Acute coronary

syndromes

Anas Salim
Asrar Abdul Ameer
Aya Ibrahim
 SLO
1. Definition of ACS
2. Atherosclerosis – pathogenesis & risk factors
3. Unstable Angina – definition, clinical features, and differentiation from Stable Angina
4. NSTEMI – definition, clinical features, risk stratification
5. STEMI – definition, clinical feature
6. Investigations – ECG, Echo, Biomarkers, coronary angiography
7. Management of ACS – Medical management including indications/contraindications
of thrombolysis, brief knowledge about Interventional mgt – PCI, CABG. EBM: PCI
intervention for ACS
8. Complications of ACS
 Definition
Acute Coronary Syndrome:
Range of conditions including unstable angina, STEMI and NSTEMI ; that are due to sudden
reduction of blood flow to the heart

Causes:
1. Atherosclerotic plague rupture and
thrombosis
2. Emboli
3. Coronary artery spasm
4. Vasculitis
 Atherosclerosis

- Is a progressive inflammatory disorder of

the arterial wall.
- Can affect any artery in the body.
- Characterized by focal lipid-rich deposits
of atheroma that remain clinically silent
until they become large enough to impair
tissue perfusion, or until ulceration and
disruption of the lesion result in
thrombotic
occlusion or distal embolization of the
vessels.
- Symptom occurs when there is more than
50% occlusion
 Risk factors
Modifiable Non Modifiable

 Age  Smoking
 Gender  HTN
 Family history  DM
 Hypercholesterolemia
 Obesity & sedentary lifestyle
 Drug & alcohol use
 Controversial risk factors include
stress, type A personality, LVH,
increased fibrinogen, hyperinsulinemia,
increased homocysteine levels, and
ACE genotype
 Unstable Angina
Definition: Clinical features :
Acute coronary syndrome in which there is  occurs at rest
myocardial ischemia without detectable  become more frequent, severe, or prolonged
myocardial necrosis. Cardiac biomarkers of than the usual pattern of angina
myocardial necrosis creatine kinase and troponin  change from the usual pattern of angina
are not released into the circulation.  not respond to rest or nitroglycerin.
 differentiation Stable/ unstable Angina
Stable Non stable
Onset Gradual Gradual

Location Central Central

Character band like / heaviness band like / heaviness

Transient Last longer than angina pain

Aggravating factor Excretion / cold / emotion / heavy Triggered by rest

meal

Reliving factor Rest / GTN spray Not relived by rest

Reperfusion therapy

Radiation Jaw / neck / arms / epigastric Jaw / neck / arms / epigastric

Severity Mild to moderate Severe

ECG Normal ECG Normal ECG /

Inverted T wave, ST depression
NSTEMI

●Non ST elevation myocardial infarction

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

●Causing unstable angina or partial thickness subendocardial MI

 NSTEMI-clinical features

●Pressure like, substernal pain on rest or minimal exertion

●Radiation: arm, neck, jaw

●Associated with: diaphoresis, dyspnea, nausea, vomiting, fatigue, syncope

NSTEMI-risk stratification-(GRACE)
 STEMI

●ST-elevation myocardial infarction

●Results from complete occlusion of one or more coronary arteries due to plaque
rupture

●Both proximal and distal portions will be affected leading to transmural infarction

●Diagnosis is made based on :

History: typical ischemic type chest discomfort
ECG: ST elevation > lead 12, often with reciprocal ST depression in the other leads
Investigations- ECG
●12 lead ECG
●Changes are best seen in leads that face the ischaemic or infracted area
●NSTEMI: ST segment depression+ T wave changes
●STEMI: ST elevation+ new LBBB
Investigations-

●Cardiac biomarkers:

Serial measurements of serum troponin

Troponin T and I concentrations are raised in MI
Levels increase within 3-6 hours and remain elevated for 36 hours and remain elevated for 2
weeks
No change in troponin in unstable angina
Serial CK-MB

●CBC: leukocytosis
●Elevated ESR & CRP
●Transient fall in cholesterol in the following 3 months
Investigations-

●Echocardiography:

