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CHEST PAIN

ANGINA PECTORIS
ACUTE CORONARY SYNDROME

MANAGEMENT

Dr. Andreas Arie, SpPD-KKV


CARDIOVASCULAR DIVISION INTERNAL MEDICINE DEPARTMENT
MEDICAL FACULTY DIPONEGORO UNIVERSITY
CHEST PAIN?
CHEST PAIN
ANGINA PECTORIS
Angina is a clinical syndrome characterized by discomfort in
the chest, jaw, shoulder, back, or arm.
 Typically aggravated by exertion or emotional stress and
relieved by nitroglycerin.
 Usually occurs in patients with CAD, but can also occur in
person with valvular heart disease, hypertrophic
cardiomyopathy, and uncontrolled hypertension.
 Also can be present in patients with normal coronary artery
and myocardial ischemia related to spasm or endothelial
dysfunction.
 And also can be present in patients with non cardiac
condition of esophagus, chest wall, or lungs.
ANGINA PECTORIS
Typical vs Atypical Chest Pain
TYPICAL CHEST PAIN ATYPICAL CHEST PAIN
• Retrosternal pressure or heaviness • Atypical presentations are not
(‘angina’) Radiating to the left arm, uncommon.
neck, or jaw, which may be
intermittent (usually lasting for • These include epigastric pain,
several minutes) or persistent. indigestion, stabbing chest pain, chest
pain with some pleuritic features, or
• These complaints may be increasing dyspnoea
accompanied by other symptoms
such as diaphoresis, nausea, • older people, diabetes, (75 years)
abdominal pain, dyspnoea, and patients, women
syncope

Hamm CW, et al. European Heart Journal (2011) 32, 2999–3054


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Grading of Angina Pectoris
by the Canadian Cardiovascular Society Classification System
Pathophysiology of coronary heart disease
Mechanisms of myocardial ischaemia
Arterial
O2 transport O2 saturation
capacity
Contractility Haematocrit

Heart rate O2 O2 Diastolic aortic


consumption supply pressure

Wall stress Coronary vascular


resistance
Coronary
blood flow Coronary
Ventri- Wall LV end-
cular thick- diastolic spasm
volume ness pressure ISCHAEMIA Organic
stenosis

Angina ST segment Impaired perfusion Impaired pump


pectoris - depression Metabolic changes function
- elevation
Recurrent ischemia and/or
ST segment shift, or
Deep T-wave inversion, or
Acute Ischemia Positive cardiac markers

Pathway Aspirin
Beta blockers
Nitrates
Antithrombin regimen
GP IIb/IIIa inhibitor
Monitoring (rhythm and ischemia)

Early invasive strategy Early conservative strategy

Immediate 12-24 hour Recurrent Patient stabilizes


angiography angiography Symptoms/ischemia
Heart failure
Serious arrhythmia

Evaluate LV
Function

EF <.40 EF >.40

Stress Test

Not low risk Low risk

Follow on
Medical Rx
Is it ACUTE CORONARY SYNDROME?
Location of chest pain

14
R
I
S
K

F
A
C
T
O
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S
Evolution of the atherosclerotic Plaque
Traditional risk factors Emerging risk factors
- Dyslipidemia - Homocystein
- Hypertension - CRP
- Smoking - Fibrinogen
- DM - etc
Likelihood That Signs and Symptoms
Represent an ACS Secondary to CAD

Fihn et al. Stable Ischemic Heart Disease. AHA Guideline 2012


EVOLUSI EKG
Time course of Serum Protein Markers

MB2/MB1
Myoglobin

048 16 24 36 48
Hour post-AMI
Acute Coronary Syndrome
• ST-segment elevation MI (STEMI)
• Non ST-segment elevation MI (NSTEMI)
• Unstable Angina
Treatment of ACS
A. Anti IschemicTherapy
• b-Blockers
• Nitrates
• Calcium channel blockers
B. Antiplatelet agents
• Aspirin
• P2Y12 receptor inhibitors (Clopidogrel, Ticagrelor, Prasugrel (not
available in Indonesia))
• Glycoprotein IIb/IIIa receptor inhibitors
C. Anticoagulants
• Indirect inhibitors of the coagulation cascade (Fondaparinux, LMWH,
UFH)
• Direct inhibitors of coagulation (Direct factor Xa inhibitors, Direct
thrombin inhibitors )
THERAPY
 General Therapy (MONACT)
 Beta-blockers
 Reperfusion
 Facilitated PCI
 Risk Factors
 Complications
Antithrombotic

Ticlopidin,
Clopidogrel,
Prasugrel
Ticagrelor

Hamm CW, et al. European Heart Journal (2011) 32, 2999–3054


CLINICAL SUSPICION OF ACS
Physical examination
ECG monitoring, Blood sample

Persistent No Persistent Undetermined


ST-elevation ST-elevation Diagnosis

Thrombolysis Nitrat, Aspirin, UFH/LMWH


PCI Ticlopidine, Clopidogrel, Ticagrelor,Betablockers,

High Risk Low Risk

Second troponin measurement

Cor-angiography Positive Twice negative


GpIIb/IIIa
Stress test
PCI, CABG or Medical management Cor-angiography
PRINCIPLES THERAPY OF THROMBOSIS
BASED ON PATHOGENESIS

PATHOGENESIS THERAPY

RISK FACTORS PREVENTION

- PLATELET ADHESION
ANTIPLATELET

-PLATELET AGGREGATION

-BLOOD COAGULATION ANTICOAGULANT

-THROMBOSIS THROMBOLYTIC
Hospital care
A. Anti Ischemic Therapy
Bed rest with continuous ECG monitoring
Supplemental O2 to maintain SaO2 > 90%
Morphine iv. (for pain, anxiety, Pulmonary congestion)
Nitrate (oral or iv.)
Betablockers if no contraindication
Non dihydropyridine calcium antagonis (Diltiazem
or Verapamil) if Betablockers contraindicated and
no severe LV dysfunction.
Ace inhibitors for hypertension LV dysfunction
after MI
Hospital care
B. Anti Thrombotic Therapy

Possible ACS Likely/Definite ACS High risk ACS/planned PCI


Aspirin Aspirin + Aspirin + LMWH
LMWH or or IV Heparin +
IV Heparin GP IIb/IIIa
+ antagonist

Clopidogrel
+
Clopidogrel
Hospital care

B. Anti Thrombotic Therapy

High risk ACS/planned PCI


Aspirin + LMWH
or IV Heparin +
GP IIb/IIIa
antagonist
+
Clopidogrel
ANAMNESIS
PEMERIKSAAN
LET’S DO OUR JOB WITH PASSION,
THANK YOU FOR YOUR ATTENTION