ILA 7: Chest

Pain

Bismillah.

Learning Objective 1

Myocardial Infarction &

Other Differential Diagnosis

Definition of Myocardial Infarction

Meaning:
A heart attack (also known as a myocardial infarction) is the death of heart
muscle from the sudden blockage of a coronary artery by blood clot.
Coronary arteries are blood vessels that supply the heart muscle with blood
and oxygen
Blockage of coronary artery deprives the heart muscle of blood and oxygen,
causing injury to the heart muscle
If blood flow is not restored to the heart muscle within 20 to 40 minutes,
irreversible death of the heart muscle will begin to occur.
The irreversible necrosis of heart muscle secondary to prolonged ischemia
Typical heart attack pain occurs in the mid to left side of the chest and may also
extend to the left shoulder, the left arm, the jaw, the stomach, or the back.
-Other associated symptoms are shortness of breath, increased sweating, nausea,
and vomiting.
-Symptoms vary considerably from person to person.
-Women may experience symptoms of heart attack similar to men (chest pain),

Severe left sided chest pain, why left sided?

Heart is located on the left side, chest wall share the same thoracic nerve with the heart that is T1 to
T4
Via upper 4 intercostal nerve
The pain radiated to the left arm, why?
Via T2 (intercostobranchial nerve) which joins medial cutenous nerve of the arm
Difficulty in breathing (dyspnea), why?
MI, affect the heart and its capacity to move blood through the lung and causes shortness of breath
Heart is unable to pump enough blood to the body organ
Damage to the heart limits the ventricular output
Epigastrium
from inferior or diaphragmatic surface of heart by sympathetic nerve enter spinal cord through T7,8
& 9 spinal nerves
Profuse sweating (diaphoresis)
Due to increase firing of sympathetic nervous system
Neck & jaw
Spread of nervous information within CNS
Nausea
Sensation of the stomach wants to empty itself

Differential Diagnosis
Potentially life-threatening causes of chest pain are as follows:
Heart attack/ MI and Angina are coronary syndrome involve coronary artery
Heart attack (acute myocardial infarction): A heart attack occurs when blood flow
to the arteries that supply the heart (coronary arteries) becomes blocked. With
decreased blood flow, the muscle of the heart does not receive enough oxygen.
This can cause damage, deterioration, and death of the heart muscle.
Angina/ JUST ISCHEMIC: Angina is chest pain related to an imbalance between the
oxygen demand of the heart and the amount of oxygen delivered via the blood.
It is caused by blockage or narrowing of the blood vessels that supply blood to the
heart. Angina is different from a heart attack in that the arteries are not
completely blocked, and it causes little or no permanent damage to the heart.
"Stable" angina occurs repetitively and predictably while exercising and goes away
with rest. "Unstable" angina results in unusual and unpredictable pain not relieved
totally by rest, or pain that actually occurs at rest. (STABLE and UNSTABLE ANGINA)

 Aortic dissection/tears: The aorta is the main artery that supplies

blood to the vital organs of the body, such as the brain, even to the
heart itself / no sufficient O2 and nutrients to kidneys, lungs, and
intestines. Dissection means a tear in the inner lining of the aorta.
This can cause massive internal bleeding and interrupt blood flow
to the vital organs.
Pulmonary embolism: A pulmonary embolus is a blood clot in one
of the major blood vessels that supplies the lungs. It is a potentially
life-threatening cause of chest pain but is not associated with the
heart.
Spontaneous pneumothorax: Often called a collapsed lung, this
condition occurs when air enters the saclike space between the
chest wall and the lung tissue. Normally, negative pressure in the
chest cavity allows the lungs to expand. When a spontaneous
pneumothorax occurs, air enters the chest cavity. When the
pressure balance is lost, the lung is unable to re-expand. This cuts
off the normal oxygen supply in the body.

