PREFACE

This project shows the original research work done by me on

role of 5th Medical Herbal (Electropathy) in coronary artery
diseases. The work is purley based on complete laboratory data
and approved by the cardiologist.
I have tried to use the nature’s power to cure of heart disease.
This work has shown tremendous results but further study is
required to see the long term effects.

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 INTRODUCTION

CORONARY HEART DISEASE

Coronary artery disease is the buildup of plaque in the arteries that
supply oxygen-rich blood to your heart. Plaque causes a narrowing or
blockage that could result in a heart attack. Symptoms include chest pain
or discomfort and shortness of breath. Treatments include lifestyle
changes and medications that target your risk factors and/or possibly
surgery

What is coronary artery disease?

Coronary artery disease is a narrowing or blockage of your coronary
arteries usually caused by the buildup of fatty material called plaque.
Coronary artery disease is also called coronary heart disease, ischemic
heart disease and heart disease

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 CORONARY HEART DISEASE
Coronary artery disease is the buildup of plaque in the arteries that
supply oxygen-rich blood to your heart. Plaque causes a narrowing or
blockage that could result in a heart attack. Symptoms include chest pain
or discomfort and shortness of breath. Treatments include lifestyle
changes and medications that target your risk factors and/or possibly
surgery.
Where are the coronary arteries? What do they do?
Coronary arteries are the blood vessels that supply oxygen-rich blood to
your heart muscle to keep it pumping. The coronary arteries are directly
on top of your heart muscle. You have four main coronary arteries:
 The right coronary artery.
 The left coronary artery.
 The left anterior descending artery.
 The left circumflex artery

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 What happens to the arteries in coronary artery disease?
Coronary artery disease is caused by atherosclerosis. Atherosclerosis is
the buildup of plaque inside your arteries. Plaque consists of cholesterol,
fatty substances, waste products, calcium and the clot-making substance
fibrin. As plaque continues to collect on your artery walls, your arteries
narrow and stiffen. Plaque can clog or damage your arteries, which

4
limits or stops blood flow to your heart muscle. If your heart does not
get enough blood, it can't get the oxygen and nutrients it needs to work
properly. This condition is called ischemia Not getting enough blood
supply to your heart muscle can lead to chest discomfort or chest pain
(called angina). It also puts you at risk for a heart attack.

How does plaque build-up in the arteries?

Coronary artery disease happens in everyone. The speed at which it
develops differs from person to person. The process usually starts when
you are very young. Before your teen years, the blood vessel walls start
to show streaks of fat. As plaque deposits in your artery’s inner walls,
your body fights back against this ongoing process by sending white
blood cells to attack the cholesterol, but the attack causes more
inflammation. This trigger yet other cells in the artery wall to form a soft
cap over the plaque. This thin cap over the plaque can break open (due
to blood pressure or other causes). Blood cell fragments called platelets
stick to the site of “the injury,” causing a clot to form. The clot further
narrows arteries.
Sometimes a blood clot breaks apart on its own. Other times the clot
blocks blood flow through the artery, depriving the heart of oxygen and
causing a heart attack

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 Who gets coronary artery disease?

You have an increased risk of coronary artery disease if you:

 Have a high cholesterol level (especially a high LDL “bad”
cholesterol level and a low HDL “good “cholesterol level).
 Have high blood pressure.
 Family history of heart disease.
 Have diabetes.
 Are a smoker.
 Are a man over 45 years of age or a post-menopausal
woman.
 Are overweight.
 Are physically inactive.
 Are Black, Mexican American, Native American, Native
Hawaiian or Asian American. The increased risks are caused
by higher rates of high blood pressure, obesity and diabetes
in these populations.

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 What are the symptoms of coronary artery disease?

You may not know you have coronary artery disease since you may not
havesymptoms at first. The buildup of plaque in your arteries takes
years to decades. Butas your arteries narrow, you may notice mild
symptoms that indicate your heart
is pumping harder to deliver oxygen-rich blood to your body. The most
commonsymptoms are chest pain or shortness of breath, especially after
light physical activitylike walking up stairs, but even at rest.
Sometimes you won’t know you have coronary artery disease until you
have a heartattack. Symptoms of a heart attack include

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 Chest discomfort (angina) described as heaviness, tightness,
pressure,
aching, burning, numbness, fullness, squeezing or a dull ache. The
discomfort canalso spread to or only be felt in your left shoulder,
arms, neck, back or jaw.
 Feeling tired.
 Dizziness, lightheadedness
 Nausea.
 Weakness.

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Symptoms of a heart attack in women can be slightly different and
include:
 Discomfort or pain in the shoulders, neck, abdomen (belly) and/or
back.
 Feeling of indigestion or heartburn.
 Unexplained anxiety.
 Cold sweat

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 What should I do if I have symptoms of coronary artery
diseas?

Because the symptoms of coronary artery disease can be symptoms of

a heart attack, you need to seek immediate help. Call 911 if you think
you are having symptoms of a heart attack.
If a blood clot in a coronary artery has broken loose and moved into
your brain, it can cause a stroke, although this is rare. Symptoms of a
stroke include
 Drooping on one side of your face. Look at your smile in a
mirror or ask someone to check your smile.
 Arm weakness or numbness.
 Difficulty speaking/slurred speech.
If you experience any of these symptoms, Every minute you spend
without treatment increases your risk of long-term damage

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 How is coronary artery disease diagnosed?

First, unless your condition is an emergency (you’re having a heart

attack or stroke), your cardiologist (heartdoctor) will ask you about
your symptoms, take your medical history, review your risk factors
and perform a physical exam.
Diagnostic tests may include:

 Electrocardiograph tests (EKG): This test records the electrical

activity of the heart. Can detect heartattack, ischemia and heart
rhythm issues.

 Exercise stress tests: This is a treadmill test to determine how well

your heart functions when it’sworking the hardest. Can detect
angina and coronary blockages.
 Pharmacologic stress test: Instead of using exercise to test your
heart when it is working its hardest,medication is given to increase
your heart rate and mimic exercise. This test can detect angina
andcoronary blockages.

 Coronary calcium scan: This test measures the amount of calcium

in the walls of your coronaryarteries, which can be a sign of
atherosclerosis.

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 Echocardiogram: This test uses sound waves to see how well the
structures of your heart are workingand the overall function of
your heart.

 Blood tests: Many blood tests are ordered for factors that affect
arteries, such as triglycerides,cholesterol, lipoprotein, C-reactive
protein, glucose, HbA1c (a measure of diabetes control) and
other tests

 Cardiac catheterization: This test involves inserting small tubes

into the blood vessels of the heart toevaluate heart function
including the presence of coronary artery disease.Other diagnostic
imaging tests may include:

 Nuclear imaging: This test produces images of the heart after

administering a radioactive tracer.Computed tomography
angiogram: Uses CT and contrast dye to view 3D pictures of the
moving heart and detect blockages in the coronary arteries.

