathogenesis of Ischemic Heart Disease.
Now the Samprapti according to Hetu is under Manasika, Sharirika, and
Aghataja Hetu. The Manasika Hetu which are responsible for Hridroga are Chinta
(sorrowful thoughts), Bhaya (fear), Krodha (anger), Shoka (grief), etc. To explain
the Samprapti according to Manasika causes we have to consider daoYa
saMbaMQa, Qaatu saMbaMQa, ]pQaatu saMbaMQa and s~aotsa
saMbaMQa. Chinta and Atidhyana (excessive thinking) are responsible for
aggravation of Prana Vayu and Vyana Vayu. Chinta is responsible for Ajirna
(indigestion). There is vitiation of Pachaka Pitta and Sadhaka Pitta. Hridaya is the
organ which is situated in the ]r and ]r is the main sqaana of Kapha. So there
will be vitiation of AvalaMbak kf and @laodk kf.
If we see the vitiation of Tridoshas there will be disturbance in the
permutation and combination of Tridoshas (AMSaaMSa klpnaa) which leads
impairment in the heart as Rasa-Rakta Vikshepana, Dhvani Vikruti and change in
the position of the heart also.for the heart diseases we have to consider the Rasa,
Rakta, Mansa and Meda Dhatu. As we considering Dhatu we have to consider
about Upadhatu. So the Upadhatu which will get vitiated will be Sira and Snayu.
Again Hridaya is the site of Ashtabindu Oja. There is relation between Oja and
Chinta.
Aaoja: xaIyaot\ k`aopxauQyaanaSaaokEamaaidiBa: l
(vaagBaT sau~sqaana 16)
In view of Hridroga, the Strotas which will get vitiated are Annavaha, Rasavaha,
Pranavaha, and Udakavaha Strotas.
Due to Manasika causes (mainly Chinta) there is aggravation and vitiation of
Tridoshas which will be responsible for the impairment of Dhatus (Rasa, Rakta,
Mansa and Meda), as Dhatus are impaired their will be no sufficient production of
Poshya Dhatu which will result in improper Upadhatu Nirmiti (Sira, Snayu). Again
there will be Agni Vaigunya due to vitiation of Annavaha Strotas. This Agni
Vaigunya will be responsible for the impairment of Oja Dhatu. As there is vitiation
of all factors the circulation (perfusion) of the heart will be disturbed which results
in manifestation of different Hridrogas e.g. mainly Hrutshula, Hrudghata and
Hridaya Ruja.
Sharirika (somatic) causes can be classified as Aharajanya and Viharajanya.
Excessive consumption of the diets which are described in the Hetu are responsible
for Kapha and Meda Sanchiti (i.e. deposition of the fat in the lumen of the vessel)

