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CHEST PAIN

ANGINA PECTORIS
ACUTE CORONARY SYNDROME

Dr. Andreas Arie, SpPD


CARDIOVASCULAR DIVISION INTERNAL MEDICINE DEPARTMENT
MEDICAL FACULTY DIPONEGORO UNIVERSITY
CHEST PAIN
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
Grading of Angina Pectoris
by the Canadian Cardiovascular Society Classification System
Guidelines for the Identification of ACS Patients
Chief Complaint
Chest pain typical of myocardial ischemia or MI
Associated : dyspnea, nausea and/or vomiting
diaphoresis
Medical History
CABG, angioplasty, CAD, angina on effort, or AMI
NTG use to relieve chest discomfort
Risk factors

Special Considerations
Women
Diabetic
Elderly patients
Initial Risk Stratification Scheme

Chest Pain
History, Physical
EKG

UA/NSTEMI/ Definite
STEMI Mod Risk Low Risk
High Risk Non-Cardiac
Acute Coronary Syndrome

No ST Elevation ST Elevation

NSTEMI

Myocardial Infarction
Unstable Angina NQMI QwMI
Braunwald E et al. J Am Coll Cardiol 2000; 36:970-1062
Acute Coronary Syndrome
ST-segment elevation MI (STEMI)
Non ST-segment elevation MI (NSTEMI)
Unstable Angina
Pembuluh darah yang mengalami aterosklerosis & trombosis
Atherosclerosis Timeline
Foam Fatty Intermediate Fibrous Complicated
Cells Streak Lesion Atheroma Plaque Lesion/Rupture

Endothelial dysfunction
From first decade From third decade From fourth decade
Growth mainly by lipid accumulation Smooth muscle Thrombosis,
and collagen haematoma

Adapted from Stary HC et al. Circulation 1995;92:1355-1374.


70 INFARCT STROKE GANGRENE ANEURYSM

60

50
CLINICAL HORIZON
AGE IN YEARS

40 CALCIFICATION
COMPLICATED LESION:
HEMORRHAGE, ULCERATION,
30 THROMBOSIS

FIBROUS PLAQUE
20

FATTY STREAK
10

0
Evolution of the atherosclerotic Plaque
Traditional risk factors Emerging risk factors
- Dyslipidemia - Homocystein
- Hypertension - CRP
- Smoking - Fibrinogen
- DM - etc
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
F non-modifiable
a usia (semakin tua semakin mudah mengalami PJK)
k gender (usia <64 tahun insidensi pria dg PJK>wanita,
namun dengan meningkatnya usia wanita menjadi lebih
t mudah mengalami PJK)
o genetik
r
modifiable
r merokok
i diabetes mellitus (DM)
s dislipidemia
i obesitas
hipertensi
k
sedentary life style
o stres
CVD disease risk factors
rokok

Diabetes

smoking

Hypertension
Hyper-
hipertensi
cholesterolae
mia

obesitas
stres
inactivity
Mayor Independent Risk Factors

Elevated Blood Presure (JNC VII)


- Hypertension : > 140/90
* Stage I : 140 159 / 90 99
* Stage II : 160 179 / 100 109
* Stage III : > 180 / 110
Dislipidemia (Framingham Criteria)
* Total cholesterol : > 200 mg%
* HDL < 35 mg%
* LDL > 130 mg%
Cigarette Smoking
DM
Advancing Age
Predisposing Risk Factors
Obesity : BMI > kg / m2
Abdominal obesity
Men : waist circ > 102 cm
Women : waist circ > 88 cm
Physical Inactivity
Family History of Premature CHD
Psychosocial factors
Conditional Risk Factors
Triglycerides > 200 mg / dl
Homocysteine
Small dense LDL
Protrombotic factor : fibrinogen
Inflamatory Markers CRP
PEMERIKSAAN
EVOLUSI EKG
Lanjutan ke hal berikutnya
Time course of Serum Protein Markers

MB2/MB1
Myoglobin

048 16 24 36 48
Hour post-AMI
Likelihood That Signs and Symptoms
Represent an ACS Secondary to CAD
CLINICAL SUSPICION OF ACS
Physical examination
ECG monitoring, Blood sample

Persistent No Persistent Undetermined


ST-elevation ST-elevation Diagnosis

Thrombolysis ASA, LMWH


PCI
Clopidogrel, betablockers, Nitrate

High Risk Low Risk

Second troponin measurement

GpIIb/IIIa Positive Twice negative


Cor.Angiography
Stress test
PCI, CABG or Medical management Coronary angiography
PRINCIPLES THERAPY OF THROMBOSIS
BASED ON PATHOGENESIS

PATHOGENESIS THERAPY

RISK FACTORS PREVENTION

- PLATELET ADHESION
ANTIPLATELET

-PLATELET AGGREGATION

-BLOOD COAGULATION ANTICOAGULANT

-THROMBOSIS THROMBOLYTIC
Algorithm for evaluation and management of patients suspected ACS
SYMPTOMS SUGGESTIVE OF ACS

Possible ACS Definite ACS

No ST elevation ST elevation

Evaluation for
Non Dx ECG ST and/or T wave changes
reperfusion
Normal initial serum cardiac marker Ongoing pain
therapy
(+) cardiac markers
Hemodynamic abnormalities
Observe
FU 4-8 h: ECG, cardiac markers

Recurrent ischemic pain


No recurrent pain (+) FU studies
(-) FU studies Diagnostic of ACS
confirmed
Stress test
Admit to hospital
Negative Positive Manage via
Nonischemic, low risk Diagnostic of ACS confirmed Acute ischemic pathway
Recurrent ischemia and/or
Acute Ischemia ST segment shift, or
Deep T-wave inversion, or
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
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