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 CARDIOVASCULAR SYSTEM

Cardiovascular system includes heart and blood vessels. Heart pumps

blood into the blood vessels.
Blood vessels circulate the blood throughout the body. Blood transports
nutrients and oxygen to the tissues and removes carbon dioxide and
waste products from the tissues.
HEART

Heart is a muscular organ that pumps blood throughout the circulatory

system. It is situated in between two lungs in the mediastinum. It is
made up of four chambers, two atria and two ventricles. The
musculature of ventricles is thicker than that of atria. Force of
contraction of heart depends upon the muscles.
RIGHT SIDE OF THE HEART

Right side of the heart has two chambers, right atrium and right
ventricle. Right atrium is a thin walled and
Low pressure chamber. It has got the pacemaker known as sinoatrial
node that produces cardiac impulses and atrioventricular node that
conducts the impulses to the ventricles.
Right atrium receives venous (deoxygenated) blood via two large veins:
1. Superior vena cava that returns venous blood from

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the head, neck and upper limbs
2. Inferior vena cava that returns venous blood from
lower parts of the body (Fig. 89.1). Right atrium communicates with
right ventricle
through tricuspid valve. Wall of right ventricle is thick. Venous blood
from the right atrium enters the right ventricle through this valve. From
the right ventricle, pulmonary artery arises. It carries the venous blood
from right ventricle to lungs. In the lungs, the deoxygenated blood is
oxygenated.

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 LEFT SIDE OF THE HEART

Left side of the heart has two chambers, left atrium and left ventricle.
Left atrium is a thin walled and low pressure chamber. It receives
oxygenated blood from the lungs through pulmonary veins. This is the
only exception in the body, where an artery carries venous blood and
vein carries the arterial blood.
Blood from left atrium enters the left ventricle through mitral valve
(bicuspid valve). Wall of the left ventricle is very thick. Left ventricle
pumps the arterial blood to different parts of the body through systemic
aorta.

SEPTA OF THE HEART

Right and left atria are separated from one another by a fibrous septum
called interatrial septum. Right
and left ventricles are separated from one another byinterventricular
septum. The upper part of this septum
is a membranous structure, whereas the lower part of it is muscular in
nature.

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 LAYERS OF WALL OF THE HEART

Heart is made up of three layers of tissues:

1. Outer pericardium
2. Middle myocardium
3. Inner endocardium.

PERICARDIUM

Pericardium is the outer covering of the heart. It is made

up of two layers:
i. Outer parietal pericardium
ii. Inner visceral pericardium.
The space between the two layers is called pericardial cavity or
pericardial space and it contains a thin film of fluid.
i. Outer Parietal Pericardium
Parietal pericardium forms a strong protective sac for the heart. It helps
also to anchor the heart within the
mediastinum.

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 Parietal pericardium is made up two layers:
a. Outer fibrous layer
b. Inner serous layer.
Fibrous layer:
Fibrous layer of the parietal pericardium is formed by thick fibrous
connective tissue. It is attached to the
Diaphragm and it is continuous with tunica adventitia (outer wall) of the
blood vessels, entering and leaving the heart. It is attached with
diaphragm below. Because of the fibrous nature, it protects the heart
from over stretching.
Serous layer:
Serous layer is formed by mesothelium, together with a small amount of
connective tissue. Mesothelium contains squamous epithelial cells which
secrete a small amount of fluid, which lines the pericardial space. This
fluid prevents friction and allows free movement of

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heart within pericardium, when it contracts and relaxes. The total
volume of this fluid is only about 25 to 35 mL.

ii. Inner Visceral Pericardium

Inner visceral pericardium lines the surface of myocardium. It is made

up of flattened epithelial cells. This layer is also known as epicardium.

MYOCARDIUM

Myocardium is the middle layer of wall of the heart and it is formed by

cardiac muscle fibers or cardiac
myocytes. Myocardium forms the bulk of the heart and it is responsible
for pumping action of the heart. Unlike skeletal muscle fibers, the
cardiac muscle fibers are involuntary in nature.
Myocardium has three types of muscle fibers:

i. Muscle fibers which form contractile unit of

heart
ii. Muscle fibers which form pacemaker
iii. Muscle fibers which form conductive system.

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 ENDOCARDIUM

Endocardium is the inner most layer of heart wall. It is a thin, smooth

and glistening membrane. It is formed by a single layer of endothelial
cells, lining the inner surface
of the heart. Endocardium continues as endothelium of the blood
vessels.

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 valves of the heart

The four valves of the heart allow blood to flow through the heart in the
right direction. The valves open or close each time the heart beats.
Problems with the heart valves can lead to palpitations, chest pain, and
other symptoms.

The four heart valves are:

 the mitral valve

 the aortic valve
 the tricuspid valve
 the pulmonic valve

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Doctors call the mitral and tricuspid valves the atrioventricular valves,
and the aortic and pulmonic valves the semilunar valves. Keep reading
to learn more about each of the four heart valves. blood flows in only
one direction. The valves close off parts of the heart, preventing
the blood from flowing backward.

1. The process begins when oxygen-depleted blood (from the

arms, legs, body, and head) enters the right atrium. This is
the upper chamber on the right side of the heart and is the
storage chamber.
2. The blood then flows through the tricuspid valve into the right
ventricle, which is the lower right pumping chamber.
3. The ventricle pumps this blood through the pulmonary valve
to the pulmonary artery, where it enters the lungs for
oxygenation.
4. Oxygen-rich blood re-enters the heart through the left atrium,
which is the upper left chamber.
5. It then flows through the mitral valve to the left ventricle, or
the left pumping chamber.
6. Finally, it moves through the aortic valve and then through
the aorta to the rest of the body.

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 The four heart valves
The four heart valvesTrusted Source all have a role in ensuring that the blood
can only flow in one direction. The four heart valves are:

Tricuspid valve

The tricuspid valve is named because it has three flaps called cusps, or leaflets.
Blood flows through this valve after leaving the right atrium. After passing
through the tricuspid valve, blood flows to the right ventricle. People with a rare
disorder Trusted Source called tricuspid atresia are born without a tricuspid
valve. Tricuspid atresia means that blood cannot flow from the right atrium to
the right ventricle. Tricuspid regurgitation means that this valve cannot fully
close, while tricuspid stenosis causes the valve to thicken, narrowing its
opening.

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 Pulmonic valve

The pulmonic, or pulmonary valve, is the next valve that deoxygenated blood
flows through. It closes off the right ventricle and opens to allow the blood to
flow to the lungs. Stenosis of the pulmonary valve causes this valve to thicken
with time, narrowing its opening and making blood flow more slowly.
Regurgitation prevents the valve from closing fully, causing blood to flow
backward into the right ventricle. A rare pulmonic valve disorderTrusted Source
called pulmonary atresia means that a person is born without this valve.

