NSTEMI Non ST Elevation Myocardial Infarction

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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PATOGENESIS
Umumnya disebabkan oleh aterosklerosis koroner Plak aterosklerosis ruptur terbentuk trombus 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

Clinical Spectrum of Acute Coronary Syndrome Acute Coronary Syndrome

Non-ST Segment Elevation

ST Segment Elevation
STEMI NSTEMI

Unstable Angina Pectoris

Non-Q-wave

Q-wave

Acute Myocardial Infarction

Risk Factors
Uncontrollable
Sex Hereditary Race Age

Controllable
High blood pressure High blood cholesterol Smoking Physical activity Obesity Diabetes Stress and anger

Myocardial infarction:
acute, evolving, recent

Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following:
a) ischemic symptoms; b) development of pathologic Q waves on the ECG; c) ECG changes indicative of ischemia (ST segment elevation or depression); or d) coronary artery intervention (e.g., coronary angioplasty).

Definition: NSTEMI

NSTEMI is an acute process of myocardial ischemia with sufficient severity and duration 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 the absence of abnormal elevation of such biomarkers in patients with UA.
ACC/AHA Guidelines

Definition: unstable angina

Unstable anginaan acute process of myocardial ischemia that is not of sufficient severity and duration to result in myocardial necrosis.

Diagnosis
Anamnesis

Pemeriksaan Fisik
Pemeriksaan Penunjang :
1. Laboratorium 2. Elektrokardiografi 3. Thoraks Foto

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,11 hand and fingers

 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 Myocardial Ischemia

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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 (increasing angina) Riwayat penyakit dahulu : Riwayat angina on effort, infark operasi pintas Riwayat penggunaan nitrogliserin Identifikasi faktor-faktor risiko

atau

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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-streaked sputum. 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 sadapan extremitas

Atau 2 mm pada 2 sadapan prekordial yang berurutan 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 sangat menyokong UAP

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ST-segment depression

T-wave inversion

ELEKTROKARDIOGRAM
Current-of-injury patterns with acute ischemia

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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 in blood versus time after onset of symptoms

A myoglobin B troponin

C CK-MB D troponin in UA

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Diagnosis Banding
1. Diseksi aorta 2. Perikarditis 3. Nyeri angina hipertrofi atipikal pada kardiomiopati

4. Penyakit esofageal, GI atas atau traktus biliaris

5. Penyakit paru-paru : pneumotoraks, emboli, pleuritis

6. Sindroma hiperventilasi

7. Gangguan neurogen
8. Psikogen

dinding

dada

muskuloskeletal,

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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 Bblocker.

Oxygen
For:
Cyanosis Resp distress High risk features

Consume resources

Evidence is lacking.

Nitrates: Decr MVO2, incr coronaries

oxygenation
Actions
Dilate venous bed: decr preload and ventricular wall tension. Smaller dilatation of arterial system: decr afterload and 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.

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

Beta-blockers
Decr sBP Decr SA node rate, contractility, AV node conduction. 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-blocker without ISA (metoprolol, atenolol, propramolol, esmolol).

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 <50 Hypotension <90

Goal is bpm of 50-60 unless side-effects

B-blockers
13% reduction of progression of UA to AMI.

Extrapolate data from use in AMI, recent MI, stable angina, heart failure.

Calcium channel blockers

Inhibit vasculature SM contracture
Coronary vasodilatation

Inhibit myocardial muscle contraction

AV block

Slow sinus node

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

Calcium channel blockers

Conclusion:
Good symptom reliever

Trend of improved outcome with nondihydropyridine agents

To use if unable to use B-blockers

Antiplatelet agents
Aspirin ASAP!
Thienopyridine (clopidogrel or ticlopidine) if hypersensitivity of major GI intolerance

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.

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

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.

Other po agents
Sulfinpyrazone Dipyridamole Prostacyclin Oral GP IIB/IIIA inhibitor:
4 studies: 1 PCI, 3 NSTEMI
2 increased mortality

None presently recommended

Anticoagulants
UFH LMW heparin

Hirudin

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;319:1105 11.

MI rate of 12% down to 0.8% in UA

LMW heparin
Molecular weight of 4200 to 6000 D Factor Xa to thrombin inhibition ratio of 1.9 to 3.8 Only 25-50% have >18 saccharides
both f2 and 10 inhibition Rest inhibits only factor Xa