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in the lumen of the coronary vessels (saMga or s~aotaoraoQa). This
deposition of Kapha and Meda in the lumen of the vessels is responsible for less
blood supply to myocytes which will result in IHD due to atherosclerosis
(QamanaIp`itcaya). Some diets are Qaatuxayajanya (e.g.-Ait$xa,
Ait]pvaasa, Ait]YNa, etc). Due to these diets there is improper nourishment of
the Dhatus which are related with Hridaya. There is aggravation of Tridoshas
which will be responsible for the functional impairment of the heart.
Viharajanya causes which are mainly Vega Vidharan and change in lifestyle
e.g.- excessive day sleep, sedimentary activities, smoking, etc. Vega Vidharana is
mainly the suppression of urge for Mutra and Purisha. Due to suppression of urge
for defecation there is vitiation of Apana Vayu which results in the cutting pain in
the abdomen. This results in abnormality in functions of heart. The normal
movements of Apana Vayu is in downward direction, due to its suppression it starts
moving in upward direction and vitiates Prana Vayu and Vyana Vayu located in
the heart thus leading to Hridroga. Similar is the case with suppression of urge for
urination.
Due to sedimentary life style e.g. excessive exercise, lack of exercise,
excessive sleep, etc. for a longer duration of time, there is disturbance in
permutation and combination of Tridoshas which will be responsible for vitiation
of Rasa, Rakta Dhatus which will results in different diseases of heart.
Ashtang Hridaya and Madhava Nidana has been described five types of
Hridrogas, these are namely- Vataja, Pittaja, Kaphaja, Sannipataja and Krimija.
Vataja Hridroga is produced due to Shoka, Upavasa, Vyayama, Ruksha, Shushka,
Alpa and Shita Ahar. Thus results in vata prakopa at the site of Hridaya by
Sthanasanshraya produce Hridroga. It shows symptoms like Hritshula,
Dhvanivikruti, different type of pain in the heart, etc. The second type, Pittaja
Hridroga is produced due to Atiushna, Amla, Lavana, Kshara, Katu rasatmaka ahar
also excessive consumption of food, ajirna bhojana, madhyapana, krodha,
atapasevana, etc. will cause pitta prakopa at the site of Hridaya leading to
Hridroga. It shows symptoms like tiktasyata, cchardi, trushna, jwara, daha
especially at Hridaya, bhrama, etc. The Kaphaja Hridroga will shows the
symptoms like heaviness at the site of heart, staimitya, kasa, tandra, jwara,
anorexia, excessive Kaphashtivana. The Sannipataja Hridroga shows the
symptoms of above three types. The main symptoms are vaivarnya, shvasa, jwara,
shula, shotha, hrid-dhvanivikruti. And last type i.e. Krimija Hridroga is produced
by, when there is a person suffering from Tridoshaja Hridroga having consumption
of tila, dugdha, guda, etc Kaphakara Ahara in excessive quantity causes Granthi
Utpatti In Heart, that part of heart becomes Vikruta which results in production of
Kleda by Rasa in that Vikruta part. Kleda causes production of Krimi that result in
Hridroga.

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 According to modern science heart diseases are mainly due to diabetes
mellitus, hypertension, obesity and smoking. Those with diabetes are at high risk
for heart and vascular disease. The heart is a muscle that pumps blood throughout
the body to supply it with nutrients and oxygen and to take away by-products of
metabolism, such as carbon dioxide. Compared to other muscles in the body, the
heart consumes a high amount of nutrients and oxygen. It pumps blood to itself
through specialized vessels called coronary arteries. These arteries are critical to
the integrity of the functioning of the heart. We know that diabetes can cause harm
to these vessels, called coronary artery disease. This disease can be in the form of
thickening of the vessels that can cause decreased blood flow through the vessel or
the formation of fatty material, commonly referred to as a plaque, that blocks the
flow of blood through the vessel. Both of these conditions can lead to a decreased
or arrested blood flow to the heart, which will cause severe impairment to this
pumping muscle. This is referred to as a myocardial infarction, or heart attack.
When blood pressure is too high and remains that way, arterial walls become
weakened and more prone to atherosclerosis (a build-up of fatty substances on the
inner walls of the arteries). The heart must then work harder to try to pump
oxygenated blood through the clogged arteries. The clogged arteries are also more
prone to blood clots that can block the flow of blood entirely. Blood pressure can
also cause arteries to bulge (aneurysm) or burst (hemorrhage). As body weight
increases, the total volume of blood in the body also increases. The cause of the
increased volume is unclear, but it forces an abnormally high output of blood from
the heart even at rest. The increased blood volume and output make the heart work
harder. The individual heart chambers stretch and expand. The added workload
causes thickening of the heart muscle of the lower left chamber, the left ventricle.
The thickening affects both contraction (squeezing) and relaxation of the heart.
Over time, the heart may not be able to keep up with the load. Congestive heart
failure with shortness of breath or fluid accumulation in the lungs may be the
result. Nicotine in tobacco smoke can increase blood pressure causing the heart to
work harder. Carbon monoxide replaces oxygen in your blood. Smoking adds to
the obstruction of the arteries which can lead to heart attack and other heart-related
conditions. And, smokers have greater risk of death from coronary heart disease
compare to non-smokers.
Aghataja causes i.e. traumatic causes means not only trauma to the
heart but also that are kRima saMËmaNa, Aamavaatjanya )d`aoga i.e.
RHD and Coagulation cascade. Kaphakara diet is p`kRitsama samavaaya in
heart diseases. So taking of those kaphakara diet which are responsible for the
production of Krimi those are having affinity to affect the heart such heart affecting
Krimis get lodgment in the heart muscles and cause Hridaya Vikruti. Again due to
Kaphakara diet there is excessive Kleda Nirmiti which is responsible for the