 Perforated viscus: A perforated viscus is a hole or tears

in the wall of any area of the gastrointestinal tract.
This allows air to enter the abdominal cavity, which
irritates the diaphragm, and can cause chest pain.
Cocaine-induced chest pain: Cocaine causes the blood
vessels in the body to constrict. This can decrease
blood flow to the heart, causing chest pain. Cocaine
also accelerates the progression of atherosclerosis, a
risk factor for a heart attack.
Causes of chest pain that are not immediately lifethreatening include the following:
Acute pericarditis: This is an inflammation of the
pericardium, which is the sac that covers the heart.

 Mitral valve prolapse: Mitral valve prolapse is an abnormality of

one of the heart in which the "leaves" of the valve bulge into the
upper heart chamber during contraction. When this occurs, a small
amount of blood flows backward in the heart. This is believed by
some to be a cause of chest pain in certain people, although this
has not been proven with certainty.
Pneumonia: Pneumonia is an infection of the lung tissue. Chest
pain occurs because of inflammation to the lining of the lungs.
Disorders of the esophagus: Chest pain from esophageal disorders
can be an alarming symptom because it often mimics chest pain
from a heart attack.
Acid reflux disease (gastroesophageal reflux disease, GERD,
heartburn) occurs when acidic digestive juices flow backward from
the stomach into the esophagus. The resulting heartburn is
sometimes experienced as chest pain.

 Esophagitis is an inflammation of the esophagus.

Esophageal spasm is defined as excessive,
intensified, or uncoordinated contractions of the
smooth muscle of the esophagus.
Costochondritis: This is an inflammation of the
cartilage between the ribs. Pain is typically located
in the mid-chest, with intermittently dull and
sharp pain that may be increased with deep
breaths, movement, and deep touch.

Learning Objective 2

Anatomical Structure &

Histology of Cardiac Muscle

The Cardiovascular System

The Heart

Valves of the Heart

Histology of Cardiac Muscle

Learning Objective 3

Blood Vessels & Its Nerve

Supply

ARTERIAL SUPPLY OF THE HEART

Branches
branches of the ascending aorta, above the aortic valve

Right coronary

Left coronary

Origin-right aortic sinus

Origin-left aortic sinus

1. Right marginal artery*

2. Posterior interventricular
branch*
3. Conus branch artery
4. SA nodal artery
5. AV nodal artery

1. Anterior interventricular
artery*
2. Circumflex artery*
3. Conus branch artery
4. Left marginal artery
5. Diagonal artery

Distribution
Right Cor onar y
Both atria & inter-atrial
septum
SA node (60%) & AV node
(90%) and bundle of His
Right ventricle except for a
narrow strip along the anterior
inter-ventricular groove
Posterior 1/2 of interventricular septum
A narrow strip of left ventricle
along the posterior interventricular groove

Left Cor onar y

Left atrium (upper part)
Left ventricle except for a
narrow strip along posterior
inter-ventricular groove
Anterior 1/2 of interventricular
septum
A narrow strip of right
ventricle along the anterior
inter-ventricular groove
SA node (40 %) and AV node
(10%)

Arterial supply of heart (summary)

*Clinical application
Right Coronary
Disorders of right coronary
artery may cause
-

Sinus bradycardia
AV nodal block

Left Coronary
Anterior interventricular
branch/Left Anterior
Descending (LAD) artery is
the most often blocked
coronary artery
Stenosis of left coronary
artery is serious because it
supplies majority of the left
ventricle

Anastomoses
1. Between termination of
right coronary artery &
circumflex artery
2. Between posterior &
anterior interventricular
arteries
3. Between right & left conal
branches

Clinical applications
Progressive blockage anastomoses collateral
circulation may form to
make the cardiac muscle
viable
Sudden blockage of one
large branch usually lead to
myocardial infarction
(death of myocardial tissue

Venous drainage of the heart

Blood return to the right
atrium by anterior cardiac
veins
Venae cordis minimae (small
cardiac veins )
- open directly into the chambers
of the heart

Coronary sinus
Continuation of great cardiac
vein
Empty into the right atrium

Coronary sinus drains

Great cardiac vein
accompanies the
anterior
interventricular artery
& circumflex artery
Middle cardiac vein
accompanies the
posterior
interventricular artery
Small cardiac vein
accompanies the right
marginal artery
Oblique vein of Lt
atrium
Posterior veins of left
ventricle

