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Acute Coronary Syndrome (ACS) (Clinical Presentation (Acute central…
Acute Coronary Syndrome (ACS)
Umbrella term which includes
ST-elevation myocardial infarction (STEMI)
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
Unstable (crescendo) angina (UA)
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
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
Biochemical markers
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
CXR
Look for cardiomegaly, pulmonary oedema or a widened mediastinum (aortic rupture)
Treatment
Beta blockers (IV & oral)
Examples include Atenolol (IV then oral) or metoprolol (IV then oral)
Side effects: avoid with asthma, heart failure, hypotension and bradyarrhythmias
Statins (oral)
HMG-CoA reductase inhibitors
Examples include simvastatin, pravastatin and atorvastin
Antiplatelets
P2Y12 inhibitors (oral)
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
Glycoprotein IIb/IIIa antagonists (IV)
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
Aspirin (oral)
COX-1 inhibitor = blocks formation of thromboxane A2 thus prevents platelet aggregation
ACE inhibitors (oral)
Examples include ramipril and lisonopril
Monitor renal function
Oxygen
Aim for 94-98% saturation
88-92% for those with COPD
Risk factor modification
Healthy diet
Treat hypertension and diabetes
Lose weight and exercise daily
Low fat diet with statins
Stop smoking
Anti-emetic
Coronary revascularisation
PCI
CABG - high risk mortality in high risk groups e.g. recent MI
Pain relief
GTN spray
IV opioid