Look for regional wall abnormalities

Performed before discharge to assess ventricular function and detect any
complications (eg. mural thrombus, mitral regurgitation ,pericardial effusion )

●Chest X-ray:

Pulmonary oedema
No cardiomegaly unless pre-existing myocardial damage is there
Investigations-coronary angiography

●Gold standard

●Done if:
 Revascularization is planned
In patients who fail to settle on medical therapy
Extensive ECG changes
Elevated plasma troponin
Patients with severe pre-existing stable angina

●Reveals disease that is amenable to PCI or urgent CABG

ACS

Unstable angina NSTEMI STEMI

Pathology Partial occlusion Partial occlusion Complete occlusion

Tissue damage No infraction Subendocardial Transmural infraction

infraction

Cardiac enzymes Normal Elevated Elevated

ECG No change ST depression ST elevation

T wave inversion New LBBB
 Immediate management – first 12 hours
● Urgent admission is necessary (12 hours from the onset of symptoms,
Bundle branch block or STEMI)
● ABC emergency management
● Keep patient in propped up position
● O2 given if saturation <92%
● Analgesia: IV opiates (Morphine sulphate 5-10mg/ Diamorphine 2.5-5mg)
● Antiemetics: Metoclopramide 10mg (titrated in small aliquots)
● Aspirin 300mg and clopidogrel 300-600mg stat (loading dose)
● Beta blockers (Metoprolol 5-15mg IV if tachycardia without heart failure)
 Thrombolysis
● Alteplase (human tissue plasminogen
activator)
● Bolus dose 15mg
● At 30min 0.75mg/kg (max. 50mg)
● At 60min 0.5mg/kg (max. 35mg)

● Tenecteplase (TNK) and Reteplase (rPA),

have a longer plasma half-life than
alteplase

● Of little net benefit or even harmful in

those who present more than 12 hours
after the onset of symptoms
 Antithrombotic therapy
Antiplatelets: Anticoagulants:
● Aspirin 300 mg daily. continued indefinitely if there ● Unfractionated heparin, LMWH and
are no side-effects fondaparinux (2.5mg subcutaneous)
● Continued for 8 days or until discharge
● Clopidogrel can be used instead (300 mg followed
by 75 mg daily)
● Warfarin: in cases with persistent atrial
● For NSTEMI – Ticagrelor (180 mg, followed by 90 fibrillation or echocardiography showing
mg twice daily) is more effective than clopidogrel in mural thrombi
reducing vascular death/MI/Stroke

● Glycoprotein IIb/IIIa receptor antagonists (Tirofiban

and Abciximab) for patients who undergo PCI, have
recurrent ischemia or high risk
 Antianginal therapy
1. Nitrates:
● Sublingual glyceryl trinitrate (300–500 μg) - Unstable angina or threatened infarction
● Intravenous nitrates (glyceryl trinitrate 0.6–1.2 mg/hr or isosorbide dinitrate 1–2 mg/hr) - Left ventricular
failure and relief of recurrent or persistent ischemic pain.

2. Beta blockers:
● Atenolol 5–10 mg/ metoprolol 5–15 mg given over 5 mins) - relieve pain, reduce arrhythmias and improve
short-term mortality
● Should be avoided in heart failure (Pulmonary edema) , hypotension (Systolic bp <105mmHg) and bradycardia
(HR <65/min)

3. Dihydropyridine calcium channel antagonist (nifedipine/amlodipine) can be added to beta blockers if there is
persistent chest discomfort.
 Reperfusion therapy - PCI
● Treatment of choice for ST segment elevation
● Combination with glycoprotein IIb/IIIa receptor antagonists and intracoronary stent implantation have the
best outcomes
● Limitation of availability of the necessary resources to provide this emergency service
● Remote areas where primary PCI cannot be achieved within 2 hours of diagnosis thrombolytic therapy
should be administered
 Late management of ACS
1. Risk stratification and further investigation:
● Using GRACE score and prognosis as it relates to :
● Left ventricular function, Ischemia and arrhythmias
● Exercise tolerance test done after 4 weeks of ACS in low-risk patients without spontaneous
ischemia

