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NSTEMI

Non ST ElevationMyocardial Infarction


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2

SKA

Suatu sindroma klinik yang menandakan

adanya iskemia miokard akut, terdiri dari :

STEMI

NSTEMI

Angina pektoris tidak stabil (UAP)

Ketiga kondisi ini sangat berkaitan erat, berbeda

hanya dalam derajat beratnya iskemi dan

luasnya miokard yang mengalami nekrosis.


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3

PATOGENESIS

Umumnya disebabkan oleh aterosklerosis

koroner

Plak aterosklerosis ruptur terbentuktrombus diatas ateroma yang secara akut

menyumbat lumen koroner

Apabila sumbatan terjadi secara total hampir seluruh dinding ventrikel akan

nekrosis


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Penyempitan

Pembuluh

darah


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Clinical Spectrum of Acute Coronary Syndrome

Acute Coronary Syndrome

Non-ST Segment

Elevation

ST Segment

Elevation

Unstable

Angina Pectoris

Non-Q-wave Q-wave

Acute Myocardial

Infarction

STEMI

NSTEMI


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Uncontrollable

Sex

Hereditary

Race

Age

Controllable

High blood pressure

High blood cholesterol

Smoking

Physical activity

Obesity

Diabetes

Stress and anger

Risk Factors


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Myocardial infarction:acute, evolving, recent

Typical rise and gradual fall (troponin) or morerapid rise and fall (CK-MB) of biochemical

markers of myocardial necrosis with at leastone of the following:

a) ischemic symptoms;

b) development of pathologic Q waves on the ECG;

c) ECG changes indicative of ischemia (ST segmentelevation or depression); or

d) coronary artery intervention (e.g., coronary angio-plasty).


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ACC/AHA Guidelines

NSTEMI is an acute process of myocardial

ischemia with sufficient severity andduration to result in myocardial necrosis.

The initial ECG in patients with NSTEMI

does not show ST-segment elevation.

NSTEMI is distinguished from UA by the

detection of cardiac markers indicative of

myocardial necrosis in NSTEMI and theabsence of abnormal elevation of such

biomarkers in patients with UA.

Definition: NSTEMI


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Definition: unstable angina

Unstable anginaan acute process of

myocardial ischemia that is not ofsufficient severity and duration to result in

myocardial necrosis.


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Diagnosis

Anamnesis

Pemeriksaan Fisik

Pemeriksaan Penunjang :

1. Laboratorium

2. Elektrokardiografi

3. Thoraks Foto


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HISTORY

PRODROMAL SYMPTOMS

History very valuable to establish D/. Prodoma : chest discomfort

unstable angina 1/3 symptoms for 1 4 wks

20% symptoms for < 24 hrs

Malaise, exhaustion

NATURE OF PAIN Most patients

severe prolonged, 30 minutes - hours Constricting, crushing, oppressing, compressing

heavy weight or squeezing in chest

Choking, vise-like, heavy pain or stabbing, knife-like, boring or

burning discomfort

Location : retrosternal, spreading frequently to both sides of the

chest with predilection to the left side

Often pain radiates down ulnar aspect of left arm, producing

tingling sensation in left wrist, hand and fingers


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NATURE OF PAIN

SOME INSTANCES : pain begins in epigastrium, and simulates

abdominal disorder

Sometimes pain radiates to shoulders, upper extremities, neck, jaw

and interscapular region favoring the left side

Elderly : no chest pain but acute left ventricular failure and chest

tightness or marked weakness or syncope

Pain arises from nerve endings in ischemic or injured, but not necrotic,

myocardium

OTHER SYMPTOMS

50% nausea or vomiting in transmural infarcts Occasionally diarrhea, profound weakness, dizziness, palpitation, cold

perspiration, sense of impending doom

Occasionally : cerebral embolism or systemic arterial embolism


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Pain Patterns with MyocardialIschemia


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Anamnesis untuk UAP

3 kategori presentasi klinik UAP:

Angina saat istirahat (resting angina)

Angina awitan baru (new onset angina)

Angina yang bertambah berat (increasingangina)

Riwayat penyakit dahulu :

Riwayat angina on effort, infark atauoperasi pintas

Riwayat penggunaan nitrogliserin

Identifikasi faktor-faktor risiko


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PHYSICAL EXAMINATION

GENERAL APPEARANCE

Anxious, considerable distress, restless, fist on chest(Levine sign)

LV failure & symp. stimulation : cold perspiration, pallor,dyspnea, cough with frothy pink or blood-streakedsputum.

