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Myocardial Ischemia and

Myocardial infarction 2009


Dr.Ira Andaningsih SpJP
2009



Myocardial Ischemia

Effects of ischemia on myocardial function
Effects of ischemia on myocardial
metabolism
Effects of ischemia on genetic expression
of spesific proteins (mRNA )



Effects of ischemia on
myocardial function
Elimination of the normal contractile
performance of localized area of myocardium
asynergic contraction
paradoxical movement in the central ischemic
zone(systolic bulging/dyskinesis)
reduced contraction in the adjacent area
(akinesis/hypokinesis)
compensatory hyperfunction of the un
involved normal myocardium.
Effects of ischemia
Effects of ischemia
Three possible outcomes
myocardial ischemia
Effects of ischemia on
myocardial metabolism
High energy phosphate metabolism
declinesADP and ATP
Glycolytic flux increasesuptake glucose
Intracellular lactate accumulates.
Oxidation of free fatty acids



Progression of cell death

Atherosclerosis Frequently
Goes Undetected for Years
Lumen size
does not change
significantly
even in the
presence of a
large lipid core
Strong JP, et al. J AMA. 1999;281:727-735. Glagov S, et al. N Engl J Med.1987;316:1371-1375.
Media
Intima
Media
Intima
Lumen
Lumen
Size of lumen
does not change
dramatically
Vascular wall remodels
to accommodate
lipid core
Atherosklerosis

Tuzcu EM, Kapadia SR, Tutar E, et al. High Prevalence of Coronary Atherosclerosis in Asymptomatic Teenagers And Young Adults: EvidenceFrom
Intravascular Ultrasound. Circulation 2001;103:2705-2710

Build-up of Plaque in the Arterial Walls
Atherosclerosis: A Progressive Disease
CRP=C-reactive protein; LDL-C=low-density lipoprotein cholesterol.
Libby P. Circulation. 2001;104:365-372; Ross R. N Engl J Med. 1999;340:115-126.
Monocyte
LDL-C
Adhesion
molecule
Macrophage
Foam cell
Oxidized
LDL-C
Plaque rupture
Smooth muscle
cells
CRP
Plaque instability
and thrombus
Oxidation Inflammation
Endothelial
dysfunction
What Characterizes Unstable
Plaque?
Libby P. Circulation. 1995;91:2844-2850.
Glagov S, et al. N Engl J Med. 1987;316:1371-1375. Hackett D. Eur Heart J . 1988;9:1317-1323. Libby
P. Lancet. 1996;348:S4-S7.
Unstable
angina
Stroke
Peripheral ischemia
Unstable Plaque Rupture Can Lead to Serious
Complications Including MI, Unstable Angina,
Stroke, and Peripheral Ischemia
Myocardial
infarction
Stable plaque can cause
systemic complications
related to vascular
narrowing & occlusion,
including:
stable angina,
stroke,
renal dysfunction,
myocardial infarction,
peripheral ischemia
Renal
dysfunction
Stroke
Stable angina
Myocardial
infarction
Virmani R et al. Arterioscler Thromb Vasc Biol. 2000;20:1262-1275. Libby P. Circulation. 1995;91:2844-2850.
Vascular Occlusion Ultimately Results in
Systemic Complications
Peripheral ischemia
Atherosclerotic progression:
Glagovs remodeling hypothesis
Normal
vessel
Progression
Glagov S, et al. N Engl J Med. 1987;316:1371-1375.
Moderate
CAD
Compensatory expansion
maintains constant lumen
Minimal
CAD
Expansion
overcome:
lumen narrows
Advanced
CAD
The clinical feature of
Atherosclerotic
Coronary Heart Disease

1. Chronic Stable Angina Pectoris
2. Acute Coronary syndrome:
Unstable Angina Pectoris
NSTEMI
STEMI
3. Silent Myocardial Ischemia
4. Ischemic Cardiomyopathy
5. Other condition

Diagnostic tools for CAD
History Taking & Physical Examination
Resting ECG & Exercise ECG
Stress Thallium Myocardial Perfusion Imaging
Echocardiography
Chest Roentgenogram
Laboratory test
CT scan
Catheterization, angiografi and coronary
arteriography
Mechanism of Angina Pectoris(1)

1.Release substances that stimulate
intracardiac symphatetic nerves
The sensory end plates are the receptors of a
network of unmyelinated nerves (lie between
cardiac muscle fibers and around coronary
vessels),
Transmitted to a cardiac plexus, and ascend
to the symphatetic ganglia.
To spinal ganglia, then via spinal cord to the
thalamus,and to cerebral cortex.

