“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.

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IHD 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

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for the 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

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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. JADHAVS.Y.B.A.M.S.Pdm.Dr.D.Y.PATIL COLLEGE OF AYURVED, NERUL

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