Nerve supply of the heart

Sympathetic
Postganglionic fibres
- SA node + AV node
- Cardiac muscle & coronary
arteries

Parasympathetic
Vagus nerve
Synapse at cardiac plexuses
Postganglionic fibres
- SA + AV nodes & coronary
arteries

Learning Objective 4

Phases of Cardiac Cycle & Its

Action Potential

Difference between Action

Potential in Myocardial Tissue
and Pace Maker & Phases of
Cardiac Cycle

Ionic basis of different phases of myocardial and pace

maker action potential
Myocardial

Pace Maker

Have a true resting potential

No true resting potential

Depolarizing current
primarily by relatively fast
Na2+ Produce rapid
depolarisation

Depolarizing current primarily

by relatively slow T-type Ca2+
Produce slower
depolarisation

Referred as
fast response
action potentials

Referred as
slow response
action potentials

Cardiac Cycle
Definition: The sequence of events that occurs when
the heart beats
2 phases: Diastole phase The heart ventricles are relaxed
and the heart fills with blood
Systole phase The ventricles contract and pump
blood to the arteries
*1 cardiac cycle is completed when the heart fills
with blood and the blood is pumped out of the heart

Slide 17 22 are the explanation for the

pressure-volume relationship mentioned in
previous slides. I
ll try my best to explain
about the Stroke Work Loop graphs okay?
J

Filling of the ventricles during diastole

During ventricular systole, large amount of
blood accumulate in the right and left atrium
because of the closed AV valves.
As soon as systole is over, ventricular pressure
drops and the increased pressure that have
developed in the atria during ventricular systole
immediately push the AV valves open and
allow blood to flow rapidly into the ventricles.

First third of diastole : Rapid filling of blood

into the ventricles
Middle third of diastole : small amount of
blood flow
Last third of diastole : Atria contract and
give an additional
thrust to the inflow of
blood into the
ventricles

Emptying of the ventricles during systole

Period of Isovolumic (Isometric) Contraction
After ventricular contraction begins, ventricular
pressure rises abruptly causing the AV valves to
close.
The ventricle also built up sufficient pressure to
push the semilunar (aortic and pulmonary) valves
open.
Contractions occurs in the ventricles but there is no
emptying of blood.
Tension is increasing in the muscle but little or no
shortening of the muscle fibers is occurring.

Period of Ejection
When the ventricular pressure rises slightly
above 80 mmHg, the ventricular pressure
push the semilunar valves open.
Immediately, blood begins to pour out of the
ventricles.

Period of Isovolumic (Isometric)

Relaxation
At the end of systole, ventricular relaxation
begins allowing both the right and left
intraventricular pressures to decrease rapidly.
The elevated pressures in the distended large
arteries that have just been filled with blood
from the contracted ventricles immediately
push blood back toward the ventricles, which
snaps the aortic and pulmonary valves closed.

 Ventricular muscle continues to relax for

another 0.03 to 0.06 second.
The intraventricular pressures decrease
rapidly back to their low diastolic levels.
The AV valves open to begin a new cycle of
ventricular pumping.

Learning Objective 5

Systole, Diastole, Mean

Arterial Pressure & Cardiac
Output

Diastole and Systole

Diastole- period of relaxation during which
the heart fills with blood
Systole - Period of contraction

 Systole represents the time during which the

left and right ventricles contract and eject
blood into the aorta and pulmonary artery,
respectively. During systole, the aortic and
pulmonic valves open to permit ejection into
the aorta and pulmonary artery. The
atrioventricular valves are closed during
systole, therefore no blood is entering the
ventricles; however, blood continues to enter
the atria through the vena cavae and
pulmonary veins.