Mechanism of Angina
Pectoris(2)
2. In various regions of the chest because
of:
Referred to the corresponding peripheral
dermatomes
Pain can be referred to medial aspects of the
arm via common connections to the brachial
plexus, and
Pain to the neck via the cervical roots.

Mechanism of Angina
Pectoris(3)
3. Silent ischemia
Perhaps because of autonomic denervation
(diabetes)
In some patients chest pain disappears after
myocardial infarction, although has transient
ischemia (ST segment depression), because
the nerve endings may have been damage.

4 types of Angina Pectoris and
Angina Equivalent

1. Stable/ Chronic Stable Angina Pectoris
2. Unstable Angina Pectoris
3. Post Infarction Angina Pectoris
4. Prinzmetals Angina Pectoris or Variant
Angina
Canadian Cardiovascular Society
Functional Classification
1. No angina with ordinary physical activity
(walking/climbing upstair), but with strenuous or
rapid or prolonged exertion
2. Slight limitation of ordinary activity.
Walking/ climbing upstairs rapidly/ after meals, walking uphill,
in cold/ in wind/ in emotional stress or only during the few
hours after awakening. Walking more than 2 blocks on the
level and climbing >one flight of ordinary stairs at a normal
pace and in normal condition.
3. Marked limitation of ordinary physical
activity.Walking 1 to 2 blocks on the level and
climbing > one flight in normal conditions.
4. Inability to carry on any physical activity without
discomfort-angina may be present at rest.

Electrocardiography
Normal (1/3 of patients)
Abnormal: the most common findings are
non specific ST-T changes.
Conducting disturbance (LBBB,LAHB)
Abnormal Q waves (old MCI)
Arrhythmia (VES)

Exercise ECG (Treadmill Test)

- The recording of an ECG during and after exercise

Class 1:
For diagnose in patient with an intermediate pre test probability of CAD
(based on age, gender, symptoms), including Complete RBBB or < 1 mm of resting ECG
For risk assessment and prognosis in patient undergoing initial evaluation

Class IIb:
For diagnosis in patient :
With a high test probability of CAD
With a low pretest probabitity of CAD
Taking digoxin with ECG < 1mm of ST depression
With ECG criteria for LVH and <1 mm of baseline ST depression

Class III:
For diagnosis in patient with:
WPW syndrome
Electronically paced ventricular rhytm
> 1mm resting ST depression
Complete LBBB

Stress Thallium Myocardial Perfusion Imaging

Give information of location and extent of
perfusion deficit.
Choice for:
Patient with abnormal baseline ECG
(LBBB, RBBB), history of myocardial
infarction, history of PTCA or CABG.
In patient with single vessel disease more
sensitive than exercise ECG.

Echocardiography

Patients with abnormal auscultation
suggesting valvular

heart

disease or
hypertrophic cardiomyopathy
Patients with suspected heart
Patients with prior MI
Patients

with LBBB, Q waves or other
significant pathological

changes

on ECG,
including electrocardiographic left anterior

hemiblock

(LVH)

Chest Roentgenogram


This is usually within normal limits,
can be cardiomegaly


Laboratory Test:

For risk factors:
Dislipidemia
Diabetes mellitus
Etc

CT Scan

Indications:
Patients with a low pre-test probability of
disease,

with a

non-conclusive exercise
ECG or stress imaging test



Coronary Arteriography
Class I
Severe stable angina(Class 3 or greater of
Canadian

Cardiovascular

Society
Classification), with a high pre-test

probability
of disease, particularly if the symptoms are
inadequately

responding

to medical treatment.
Survivors

of cardiac arrest
Patients with serious

ventricular arrhythmias
Patients previously

treated by myocardial
revascularization

(PCI, CABG), who develop

early recurrence of moderate or severe
angina pectoris
Coronary Angiography
Class IIa
Patients with an inconclusive diagnosis on non-
invasive

testing

or conflicting results from different
non-invasive modalities

at intermediate to high risk of
coronary disease
Patients with a high risk of restenosis after PCI, if PCI

has

been performed in a prognostically important site


Management Chronic Stable Angina
(the guideline of ESC 2007)

