Myocardial Ischemia and Myocardial infarction 2009.ppt

8/11/2019 Myocardial Ischemia and Myocardial infarction 2009.ppt

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Myocardial Ischemia and

Myocardial infarction 2009

Dr.Ira Andaningsih SpJP

2009


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Myocardial Ischemia

Effects of ischemia on myocardial function

Effects of ischemia on myocardialmetabolism

Effects of ischemia on genetic expression

of spesific proteins (mRNA )


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Effects of ischemia on

myocardial function

Elimination of the normal contractileperformance 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.


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Effects of ischemia


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Effects of ischemia


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Three possible outcomes

myocardial ischemia


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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


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Progression of cell death


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Atherosclerosis Frequently

Goes Undetected for Years

Lumen size

does not changesignificantly

even in the

presence of a

large lipid core

Strong JP, et al. JAMA . 1999;281:727-735. Glagov S, et al. N Engl J Med.1987;316:1371-1375.

Media

Intima

MediaIntima

Lumen Lumen

Size of lumen

does not change

dramatically

Vascular wall remodels

to accommodate

lipid core


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Atherosklerosis

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


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Build-up of Plaque in the Arterial Walls


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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 instabilityand thrombus

OxidationInflammationEndothelialdysfunction


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What Characterizes Unstable

Plaque?

Libby P. Circulation.1995;91:2844-2850.


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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


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Stable plaquecan cause

systemic complications

related to vascular

narrowing & occlusion,

including:stable angina,

stroke,

renal dysfunction,

myocardial infarction,peripheral ischemia

Renaldysfunction

Stroke

Stable anginaMyocardial

infarction

Virmani R et al. Arter ioscler Thromb Vasc Biol .2000;20:1262-1275. Libby P. Circulat ion. 1995;91:2844-2850.

Vascular Occlusion Ultimately Results in

Systemic Complications

Peripheral ischemia


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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


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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


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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


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Mechanism of Angina Pectoris(1)

1.Release substances that stimulateintracardiac symphatetic nerves

The sensory end plates are the receptors of a

network of unmyelinated nerves (lie betweencardiac muscle fibers and around coronaryvessels),

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.


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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.


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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.


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4 types of Angina Pectoris and

Angina Equivalent

1. Stable/ Chronic Stable Angina Pectoris

2. Unstable Angina Pectoris3. Post Infarction Angina Pectoris

4. Prinzmetals Angina Pectoris or Variant

Angina


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Canadian Cardiovascular Society

Functional Classification1. No angina with ordinary physical activity

(walking/climbing upstair), but with strenuous orrapid 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 fewhours after awakening. Walking more than 2 blocks on thelevel and climbing >one flight of ordinary stairs at a normalpace and in normal condition.

3. Marked limitation of ordinary physicalactivity.Walking 1 to 2 blocks on the level andclimbing > one flight in normal conditions.

4. Inability to carry on any physical activity withoutdiscomfort-angina may be present at rest.


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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)


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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 1mm resting ST depression

Complete LBBB


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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.


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Echocardiography

Patients with abnormal auscultationsuggesting valvularheartdisease orhypertrophic cardiomyopathy

Patients with suspected heart Patients with prior MI

Patientswith LBBB, Q waves or other

significant pathological

changes

on ECG,including electrocardiographic left anterior

hemiblock(LVH)


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Chest Roentgenogram

This is usually within normal limits,

can be cardiomegaly


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Laboratory Test:

For risk factors:

Dislipidemia

Diabetes mellitus Etc


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CT Scan

Indications:

Patients with a low pre-test probability of

disease,with anon-conclusive exercise

ECG or stress imaging test


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Coronary Arteriography

Class I Severe stable angina(Class 3 or greater of

CanadianCardiovascularSocietyClassification), with a high pre-testprobability

of disease, particularly if the symptoms areinadequatelyrespondingto medical treatment.

Survivors of cardiac arrest

Patients with seriousventricular arrhythmias

Patients previouslytreated by myocardialrevascularization(PCI, CABG), who develop

early recurrence of moderate or severeangina pectoris


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Coronary Angiography

Class IIa Patients with an inconclusive diagnosis on non-

invasivetestingor conflicting results from differentnon-invasive modalitiesat intermediate to high risk ofcoronary disease

Patients with a high risk of restenosis after PCI, if PCIhasbeen performed in a prognostically important site

Management Chronic Stable Angina


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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


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Precipitating factors of unstable

angina

Anemia

Infection

Thyrotoxicosis

Fever

Hypotension

Hypoxia secondary due to respiratory

failure Tachyarrhythmia


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Classification of unstable angina(1)

1.Severity Class I: New onset, severe, or accelerated.

Patient with angina < 2 months duration,severe oroccurring 3 or more times/day, more frequent and

precipitated by less exertion.No rest pain in the last 2months.

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.


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Classification of unstable

angina(2)2.Clinical circumstance

Class A: Secondary unstable angina

Identified extrinsic condition to the coronary

vascular bed,which intensified myocardialischemia (precipitating factors)

Class B: Primary Unstable angina

Class C: Post infarction unstable angina

(within 2 weeks)


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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,andcalcium antagonist)

Occuring in maximal therapy (including

nitroglycerine iv).