 Diastole represents the period of time when the

ventricles are relaxed. Blood is passively flowing
from the left atrium and right atrium into the left
ventricle and right ventricle respectively . The blood
flows through atrioventricular valves (mitral and
tricuspid) that separate the atria from the ventricles.
The right atrium receives venous blood from the
body through the superior vena cava and inferior
vena cava . The LA receives oxygenated blood from
lungs through four pulmonary veins that enter the LA.
At the end of diastole, both atria contract, which
propels an additional amount of blood into the
ventricles.

Mean Arterial Pressure (MAP)

Definition : Average arterial pressure during
single cardiac cycle.
MAP = (Q x SVR) + CVP
Q - cardiac output
SVR - systemic vascular resistance
CVS - central venous pressure

 Because CVP is or near 0 mmHg,so

MAP approx = Q x SVR
At normal resting heart rates, MAP can be
approximated by the following equation:

Systemic Vascular Resistance (SVR)

Resistance to blood flow offered by all of the
systemic vasculature.
Resistance to blood flow within a vascular
network is determined by the size of
individual vessels, the organization of the
vascular network and physical characteristics
of the blood (viscosity, laminar flow versus
turbulent flow).

Cardiac Output (Q)

Q is the volume of blood pumped by the heart
per minute ( ml / min ).
Q is controlled by heart rate ( HR) and stroke
volume (SV).
Measurement of Cardiac Output
Q (ml/min) = HR (beats/min) x SV (ml/beat)

HR and SV
Heart rate- number of heartbeats per unit of
time. (bpm)
Stroke volume - volume of blood pumped
from one ventricle of the heart with each beat.
SV calculation - SV = EDV - ESV
EDV : Volume of blood just prior to the beat
ESV : Volume of blood in ventricle at end of
beat

Factors affecting Q
ANS
Cause bp changes.
Age
Infant HR 115 bpm, decrease to 100 bpm.
Epinephrine and norepinephrine
HR and SV, Q.
Gender
Female higher resting HR.
Physical fitness
Active person around 50 bpm resting HR.
Body temperature
temperature, Q.

Learning Objective 6

Acute & Chronic Cases

Related to Chest Pain

Noncardiac chest pain (NCCP) is recurrent chest pain,

resembling angina, that is not caused by heart disease
Chest pain may also be caused by problems in your
lungs, esophagus, muscles, ribs, or nerves, for
example. Some of these conditions are serious and
life threatening. Others are not.
Most chest pain is not heart-related and isn't a sign of a
life threatening problem.

Gastro-oesophageal reflux disease (GORD)

Gastro-oesophageal reflux disease (GORD) is a

common condition where acid from the stomach
comes up into the oesophagus (gullet).
Common symptoms of GORD include:
- burning chest pain (heartburn)
- an unpleasant taste in the mouth caused by
stomach acid coming back up into your mouth
These symptoms usually occur soon after you've
eaten and get worse if you bend over or lie down.
GORD can often be treated by making lifestyle
changes and, if necessary, using medication.

Bone or muscle problems

If your chest is painful and tender to touch, it may be

caused by a strained muscle in your chest wall. This
can be surprisingly painful, but with rest the pain
should ease and the muscle will heal in time.
If you have pain, swelling and tenderness around
your ribs, and the pain is made worse by lying down,
breathing deeply, coughing or sneezing, you may
have a condition called costochondritis.
This is caused by inflammation in the joints between
the cartilage that joins the ribs to the breastbone
(sternum). The symptoms often improve after a few
weeks and may be relieved by painkillers.

 Some types of chest pain are associated with injuries

and other problems affecting the structures that
make up the chest wall. Examples include:
- Sore muscles. Chronic pain syndromes, such as
fibromyalgia, can produce persistent muscle-related
chest pain.
- Injured ribs. A bruised or broken rib can cause
chest pain.

Anxiety and panic attacks

Some episodes of chest pain occur as part of an
anxiety or panic attack.
In addition to chest pain and overwhelming feelings
of anxiety, these attacks can cause symptoms such
as heart palpitations, sweating, breathlessness and
dizziness.
Most panic attacks last for 5 to 20 minutes. In the
long-term, you may benefit from psychological
therapy and medication, or both.