1.Correction of specific coronary risk factors
2.General and non pharmacological
methods (lifestyle)
3.Medications
4.Revascularization (PTCA/CABG)

Precipitating factors of unstable
angina

Anemia
Infection
Thyrotoxicosis
Fever
Hypotension
Hypoxia secondary due to respiratory
failure
Tachyarrhythmia
Classification of unstable angina(1)

1.Severity
Class I: New onset, severe, or accelerated.
Patient with angina < 2 months duration,severe or
occurring 3 or more times/day, more frequent and
precipitated by less exertion.No rest pain in the last 2
months.
Class II: Angina at rest. Subacute.
Patient with 1 or more episodes of angina at rest during
preceding month but not within preceding 48 hours.
Class III: Angina at rest. Acute
Patient with 1 or more episodes at rest within the
preceding 48 hours.


Classification of unstable
angina(2)
2.Clinical circumstance
Class A: Secondary unstable angina
Identified extrinsic condition to the coronary
vascular bed,which intensified myocardial
ischemia (precipitating factors)
Class B: Primary Unstable angina
Class C: Post infarction unstable angina
(within 2 weeks)
Classification of unstable
angina(3)
3. Intensity of treatment
Absence of treatment or minimal treatment
Occuring in presence of standard therapy for
chronic AP(oral nitrates, beta blockers,and
calcium antagonist)
Occuring in maximal therapy (including
nitroglycerine iv).
Diagnostic Tools of Unstable
Angina

Early risk stratification
Rapid clinical assessment
12 leads ECG, repeat 15-30 min interval to detect
development of ST elevation/depression
Cardiac biomarkers/Cardiac Troponin
< 6 h of the onset, remeasure 8-12 h after onset
Repeat biomarkers 6-8 h (2 to 3 times) until
level peaked
Repeat ECG 12 leads
Continuous ECG monitoring

Treatment of Unstable Angina
Pectoris/Acute Coronary Syndrome


Depends upon the guideline of ESC 2007
Immediate management
Early hospital care
Primary PCI

Immediate management

1.Probable/ possible ACS but ECG normal, make
continuous ECG
2.Follow up 12 leads normal, make exercise stress
test
3.Before stress test give the patient ASA, nitrate,
beta blockers
4.If definite ACS (ECG + biomarkers),going to critical
care unit
5.If <6 h give perfusion therapy
6.If the patient discharge, give specific instruction

Early hospital care(1)

1.Anti ischemic and analgesic therapy
Bed rest
Oxigen therapy
Sublingual nitroglycerin every 5 min (total 3
doses)
Nitroglycerine iv first 48 h after UA/NSTEMI
persistent ischemia.
Nitrate should not be admitted if BP<90/30
mmHg

Early hospital care(2)
2.Antiplatelet therapy
ASA as soon as possible
Clopidogrel (loading dose)
protect the gaster with proton pump inhibitor
Before diagnostic angiography + anti
coagulant therapy

Early hospital care(3)
3.Anticoagulant therapy
As soon as possible
Unless CABG is planned within 24 h

Indication for coronary angioplasty

Generally accepted indication is:
Chronic stable angina unresponsive to
medical therapy or Unstable Angina
a. with objective evidence of ischemia
b. with normal or mildly reduced LV function
c. with significant coronary artery stenoses
(1 or 2 vessels)

Indication for coronary
angioplasty(2)

2.Evolving indications:
Chronic stable angina unresponsive to medical
therapy with multivs disease
Acute myocardial infarction complicated by continuing
UA or cardiogenic shock
No/mild angina, taking medication, and with strongly
positive stress test
Angina in patient with a recent cor artery occlusion (<3
mo)
Angina after CABG
Documented variant angina, taking medication, with
significant cor.stenosis
Angina in operable/ high risk patient
Recurrent angina after myocardial infarction

Indication for coronary
angioplasty(3)