2. Lifestyle and Risk factor modification:

● Smoking cessation
● Statin therapy (LDL >3.2 mmol/L require high intensity therapy – Atorvastatin 80mg daily)
● Diet and regular exercise
● Good control on hypertension and diabetes
 Late management of ACS
3. Mobilization and rehabilitation:
● Restricted activities for 4-6 weeks until fibrosis of necrotic muscle
● If uncomplicated – mobilization on day 2 and return home in 3-5 days

4. Secondary prevention:
● Aspirin and clopidogrel – combination for 3 months, and lifelong aspirin)
● Beta blockers (Cardioselective) – lifelong
● ACE inhibitors in hypertensive patients – Enalapril 10mg BID, Ramipril 2.5-5mg BID
● ACE inhibitors counteract ventricular remodeling and prevent onset of heart failure
● Mineralocorticoid receptor antagonist – eplerenone 25-50mg OD in cases of Acute MI with left
ventricular dysfunction and pulmonary edema
 Late management of ACS
Coronary revascularization:
Coronary angiography considered in all patients at moderate or high risk to view revascularization (fail
to settle on medical therapy, extensive ECG changes, markedly elevated troponin levels and severe
pre-existing stable angina)

Coronary artery bypass grafting done in patients with:

1. Three vessel disease
2. Over 50% left main coronary artery stenosis
3. Unsuccessful treatment with PCI
4. Complications developed post MI
 Complications – Arrhythmias
● Most cases transient and of no hemodynamic or prognostic importance
● Pain relief, rest and the correction of hypokalemia may help prevent arrhythmias

1. Ventricular fibrillation: Major cause of death in those who die before receiving medical
attention. Managed by defibrillation

2. Atrial fibrillation: common but mostly transient. Doesn’t require emergency treatment. Only
need management when presents with high ventricular rate (with hypotension) or circulatory
collapse (Cardioversion with DC shock or medically with digoxin and beta blockers)

3. Bradycardia: usually no treatment required, except when there is hypotension or hemodynamic

deterioration (atropine 0.6-1.2mg/IV)
 Complications
2. Ischemia: recurrent angina at rest or minimal exertion, may require coronary angiography to assess
revascularization.
● Post-infarct angina occurs in up to 50% of patients treated with thrombolysis.
● Angina is felt when there is viable myocardium downstream the stenosed vessel

3. Acute circulatory failure: reflects extensive myocardial damage and indicates a bad prognosis
● All other complications of MI can occur when heart failure is present

4. Pericarditis: only occurs following infarction and is particularly common on the second and third
days.
● Pain is positional and tends to be worse on inspiration.
● pericardial rub may be audible
● Non-steroidal (NSAIDs) and steroidal anti-inflammatory drugs may increase the risk of
aneurysm formation and myocardial rupture in the early recovery period, and so should be
avoided.
 Complications
5. Mechanical complications:
● Rupture of the papillary muscle - causes acute pulmonary oedema and shock due to the
sudden onset of severe mitral regurgitation
● Rupture of the interventricular septum - causes left to right shunting through a ventricular septal
defect.
● Rupture of the ventricle – causes cardiac tamponade, usually fatal

6. Embolism: Thrombus often forms on the endocardial surface of freshly infarcted myocardium
● Leads to systemic embolism and occasionally causes a stroke or ischemic limb.
● Venous thrombosis and pulmonary embolism are less common (prophylactic
anticoagulants and early mobilization)

7. Impaired ventricular function, remodeling and ventricular aneurysms:

● Transmural MI is often followed by thinning and stretching of the infarcted segment
EBM
 MCQ’s

●A patient presents with crushing chest pain that is not relieved with rest. `The patient has a five year history of controlled
stable angina. He has no ischaemic ECG changes, but cardiac troponin is raised. Which of the following is the best
supported diagnosis?
A. STEMI
B. NSTEMI
C. Unstable angina
D. Stable angina

●Which sign below is less likely on physical examination of an ACS patient?

A. S3 heart sound
B. Bibasal lung field crackles
C. Central cyanosis
D. Pain not relieved with rest or ISMN administration
E. Relieved when leaning forward