Diagnostic Tools of Unstable


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Diagnostic Tools of UnstableAngina

Early risk stratification Rapid clinical assessment

12 leads ECG, repeat 15-30 min interval to detectdevelopment 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) untillevel peaked

Repeat ECG 12 leads Continuous ECG monitoring

Treatment of Unstable Angina


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Treatment of Unstable AnginaPectoris/Acute Coronary Syndrome

Depends upon the guideline of ESC 2007

Immediate management Early hospital care

Primary PCI


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Immediate management

1.Probable/ possible ACS but ECG normal, makecontinuous ECG

2.Follow up 12 leads normal, make exercise stresstest

3.Before stress test give the patient ASA, nitrate,beta blockers

4.If definite ACS (ECG + biomarkers),going to criticalcare unit

5.If


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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


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2.Antiplatelet therapy

ASA as soon as possible

Clopidogrel (loading dose)

protect the gaster with proton pump inhibitor

Before diagnostic angiography + anti

coagulant therapy


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3.Anticoagulant therapy

As soon as possible

Unless CABG is planned within 24 h

f


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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


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Indication for coronaryangioplasty(2)

2.Evolving indications:Chronic stable angina unresponsive to medical

therapy with multivs disease

Acute myocardial infarction complicated by continuing

UA or cardiogenic shockNo/mild angina, taking medication, and with strongly

positive stress test

Angina in patient with a recent cor artery occlusion (


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Indication for coronaryangioplasty(3)

3.Relative contra indications

a. No/mild angina without evidence of ischemia

b. Significant LM coronary artery stenosis

c. Coronary stenosis with 3

moe.Severe LV dysfunction (EF


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Indications for coronaryrevascularization /CABG

1.Angina is severe, disabling, or interfering with lifestyle on max.medical therapy

2.Results of non invasive stress test indicateextensive 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 inducibleischemia/poor exercise tolerance

5.Critical obstruction of proximal LAD with significantobstruction of 1 other major vsl + moderate angina

P t I f ti A i


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Post Infarction Angina

Very serious forms of APIf occur immediately post infarctionimmediate post

infarction AP

If occur a few days to several weeksdelayed postinfarction AP

After myocardial infarction (dead myocardial cells) there is nopainContinuing angina is due to myocardial ischemia

Treatment of Post Infarction Angina

Usually same with unstable angina

1. Immediate AP

2. Delayed AP

P i t l A i


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Prinzmetals Angina

Episodes ot myocardial ischemia at rest- During the episode,the ECG are:

a. Transient ST-segment elevation suggesting an acuteinfarction

b. Transient abnormal Q waves (rare)

c. AV block and another arrhythmia may occur during theepisodes

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 ofchest pain at rest

T t t f P i t l A i


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Treatment of Prinzmetals Angina

1. With normal coronary arterya. Nitroglycerine, isosorbide dinitrate, or intravenous

nitroglycerine

b. Nifedipine and diltiazem

c. Some patients are made worse by betablockers suchas propanolol

2. With obstructive coronary disease + coronaryspasm

a. CABGb. PTCA

c. Medical therapy

A i E i l t


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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 extensivemultivessels coronary disease)

Prolonged Myocardial Ischemia


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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 afterepisode

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 coronaryinsufficiency, to be between AP and myocardial

infarction

T t t


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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

A t M di l I f ti


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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 feat re of AMI(1)


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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,gaspingfor breath. Heart rate: bradycardia, rapid regular or no regular

tachycardia

BP: uncomplicated patient is normotensive, in cardiogenicshock is hypotension

Cardiac Examination: unremarkable findings on palpation andauscultation.


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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 8-14days

White blood cells: increased 2 h after theonset,peaks 2-4 days and normal in 1 weeks

ESR increased


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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


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Clinical feature of AMI

Imaging in AMI

Roentenography

Normal

Pulmonary edema (LV failure) Cardiomegaly

Nuclear cardiac imaging

Echocardiography Coronary angiography

Management of AMI


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Management of AMI

Prehospital care:

Most death occur within the first hour after itsonset 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:


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Speeding time to treatment:

Patient with chest pain at Emergency Rooms 10 min ECG assess for ST elevation,

10 min assess for contra indication tothrombolysis,

10 min: if no contra indication: Streptokinase (1.5MU over 60 min) or rTPA (15 mg bolus, 50mg/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


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General measure

1.Bed rest2.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


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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


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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


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Thrombolytic Therapy

1.BP > 180/110 mmHg

2.History chronic,severe hypertension with or withoutmedicine

3.Active peptic ulcer

4.History of CVA

5.Prolonged or traumatic CPR

6.Bleeding diathesis or current use anticoagulant

7.Diabetic hemorrhagic retinopathy8.Pregnancy

9.Thrombolytic 6-9 months ago

Primary PTCA


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Primary PTCA

90 % versus 65 % for thrombolysis

1.Infarct size reduced 23%

2.LV function global and regional improved

Complication of Myocardial


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Complication of Myocardial

Infarction

LV failure-Acute Pulmonary Edema

Cardiogenic Shock

Arrhythmia

Others

Management of LV failure- Acute


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gPulmonary Edema

1.Diuretics

2.Nitrate (vasodilator)

3.Digitalis

4.Beta adreno receptors:Dopamin,

dobutamin

5.Positive inotropic agents: amrinon/milrinon

Cardiogenic shock:


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Cardiogenic shock:

1.Medicamentosa: inotropic agent

2.Reperfusion (Primary PCI/CABG)

3.IABP (Intra Aortic Balloon Pump)


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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

extension6.Pericardial effusion and pericarditis


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