3.Relative contra indications
a. No/mild angina without evidence of ischemia
b. Significant LM coronary artery stenosis
c. Coronary stenosis with <50 % diameter
narrowing
d. Chronic,total/difuse coronary.occlusion > 3
mo
e.Severe LV dysfunction (EF <25 %)
f. Absence of on site surgical back up


Indications for coronary
revascularization /CABG

1.Angina is severe, disabling, or interfering with life
style on max.medical therapy
2.Results of non invasive stress test indicate
extensive ischemia, poor LV function, associated
with critical (>70%) occlusion in 1 or more vessels.
3.Left Main coronary artery stenoses (>60%)
4. Critical obstruction (>70%) in 3 major cor.artery,
with:
Resting LV dysfunction
Normal resting LV function + evidence of inducible
ischemia/poor exercise tolerance
5.Critical obstruction of proximal LAD with significant
obstruction of 1 other major vsl + moderate angina

Post Infarction Angina

Very serious forms of AP
If occur immediately post infarction immediate post
infarction AP
If occur a few days to several weeks delayed post
infarction AP
After myocardial infarction (dead myocardial cells) there is no
painContinuing angina is due to myocardial ischemia

Treatment of Post Infarction Angina
Usually same with unstable angina
1. Immediate AP
2. Delayed AP

Prinzmetals Angina

Episodes ot myocardial ischemia at rest
- During the episode,the ECG are:
a. Transient ST-segment elevation suggesting an acute
infarction
b. Transient abnormal Q waves (rare)
c. AV block and another arrhythmia may occur during the
episodes
Due to coronary artery spasm
May occur in partially occluded or normal artery.
Need Coronary arteriography and left ventriculography
(with special care)
An exercise ECG is a great caution
The goal is to record the ECG during an episodes of
chest pain at rest

Treatment of Prinzmetals Angina

1. With normal coronary artery
a. Nitroglycerine, isosorbide dinitrate, or intravenous
nitroglycerine
b. Nifedipine and diltiazem
c. Some patients are made worse by betablockers such
as propanolol

2. With obstructive coronary disease + coronary
spasm
a. CABG
b. PTCA
c. Medical therapy

Angina Equivalents

Symptoms associated with
Diminished LV compliance
Decrease myocardial contractility, and
Increased LV end diastolic pressure, due to ischemia.
The symptoms are:
Dyspnea
Exhaustion or chronic fatique
The complaint may occur while the patient is inactive

Treatment of Angina Equivalent
Is similar to that angina pectoris
Revascularization procedure (usually due to extensive
multivessels coronary disease)

Prolonged Myocardial Ischemia
with no evidence of Myocardial
Infarction)

Definition:
Features are similar to AP
Episode often at rest, may awaken the patient at night
Lasts 20 to 30 min
May not be associated with ECG abnormality after
episode
May produce ST-segment depression during attack
May produce ST-segment elevation (Prinzmetals)
May produce T-wave inversion that requires minutes
or hours to return to normal
In years past later was labeled as acute coronary
insufficiency, to be between AP and myocardial
infarction

Treatment
of Prolonged Myocardial Ischemia

Similar with unstable AP
1. Admitted to the coronary care unit
2. Sublingual / intravenous nitroglycerine
3. Heparin or thrombolytic therapy
4. Revascularization procedure


Acute Myocardial Infarction

WHO criteria for AMI:
Have 2 of 3 elements,
History of ischemic type chest discomfort
Evolutionary changes on serially ECG
A rise and fall in serum cardiac marker

Clinical feature of AMI(1)

1.Symptoms
Pain: prolonged, severe, some intolerable,
Lasting for more 30 min
2.Physical Examination
Anxious and distress, cold perspiration, skin pallor,gasping
for breath.
Heart rate: bradycardia, rapid regular or no regular
tachycardia
BP: uncomplicated patient is normotensive, in cardiogenic
shock is hypotension
Cardiac Examination: unremarkable findings on palpation and
auscultation.