Mitral valve

The mitral valve closes off the left atrium, allowing oxygenated blood from the
lungs to flow through to the left ventricle. One of the most common
typesTrusted Source of mitral valve issues is mitral valve prolapse (MVP). This
causes the leaflets of the mitral valve to fit together poorly or buckle backward,
allowing blood to flow back to the left atrium. Some connective tissue disorders
may also damage the mitral valve, causing MVP. Mitral valve prolapse can
result in mitral valve regurgitation, which causes blood to flow backward. A
heart attack or enlargement of the heart can cause the leaflets of the valve to
spread apart, leading to mitral regurgitation.
Mitral valve stenosis hardens and thickens the walls of the mitral valve,
narrowing the opening and causing blood to flow more slowly.

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 Aortic valve

The aortic valve is the final valve that oxygen-rich blood passes through before
exiting the heart and coursing through the rest of the body. The valve prevents
blood from flowing back to the left ventricle. Aortic regurgitation, or aortic
insufficiency, means that the aortic valve does not fully close, allowing blood to
flow backward. Aortic stenosis means that the aortic valve thickens or hardens,
narrowing the path through which blood can flow. This delays or prevents
adequate blood flow to the rest of the body.

Coronary Arteries

Coronary arteries supply blood to the heart muscle. Like all other tissues in the
body, the heart muscle needs oxygen-rich blood to function. Also, oxygen-
depleted blood must be carried away. The coronary arteries wrap around the
outside of the heart. Small branches dive into the heart muscle to bring it blood.
Exterior of the heart and coronary arteries

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 What are the different coronary arteries?

The 2 main coronary arteries are the left main and right coronary arteries.

Left main coronary artery (LMCA). The left main coronary artery supplies
blood to the left side of the heart muscle (the left ventricle and left atrium). The
left main coronary divides into branches:

The left anterior descending artery branches off the left coronary artery and
supplies blood to the front of the left side of the heart.

The circumflex artery branches off the left coronary artery and encircles the
heart muscle. This artery supplies blood to the outer side and back of the heart.

Right coronary artery (RCA). The right coronary artery supplies blood to the
right ventricle, the right atrium, and the SA (sinoatrial) and AV
(atrioventricular) nodes, which regulate the heart rhythm. The right coronary
artery divides into smaller branches, including the right posterior descending
artery and the acute marginal artery. Together with the left anterior descending
artery, the right coronary artery helps supply blood to the middle or septum of
the heart.
Smaller branches of the coronary arteries include: obtuse marginal (OM), septal
perforator (SP), and diagonals.

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 Why are the coronary arteries important?

Since coronary arteries deliver blood to the heart muscle, any coronary artery
disorder or disease can have serious implications by reducing the flow of
oxygen and nutrients to the heart muscle. This can lead to a heart attack and
possibly death. Atherosclerosis (a buildup of plaque in the inner lining of an
artery causing it to narrow or become blocked) is the most common cause of
heart disease.

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 conduction system of the heart
The cardiac conduction system is a collection of nodes and specialised
conduction cells that initiate and co-ordinate contraction of the heart muscle. It
consists of:
 Sinoatrial node
 Atrioventricular node
 Atrioventricular bundle (bundle of His)
 Purkinje fibres
In this article, we shall look at the anatomy of the cardiac conduction system –
its structure, function and clinical correlations.

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 Components of the Cardiac Conduction System
Sinoatrial Node

The sinoatrial (SA) node is a collection of specialised cells (pacemaker cells),

and is located in the upper wall of the right atrium, at the junction where the
superior vena cava enters.

These pacemaker cells can spontaneously generate electrical impulses. The

wave of excitation created by the SA node spreads via gap junctions across both
atria, resulting in atrial contraction (atrial systole) – with blood moving from the
atria into the ventricles.

The rate at which the SA node generates impulses is influenced by the

autonomic nervous system:

Sympathetic nervous system – increases firing rate of the SA node, and thus
increases heart rate.
Parasympathetic nervous system – decreases firing rate of the SA node, and
thus decreases heart rate.

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Atrioventricular Node
After the electrical impulses spread across the atria, they converge at the
atrioventricular node – located within the atrioventricular septum, near the
opening of the coronary sinus.

The AV node acts to delay the impulses by approximately 120ms, to ensure the
atria have enough time to fully eject blood into the ventricles before ventricular
systole.
The wave of excitation then passes from the atrioventricular node into the
atrioventricular bundle.

Atrioventricular Bundle
The atrioventricular bundle (bundle of His) is a continuation of the specialised
tissue of the AV node, and serves to transmit the electrical impulse from the AV
node to the Purkinje fibres of the ventricles.

It descends down the membranous part of the interventricular septum, before

dividing into two main bundles:

Right bundle branch – conducts the impulse to the Purkinje fibres of the right
ventricle
Left bundle branch – conducts the impulse to the Purkinje fibres of the left
ventricle.

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Purkinje Fibres

The Purkinje fibres (sub-endocardial plexus of conduction cells) are a network

of specialised cells. They are abundant with glycogen and have extensive gap
junctions.

These cells are located in the subendocardial surface of the ventricular walls,
and are able to rapidly transmit cardiac action potentials from the
atrioventricular bundle to the myocardium of the ventricles.

This rapid conduction allows coordinated ventricular contraction (ventricular

systole) and blood is moved from the right and left ventricles to the pulmonary
artery and aorta respectively.

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 Cardiac Cycle

The human heart is a muscular organ that is about the size of a fist. It pumps
blood through a set of connections between arteries and veins, known as the
cardiovascular system. It involves systemic and pulmonary circulation.

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Table of Contents

 Meaning
 Diagram
 Physiology
 Phases
 Duration
Cardiac Cycle Definition
“Cardiac cycle refers to the sequence of events that take place when the heart
beats.”

What is Cardiac Cycle?

The cardiac cycle attributes to a comprehensive heartbeat from its production to

the commencement of the next beat. It comprises diastole, the systole, and the
intervening pause. The occurrence of a cardiac cycle is illustrated by a heart
rate, which is naturally indicated as beats per minute. A healthy human heart
beats 72 times per minute which states that there are 72 cardiac cycles per
minute. The cardiac cycle involves a complete contraction and relaxation of
both the atria and ventricles and the cycle last approximately 0.8 seconds.

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Cardiac Cycle Diagram
The diagram below represents the different phases of the cardiac cycle. The
atrial systole, ventricular systole, atrial diastole, and ventricular diastole are
clearly mentioned in the cardiac cycle diagram given below.

