• Coronary Artery Disease 411

• Coronary artery disease is one of the most common

and serious effects of aging. Bloodvessels lasers
• Fatty deposits build up in blood vessel walls and
narrow the passageway for the movement of blood.
• The resulting condition, called atherosclerosis often
leads to eventual blockage of the coronary arteries
and a “heart attack”.
atherosclerosis
Atherosclerosis
 60%
Narrowing
Normal of
Coronary
Coronary Artery
Artery Cross
Section
 Risk Factors
Uncontrollable Controllable
•High blood pressure
•Sex
a •High blood cholesterol
•Hereditary to fi xauox

sick 2 •Smoking
monoxis raising
canon
•Race
•Physical activity
•Age
•Obesity
•Diabetes
•Stress and anger
• Arteriosclerosis:
post
– Chronic disease of the arterial system,
characterized by:
• Abnormal thickening and hardening of vessel
walls
• Decrease in the artery’s ability to change lumen
size, lumen is gradually narrowed
• Pathophysiologic conditions;
–High blood pressure
GI
–Insufficient perfusion of tissues
–Weakening of arterial walls
• Atherosclerosis:
– Form of arteriosclerosis, thickening and
fat
hardening of the vessel walls are caused by soft
deposits of intra-arterial fat and fibrin that harden
over time
– Leading contributor to coronary artery and
cerebrovascular disease
– Inflammatory disease that begins with injury to
the endothelial cells that line arterial walls
• Atherosclerosis - injury hypothesis
• Injury to coronary artery endothelium (artery
lining) caused by:
• Flow turbulence (shear A
wd.wsstress), CO toxicity
(smoking), Inflammation, low Jinserty labboprotein

• Hypertension, Hyperinsulinemia, LDL-C

accumulation in artery wall.
is SW
•µOxidative stress ( free radical)
• Endothelial dysfunction (collagen & smooth
muscle exposed to blood).
• Platelets adhere to injury & release growth factors
55
• Macrophages engulf oxidized LDL (Foam cells).
 I
• Accumulation & Proliferation of Smooth Muscle
and Fibrous Tissue
• Lipid Accumulation & Mature Plaque Formation.
• Notes on atherosclerosis:
• Plaque formation is a ongoing dynamic process that
begins in infancy 45% of infants up to 8 months old
and 65% of teenagers.
• A plaque is hemodynamically significant (may cause
symptoms) if it covers 60%--70% the diameter of
the coronary artery lumen.
• Reversal of the atherosclerotic process has be found
in patients whose Total-C level is < 150 mg/dl &
HDL-C is > high (> 45 - 55 mg/dl).
plate hemodynamically siamificant
 Coronary Artery Disease (CAD)

Normal Narrowed Blood Clot

Occluded
• Ischemic Heart Disease
• A result of CAD
(atherosclerosis):
• Imbalance between supply
and demand of the heart.
• Narrowing and hardening
of the arteries leads to
• imbalance between the
supply and demand of
• blood for cardiac muscle =
(Ischemia).
• Ischemia is either detected
by a symptom such as chest
pain: chest Pain
• (angina) or indirectly by
electrocardiogram
• Types of Angina and
• Associated Pathophysiology
141
• Typical Angina – evoked by exertion, emotions,
cold/heat exposure, and meals;
relieved by rest or nitroglycerin
• – Stable Angina – reproducible and predictable in
onset 96W if
•2 Atypical Angina – no relationship to exertion
• – Unstable Angina – new onset of typical angina,
increasing in intensity or occurs at rest
ischemia
Wb
• 3 – Variant (Prinzmetal’s angina) - coronary artery spasms
 no
• TESTS:
Many tests help diagnose CHD. Usually, the doctor
will order more than one test before making a
definite diagnosis.
• Electrocardiogram (ECG)
• Exercise stress test
• Echocardiogram
• Nuclear scan SHY
• Electron-beam computed tomography (EBCT) to
look for calcium in the lining of the arteries -- the
more calcium, the higher your chance for CHD
• CT angiography -- a noninvasive way to perform
coronary angiography vessels
blood
• Magnetic resonance angiography MRA
• Coronary angiography /arteriography -- an invasive
procedure designed to evaluate the heart arteries
under x-ray
• Treatment
• Pharmacologically manipulate blood pressure, heart
rate, and contractility to decrease oxygen demands
6 pA
X
• Aspirin. daily dose of aspirin makes the blood less
likely to form clots in the coronary arteries.
• Statins. These drugs help to lower the cholesterol
levels. LOL
– Beta-blockers block sympathetic input, so
– Decrease heart rate,
– Decrease oxygen demand
• ACE inhibitors. These drugs are often used in
people with heart failure or after a heart attack.
• They lower your blood pressure.
 Nitroblyslen
• Nitrates dilate peripheral blood vessels and
• Decrease oxygen demand
• Increase oxygen supply
• Relieve coronary spasm
• Digitalis
– Increases the force of contraction
• Calcium channel blockers spasm.si I
• Antiplatelet agents
II 8
 Myocardial
infarction MI
Heartattack
• Necrosis of cardiac
myocytes
–GO.U.IN
Irreversible
– Commonly affects
left ventricle
IT
– Follows after more
than 20 minutes of
ischemia
authemia
 Structural, functional changes
6
• Decreased contractility
S
• Decreased LV compliance
s
• Decreased stroke volume
• Dysrhythmias
• Inflammatory response is severe
• Scarring results –Replacement
resentation
– Strong, but stiff; can’t contract like healthy cells
 Clinical manifestations
• Sudden, severe chest pain
– Similar to pain with ischemia, but stronger
– Not relieved by nitrates except in some condition
– Radiates to neck, jaw, shoulder, left arm
• Indigestion, nausea, vomiting
• Fatigue, weakness, anxiety, restlessness and
die
feelings of impending doom.
• Abnormal heart sounds possible (S3,S4)
51,52 lab Jab
• Blood test show several markers:
– Leukocytosis Inflammation vespons
– Increased blood sugar healink
– Increased plasma enzymes
• Creatine kinase
• Lactic dehydrogenase
• Aspartate aminotransferase (AST or SGOT)
– Cardiac-specific troponin
Troponin