Lung conditions
If you have sharp chest pain that gets worse when you
breathe in and out, and is accompanied by other symptoms
such as a cough and breathlessness, it may be caused by a
condition affecting the lungs or surrounding tissue, such as:
- pneumonia inflammation of the lungs, usually caused
by an infection
- pleurisy inflammation of the membrane surrounding
the lungs, also usually caused by an infection
Mild cases of pneumonia can usually be treated with
antibiotics, rest and fluids. For people with other health
conditions, the condition can be severe and they may need to
be treated in hospital.
Treatment for pleurisy will depend on the underlying cause.
Pleurisy caused by a viral infection will often resolve without
needing treatment, whereas pleurisy caused by a bacterial
infection will usually need to be treated with antibiotics.

Other possible causes

There are many other potential causes of chest pain,

including:
shingles a viral infection of a nerve and the area of
skin around it, which causes a painful rash that
develops into itchy blisters
mastitis pain and swelling of the breast, which is
usually caused by an infection, most commonly
during breastfeeding
acute cholecystitis inflammation of the gallbladder,
which can cause a sudden sharp pain in the upper
right side of your tummy that spreads towards your
right shoulder
stomach ulcers a break in the lining of the stomach,
which can cause a burning or gnawing pain in your
tummy

 a pulmonary embolism a blockage in the blood

vessel that carries blood from the heart to the lungs,
which can cause sharp, stabbing chest pain that may
be worse when you breathe in, as well as
breathlessness, a cough and dizziness
pericarditis inflammation of the sac surrounding
your heart, which can cause a sudden, sharp and
stabbing pain in your chest, or more of a dull ache;
the pain usually worsens when lying down
Some of these conditions can be very serious. Make
sure you seek medical advice so you can be correctly
diagnosed and treated.

Learning Objective 7

Biomarkers of MI & Its

Diagnostic Test

Biomaker
What is biomarker?
In medicine, a biomarker is a term often used to refer
to a protein measured in blood whose concentration
reflects the severity or presence of some disease state.
More generally a biomarker is anything that can be
used as an indicator of a particular disease state
Biomarker that is being used in diagnose MI is called
cardiac marker. Example of cardiac marker is:

Chest X-ray
A doctor may be looking for specific features on a
chest x-ray. A posterior-anterior (PA) and lateral x-rays
will be conducted. Some of the common features that
may be noted include :
Tracheal alignment, lung segments and any signs of
effusions (fluid in the lungs).
Widening of the mediastinum, cardiothoracic ratio,
cardiac size and shape and major blood vessels shape,
size and position
Sternal, clavicle, scapula or rib fracture.
Vertebral body height and disc spaces.
Any foreign objects or abnormal, opaque mass.
Basically, doctor look for cardiac size and
cardiothoracic ratio if any heart disease is suspected.

Lipid profile
Lipid profile is the collective term given to the estimation of, typically,
Total cholesterol
High density lipoprotein cholesterol (HDL-C) often called good
cholesterol
Low density lipoprotein cholesterol (LDL-C) often called bad cholesterol
Triglycerides
An extended profile may also include:
Very low density lipoprotein cholesterol (VLDL-C), IDL, chylomicron
The lipid profile is used to help determine your risk of heart disease and to help guide
you and your health care provider in deciding what treatment may be best for you if
you have borderline or high risk

 This is used to identify hyperlipidemia which many

forms of which are recognized risk factors for
cardiovascular disease and sometimes pancreatitis.
Lipid profile needs to be obtained at presentation
because levels can change after 12-24 hours of an
acute illness
During myocardial infarction:
- From day 1 post-MI to day 4 post-MI, the mean serum levels
of total cholesterol, LDL cholesterol, and HDL cholesterol
decreased
- but the mean serum level of triglycerides increased.
- The cholesterol ratios, however, remained unchanged
between day 1 post-MI and day 4 post-MI.

Learning Objective 8

Cholesterol &
Lipoprotein Metabolism

 Cholesterol is an essential component of

mammalian cell membranes as well as a
precursor of bile acids and steroid hormones.