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34
Cardiac Cycle
Cardiac Cycle Physiology
The human heart consists of four chambers, comprising left and right halves.
Two upper chambers include left and right atria; lower two chambers include
right and left ventricles. The key function of the right ventricle is to pump
deoxygenated blood through the pulmonary arteries and pulmonary trunk to the
lungs. While the left ventricle is responsible for pumping newly oxygenated
blood to the body through the aorta.
Cardiac Cycle Phases
Following are the different phases that occur in a cardiac cycle:

Atrial Diastole: In this stage, chambers of the heart are calmed. That is when the
aortic valve and pulmonary artery closes and atrioventricular valves open, thus
causing chambers of the heart to relax.

Atrial Systole: At this phase, blood cells flow from atrium to ventricle and at
this period, atrium contracts.

Isovolumic Contraction: At this stage, ventricles begin to contract. The

atrioventricular valves, valve, and pulmonary artery valves close, but there
won’t be any transformation in volume.

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Ventricular Ejection: Here ventricles contract and emptying. Pulmonary artery
and aortic valve close.
Isovolumic Relaxation: In this phase, no blood enters the ventricles and
consequently, pressure decreases, ventricles stop contracting and begin to relax.
Now due to the pressure in the aorta – pulmonary artery and aortic valve close.

Ventricular Filling Stage: In this stage, blood flows from atria into the
ventricles. It is altogether known as one stage (first and second stage). After that,
they are three phases that involve the flow of blood to the pulmonary artery
from ventricles.

Duration of Cardiac Cycle

In a normal person, a heartbeat is 72 beats/minute. So, the duration of one
cardiac cycle can be calculated as:

1/72 beats/minute=.0139 minutes/beat

At a heartbeat 72 beats/minute, duration of each cardiac cycle will be 0.8
seconds.
Duration of different stages of the cardiac cycle is given below:
Atrial systole: continues for about 0.1 seconds
Ventricular systole: continues for about 0.3 seconds
Atrial diastole: continues for about 0.7 seconds
Ventricular diastole: continues for about 0.5 seconds

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 OBJECTIVE: To study the various types of heart diseases

MATERIALS REQUIRED:
1) A sample of heart
2) A white paper to note down observations
3) A pen

Procedure: 1. STUDY OF A HEART WITH CORONARY ARTERY

DISEASE

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Coronary artery disease (CAD), also known as ischemic heart disease (IHD),
refers to a group of diseases which includes stable angina, unstable angina,
myocardial infarction, and sudden cardiac death. It is within the group of
cardiovascular diseases of which it is the most common type. A common
symptom is chest pain or discomfort which may travel into the shoulder, arm,
back, neck, or jaw. Occasionally it may feel like heartburn. Usually symptoms
occur with exercise or emotional stress, last less than a few minutes, and
improve with rest. Shortness of breath may also occur and sometimes no
symptoms are present. Occasionally, the first sign is a heart attack. Other
complications include heart failure or an abnormal heartbeat.

Risk factors include high blood pressure, smoking, diabetes, lack of exercise,
obesity, high blood cholesterol, poor diet, depression, and excessive alcohol.
The underlying mechanism involves reduction of blood flow and oxygen to the
heart muscle due to atherosclerosis of the arteries of the heart. A number of tests
may help with diagnoses including:
electrocardiogram, cardiac stress
testing, coronary computed
tomographic angiography, and coronary
angiogram, among others.

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Ways to reduce CAD risk include eating a healthy diet, regularly exercising,
maintaining a healthy weight, and not smoking. Medications for diabetes, high
cholesterol, or high blood pressure are sometimes used. There is limited
evidence for screening people who are at low risk and do not have symptoms.
Treatment involves the same measures as prevention. Additional medications
such as antiplatelets (including aspirin), beta blockers, or nitroglycerin may be
recommended. Procedures such as percutaneous coronary intervention (PCI) or
coronary artery bypass surgery (CABG) may be used in severe disease. In those
with stable CAD it is unclear if PCI or CABG in addition to the other treatments
improves life expectancy or decreases heart attack risk.

In 2015 CAD affected 110 million people and resulted in 8.9 million deaths. It
makes up 15.9% of all deaths making it the most common cause of death
globally. The risk of death from CAD for a given age has decreased between
1980 and 2010, especially in developed countries. The number of cases of CAD
for a given age has also decreased between 1990 and 2010.In the United States
in 2010 about 20% of those over 65 had CAD, while it was present in 7% of
those 45 to 64, and 1.3% of those 18 to 45. Rates are higher among men than
women of a given age.

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2. STUDY OF HEART WITH ISCHEMIA

ISCHEMIA is a condition where the flow of oxygen-rich blood to a part of the

body is restricted. Cardiac ischemia refers to lack of blood flow and oxygen to
the heart muscle.
Cardiac ischemia happens when an artery becomes narrowed or blocked for a
short time, preventing oxygen-rich blood from reaching the heart. If ischemia is
severe or lasts too long, it can cause a heart attack (myocardial infarction) and
can lead to heart tissue death. In most cases, a temporary blood shortage to the

40
heart causes the pain of angina pectoris. But in other cases, there is no pain.
These cases are called silent ischemia.
Silent ischemia may also disturb the heart’s rhythm. Abnormal rhythms such as
ventricular tachycardia or ventricular fibrillation can interfere with the heart’s
pumping ability and can cause fainting or even sudden cardiac death.

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 3. STUDY OF ANGINA OF HEART

Angina, also known as angina pectoris, is chest pain or pressure, usually due to
not enough blood flow to the heart muscle.

Angina is usually due to obstruction or spasm of the coronary arteries. Other

causes include anemia, abnormal heart rhythms, and heart failure. The main
mechanism of coronary artery obstruction is an atherosclerosis. The term
derives from the Latin angere ("to strangle") and pectus ("chest"), and can
therefore be translated as "a strangling feeling in the chest".

42
There is a weak relationship between severity of pain and degree of oxygen
deprivation in the heart muscle (i.e., there can be severe pain with little or no
risk of a myocardial infarction (heart attack) and a heart attack can occur
without pain). In some cases, angina can be quite severe, and in the early 20th
century this was a known sign of impending death. However, given current
medical therapies, the outlook has improved substantially. People with an
average age of 62 years, who have moderate to severe degrees of angina
(grading by classes II, III, and IV) have a 5-year survival rate of approximately
92%.
Worsening angina attacks, sudden-onset angina at rest, and angina lasting more
than 15 minutes are symptoms of unstable angina (usually grouped with similar
conditions as the acute coronary syndrome). As these may precede a heart
attack, they require urgent medical attention and are, in general, treated in
similar fashion to myocardial infarction.

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 Stable angina

Also known as 'effort angina', this refers to the classic type of angina related to
myocardial ischemia. A typical presentation of stable angina is that of chest
discomfort and associated symptoms precipitated by some activity (running,
walking, etc.) with minimal or non-existent symptoms at rest or after
administration of sublingual nitroglycerin. Symptoms typically abate several
minutes after activity and recur when activity resumes. In this way, stable
angina may be thought of as being similar to intermittent claudication
symptoms. Other recognized precipitants of stable angina include cold weather,
heavy meals, and emotional stress.