itin.si ff
troponin 0.05
MI
 ECG changes
• Pronounced, persisting Q waves
• ST elevation If
• T wave inversion
a

AV

Pronounced a wave

1 elevation
T inversion
 Treatment
Thrombolytic
291115
• First 24 hours crucial
Thrombolytic
• Hospitalization, bed rest e

• ECG monitoring for arrhythmias

• Pain relief (morphine, nitroglycerin)
• Thrombolytics to break down clots Asprine
• Administer oxygen
• Revascularization interventions: by-pass
selfie
grafts, stents or balloon angioplasty
Thrombolistic
• Heart Failure I
MI 1st
• Is a complex clinical syndrome in which the heart is
incapable of maintaining a cardiac output adequate
to accommodate metabolic requirements and the
w̅
venous return. will need to decrease or output
swelling

RV LV
Biv
Backworktilute
asapnedfluide inalveloi
majorsymptoms

A
6
• What causes heart failure?
• The loss of a critical quantity of functioning
myocardial cells after injury to the heart due to:
3 major causes
decrease contic output decrease rine
vineantiot

48
 LV Dysfunction causes Decreased Blood Pressure and
Decreased cardiac output Decreased Renal perfusion

Stimulates the Release

of renin, Which allows
conversion of
Angiotensin
to Angiotensin II.
Angiotensin II stimulates
Aldosterone secretion which
causes retention of
Na+ and Water,
increasing filling pressure
• The heart compensates to cope with and hide the
effects of heart failure.
– Enlargement (dilation): Allows more blood into the
heart.
– Thickening of muscle fibers (hypertrophy) to strengthen
the heart muscle: Allows the heart to contract more
forcefully and pump more blood.
– More frequent contraction: Increases circulation.
– Pathophysiology
– When cardiac output is not sufficient to meet the
metabolic needs of the body, compensatory mechanisms,
including neurohormonal responses, become activated.
– Mechanisms initially help improve contraction and
maintain circulation
• Renin-Angiotensin-Aldosterone System 8490464
• The decreased cardiac output in HF results in
decreased renal blood flow.
– Activates the release of renin which converts to
angiotensin I, and then angiotensin II, which is a direct
vasoconstrictor.
• This system promotes fluid retention
• Adrenergic System
• Decreased cardiac output causes increased
sympathetic activity and increased catecholamine's.
– Results in vasoconstriction, leading to the shunting of
blood.
• Tachycardia Cassi arrest of
• This initial compensatory response eventually
becomes detrimental, as it increases myocardial
oxygen demand and shortens the time for coronary
perfusion.
• In addition, sympathetic stimulation reduces renal
blood flow and stimulates the renin-angiotensin
system.
IT
• Heart Failure Classifications 2types acute andCronic
• I Normal daily activity does not initiate
symptoms.
• II Normal daily activities initiate onset of
symptoms, but symptoms subside with rest.
• III Minimal activity initiates symptoms; patients are
usually symptom free at rest.
• IV Any type of activity initiates symptoms and
symptoms are present at rest.
• Right Heart Failure
nonsense
• Ineffective right ventricular contractile function.
• Pure failure of the right side of the heart can occur
embolism
acutely (as in pulmonary embolus or a right
ventricular infarction).
• Most commonly caused by left sided failure or
severe pulmonary disease.COPD ephsiuna
Pulmonary

