Acute Coronary Syndrome (ACS)

Umbrella term which includes

ST-elevation myocardial infarction (STEMI)

Unstable (crescendo) angina (UA)

This causes full thickness damage of heart muscle

Can usually be diagnosed on ECG at presentation

Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis

Will produce a pathological Q wave some time after MI so also known as Q-wave infarction

Cardiac chest pain with crescendo pattern

Deterioration in previously stable angina, with symptoms frequently occurring at rest

Angina of recent onset (less than 24hrs) or

Angina of increasing frequency or severity, occurs on minimal exertion or even at rest - form of ACS

Non ST-elevation myocardial infarction (NSTEMI)

Is a retrospective diagnosis made after troponin results and sometimes other investigation results are available

This causes partial thickness damage of heart muscle

Occurs by developing a complete occlusion of a MINOR or a partial occlusion of a major coronary artery previously affected by atherosclerosis

Also known as non-Q wave infarction will see ST depression and/or T wave inversion

Epidemiology

5/1000 per annum in UK of STEMI

Risk factors

Family history of ischaemic heart disease (IHD) - MI in first degree relative below 55

Smoking

Male

Hypertension, diabetes mellitus, hyperlipidaemia

Age

Obesity & sedentary lifestyle

Pathophysiology

Leading to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation

Rupture or erosion of the fibrous cap of a coronary artery plaque

Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow

Fatty streak - fibrotic plaque - atherosclerotic plaque - plaque rupture/fissure and thrombosis - MI or ischaemic stroke or critical leg ischaemia or sudden CVS death

In unstable angina the plaque has a necrotic centre and ulcerated cap and the thrombus results in PARTIAL OCCLUSION

In myocardial infarction the plaque also has a necrotic centre but the thrombus results in TOTAL OCCLUSION

Clinical Presentation

Unstable angina

Breathlessness

Pleuritic pain

Chest pain; new onset, at rest with crescendo pattern

Indigestion

New onset angina

Acute central chest pain, lasting more than 20 minutes, associated with:

Dyspnoea

Fatigue

Nausea and vomiting

Shortness of breath

Sweating

Palpitations

May present without chest pain (silent infarct) e.g. in elderly or diabetics

Distress and anxiety

Pallor

Increased pulse and reduced BP

Reduced 4th heart sound

Tachycardia or bradycardia

May be signs of heart failure (increase in jugular venous pressure)

Peripheral oedema

Differential Diagnosis

Myocarditis

Aortic dissection

Pericarditis

Pulmonary embolism

Angina

Oesophageal reflux/spasm

Diagnosis

12 lead ECG

Biochemical markers

Treatment

Can get hyper acute (tall) T waves

ST depression and T-wave inversion (this tends to occur hours/days after in NSTEMI) are highly suggestive of an ACS, particularly if associated with anginal chest pain

With a STEMI, complete occlusion of a coronary vessel will result in a persistent ST-elevation, hyper acute (tall) T waves or new left bundle branch block pattern - may see pathological Q waves a few days after MI (sign of previous MI)

Can be normal

CXR

CK-MB

Myoglobin

Troponin (T & I)

Serum levels increase within 3-12 hours from the onset of chest pain and peak at 24-48 hours

They then fall back to normal over 5-14 days

The most sensitive and specific markers of myocardial necrosis

Can act as a prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation

Look for cardiomegaly, pulmonary oedema or a widened mediastinum (aortic rupture)

Beta blockers (IV & oral)

Statins (oral)

Antiplatelets

ACE inhibitors (oral)

Oxygen

Risk factor modification

Anti-emetic

Coronary revascularisation

Pain relief

GTN spray

IV opioid

Aim for 94-98% saturation

88-92% for those with COPD

P2Y12 inhibitors (oral)

Glycoprotein IIb/IIIa antagonists (IV)

Aspirin (oral)

COX-1 inhibitor = blocks formation of thromboxane A2 thus prevents platelet aggregation

Can be used if allergic to aspirin

Can also be used alongside aspirin as a dual anti-platelet therapy

Inhibit ADP-dependent activation of IIb/IIIa glycoproteins thereby preventing amplification response of platelet aggregation

Examples include clopidogrel, prasugrel and ticagrelor

Side effects: neutropenia (low neutrophils), thrombocytopenia (low platelets) and INCREASED RISK OF BLEEDING

AVOID if CABG planned

Used in combination with aspirin and oral P2Y12 inhibitors in patients with ACS undergoing PCI

INCREASES RISK OF MAJOR BLEEDING

Only IV available

Examples include Abciximab, Tirofiban and Eptifbatide

Examples include Atenolol (IV then oral) or metoprolol (IV then oral)

Side effects: avoid with asthma, heart failure, hypotension and bradyarrhythmias

HMG-CoA reductase inhibitors

Examples include simvastatin, pravastatin and atorvastin

Examples include ramipril and lisonopril

Monitor renal function

PCI

CABG - high risk mortality in high risk groups e.g. recent MI

Healthy diet

Treat hypertension and diabetes

Lose weight and exercise daily

Low fat diet with statins

Stop smoking