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 Unstable angina

Unstable angina (UA) (also "crescendo angina"; this is a form of acute coronary
syndrome) is defined as angina pectoris that changes or worsens.
It has at least one of these three features:
it occurs at rest (or with minimal exertion), usually lasting more than 10 minutes
it is severe and of new onset (i.e., within the prior 4–6 weeks)
it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or
frequent than before).UA may occur unpredictably at rest, which may be a
serious indicator of an impending heart attack. What differentiates stable angina
from unstable angina (other than symptoms) is the Pathophysiology of the
atherosclerosis. The Pathophysiology of unstable angina is the reduction of
coronary flow due to transient platelet aggregation on apparently normal
endothelium, coronary artery spasms, or coronary thrombosis. The process
starts with atherosclerosis, progresses through inflammation to yield an active
unstable plaque, which undergoes thrombosis and results in acute myocardial
ischemia, which, if not reversed, results in cell necrosis (infarction). Studies
show that 64% of all unstable anginas occur between 22:00 and 08:00 when
patients are at rest.

45
 4. STUDY A HEART WITH MYOCARDIAL INFARCTION

Myocardial infarction (MI), commonly known as a heart attack occurs when

blood flow decreases or stops to a part of the heart, causing damage to the heart
muscle. The most common symptom is chest pain or discomfort which may
travel into the shoulder, arm, back, neck, or jaw. Often it occurs in the centre or
left side of the chest and lasts for more than a few minutes. The discomfort may
occasionally feel like heartburn. Other symptoms may include shortness of
breath, nausea, feeling faint, a cold sweat, or feeling tired. About 30% of people
have typical symptoms. Women more often have atypical symptoms than men.
Among those over 75 years old, about 5% have had an MI with little or no
history of symptoms. An MI may cause heart failure, an irregular heartbeat,
carcinogenic shock, or cardiac arrest.

46
Most MIs occur due to coronary artery disease. Risk factors include high blood
pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol,
poor diet, and excessive alcohol intake, among others. The complete blockage
of a coronary artery caused by a rupture of an atherosclerotic plaque is usually
the underlying mechanism of an MI. MIs are less commonly caused by
coronary artery spasms, which may be due to cocaine, significant emotional
stress, and extreme cold, among others. A number of tests are useful to help
with diagnosis, including electrocardiograms (ECGs), blood tests, and coronary
angiography. An ECG, which is a recording of the heart's electrical activity,
may confirm an ST elevation MI (STEMI) if ST elevation is present.
Commonly used blood tests include trooping and less often creatine kinase MB.

Treatment of an MI is time-critical. Aspirin is an appropriate immediate

treatment for a suspected MI. Nitroglycerin or opioids may be used to help with
chest pain; however, they do not improve overall outcomes. Supplemental
oxygen is recommended in those with low oxygen levels or shortness of breath.
In a STEMI, treatments attempt to restore blood flow to the heart, and include
percutaneous coronary intervention (PCI), where the arteries are pushed open
and may be stented, or thrombolysis, where the blockage is removed using
medications. People who have a non-ST elevation myocardial infarction
(NSTEMI) are often managed with the blood thinner heparin, with the
additional use of PCI in those at high risk. In people with blockages of multiple

47
coronary arteries and diabetes, coronary artery bypass surgery (CABG) may be
recommended rather than angioplasty. After an MI, lifestyle modifications,
along with long term treatment with aspirin, beta blockers, and statins, are
typically recommended.

Instable angina, the developing atheroma is protected with a fibrous cap. This
cap may rupture in unstable angina, allowing blood clots to precipitate and
further decrease the area of the coronary vessel's lumen. This explains why, in
many cases, unstable angina develops independently of activity.

48
 5. STUDY OF HEART FAILURE

Heart failure (HF), often referred to as congestive heart failure (CHF), is when
the heart is unable to pump sufficiently to maintain blood flow to meet the
body's needs. Signs and symptoms commonly include shortness of breath,
excessive tiredness, and leg swelling. The shortness of breath is usually worse
with exercise, while lying down, and may wake the person at night. A limited
ability to exercise is also a common feature. Chest pain, including angina, does
not typically occur due to heart failure.

49
Common causes of heart failure include coronary artery disease including a
previous myocardial infarction (heart attack), high blood pressure, atrial
fibrillation, valvular heart disease, excess alcohol use, infection, and
cardiomyopathy of an unknown cause. These cause heart failure by changing
either the structure or the functioning of the heart. There are two main types of
heart failure: heart failure due to left ventricular dysfunction and heart failure
with normal ejection fraction depending on whether the ability of the left
ventricle to contract is affected, or the heart's ability to relax. The severity of
disease is usually graded by the degree of problems with exercise. Heart failure
is not the same as myocardial infarction (in which part of the heart muscle dies)
or cardiac arrest (in which blood flow stops altogether). Other diseases that may
have symptoms similar to heart failure include obesity, kidney failure, liver
problems, anemia, and thyroid disease.

50
The condition is diagnosed based on the history of the symptoms and a physical
examination with confirmation by echocardiography. Blood tests,
electrocardiography, and chest radiography may be useful to determine the
underlying cause. Treatment depends on the severity and cause of the disease.
In people with chronic stable mild heart failure, treatment commonly consists of
lifestyle modifications such as stopping smoking, physical exercise, and dietary
changes, as well as medications. In those with heart failure due to left
ventricular dysfunction, angiotensin converting enzyme inhibitorsor angiotensin
receptor blockers along with beta blockers are recommended. For those with
severe disease, aldosterone antagonists, or hydralazine with a nitrate may be
used. Diuretics are useful for preventing fluid retention. Sometimes, depending
on the cause, an implanted device such as a pacemaker or an implantable
cardiac defibrillator may be recommended. In some moderate or severe cases,
cardiac resynchronization therapy (CRT) or cardiac contractility modulation
may be of benefit. A ventricular assist device or occasionally a heart transplant
may be recommended in those with severe disease that persists despite all other
measures.

51
 6. TO STUDY A HEART WITH Heart arrhythmia

Heart arrhythmia (also known as arrhythmia, dysrhythmia, or irregular

heartbeat) is a group of conditions in which the heartbeat is irregular, too fast, or
too slow. A heart rate that is too fast – above 100 beats per minute in adults – is
called tachycardia and a heart rate that is too slow – below 60 beats per minute –
is called bradycardia. Many types of arrhythmia have no symptoms. When
symptoms are present these may include palpitations or feeling a pause between
heartbeats. In more serious cases there may be lightheadedness, passing out,
shortness of breath, or chest pain. While most types of arrhythmia are not
serious, some predispose a person to complications such as stroke or heart
failure. Others may result in cardiac arrest.