It is a multi-ringed lipid of 27 carbons.

 The
OH group at carbon 3 makes cholesterol
amphipathic (both hydrophilic & hydrophobic);
allowing cholesterol to insert itself into
membranes.
Cholesterol has several functions, one of
which being an essential component of
eukaryotic membranes and that it modulates
the fluidity of these membranes.

 Cholesterol is synthesized de novo from acetyl CoA.

The synthesis is a multi-step process but the key

step is the conversion of 3-hydroxy-3methylglutaryl CoA (HMG CoA; made from 3 acetyl
CoA molecules) to mevalonate.

 This reaction is catalyzed by HMG CoA

reductase; of which is the committed and rate
-limiting step in cholesterol synthesis.
It is subjected to negative feedback regulation
at two levels: increased mevalonate decreases
the transciption of HMG CoA reductase,
leading to lower mRNA levels and mevalonate
also increases degradation of HMG CoA
reductase protein.

Summary of Cholesterol Synthesis

Composition of Plasma Lipoprotein

Composed of a neutral lipid core (containing

triacylglycerols & cholesteryl esters)
surrounded by a shell of amphipathic
apolipoproteins, phospholipid &
nonesterified cholesterol.

 Lipoproteins function both to keep their

component lipids soluble as they transport
them in the plasma and to provide an efficient
mechanism for transporting their lipid
contents to the tissues.
Its particles include chylomicrons, VLDLs, LDLs,
and HDLs. Each differing in lipid and protein
composition, size, density and site of origin.

HDL Metabolism
HDL is the smallest lipoprotein, containing the
least amount of lipid. It contains of a lipid core
of CE and TG, surrounded by PLs and apo A-I.
Its particles are formed in blood by the
addition of lipid to apo A-I, an apolipoprotein
made by the liver and intestine and secreted
into the blood. Apo A-I accounts for 70% of
the apoproteins in HDL.

 HDL is a reservoir of apolipoproteins, primarily

apo C-II (transferred to VLDL and chylomicrons;
activator of LPL) and also apo E (required for
receptor-mediated endocytosis of IDLs and
chylomicron remnants).
It also plays an important role in the
esterification of cholesterol. When cholesterol
is taken up by HDL, it is immediately esterified
by the plasma enzyme LCAT, which binds and
transfers the fatty acid from carbon 2 of
phosphatidylcholine to cholesterol.

Learning Objective 9

Treatment & Prevention

for Myocardial Infarction

Treatment and Prevention for MI

Treatment :
Platelets aggregation
inhibitors
Anti-coagulants
Surgery
Balloon angioplasty

Prevention :
Lifestyle modification
Anti-hyperlipidemic
drugs (atherosclerosis
prevention)

Platelets aggregation inhibitors

Decrease the formation or the action of chemical signals that promote
platelet aggregation.
By :
inhibits the activity of the enzyme cyclo-oxygenase inside platelets.
Cyclo-oxygenase is an enzyme whose activity is necessary for the
formation of a chemical, thromboxane A2, that causes platelets to
aggregate. Thus by inhibiting the formation of thromboxane A2,
prevents platelets from aggregating and thereby prevents the
formation of blood clots.
Examples : Aspirin, Thienopyridines (Ticlopidine, Clopidogrel) and
Glycoprotein 2b/3a inhibitor (Abciximab)
For reducing incidence of recurrent MI

Anti-coagulants/anti-thrombotic
Binding to antithrombin 3, with the subsequent rapid
inactivation of coagulant factors. Also include inhibition of
serine proteases, thrombin clotting factor (factor 2a & factor
5a)
Thus limit the expansion of thrombi by preventing fibrin
formation
Example : Heparin, low-molecular weight heparins LMWHs
For acute phase of MI

Balloon angioplasty

Surgery

Anti-hyperlipidemic
Treatment goals :
reduction of LDL level
Reducing total serum cholesterol and
triglycerides
Increasing HDL level

