ACUTE CORONARY SYNDROME

MARYAM JAMILAH BINTI ABDUL HAMID082013100002

IMS BANGALORE

LEARNING OUTCOME•Definition•Etiology•Pathogenesis•Clinical features• Investigation•Management•Prognosis

INTRODUCTIONAcute coronary syndrome: Encompasses both

unstable angina and myocardial infarction (MI)

Unstable angina: Characterized by new-onset or rapidly worsening angina (crescendo angina),

angina on minimal exertion or angina at rest in the absence of myocardial damage

MI: Symptoms occur at rest and there is evidence of myocardial necrosis, as demonstrated by an

elevation in cardiac troponin or CK-MB isoenzyme

ETIOLOGY•Atherosclerosis•Arteritis•Coronary dissection• Embolism•Coronary mural thickening•Causes of coronary luminal narrowing•Congenital coronary artery disease

PATHOGENESIS

UNSTABLE ANGINA• Pattern of pain that is progressive with increasing frequency

• Precipitated by less effort

• Often occurs at rest. Tends to be long duration.• Induced by disruption of atherosclerotic plaques, with

superadded thrombosis, embolization & vasospasm.• Pre Infarction Angina

MYOCARDIAL INFARCTION

TYPES•TRANSMURAL •SUBENDOCARDIAL

LOCATION OF INFARCT

•LAD Anterior & Apical LV& 2/3 IV Septum [40--50%]

•RCA Post & Basal LV & Post 1/3 of IV Septum [30--40%]

•LCA Lateral wall of LV [15 - 20% ]

CLINICAL FEATURESSYMPTOMS

• Prolonged cardiac pain: chest, throat, arms, epigastrium or back

• Anxiety and fear of impending death

• Nausea & vomiting

• Breathlessness

• Collapse/syncope

PHYSICAL SIGNS• Signs of sympathetic activation: pallor, sweating,

tachycardia• Signs of vagal activation: vomiting, bradycardia• Signs of impaired myocardial function

Hypotension, oliguria, cold peripheriesNarrow pulse pressureRaised JVPS3S1 –quietApical impulse: diffuseLung crepitation

• Signs of tissue damage: fever• Signs of complications: mitral regurgitation,

pericarditis

Condition Duration Quality Location Associated features

Unstable

angina10-20 min Pressure,

tightness, heaviness, burning

Retrosternal, often with radiation to or isolated discomfort in neck, jaw, sholders, or arms- freq. left

Precipitated by low exertion, at rest, exposure to cold, psychologic stressS4 gallop or mitral regurgitation murmur during pain

Acute MI

Variable; often >30 min

Unrelieved with nitroglycerinMay be associated with heart failure or arrhythmia

KILLIP CLASS• 1967, Acute myocardial infarction

• Focus on physical examination & development of heart failure to predict risk

• Class I: No evidence of heart failure (mortality 6%)

• Class II: Mild to moderate heart failure (S3 gallop, rales < half-way up lung fields or elevated JVP)

• Class III: Pulmonary edema (mortality 38%)

• Class IV: Cardiogenic shock defined as SBP <90 mmHg, signs of hypoperfusion; oligouria, cyanosis, swelling (mortality 67%)

RISK STRATIFICATION

INVESTIGATION• Electrocardiography

•Plasma cardiac biomarkers

•Other blood tests

•Chest X-Ray

• Echocardiography

ECG

• Confirming diagnosis

• To be repeated

• Limitation: difficult to interpret if bundle branch block (BBB) or

previous MI present

• Best seen in the leads ‘face’ ischaemic or infected area

• Anteroseptal infarction: V1 to V4

• Anterolateral infarction: V4 to V6, aVL, lead I

• Inferior infarction: lead II, lead III, aVF, ‘reciprocal’ changes of ST depression on lead I, aVL and anterior chest lead

if involve RV– need additional leads on right pericardium• Posterior wall infarction: no ST elevation or Q waves in

standard leads, ‘reciprocal’ changes (ST-segment depress), tall R wave V1-V4

Transmural MI

1. Proximal occlusion of a major coronary artery; ST-segment elevation (or new BBB)

2. Diminution size of R wave

3. Transmural develop Q wave

4. T wave inverted; change in ventricular repolarisation

Subendocardial MI

• Non ST-segment elevation

• Partial occlusion of a major vessel or complete occlusion of a minor vessel

• Unstable angina, subendothelial MI

• T wave inversion

• Loss of R wave

• Absence of Q wave

MARKER ONSET PEAK DURATION NORMAL VALUE

CK-MB 3-6 hours 18-24 hours 36-72 hours 0-5.5 ng/mlTroponins 4-10 hours 18-24 hours 8-14 days 0-0.1 ng/mlMyoglobin 1-4 hours 6-7 hours 24 hours 10-95 ng/ml (M)

10-65 ng/ml (F)LDH 6-12 hours 24-72 hours 6-8 days 125-220 U/LAST 24-36 hours 4-5 days 10-12 days 10-45 U/L

IMMEDIATE MANAGEMENT- FIRST 12 HOURS

•Analgesia

•Antithrombotic therapy

•Anti-angina therapy

•Reperfusion therapy

COMPLICATIONS OF ACUTE CORONARY

SYNDROME• Arrhythmias• Ischemia• Acute circulatory failure• Pericarditis• Mechanical complication• Embolism• Impaired ventricular function, remodeling and ventricular aneurysm

LATE MANAGEMENT IN MI•Risk stratification and further investigation•Lifestyle modification•Secondary prevention drug therapy•Rehabilitation•Device

PROGNOSIS• ¼ cases, death within few minutes without medical care• ½ death within 24 hours of onset• 40% affected patients die within first month• Reach hospital & receive medication; 28-day survival >85%• Worse prognosis with anterior and inferior infarction• Who survive acute attack;>80% live a further year75% for 5 years50% for 10 years25% for 20 years

CONCLUSION

REFERENCES•BRIAN R. WALKER, NICKI R. COLLEDGE, STUART H. RALSTON, IAN D. PENMAN, Davidson’s Principles & Practice of Medicine, 22nd Edition

•MICHAEL GLYNN, WILLIAM DRAKE, Hutchinson’s Clinical Methods, 23rd Edition

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