Shock : cool, clammy skin, facial pallor, cyanosis,confusion or disorientation

HEART RATE Variable depending on underlying rhythm and degree or

ventr. failure

Most commonly, HR 100 110/min; > 95% patients :

VPBs within first 4 hours


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BLOOD PRESSURE

Majority normotensive, but syst. BP may decline and

diast. BP may rise Half of pts with inferior MI parasympathetic

stimulation : hypotension, bradycardia or both (Bezold Jarisch reflex)

half of pts with anterior MI, sympathetic excess :hypertension, tachycardia or both

TEMPERATURE AND RESPIRATION

Most pts with extensive MI fever within 24-48 hrs,fever resolves by 4th or 5th day

Respiration due to anxiety and pain, in LV failure : resp.rate correlates with degree of heart failure


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JUGULAR VENOUS PULSE

JVP usually normal

RV infarction : marked jug. venous distension

CAROTID PULSE

Small pulse reduced stroke volume

Pulse alternans : severe LV dysfunction


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CHEST

LV failure and/or LV compliance : moist rales

Severe failure : diffuse wheezing, cough + hemopthysis

1967 : Killip & Kimball : prognostic classification

Class I : patients free of rales or S3

II : rales < 50% lung fields +/- S3

III : rales > 50% lung fields, frequently

pulm. edema IV : cardiogenic shock


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Pemeriksaan Penunjang

Pemeriksaan EKG

Gambaran EKG infark miokard akut Q-wave (STEMI):

Elevasi segmen ST 1 mm pada 2 sadapanextremitas

Atau 2 mm pada 2 sadapan prekordial yangberurutan

Atau gambaran LBBB baru atau diduga baru


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Gambaran EKG infark miokard akut non-Q-wave

(NSTEMI) atau angina pektoris tidak stabil

(UAP) :

Depresi segment ST atau gelombang T

terbalik pada 2 sadapan berurutan

Inversi gelombang T minimal 1 mm pada 2

sadapan atau lebih yang berurutan.

Perubahan segment ST saat keluhan dan

kembali normal saat keluhan hilang sangatmenyokong UAP


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ST-segment depression


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T-wave inversion


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Current-of-injury patterns with acuteischemia

ELEKTROKARDIOGRAM


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Pemeriksaan Penanda Jantung/Enzim jantung

(Cardiac Markers):

Yang lazim adalah CKMB, dapat pula troponin T

(TnT) atau troponin I (TnI)

Peningkatan marka jantung akan terlihat pada

infark miokard akut Q-wave (STEMI) dan non-Q-wave

(NSTEMI)


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Plot of the appearance of cardiac markers inblood versus time after onset of symptoms

A myoglobin C CK-MB

B troponin D troponin in UA


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1. Diseksi aorta

2. Perikarditis

3. Nyeri angina atipikal pada kardiomiopati

hipertrofi

4. Penyakit esofageal, GI atas atau traktus biliaris

5. Penyakit paru-paru : pneumotoraks, emboli,

pleuritis

6. Sindroma hiperventilasi7. Gangguan dinding dada : muskuloskeletal,

neurogen

8. Psikogen

Diagnosis Banding


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Recommended Class I:

Aspirin, Nitrate, B-blockers, morphine, O2 (prn).

Nondihydropyridine (cardizem/verapamil).

ACEi for specifics.

Class 2a:

ACEi for all.

Long-acting CCB for recurrent ischemia.

IABP if all fails.

Class 2b:

Extended form of Nondihydropyridine.

Short acting dihydropyridine in the presence of B-blocker.


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Oxygen

For:

Cyanosis

Resp distress

High risk features

Consume resources Evidence is lacking.

Nit t


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Nitrates: Decr MVO2, incr coronariesoxygenation

Actions

Dilate venous bed: decr preload and ventricular walltension.

