HO CME : Acute Coronary

SyndromePresenters:

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)

Outline 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

Pathogenesis of AtherosclerosisAccumulation 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)

Diagnosis History Physical examination Electrocardiography Cardiac biomarkers Other diagnostic

modalities. E.g. echocardiogram

4.3 ElectrocardiographyThe ECG adds support to the diagnosis and provides prognosticinformation6-11. A recording made during an episode of chest pain isparticularly valuable.It should be performed within 10 minutes of the patients arrival atthe Emergency Department.Features suggestive of UA/NSTEMI are:Dynamic ST/T changesST depression > 0.5 mm in 2 or more contiguous leadsT-wave inversion deep symmetrical T-wave inversionOther ECG changes include new or presumed new onset bundlebranch block (BBB)* and cardiac arrhythmias, especially sustainedventricular tachycardia. Evidence of previous infarctions such as Qwaves may be present.However, a completely normal ECG does not exclude the diagnosisof UA/NSTEMI. Serial ECGs should be done as the ST changesmay evolve.* New LBBB should be treated as STEMI

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

ManagementThe 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

Oral antiplatelet agents7.2.2.1.1 Acetylsalicylic acid (ASA)Recommended loading dose: 300 mg of soluble/chewableaspirin 26,27. Enteric coated aspirin is not recommended forinitial loading dose because of its slow onset of actionMaintenance dose: 75-150 mg daily of soluble or entericcoated aspirin 26,27Aspirin in excess of 300-325 mg per day is associated withincreased risk of minor bleeding without greater efficacy

UA/NSTEMI in (CKD)

-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.

ACE-I / ARB in UA/NSTEMI

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

DEMOGRAPHIC DETAILS

Chief ComplaintMr 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 IllnessOn 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 HistoryPatient 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 HistoryMultiple 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

4/23/2014

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

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Echocardiogram done on 25/03/2014 15:26

Physical Examination

Physical ExaminationAlert, comfortable, not in respiratory distress. Pink. Fair hydrational status. No xanthelasma/xanthomata

V/S:AfebrileBP 130/70PR 60, regular, good volumeRR 20sPO2 99% under R/ADXT 5.0

JVP not raisedCVS S1, S2, no added heart sounds, no murmursLungs clear, equal air entryP/A soft, non-tenderNo pedal edema

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Investigations

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Serial ECGs ECG STAT in KK

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ECG STAT in ED

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ECG STAT in ED (II)

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ECG in ward

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Daily ECG in ward

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Daily ECG in ward

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Management in the Ward

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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

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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

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Thank You