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can, and
does, occur in almost any artery in the
body. But in the heart its effects can be
crucial. The body depends on a strong
pumping heart to circulate life-giving
blood, and this includes to the heart
muscle itself. If the coronary arteries
become blocked, the cardiac muscle
begins to fail, and so the blood circulation
decreases, which includes the circulation
to the heart muscle itself. (Thibodeau,
494)
IHD: Pathophysiology
Oxygen supply decreases due to :
a. Atherosclerotic plaque obstruction
IHD: Pathophysiology
b. Coronary Vasospasm : prinzmetal or
variant angina
c. Mixed atherosclerotic diseases and
coronary spasm
d. Platelet activation occurs in
response to
plaque formation, plaque rupture,
endothelial damage
which lead to thrombus formation,
unstable angina or acute MI
IHD: Pathophysiology
OTHER FACTORS:
Increased O2
demand
Tachycardia
Hypertension
Anxiety
LVH
Aortic stenosis
Hyperthyroidism
Exertion
Volume overload
Decreased O2
supply
Atherosclerosis
Hypoxemia
Anemia
LVH
Aortic stenosis
Chest
Pain
None
Signs &
Symptoms
Shortness
Of Breath
Heart
Attack
ANGINA
Transient discomfort in the:
-Chest
-Shoulder
-Arm
-Back
Aggravated by:
-Exertional stress
-Emotional stress
Relieved by:
-Nitroglycerin
-Rest
Location
Near the sternum
Limited to left shoulder and arm
Precipitating factors
Exercise, Cold environment, Eating,
Walking against wind or after large
meal, Emotional factors,
Risk Factors
Uncontrollable
Sex
Hereditary
Controllable
High blood
pressure
Race
High blood
cholesterol
Age
Smoking
Physical activity
Obesity
Diabetes
Stress and anger
Evaluation
Patients history
Lipid profile
BP & HR
Stress test
Treadmill test (TMT)
Dobutamine stress echocadiogram (DSE) :
ejection fraction, LV function abnormality
EKG
T-wave inversion
ST depression
ST elevation
Coronary angiogram (cardiac cath)
12 Lead ECG
Assess for RVI
RCA
inferior, right ventricle
Evolution of AMI
Anatomy of Plaque Disruption
Shoulder region
Lipid core
Media
Lumen
Lumen
Lipid core
Fibrous cap
Vulnerable Plaque
Thin, friable fibrous cap
separating substantial
thrombogenic lipid core
from blood
Stable Plaque
Thick fibrous cap
protecting thrombogenic
lipid core from blood
More luminal narrowing
Evolution of AMI
Plaque Rupture, Stenosis, and Thrombosis
Plaque rupture
intraplaque thrombus
Mural
thrombus
Occlusive
thrombosis
Total chronic
occlusion
Recanalized
lumen
Healed plaque
increased
stenosis
Healed plaque
decreased stenosis
Ada pte d from Davies MJ . In: Schla nt RC, Alexander RW, eds. The Heart, Arteries
and Ve ins. 8th ed. 1994:1 009-102 0, with permission.
Evolution of AMI
Plaque Rupture and Thrombus Progression
Complete
occlusion
Disease
progression
AMI
Lipid- Plaque
rich disruptio
plaque
n
Reocclusion
Unstable
angina
Thrombus
Ada pte d from Fus ter V. N Engl J Med. 199 2;326:2 42-250 , with perm iss ion.
The
external
anterior
view of the
heart
shows a
dark clot
formation
in this
artery
Source: University of Utah WebPath
Evolution of Infarction/Necrosis
Coronary Artery Occlusion:
The Evolution of Infarction
Progression of myocardial necrosis with time since occlusion
30 min
4h
Normal
myocardium
Normal
myocardium
At risk
myocardium,
ischemic but viable
Necrosis starting
subendocardially
6 - 12 h
Normal
myocardium
At risk
myocardium,
ischemic but viable
Necrosis extending
towards
subepicardium
Completed infarct
involving whole area
at risk
Ada pte d from Sa ltissi S , Mushahwar S S. Postgrad Med J. 1995;71 :534-54 1, with permission.
Last longer
Not easily relieved with rest or NTG
Sx/Sx may be more severe (feeling of impending doom)
Pain often radiates to arms, neck, jaw, back, epigastrium
Therapies
Goals for AMI Therapy
Shorten time to reperfusion
Preserve
LV function
Limit
Infarct Size
REDUCE MORTALITY
IMPROVE OUTCOME
Resolve
ST-segment
elevation
12 Lead ECG
Diagnostic evidence of AMI present
Assess for RVI
Aspirin, 160-325 mg PO
Chewed & swallowed if possible
Determine if hypersensitive to ASA
Thrombolytics Checklist
Exclusions for thrombolysis
Surgery or trauma in
past 3 weeks
Terminal illness
Jaundice, hepatitis,
kidney failure
Use of anticoagulants
Systolic BP < 180 mm
Hg
Diastolic BP < 110
mm Hg
Time is
Muscle!!!
Treatment (continued)
1) Stenting
a stent is introduced into a blood vessel on a balloon
catheter and advanced into the blocked area of the artery
the balloon is then inflated and causes the stent to expand
until it fits the inner wall of the vessel, conforming to
contours as needed
the balloon is then deflated and drawn back
The stent stays in place permanently, holding the vessel
open and improving the flow of blood.