Smaller dilatation of arterial system: decr afterloadand ventricular wall tension.

Need B-blocker

Dilatation of atherosclerotic coronaries

Decreased platelets adhesiveness.

For

ischemia despite nitro X 3 and iv B-blockade

high-risk patients (non-hypotensive).

Prethrombolytics: 35% mortality reduction.


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Morphine

Potent anxiolytic and analgesic action

Potentially beneficial

Venous dilatation

Decr HR

Decr sBP (Decr MVO2)

Activates neutral endopeptidases

Ann Emerg Med. May 2001;37:445-449.

Nausea and vomiting in 20%

Hypotension

Meperidine if allergic


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Beta-blockers Decr sBP

Decr SA node rate, contractility, AV nodeconduction.

Incr diastole filling time.

iv form for high-risk pts/on going pain.

Oral for intermediate/low risks patients.

No preferred agents except better if B-blockerwithout ISA (metoprolol, atenolol, propramolol,esmolol).


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B-blockers Contraindications (consensus):

1st degre AV block >24 msec

2nd or 3rd degre AV block without pacemaker

Asthma

Severe LV dysfunction with CHF

Caution with:

COPD

Bradycardia


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B-blockers

13% reduction of progression of UA to

AMI.

Extrapolate data from use in AMI, recent

MI, stable angina, heart failure.


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Calcium channel blockers

Inhibit vasculature SM contracture

Coronary vasodilatation

Inhibit myocardial muscle contraction

AV block

Slow sinus node


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Calcium channel blockers Dihydropyridines: nifedipine and amlodipine

peripheral vasodilatation

Verapamil: DAVIT study (3200 pts)

Only favorable trend

Nifedipine: HINT study (500 pts)

Incr MI by 16%, decr by 20% if with metoprolol

But metoprolol alone decr by 24%!!!

Diltiazem showed trends of improved outcome

CKMB level, reinfarction rate

Same mortality

except in LV dysfunction ACS


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Calcium channel blockers

Conclusion:

Good symptom reliever Trend of improved outcome with non-

dihydropyridine agents

To use if unable to use B-blockers


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Antiplatelet agents

Aspirin ASAP!

Thienopyridine (clopidogrel or ticlopidine) ifhypersensitivity of major GI intolerance


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Aspirin

Cyclooxygenase-1 inhibitor

Prevents thromboxane A2 formation

Dosing: 160 mg or 325 mg

Based on ISIS-2 which definetly established

its efficacy.

Can use pr route.


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Adenosine diphosphate

inhibitors Clopidogrel acts faster than ticlopidine.

Ticlodipine: Gi se, neutropenia, TTP

Clopidogrel: minimal rash and diarrhea

11 TTP within 14 days (3 millions pts)

CURE study: NEJM Aug 2001 12000 pts, plavix 300mg po

9.3 vs 11.4, 16.5 vs 18.8

ST changes or + markers

No GP2b3a inh or angio


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Plavix:Safety if angio or used with

Gp2b3A inh Lancet August 2001: PCI-CURE study

2600 pts.

Plavix 300mg loading

No increased bleeding problem whether

plavix +/- GPIIb/IIIa inh were used.

Better outcome before an after PCI.


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Other po agents

Sulfinpyrazone

Dipyridamole

Prostacyclin

Oral GP IIB/IIIA inhibitor:

4 studies: 1 PCI, 3 NSTEMI 2 increased mortality

None presently recommended


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Anticoagulants

UFH

LMW heparin

Hirudin


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UFH Activates antithrombin III

Inactives thrombin (f2), f9a and f10a

Molecular weight: 5 000 to 30 000 D

Binds to various proteins, cells , endothelium

Unpredictable.

Weight adjusted dosage

Incr need in DM and smoking, lower with age

Theroux et al. N Engl J Med 1988;319:110511.

MI rate of 12% down to 0.8% in UA


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LMW heparin

Molecular weight of 4200 to 6000 D

Factor Xa to thrombin inhibition ratio of1.9 to 3.8

Only 25-50% have >18 saccharides

both f2 and 10 inhibition

Rest inhibits only factor Xa


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