52
There are four main types of arrhythmia: extra beats, supraventricular
tachycardias, ventricular arrhythmias, and bradyarrhythmias. Extra beats
include premature atrial contractions, premature ventricular contractions, and
premature junctional contractions. Supraventricular tachycardias include atrial
fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia.
Ventricular arrhythmias include ventricular fibrillation and ventricular
tachycardia. Arrhythmias are due to problems with the electrical conduction
system of the heart. Arrhythmias may occur in children; however, the normal
range for the heart rate is different and depends on age. A number of tests can
help with diagnosis including an electrocardiogram(ECG) and Holter monitor.
Most arrhythmias can be effectively treated. Treatments may include
medications, medical procedures such as inserting a pacemaker, and surgery.
Medications for a fast heart rate may include beta blockers or agents that
attempt to restore a normal heart rhythm such as procainamide. This latter group
may have more significant side effects especially if taken for a long period of
time. Pacemakers are often used for slow heart rates. Those with an irregular
heartbeat are often treated with blood thinners to reduce the risk of
complications. Those who have severe symptoms from an arrhythmia may
receive urgent treatment with a controlled electric shock in the form of
cardioversion or defibrillation.
Arrhythmia affects millions of people. In Europe and North America, as of
2014, atrial fibrillation affects about 2% to 3% of the population. Atrial
fibrillation and atrial flutter resulted in 112,000 deaths in 2013, up from 29,000

53
in 1990. Sudden cardiac death is the cause of about half of deaths due to
cardiovascular disease or about 15% of all deaths globally. About 80% of
sudden cardiac death is the result of ventricular arrhythmias. Arrhythmias may
occur at any age but are more common among older people.

54
 Risk factors

Coronary artery disease is common. Age, genetics, other health conditions and
lifestyle choices can affect the health of the heart arteries.

Coronary artery disease risk factors include:

Age. Getting older increases the risk of damaged and narrowed arteries.

Sex. Men are generally at greater risk of coronary artery disease. However, the
risk for women increases after menopause.

Family history. A family history of heart disease makes you more likely to get
coronary artery disease. This is especially true if a close relative (parent, sibling)
developed heart disease at an early age. The risk is highest if your father or a
brother had heart disease before age 55 or if your mother or a sister developed it
before age 65.

Smoking. If you smoke, quit. Smoking is bad for heart health. People who
smoke have a significantly increased risk of heart disease. Breathing in
secondhand smoke also increases the risk.

55
High blood pressure. Uncontrolled high blood pressure can make arteries hard
and stiff (arterial stiffness). The coronary arteries may become narrow, slowing
blood flow.

High cholesterol. Too much bad cholesterol in the blood can increase the risk
of atherosclerosis. Bad cholesterol is called low-density lipoprotein (LDL)
cholesterol. Not enough good cholesterol — called high-density lipoprotein
(HDL) — also leads to atherosclerosis.

Diabetes. Diabetes increases the risk of coronary artery disease. Type 2

diabetes
and coronary artery disease share some risk factors, such as obesity and high
blood pressure.
Overweight or obesity. Excess body weight is bad for overall health. Obesity
can lead to type 2 diabetes and high blood pressure. Ask your health care
provider what a healthy weight is for you.

Chronic kidney disease. Having long-term kidney disease increases the risk of
coronary artery disease.
Not getting enough exercise. Physical activity is important for good health. A
lack of exercise (sedentary lifestyle) is linked to coronary artery disease and
some of its risk factors.

56
A lot of stress. Emotional stress may damage the arteries and worsen other risk
factors for coronary artery disease.

Unhealthy diet. Eating foods with a lot of saturated fat, trans fat, salt and sugar
can increase the risk of coronary artery disease.

Alcohol use. Heavy alcohol use can lead to heart muscle damage. It can also
worsen other risk factors of coronary artery disease.

Amount of sleep. Too little and too much sleep have both been linked to an
increased risk of heart disease.
Risk factors often occur together. One risk factor may trigger another.

When grouped together, certain risk factors make you even more likely to
develop coronary artery disease. For example, metabolic syndrome — a cluster
of conditions that includes high blood pressure, high blood sugar, excess body
fat around the waist and high triglyceride levels — increases the risk of
coronary artery disease.

Sometimes coronary artery disease develops without any classic risk factors.
Other possible risk factors for coronary artery disease may include:

57
Breathing pauses during sleep (obstructive sleep apnea). This condition causes
breathing to stop and start during sleep. It can cause sudden drops in blood
oxygen levels. The heart must work harder. Blood pressure goes up.
High-sensitivity C-reactive protein (hs-CRP). This protein appears in higher-
than-usual amounts when there's inflammation somewhere in the body. High
hs-CRP levels may be a risk factor for heart disease. It's thought that as coronary
arteries narrow, the level of hs-CRP in the blood goes up.

High triglycerides. This is a type of fat (lipid) in the blood. High levels may
raise the risk of coronary artery disease, especially for women.
Homocysteine. Homocysteine is an amino acid the body uses to make protein
and to build and maintain tissue. But high levels of homocysteine may increase
the risk of coronary artery disease.

Preeclampsia. This pregnancy complication causes high blood pressure and

increased protein in the urine. It can lead to a higher risk of heart disease later in
life.

Other pregnancy complications. Diabetes or high blood pressure during

pregnancy are also known risk factors for coronary artery disease.

58
Certain autoimmune diseases. People who have conditions such as
rheumatoid arthritis and lupus (and other inflammatory conditions) have an
increased risk of atherosclerosis.

59
 Prevention

Up to 90% of cardiovascular disease may be preventable if established

risk factors are avoided. Currently practiced measures to prevent
cardiovascular disease include:
Tobacco cessation and avoidance of second-hand smoke. Smoking
cessation reduces risk by about 35%.
A low-fat, low-sugar, high-fiber diet including whole grains and fruit
and vegetables. Dietary interventions are effective in reducing
cardiovascular risk factors over a year, but the longer term effects of
such interventions and their impact on cardiovascular disease events is
uncertain.
At least 150 minutes (2 hours and 30 minutes) of moderate exercise per
week. Exercise-based cardiac rehabilitation reduces risk of subsequent
cardiovascular events by 26%, but there have been few high quality
studies of the benefits of exercise training in people with increased
cardiovascular risk but no history of cardiovascular disease.
Limit alcohol consumption to the recommended daily limits; People who
moderately consume alcoholic drinks have a 25–30% lower risk of
cardiovascular disease.
Lower blood pressure, if elevated. A 10 mmHg reduction in blood
pressure reduces risk by about 20%.
Decrease non-HDL cholesterol. Statin treatment reduces cardiovascular
mortality by about 31%.