Treatment
(continued)
2) Angioplasty
a balloon catheter is passed through the guiding catheter to the
area near the narrowing. A guide wire inside the balloon catheter is
then advanced through the artery until the tip is beyond the
narrowing.
the angioplasty catheter is moved over the guide wire until the
balloon is within the narrowed segment.
balloon is inflated, compressing the plaque against the artery wall
once plaque has been compressed and the artery has been
sufficiently opened, the balloon catheter will be deflated and
removed.
Treatment (continued)
3) Bypass surgery
healthy blood vessel is removed from leg, arm or chest
blood vessel is used to create new blood flow path in your heart
the bypass graft enables blood to reach your heart by flowing
around (bypassing)
the blocked portion
of the diseased
artery. The increased
blood flow reduces
angina and the risk
of heart attack.
Complication
Cardiomyopathy / Congestive
heart failure
Cardiac Arrthymia
Death
Nitrates
Mechanism of Action:
Metabolized to endogenous EDRF (nitric
oxide) which increase cGMP
smooth
muscle relaxation & vasodilation
Antianginal effect
Venodilation
decrease preload
(venous return), ventricular wall stress and
O2 demand
Coronary vasodilation improves blood flow
to the myocardium and relieves vasospasm
Nitrates
Adverse Effects
Nitrate tolerance
Reflex tachycardia
:*combine with
drugs controlling HR
Headache
Most common,
usually subsides after
few days
Dizziness, presyncope
Worse with alcohol
Contraindications
Aortic valve
stenosis
Hypertrophic
obstructive
cardiomyopathy
Patient education
Beta-Blockers
Mechanism of action
Antagonize effect of catecholamine
by blocking beta receptor
reduce BP, HR and contractility
Decrease myocardial oxygen demand
Negative Inotropic
Beta-Blockers
Adverse Effects
Bradycardia
Hypotension
Fatigue
Sexual
dysfunction
Contraindications
Absolute
HR<50 BPM, heart
block : AV block,
severe LV failure,
acute HF,
vasospastic angina
Relative
Asthma, COPD,
severe depression,
PVD, DM,
dyslipidemia
Beta-Blockers
Withdrawal symptom from
abruptly discontinuing therapy
AMI
Sudden death
Calcium-Channel Blockers
Mechanism of Action
Block calcium entry into myocardial and smooth
muscle cells=variable negative inotropic effects
Diltiazem/Verapamil Vs.
Dihydropyridines
Dihydropyridines: Amlodipine,
Nifedipine
No effect on AV-node conduction and
may result in reflex tachycardia
Calcium-Channel Blockers:
Clinical Effectiveness
Calcium-Channel Blockers
Adverse Effects
Reflex tachycardia
Headache/flushing
Peripheral edema
Gingival
hyperplasia (N)
Hypotension
Bradycardia (D/V)
Constipation (V)
Contraindications
Heart Failure (D/V)
Bradycardia, heart
block ,AV block:
(D/V only)
CHF exarceration
(D/V)
Combination Therapy
Beta-blockers often combined with
nitrates or dihydropyridine CCBs
Diltiazem or verapamil often
combined with nitrates
Rarely used with beta-blockers but
some patients may benefit: monitor
heart rate
Pharmacotherapy to Prevent
MI and Death
Antiplatelet Agents
Lipid-lowering Therapy
ACEIs
Pharmacotherapy to Prevent
MI and Death
Antiplatelet agents
Aspirin
81-325 mg daily is indicated for all patients
lacking contraindications / EC reduce GI irritation
Clopidogrel (Plavix)
75 mg daily for patients unable to take aspirin
Avoid: ticlopidine and dipyridamole
Ticlopidine
250 mg bid with food
Pharmacotherapy to Prevent
MI and Death
Lipid-lowering therapy
Pharmacotherapy to Prevent
MI and Death
Patient Education
Take an active role!
Educated patients are happier patients
Poor adherence = poor outcomes
Multi-disciplinary approach is strongly
encouraged by ACC/AHA
Coronary Intervention
PTCA (percutaneous transluminal
coronary angioplasty)
CABG (Coronary Artery Bypass
Graft)
QUICK REVIEW
BBs: decrease oxygen demand
Nitrates: decrease oxygen demand and
increase oxygen supply
CCBs: decrease oxygen demand and
increase oxygen supply-D/V vs. DHP
Preventive therapy : ASA, lipid lowering
agents, ACEIs
ABCDE
QUICK REVIEW
LG is a 59 y.o. male with a PMH of HTN, mild
asthma, HL and CAD. Allergy: NKA. Current
meds include: lisinopril 10 mg QD, lovastatin 20
mg QD, atenolol 100 mg QD, albuterol inhaler
PRN, 0.4 mg NTG SL prn. BP=128/76;
pulse=60.
Since increasing the dose of
atenolol, he has noticed an increase in the use
of his albuterol. His anginal symptoms are well
controlled with his current regimen. Dr. Johnson
would like to know your assessment and
recommendations regarding LGs current
therapy.
QUICK REVIEW
A) Continue current therapy as there are no
other therapeutic options
B) Add isosorbide dinitrate 10 mg TID and
aspirin 81 mg QD
C) Gradually taper atenolol over the course of 12 weeks and add diltiazem CR 120 mg QD and
aspirin 81 mg QD
D) Add steroid inhaler due to increased use of
albuterol
E) Gradually taper atenolol over the course of 12 weeks and add isosorbide mononitrate ER 30
mg daily