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increasing the virulence of Krimi. This Krimija Hridroga can be correlated with
infectious causes. E.g.-SABE (Sub Acute Bacterial Endocarditis), Aortitis,
Myocarditis,etc. In Amavatajanya Hridroga there is excessive Amotpatti,
Strotorodha. The quqlities of Ama are somewhat similar to that of Kapha so both
gets mixed and the Kapha excides its normal quantity. As heart is the site for
kapha, it causes Rasa dushti which results in Hridgraha.
Samprapti of Hridroga can also be illustrated with the help of
YaT\iËyaakala. Due to improper Ahara, Vihara and instable mental status there
is accumulation of Kapha in its site of predominance i.e. ]rxao~ or ]rsqaana
i.e. chest region. These increased Doshas on further aggravation overflow their site
and spread all over the body thus vitiating Rasavaha Strotas and Pranavaha Strotas.
The increased Doshas spreading to different parts of the body gets lodged into
various parts of the body like coronary arteries, valves of the heart, muscles of the
heart leading to heart diseases- Coronary Artery Disease (CHD), Valvar
abnormality, Myocardiatis respectively. The disease if untreated leads to complete
manifestation resulting in different kinds of Hridrogas e.g.- Hrutshula, Hrud-drava,
etc.
Now lastly the SAMANYA SAMPRAPTI OF HRIDROGA IS DESCRIBED
AS FOLLOWS
dUYaiya%vaa rsaM daoYaa ivagauNaa )dM gata: l
)id baaQaaM p`kuva-int )d`aogaM tM p`caxato l l
(sauEaut ]<ar KMD)

Due to vitiation of principles of diet and other Nidana which causes

Mandagni .this mandagni will results in production of Ama. Ama mixes with Rasa
Dhatu and causes its Vikruti, then rasa Dhatu gets vitiated. If that vitiated rasa gets
mixed with Vayu then it will result in Ruja (pain) in Hridaya. Otherwise if that
vitiated rasa gets mixed with Kapha and Pitta it will result in strotorodha which
causes obstruction of Prana Vayu. So that will result in HridaBadha.

“PATHOGENESIS OF ISCHEMIC HEART

DISEASE”
IHD is the generic designation for a group of closely related syndromes
resulting from myocardial ischemia an imbalance between supply & demand of the
heart for oxygenated blood .In more than 90% of cause of myocardial ischemia is
reduction in coronary blood flow due to atherosclerotic coronary arterial
obstruction .Thus IHD is often termed as coronary artery disease (CAD).

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 The clinical manifestations of IHD can be divided into four syndromes-
Myocardial Infarction (MI), Angina Pectoris, Chronic IHD with heart failure and
Sudden cardiac death,
The dominant influence in the causation oh IHD syndromes is diminished coronary
perfusion relative to myocardial demand owing largely to a complex and dynamic
interaction among fixed atherosclerotic narrowing of the epicardial coronary
arteries interluminal thrombosis over lying a disrupted atherosclerotic plaque,
platelet aggravation and vasospasm.

More than 90% of patients with IHD have atherosclerosis of coronary

arteries. The clinical manifestations of coronary atherosclerosis are generally due
to progressive encroachment of the lumen leading to stenosis or to acute plaque
disruption, which compromises blood flow.
Although only a single major coronary epicardial trunk may be affected, two
or all three- lateral anterior descending (LAD), lateral circumflex (LCX), and right
coronary artery (RCA) - are often involved.