60
Decrease body fat if overweight or obese. The effect of weight loss is
often difficult to distinguish from dietary change, and evidence on
weight reducing diets is limited. In observational studies of people with
severe obesity, weight loss following bariatric surgery is associated with
a 46% reduction in cardiovascular risk.
Decrease psychosocial stress. This measure may be complicated by
imprecise definitions of what constitute psychosocial
interventions. Mental stress–induced myocardial ischemia is associated
with an increased risk of heart problems in those with previous heart
disease. Severe emotional and physical stress leads to a form of heart
dysfunction known as Takotsubo syndrome in some people. Stress,
however, plays a relatively minor role in hypertension. Specific
relaxation therapies are of unclear benefit.

Diet
A diet high in fruits and vegetables decreases the risk of cardiovascular
disease and death. Evidence suggests that the Mediterranean diet may
improve cardiovascular outcomes. There is also evidence that a
Mediterranean diet may be more effective than a low-fat diet in bringing
about long-term changes to cardiovascular risk factors (e.g.,
lower cholesterol level and blood pressure). The DASH diet (high in
nuts, fish, fruits and vegetables, and low in sweets, red meat and fat) has
been shown to reduce blood pressure, lower total and low density

61
lipoprotein cholesterol and improve metabolic syndrome; but the long-
term benefits outside the context of a clinical trial have been
questioned. A high fiber diet appears to lower the risk.
Total fat intake does not appear to be an important risk factor. A diet
high in trans fatty acids, however, does increase rates of cardiovascular
disease. Worldwide, dietary guidelines recommend a reduction
in saturated fat. However, there are some questions around the effect of
saturated fat on cardiovascular disease in the medical literature. Benefits
from replacement with polyunsaturated fat appears greatest; however,
supplementation with omega-3 fatty acids (a type of polysaturated fat)
does not appear to have an effect.

Medication
Blood pressure medication reduces cardiovascular disease in people at
risk, irrespective of age, the baseline level of cardiovascular risk, or
baseline blood pressure. The commonly-used drug regimens have
similar efficacy in reducing the risk of all major cardiovascular events,
although there may be differences between drugs in their ability to
prevent specific outcomes. Larger reductions in blood pressure produce
larger reductions in risk, and most people with high blood pressure
require more than one drug to achieve adequate reduction in blood
pressure.

62
Statins are effective in preventing further cardiovascular disease in
people with a history of cardiovascular disease. Anti-diabetic
medication may reduce cardiovascular risk in people with Type 2
Diabetes, although evidence is not conclusive. Aspirin has been found to
be of only modest benefit in those at low risk of heart disease as the risk
of serious bleeding is almost equal to the benefit with respect to
cardiovascular problems. In those at very low risk it is not
recommended. The United States Preventive Services Task
Force recommends against use of aspirin for prevention in women less
than 55 and men less than 45 years old; however, in those who are older
it is recommends in some individuals.

63
The use of vasoactive agents for people with pulmonary hypertension
with left heart disease or hypoxemic lung diseases may cause harm and
unnecessary expense.

Physical activity
A systematic review estimated that inactivity is responsible for 6% of
the burden of disease from coronary heart disease worldwide. The
authors estimated that 121,000 deaths from coronary heart disease could
have been averted in Europe in 2008, if physical inactivity had been
removed. A Cochrane review found some evidence that yoga has
beneficial effects on blood pressure and cholesterol, but studies included
in this review were of low quality.

64
 How is coronary artery disease treated?

Your healthcare provider will talk to you about the best treatment plan
for you. Follow your treatment planto reduce your risk of problems that
can result from coronary artery disease, like heart attack and stroke.
Lifestyle changes The first step in treating coronary artery disease is to
reduce your risk factors. This involves making changes in your lifestyle.
 Don’t smoke. If you smoke or use tobacco products, quit. Ask your
healthcare providers about ways to quit, including programs and
medications.
 Manage health problems like high cholesterol, high blood pressure
and diabetes
 Eat a heart-healthy diet. Talk to your healthcare provider or a
registered dietitian about ways
tochange your diet to reduce your risk of heart disease. Good dietar
y choices include theMediterranean and DASH diets.
 Limit alcohol use. Limit daily drinks to no more than one drink per
day for women and two drinks per day for men.
 Increase your activity level. Exercise helps you lose weight,
improve your physical condition andrelieve stress. Most people
can reduce their risk of heart attack by doing 30 minutes of
walking fivetimes per week or walking 10,000 steps per day. Talk
to your healthcare provider before you startany exercise

65
 program.MedicationsYour healthcare provider will recommend
medications to best manage your risk factors for heart
disease.Types of heart-related medications that may be selected for
you include:
 Medication to lower your cholesterol levels, such as stati
ns, bile acid sequestrants, niacin andfibrates.
 Medications to lower blood pressure, such as beta blockers,
calcium channel blockers, angiotensin-converting enzyme (ACE)
inhibitors or angiotensin II receptor blockers.
 Medications to stop angina, such as nitrates/nitroglycerin or
ranolazine.
 Medications to reduce the risk of blood clots, such as ant
icoagulants (including aspirin) andantiplatelets.If you have
diabetes and coronary artery disease, you’ll be prescribed
medications to lower your blood sugar level.

It's important to take all medications as prescribed, including those for

heart disease and all other healthconditions. Talk to your healthcare
provider if you have any questions or concerns about which
medicationsto take or how to take them.Interventional procedures are
nonsurgical treatments to get rid of plaque buildup in the arteries and
prevent blockages. Common procedures are balloon angioplasty and sten

66
ting. These procedures are done with along, thin tube called a catheter. It
is inserted into an artery in the wrist or the top of the leg through a
smallincision and guided to the blocked or narrowed area of the artery.
The balloon widens the diameter of theartery to restore blood flow to the
heart. A stent (a small metal spring-like scaffold) is left in place
to keepyour artery open.Coronary artery bypass graft (CABG) surgery
involves creating a new path for blood to flow when there is a blockage
in the coronary arteries. In most cases, the surgeon removes blood
vessels from your chest, arm or leg, and creates a new pathway to
deliver oxygen-rich blood to the
heart.If traditional treatment options are not successful, your c
ardiologist may recommend other treatmentoptions, such as
enhanced external counterpulsation (EECP). In this procedure, inflatable
cuffs (like blood pressure cuffs) are used to squeeze the blood vessels in
your lower body. This helps improve blood
flow tothe heart and helps create natural bypasses (collateral ci
rculation) around blocked coronary arteries.Enhanced external
counterpulsation is a possible treatment for those with chronic
stable angina who can’thave an invasive procedure or bypass surgery
and don't get relief from medication.

67
 OBSERVATIONS

This study was conducted in 25 patients.

Patients varied in the age group of 35 years to 70 years.

 15 patients were males & 10 were females.

 18 patients had severe coronary artery disease, out of which 8 had

already suffered from myocardial infarction, 10 patients had
angina on effort & their treadmill test before instituting the therapy
was strongly positive.

 7 patients were having hypertension.

 3 patients diabetes.

 All the atients were taken up for lipid profile before instituting the
therapy was shown positive.

 20 patients had high cholesterol level & high triglycerides and low
hdr levels.