Drugs used :
Statins (HMG-CoA reductase inhibitors)
Atorvastatin,rosuvastatin, simvastatin, Lovastatin, Pravastatin,
fluvastatin
Bile Acid BindingResins:
Cholestyramine, Colestipol, colesevelam
Nicotinic acid
Niacin
FibricAcid Derivatives
Gemfibrozil, clofibrate, Fenofibrate, bezafibrate& ciprofibrate
Ezetimibe

Lifestyle modification

Fat & total calorie intake & body weight

Judicious consumption of alcohol (low dose BP)
Regular dynamic physical exercise, such as brisk
walking and swimming
Cessation of smoking
Adequate nutritional intake of minerals & vitamins

Learning Objective 10

Epidemiology, Risk Factors

& Management of MI

Epidemiology of MI
Myocardial infarction is a common presentation of
coronary artery disease.
The World Health Organization estimated in 2004, that
12.2% of worldwide deaths were from ischemic heart
disease.
Rates of death from ischemic heart disease (IHD) have
slowed or declined in most high-income countries.
In contrast, IHD is becoming a more common cause of
death in the developing world. For example in India,
IHD had become the leading cause of death by 2004.

Risk Factors of MI
High blood pressure
- Alone or in association with obesity, smoking, high blood
cholesterol levels or diabetes, high blood pressure increases
the risk of myocardial infarction and stroke.
Smoking
- Smoking appears to be the cause of 20% of coronary artery
disease.
- Tobacco smoking (including secondhand smoke) and shortterm exposure to air pollution such as carbon monoxide,
nitrogen dioxide, and sulfur dioxide have been associated
with MI.
- Smokers also have a two to four time higher risk of sudden
cardiac death (within an hour of a heart attack).

 High blood cholesterol

- High total and low-density lipoprotein (LDL cholesterol) levels
and low HDL cholesterol levels increase the risk of myocardial
infarction.
- Cholesterol levels can be lowered with dietary/lifestyle
modifications such as exercise or medications.
Obesity
- Obesity increases coronary artery disease, myocardial
infarction, and stroke risk.
- Obesity increases strain on the heart, raises blood pressure
and cholesterol, and increases diabetes risk. Weight reduction
can be achieved with modifications to diet and increased
physical activity.

 Diabetes
- Approximately two-thirds of patients with
diabetes die from heart or blood vessel
disease. Adults with diabetes are three to
seven times more likely to develop heart
disease.
- A recent recommendation from the U.S.
government advocates aggressive treatment
of high cholesterol in people with diabetes.

Management of MI
Ways to reduce the risk of MI:
Quit smoking
- Smokers have more than twice the risk for heart attack as
nonsmokers.
- If you smoke, quit. Better yet, never start smoking at all.
- Nonsmokers who are exposed to constant smoke (such as living
with a spouse who smokes) also have an increased risk.
Control diabetes
- If not properly controlled, diabetes can contribute to significant
heart damage, including heart attacks and death.
- Control diabetes through a healthy diet, exercise, maintaining a
healthy weight, and taking medications as prescribed by your
doctor.

 Get active
- Many of us lead sedentary lives, exercising infrequently or
not at all.
- People who don't exercise have higher rates of death and
heart disease compared to people who perform even mild to
moderate amounts of physical activity.
- Even leisure-time activities like gardening or walking can
lower your risk of heart disease. Most people should exercise
30 minutes a day, at moderate intensity, on most days.
Control high blood pressure
- Nearly one in three adults has systolic blood pressure (the
upper number) over 140, and/or diastolic blood pressure (the
lower number) over 90, which is the definition of
hypertension.
- Control blood pressure through diet, exercise, weight
management, and if needed, medications.

 Manage stress
- Poorly controlled stress and anger can lead to
heart attacks and strokes.
- Use stress and anger management techniques to
lower your risk.
- Learn to manage stress by practicing relaxation
techniques, learning how to manage your time,
setting realistic goals, and trying some new
techniques such as guided imagery, massage, Tai
Chi, or yoga.