• Left Heart Failure

• Disturbance of the contractile function of the left
ventricle.
Necrosis
• Most frequently caused by left ventricular infarction,
hypertension, and aortic and/or mitral valve disease.
• Forward Failure Inability to Push forward 4
• Inadequate delivery of blood into the arterial system.
• Occurs when systemic vascular resistance is
increased, producing decreased blood flow out of
the ventricles.
• Results in reduced cardiac output and hypoperfusion
of vital organs.
• Most often occurs with aortic stenosis or systemic
hypertension. in pressure atchest a
poet
• Backward Failure
• Failure of the ventricle to empty.
• Usually a result of left ventricular systolic
dysfunction caused by infarction or cardiomyopathy.
breathing
• Systolic Dysfunction
• More familiar classic type of heart failure.
– Due to the heart’s depressed contractility, a
reduction in the force of contraction occurs.
– Ejection Fraction usually drops below 40%
(normal 50-70%).
– The heart cannot pump with enough force to push
a significant amount of blood into circulation.
– Blood coming into the heart from the lungs may
back up and cause fluid to leak into the lungs.
• Known as pulmonary congestion.
• Diastolic Dysfunction
6599Necrosis f
• Due to slowed or incomplete ventricular relaxation.
• The heart cannot properly fill with blood because
the muscle has become stiff, losing its ability to
relax.
• This form may lead to fluid accumulation, especially
in the feet, ankles, and legs. water retention
I
• Symptoms I 4,14
• Dyspnea
• Fatigue
• Edema
• Persistent Coughing
• Raspy Breathing or WheezingA
 t
• Pharmacology
• ACE Inhibitors
– Prevent the production of a chemical that causes
blood vessels to narrow.
• Inhibits the conversion of angiotensin I to
angiotensin II.
WS ¼ ms
– As a result, BP drops and the heart doesn’t have to
work as hard to pump blood.
• Side Effects
– Coughing, skin rashes, fluid retention, excess K+
in the bloodstream, kidney problems, and an
altered or lost sense of taste.
• Digitalis
Prevent overload for heart
– Decreases the force of the heart’s contractions.
– Also slows certain fast heart rhythms.
– As a result, the heart beats less frequently but
more effectively, and more blood is pumped into
the arteries.
• Side Effects
– Nausea, vomiting, loss of appetite, diarrhea,
confusion, and new heartbeat irregularities.
• Diuretics
– Help the body to rid itself of extra fluid and
sodium.
– Commonly prescribed to reduce high blood
pressure.
• Side Effects
– Loss of too much potassium, weakness, muscle
cramps, joint pains, and impotence.
• Beta Blockers
– Reduce the heart’s workload.
– Work on the body’s sympathetic nervous system,
which pours hormones like adrenaline into the
bloodstream in response to stress.
– In response to high levels of the hormones, the
heart beats faster and has to work harder.
– Patients with heart failure have high levels of
these stress-related hormones, a sort of chronic
panic mode.
– By blocking that response, beta blockers make the
heart beat more efficiently.
• Nitrates Dilate Periphral
Antina
– Used mostly for chest pain, but may also help
diminish heart failure symptoms.
– Relax smooth muscle and widen blood vessels.
– They act to lower primarily systolic blood
pressure.
• Side Effects
– Headaches.
• Cardiac hypertrophy
Cardiac Hypertrophy andand dilatation
dilatation

I
6.046
•The heart may undergo compensatory enlargement
in the form of
•Hypertrophy
•Dilatation
•Or both
• Compensatory hypertrophy;
• Definition; increase in the size and weight of
myocardium.
• Results usually from increased pressure load
• Causes of left ventricular hypertrophy:
• 1. Systemic hypertension
Aorta 0940 IN
• 2. Aortic stenosis
• 3. Mitral insufficiency
• Causes of right ventricular hypertrophy
• 1. Chronic lung disease
• 2. Pulmonary stenosis
• 3. Tricuspid insufficiency
weakness
• Compensatory dilatation;
• In this case stress leading to accumulation of
excessive volume of blood in the heart chamber
causes increase in the length of the myocardial
fibers and hence cardiac dilatation;
• Causes;
• 1. valvular insufficiency (mitral and or aortic).
• 2. left to right shunts e.g. in VSD (ventricular septal
defect)
• 3. conditions with high cardiac output
(thyrotoxicosis, arteriovenous shunt)
• 4. systemic hypertension
• 5. cardiomyopathy and myocarditis
 dec 4
• Congenital heart disease (CHD)
• is a problem with the heart's structure and function
that is present at birth.
• Causes;
• Multifactorial inheritance involving genetic and
environmental influences
• Other factors like
IN IN
• Rubella infection to
mother during pregnancy
• Drugs taken by the mother1 19 08
• Heavy alcohol drinking
by the mother
• Classification:

Righttoleft
Lrhypertrop
LSRsifect
cynosis
ME 5 0
numyas

RV
saowor LVSPulmono.rs
Gnosis
mostcommon ix

LARID
ane

IA
• A cyanotic
• Left to right shunt
• VSD Ventricular septal defect;
• Most common congenital anomaly of the heart.
• The smaller defect often close spontaneously, while
larger defects remain and produce significant
effects: which are (result from left to right shunt)
• 1. volume hypertrophy of the right ventricle.
• 2. haemodynamic changes in the tricuspid and
pulmonary valves.
• 3. pressure hypertrophy of the right atrium
• 4. volume hypertrophy of the left heart.
 •Right TO Left shunt (Cyanotic group)
•In such conditions there is entry of poorly oxygenated blood
into systemic circulation resulting in early cyanosis
•Most common example is
•Tetralogy of Fallot
• Tetralogy of Fallot

•The most common cyanotic

congenital heart disease