Five patients had only hypertriglyceridemia

68
Arjuna +Allium satvum + Amlaki + L1 medicine was given for
3 months & lipid profile was repeated at one month interval.

69
 PROGRESS

1. All the patients having angina improved remarkably. Out

of ten patiemts with angina, 8 patients ere selected to TMT
after 3 months of therapy . all the patients did well on
TMT & test through positive at the nd of months, showed
significant on improvements in their exercise tolerance,
depression in St segment & symptomatic improvement.

2. Patients with myocardial infarction did show improvement

in system improvement but those with did not much
improvement.

3. All the patients with dyslipidemia were previously taking

over cholesterol lowering agents like simvastatin,
atorvastatin & finofibrate with no improvement in lipid
profile. they were subjected to mono therapy & all the
pervious medicines were withdrawn. Their lipid profile
also showed saifnicant improvement.

70
4. All the patients with dyslipdemia, showed remarkable &
significant improvement in their lipid profile. Cholesterol
level decreased by 50% triglyceride levels decreased by 47
% & Hdl levels by 24%.

5. 40% of patients showed weight loss of about 5- 10 kg in

space were 3 times.

71
 Summary
 Treatment with arjuna + allium sativum + amlaki + L1 medicine
shows significant effects in reducing high holesterol, high
triglycerdes levels
 There is significant increase in hdl level
 There significant symptomatic improvement in efforts angina in
patients with CAD.there is improvement in hyperliidemia
 The patients with LHF did not show much improvement
 There is marked weight reucing effect with medicine

72
 Used medicinal herbs & its effect
S1 it is quite useful for lymphatic patients the higher does in
agina, constipation & indigestion. It works nervous system, brain,
heart, and muscclar system
A3 on acts left & right side the heart. C1 on act on tissue
degeneration so it acts on oedema & chronic inflammation. F1 on
acts on the entire motors & sensory nerves iits act all heart
disorder. C5 on acts all skin disease external and internal this is
good varicose vein and neuralgic pain killer, WE on works on any
pain it is good pain killer L1 on tissue medicine, & it reduces the
weight, we give it in obese & high lipid levels.
A3 on acts lfet & right side the heart. C1 on acts on tissue
degeneration So it acts on oedema & chronic inflammation. F1 on
acts on the entire motor & sensory nerves it acts all heart disorder.
Vein & neuraligic pain killer. WE on works on any pain it is good
pain killer. L1 on is tissue medicine, & it reduces the weight, we
give it in obese & high lipid levels.
Arjuna - It is very good for heart it acts oncardic muscle & it
regulate the cardic blood flow it reduces the fat also it decrease the
TG levels & increase the HDL levels. It is good tonic for cardiac
disorder.

73
Amalaki – It is good expectorant & good for fat burner when we
give it before meal. It reduce the Triglyceride & increase HDL
levels.
Climicifuga Racemose- This is the very good medicin for Angina
pectoris, Stiffiness & contraction in neck & back, sleeplessness
brain irritation.
Fucus Vesiculosus – It is good for obesity & non –toxic goiter, &
obese patients. It reduce the fat it is good fat burner.

74
 MEDICINE OBSERVATION

ANGINA :

On angina we use combination A3+C1+F1+C5. Those medicine

acts on cardiac muscle & blood vessels. It increase the blood
supply of cardiac muscle. It balance between demand & supply of
blood flow to the heart. 81 is main role is to cure the constipation
& indigestion.

Supplementation –
Arjuna, Amalki, Galric, Cimicifuga Racemase.
The major role of this medicine is on heart it curse the obstruction
of the all vessels & regulate oxygenated blood supply in the heart.

MYOCARDIAL INFRACTION:

On Myocradial infraction we use the Medicine A2+C5+WE

compress & apply of heart. It dissolve any thrombus in the
Coronary artery & suppress the pain. In dilution A3+S10. In M.I.
Case it cure the indigestion & regulate supply of blood in the Left
& Right side of heart & cure the nervousness.

75
Supplementation –
Arjuna – Amalki, Garlic, A2.
If we use it I n2nd Dilution then it increase the cardiac ejection
(pumping of heart) and it Cure the thrombosis in vessels. It
decrease thelipid levels those which are responsbible for thrombus
formation & hence act as cardic friendly.
HYPERLIPIDEMIA :
In Hyperlipidemia we can use the combination of Arjune + Amalki
+ Garlic + L2. This reduces the cholestorl + triglyceride levels & it
increases the HDL levels which is good for heart. It takes care of
blood vessles & cardic muscle.
Supplementation –
On hyperlipidemia we give the dilution which reduce the CHO &
TRIG. Levels & increase the HDL . levels on supplementation we
give it ofr 4 months then one month gap then again 3 months ligher
dilution.

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 TREATMENT
Angina Pectoris—
15 tables of S1 is to be taken after every 20 to 25 minutes. Beside
this 3rd dilution of A3+C1+F1+C5 be given after 1 Hrs interval .On
heart apply ointment of C5+WE
The Supplimentation : Amlaki +Arjuna+Alluim Sativum +
Cimicifuga Racemose. 3rd dilution given for 2-3 monts.

Myocardial Infarction—
A2+ C5+WE compress & applied on Heart. Higher dilution
A3+S10 should be given two times a day.
The Suplimentation Amlaki+Arjuna+Allium Sativum + A2 2nd
dilution given for 2-3 months.
Hyperlipidemia--
2nd dilution Arjuna+Amlaki+ Alium Sativum+L1. 15 min. before
meals two times a day total 30 to 40 days then check the lipid
levels.

77
 REPORTS
CASE NO CHO TG HDL TIME CHO TG HDL
1. 215.6 595.6 44.2 After 30 days 199.2 219.6 46.8
2 315.1 325.2 41.0 After 40 days 206.8 223.9 43.3
3 285.3 260.9 42.1 After 35 days 169.0 256.7 46.8
4 398.5 458.4 45.3 After 35 days 210.4 199.5 47.6
5 359.8 323.7 42.9 After 25 days 225.00 215.0 44.6
6 346.8 295.9 41.2 After 15 days 249.8 201.9 43.3
7 303.6 356.6 47.5 After 20 days 265.0 254.7 47.8
8 260.5 265.5 43.6 After 30 days 178.0 160.6 44.9
9 287.9 298.0 41.0 After 30 days 199.8 202.0 44.8
10 234.8 286.5 48.6 After 40 days 201.9 189.0 49.9
11 298.9 278.0 43.5 After 30 days 213.3 210.8 44.9
12 239.9 260.6 44.1 After 25 days 202.2 200.1 45.90
13 225.9 265.9 42.2 After 20 days 200.3 199.9 44.9
14 222.2 254.3 43.2 After 25 days 189.0 179.7 44.0
15 345.5 278.3 42.1 After 30 days 226.2 201.1 44.3

78