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Clinically significant stenosis plaque may be located anywhere within these vessels
but tend to predominate within the first several centimeters of the LAD and LCX
and along the entire length of RCA. Sometimes the major secondary epicardial
branches are also involved (i.e. diagonal branches of the LAD, obtuse marginal
branches the LCX or posterior descending branch of the RCA), but atherosclerosis
of the intramural branches is rare. However, as mentioned above, the onset of
symptoms and prognosis of IHD depend not only on the extent and severity of
fixed, chronic anatomic disease, but also critically on dynamic changes in coronary
plaque morphology.
ANGINA PECTORIS is a symptom complex of IHD characterized by
paroxysmal and usually recurrent attacks of substernal or precordial chest
discomfort (variously described as constricting, squeezing, choking, or knifelike)
caused by transient (15 seconds to 15 minutes) myocardial ischemia that falls short
of inducing the cellular necrosis that defines infarction. There are three over
lapping patterns of angina pectoris- Stable or typical angina, Prinzmetal or variant
angina and Unstable or crescendo angina. They are caused by varying combination
of increased myocardial demand and decreased myocardial perfusion, owing to
fixed stenosing plaques, disrupted plaques, vasospasm, thrombosis, platelet
aggregation, and embolization. Moreover, it is being increasingly recognized that
not all ischemic event are perceived by patients, even though such event may have
adverse prognostic implications (silent ischemia).
Stable angina, the most common form and therefore called
typical angina pectoris, appears to be caused by the reduction of coronary
perfusion to a critical level by chronic stenosing coronary atherosclerosis; this
renders the heart vulnerable to further ischemia whenever there is increased
demand such are that produced by physical activity, emotional, excitement or any
other cause of increased cardiac workload typical angina pectoris is usually
relieved by rest(thereby decreasing demand) or nitroglycerin, a strong vasodilator.

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Although the coronary arteries usually maximally dilated by intrinsic regulatory
influences, nitroglycerin also decrease cardiac work by dilating the peripheral
vasculature. In particular instances, local vasospasm may contribute to the
imbalance between supply and demand
Prinzmetal variant angina is an uncommon pattern of episodic
angina that occurs at rest and is due to coronary artery spasm usually there is an
elevated ST segment on the electrocardiogram (ECG), indicating of transmural
ischemia. Although individual with this form angina may well have significant
coronary atherosclerosis, the anginal attacks are unrelated to physical activity, heart
rate, or blood pressure. Prinzmental angina generally responds promptly to
vasodilators, such as nitroglycerin and calcium channel blockers.
Unstable or crescendo angina refers to a pattern of pain that
occurs progressively increasing frequent, is precipitated with less effort, often
occurs at rest, and tends to be of more prolonged duration. As discussed above, in
most patients, unstable angina is induced by disruption of an atherosclerotic plaque
with superimposed partial (mural) thrombosis and possibly embolization or
vasospasm (or both). Although ischemia that occurs in unstable angina falls
precariously close to inducing clinically detectable infarction, unstable angina is
often the prodrome of subsequent acute MI. Thus this syndrome is sometimes
referred to as preinfaction angina, and in the spectrum of IHD unstable angina lies
intermediate between stable angina on the one hand and MI on the other.
MYOCARDIAL INFARCTION is also known as ‘Heart attack’, is the
death of cardiac muscles resulting from ischemia. It is by far the most important
form of IHD and alone is the leading cause of death. Most myocardial infarcts are
transmural, in which the ischemic necrosis involves the full or nearly full thickness
of the ventricular wall in the distribution of a single coronary atherosclerosis, acute
plaque changes, and superimposed thrombosis.

