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HO CME : Acute Coronary Syndrome

Presenters: Hakimah Khani' Binti Suhaimi Nurul 'Izzah Binti Sodri Supervisor: Dr Patrick

23/4/14 Seminar Room Wad Kenanga 12 Hospital Sultan Haji Ahmad Shah (HoSHAS)

Introduction Pathogenesis Diagnosis Risk stratification Management
Pre-Hospital In-Hospital Post-Hospital

Case file

ACS - An Introduction
Incidence: 141 per 100,000 population/year, and the inpatient mortality rate is approximately 7%. Definition: A spectrum of UA / NSTEMI and STEMI. The clinical presentation will depend on the acuteness and severity of coronary occlusion.


Pathogenesis of Atherosclerosis
Accumulation of lipid-laden macrophages and smooth muscle cells, so-called foam cells

The oxidized (LDL-C) in foam cells is cytotoxic, procoagulant, and chemotactic.

As the atherosclerotic plaque grows, production of macrophage proteases and neutrophil elastases within the plaque can cause thinning of the fibromuscular cap that covers the lipid core.

Increasing plaque instability coupled with blood-flow shear and circumferential wall stress lead to
plaque fissuring or rupture, especially at the junction of the cap and the vessel wall activation, adhesion and aggregation of platelets + activation of clotting cascade formation of occlusive thrombus

Pathogenesis of ACS
Atherosclerotic plaque rupture, fissure or ulceration with superimposed thrombosis and coronary vasospasm Etiology of plaque fissure or rupture is still unclear. Possible causes: inflammation, infection, uncontrolled BP and smoking. Primary UA/NSTEMI = ACS occurring de novo Secondary UA/NSTEMI can occur due to: - increased myocardial oxygen demand (eg fever, tachycardia, thyrotoxicosis) - reduced coronary blood flow (hypotension) - reduced myocardial oxygen delivery (eg anaemia or hypoxemia)

of UA/N may evo * New L

History Physical examination Electrocardiography Cardiac biomarkers Other diagnostic modalities. E.g. echocardiogram

Diagnosis - Key message

The diagnosis of UA/NSTEMI is based on history + dynamic ECG changes (without persistent ST elevation), + raised cardiac biomarkers. In UA cardiac biomarkers are normal while in NSTEMI it is elevated. A raised troponin level has diagnostic and prognostic significance

Risk Stratification - TIMI Risk Score

Less accurate in predicting events, but is simple and widely accepted Intermediate/high risk patients benefit from early angiography and revascularization

TIMI Risk Score

The goals of management are: Immediate relief of ongoing ischemia and angina Prevention of recurrent ischemia and angina Prevention of serious adverse cardiac events

Pre-hospital Management

Non-invasive Investigations of Low Risk Patients

In-Hospital Management

ciated with efficacy


-blockers in UA/NSTEMI

Contraindications for -blockers

Marked first-degree AV block (PR interval >0.24s). Second- or third-degree AV block. History of bronchial asthma Severe peripheral arterial disease Acute decompensated LV dysfunction Cardiogenic shock.


Lipid-lowering drugs

Post Hospital Discharge

Education on medication Lifestyle change and CV risk factors modification Timely follow-up appointment and further ix Referral to a cardiac rehabilitation program where appropriate

Case File


Chief Complaint
Mr Mohd Ali, 64-year-old gentleman, with underlying DM, HPT, IHD, COPD, and gastritis was admitted with the chief complaint of left-sided chest pain for 3 days prior to admission.

History Of Presenting Illness

On 19/4/14 - presented to KK with:

Left-sided chest pain X 3/7 - occurs at rest, radiated to left jaw and arm, heaviness in nature - lasted for >20mins - S/L GTN X4 per day - partially relieved - pain score 4-5, on 19/4/14 - pain score 10/10 - a/w diaphoresis, SOB, palpitation, and failure sx: orthopnea, PND In KK, BP 132/67, PR 63, given T. aspirin 300mg STAT

Past Medical & Surgical History

Patient has HPT, DM, COPD since many years. In 2006, diagnosed to have IHD (age at that time 57 y/o) - done angiogram in IJN 2006 - claims had 3-vessel blockage, one of them >80% Patient was symptom-free since 2006. Under KK follow up, compliant to aspirin and other meds. In 2013 - diagnosed to have gastritis - OGDS done by Miss Suleka on 14/8/13: normal findings - on lifelong PPI

Past Medical & Surgical History

Multiple admissions in 2014: 23-27/3/14 - USA Completed S/C fondaparinux 2.5mg OD X 5/7 TCA HTAA cardio: 27/8/14 8am 2-8/4/14 - USA On day 2 of admission, he developed one episode of chest pain, and the ECG during that time showed ST elevation (anterior) Completed S/C fondaparinux 2.5mg OD X 1/52 TCA HTAA cardio: 6/5/14 8am 12-16/4/14 - USA Completed S/C fondaparinux 2.5mg OD X 3/7 No need for inpatient angiogram or earlier TCA

Meds upon discharge:

Tab Aspirin 150mg od Tab Clopidogrel 75mg od Tab Isordil 10mg tds S/L GTN prn Tab talmesartan 40mg od Tab Metoprolol 25mg od Tab Simvastatin 40mg on Tab Pantoprazole 40mg od Tab Glicazide 40mg bd MDI Budesonide ii/ii BD MDI Berodual prn


Echocardiogram done on 25/03/2014 15:26


Physical Examination

Physical Examination
Alert, comfortable, not in respiratory distress. Pink. Fair hydrational status. No xanthelasma/xanthomata V/S: Afebrile BP 130/70 PR 60, regular, good volume RR 20 sPO2 99% under R/A DXT 5.0 JVP not raised CVS S1, S2, no added heart sounds, no murmurs Lungs clear, equal air entry P/A soft, non-tender No pedal edema



Serial ECGs






ECG in ward


Daily ECG in ward


Daily ECG in ward






Management in the Ward


Management in the ward

Treat as unstable angina - TIMI score: ?
S/C fondaparinux 2.5mg OD X 3/7 Dual antiplatelet ECG/CE daily and per chest pain Inform STAT if chest pain S/L GTN I/I PRN Cont beta blocker, ARB, nitrate Cont other old meds Allowed discharge on 21/4/14 TCA IJN 28/4/14

Surely there is in the body a small piece of flesh; if it is good, the whole body is good, and if it is corrupted, the whole body is corrupted, and that is surely the heart.
- Prophet Muhammad SAW, narrated by Abu Abdullah an-Nu'maan ibn Basyiir RA


Thank You