Clinical feature of AMI(2)
Laboratory Examination
Creatine Kinase (CK): 4-8 h following AMI,
declines to normal 2-3 days.Peak about 24 h
CK isoenzymes (CK MB): 2-4 h after the onset
Troponins (cTnT, cTnI): is qualitative
Lactic dehydogenase (LDH): 24-48 h after the
onset, peaks 3-6 days,return to normal 8-14
days
White blood cells: increased 2 h after the
onset,peaks 2-4 days and normal in 1 weeks
ESR increased



Clinical feature of AMI
ECG findings:
Q wave (Transmural) and non Q wave infarction
(subendocardial)
ST segment elevation or/and depression
Location:
Inferior-II, III, avF
Anterior V1-V3
Anteroseptal V2-V4
Anterior extensive V1-V6
Anterolateral V4-V6,I-avL
Lateral I-avL,V5-6
Posterior V7-9
RV V3R, V4R, V5R, V6R
Clinical feature of AMI
Imaging in AMI
Roentenography
Normal
Pulmonary edema (LV failure)
Cardiomegaly
Nuclear cardiac imaging
Echocardiography
Coronary angiography

Management of AMI

Prehospital care:
Most death occur within the first hour after its
onset and death usually is due to VF

Hemodynamic disturbance:
1.Hypotension
2.Hypovolemic hypotension (low ventricular filling)
3.Hyperdynamic state
4.LV failure: Acute pulmonary edema


Speeding time to treatment:

Patient with chest pain at Emergency Rooms
10 min ECG assess for ST elevation,
10 min assess for contra indication to
thrombolysis,
10 min: if no contra indication: Streptokinase (1.5
MU over 60 min) or rTPA (15 mg bolus, 50
mg/30min, 35 mg/60 min),
if have contra indication do primary PTCA.
Admission to CCU
AMI (12-24 h)
Severe UA, if AMI ruled out, 12 h discharge from CCU
Uncomplicated AMI: discharge from CCU 24-36 h
Complicated AMI: discharge by need for CCU

General measure
1.Bed rest
2.Oxigenation
3.Diet: 4-12 h fasting and after that low calories
4.Balance electrolyte
5.Tranquilizer
6.Analgetic: Morphine sulfate
7.Medicamentosa:
Thrombolytic
Beta blockers
ACE inhibitors
Nitrate
Ca antagonist
Magnesium
8.Another approach:
- Primary PTCA
- IABP

Criteria for thrombolytic therapy

Indications:
1.Chest pain consistent with AMI
2.ECG changes : ST elevation > 0,1 mV in
at least 2 contiguous leads, or new or
presumably new LBBB
3.Time from onset the symptoms:
< 6 h most beneficial
6-12 h lesser but still important benefit
> 12 h diminishing benefits, but may still useful

Absolute Contra Indication for
Thrombolytic Therapy

1.Active internal bleeding
2.Suspected aorta dissection
3.Recent head trauma or known intra cranial
neoplasma
4.History of CVA
5.Major surgery or trauma < 2 weeks

Relative Contra Indication for
Thrombolytic Therapy

1.BP > 180/110 mmHg
2.History chronic,severe hypertension with or without
medicine
3.Active peptic ulcer
4.History of CVA
5.Prolonged or traumatic CPR
6.Bleeding diathesis or current use anticoagulant
7.Diabetic hemorrhagic retinopathy
8.Pregnancy
9.Thrombolytic 6-9 months ago

Primary PTCA


90 % versus 65 % for thrombolysis
1.Infarct size reduced 23%
2.LV function global and regional improved

Complication of Myocardial
Infarction

LV failure-Acute Pulmonary Edema
Cardiogenic Shock
Arrhythmia
Others


Management of LV failure- Acute
Pulmonary Edema

1.Diuretics
2.Nitrate (vasodilator)
3.Digitalis
4.Beta adreno receptors:Dopamin,
dobutamin
5.Positive inotropic agents: amrinon/milrinon

Cardiogenic shock:


1.Medicamentosa: inotropic agent
2.Reperfusion (Primary PCI/CABG)
3.IABP (Intra Aortic Balloon Pump)

Other complications of AMI
1.Rupture of the free wall
2.Rupture of the interventricular septum
3.Rupture of the papillary muscle
4.LV thrombus and arterial embolism
5.Post infarction ischemia and infarct
extension
6.Pericardial effusion and pericarditis