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In contrast, a subendocardial (nontransmural) infarct constitutes an area of
ischemic necrosis limited to the inner one third or at most one half of the
ventricular wall; under some circumstances, it may extend laterally beyond the
perfusion territory of a single coronary artery. The subendocardial zone is normally
the least well-perfused region of a myocardium and therefore is most vulnerable to
any reduction in coronary flow. A subendocardial infarct can occur as a result of
plaque disruption followed by coronary thrombus that becomes lysed before
myocardial necrosis extents across the major thickness of the wall; in this case the
infarct will be limited to the distribution of one coronary artery with plaque
change. However, subendocardial infarct can also result from sufficiently
prolonged and severe reduction in systemic blood pressure, as in shock, often
superimposed on chronic, otherwise noncritical, coronary stenosis.
MI may occur at virtually any age. But the frequency rises progressively
with increasing age and when predispositions to atherosclerosis are present, such as
hypertension, cigarette smoking, diabetes mellitus, genetic hypercholestoremia,
and other causes of hyperlipoproteinemia.
Now consider the basis for and subsequent consequences of myocardial
ischemia, particularly among they relate to the typical transmural myocardial
infarct. As discussed above, transmural acute MI results from a dynamic
interaction among several or all of the following- coronary atherosclerosis, acute
atheromatous plaque change (such as rupture), superimposed platelet activation
thrombosis and vasospasm- resulting in an occlusive intramural thrombus
overlying a disrupted plaque. In addition, either increased myocardial demand or
hemodynamic compromise (as with a drop in blood pressure) can worsen the
situation. Recall also that collateral circulation may provide perfusion to ischemic
zones from a relatively unobstructed branch of the coronary tree, bypassing the
point of obstruction and protecting against the effect of an acute coronary
occlusion.
In the typical cases of MI, the following sequence of events can be
proposed: The initial event is a sudden change in morphology of an atheromatous
plaque, that is, disruption-manifest as intraplaque hemorrhage, erosion or
ulceration, or rupture or fissuring. Exposed to subendothelial collagen and necrotic
plaque contents, undergo adhesion, aggregation, activation, and release of potent
aggregators including thrombaxone A2, serotonin and platelet factors 3 and 4.
Vasospasm is stimulated by platelet aggregation and the release of mediators. Other
mediators activate the extrinsic pathway of coagulation, adding to the bulk of the
thrombus. Frequently within minute, the thrombus evolves to completely occlude
the human of the coronary vessel.
THE DESIGNATION CHRONICISCHEMIC HEART DISEASE
(CIHD) is used here to describe the cardiac finding in patient, often but not

10
exclusively elderly, who develop progressive heart failure as a consequence of
ischemic myocardial damage. In most instances, there has been prior MI and some
time previous coronary arterial bypass graft surgery or other intervention. CIHD
usually constitute post infarction cardiac decompensation owning to exhaustion of
the compensatory hypertrophy noninfarcted viable myocardium i.e. itself in
jeopardy of ischemic injury. However, in other cases severe obstructive CAD may
be present without acute or healed infarction but with diffuse myocardial
dysfunction.
SUDDEN CARDIAL DEATH (SCD) is most commonly defined as
unexpected death from cardiac causes early after symptom onset (usually within
one hour) or without onset of symptom in many adults, SCD is a completion and
often the first clinical manifestation of IHD. With decreasing age of the victim, the
following nonatherosclerotic causes of SCD become increasingly probable –
congenital structural or coronary arterial abnormalities, Aortic valve stenosis,
Mitral valve prolapse, Myocarditis, Dilated or hypertrophic Cardiomyopathy,
Pulmonary hypertension, Hereditary or acquired abnormalities of the cardiac
conduction system, Isolated hypertrophy, hypertensive or unknown causes.
Increased cardiac mass is an independent risk factor for cardiac death; thus, some
young patient who die suddenly including athletes, have hypertensive hypertrophy
or unexplained increased cardiac mass as a only finding.
This was all regarding the Pathogenesis of IHD. Though the severity of IHD
is notifying yet taking strict preventive measures at the earliest and following a
disciplined lifestyle can prevent it. Then definitely Hrudroga can be Prevented and
Conquered!

• SUBMITTED BY:-
GAURAV M. JADHAV
S.Y.B.A.M.S.
Pdm.Dr.D.Y.PATIL COLLEGE OF
AYURVED, NERUL

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