Ischaemic Heart Disease (angina pectoris, acute coronary syndrome, myocardial infarction) Flashcards
Definition
Characterised by decreased blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome.
Acute coronary syndrome subdivisions
o Unstable angina - chest pain at rest due to ischaemia but without cardiac injury
o NSTEMI
o STEMI - ST elevation with transmural infarction
o NOTE: MI = cardiac muscle necrosis resulting from ischaemia
Epidemiology
· COMMON
· Prevalence: > 2 %
· More common in males
· Annual incidence of MI in the UK ~ 5/1000
Aetiology
· Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply
· This is usually due to atherosclerosis
· Rarer causes of angina pectoris include coronary artery spasm (e.g. induced by cocaine), arteritis and emboli
Atherosclerosis pathophysiology
o Endothelial injury leads to migration of monocytes into the subendothelial space
o These monocytes differentiate into macrophages
o Macrophages accumulate LDL lipids and become foam cells
o These foam cells release growth factors that stimulate smooth muscle proliferation, production of collagen and proteoglycans
o This leads to the formation of an atherosclerotic plaque
Risk factors
o Male o Diabetes mellitus o Family history o Hypertension o Hyperlipidaemia o Smoking
Presenting symptoms (acute coronary syndrome)
o Acute-onset chest pain
o Central, heavy, tight, crushing pain
o Radiates to the arms, neck, jaw or epigastrium
o Occurs at rest
o More severe and frequent pain that previously occurring stable angina
o Associated symptoms: · Breathlessness · Sweating · Nausea and vomiting · SILENT INFARCTS occur in the elderly and diabetics
Presenting symptoms (stable angina)
o Chest pain brought on by exertion and relieved by rest
Signs on physical examination (stable angina)
Check for signs of risk factors
Signs on physical examination (acute coronary syndrome)
o There may be NO CLINICAL SIGNS o Pale o Sweating o Restless o Low-grade pyrexia o Check both radial pulses to rule out aortic dissection o Arrhythmias o Disturbances of BP o New heart murmurs o Signs of complications (e.g. acute heart failure, cardiogenic shock)
Investigations (bloods)
o FBC o U&Es o CRP o Glucose o Lipid profile o Cardiac enzymes (troponins and CK-MB) o Amylase (pancreatitis could mimic MI) o TFTs o AST and LDH (raised 24 and 48 hours post-MI, respectively)
Investigations (ECG)
Unstable Angina or NSTEMI:
· May show ST depression or T wave inversion
o STEMI: · Hyperacute T waves · ST elevation (> 1 mm in limb leads, > 2 mm in chest leads) · New-onset LBBB · Later changes: § T wave inversion § Pathological Q waves
o Relationship between ECG leads and the side of the heart
· Inferior: II, III, aVF
· Anterior: V1-V5/6
· Lateral: I, aVL, V5/6
· Posterior: Tall R wave and ST depression in V1-3
Investigations (CXR)
Check for signs of heart failure
Investigations (exercise ECG)
o Indications
· Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease
· Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender
· NOTE: digoxin is associated with giving a false-positive result
o Results:
· Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex
· Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes)
§ NOTE: beta-blockers reduce heart rate and so should be stopped before the test
· Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm
Investigations (radionuclide myocardial perfusion imaging (rMPI))
o Uses Technetium-99m sestamibi or tetrofosmin
o Can be performed under stress or at rest
o Stress testing shows low uptake in ischaemic myocardium
Investigations (echocardiogram)
o Measures left ventricular ejection fraction
o Exercise or dobutamine stress echo may detect regional wall motion abnormalities
Investigations (pharmacological stress testing)
o This is used in patients who are unable to exercise
o Pharmacological agents can be used to induce a tachycardia, such as:
· Dipyridamole
· Adenosine
· Dobutamine
o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium
o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease
Investigations (cardiac catheterisation/angiography)
Performed if ACS with positive troponin or if high risk on stress testing
Investigations (coronary calcium scoring)
o Uses specialised CT scan
o May be useful in outpatients with atypical chest pain or in acute chest pain that isn’t clearly due to ischaemia
Management plan (stable angina)
o Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes)
· All patients should receive aspirin 75 mg/day unless contraindicated
o Immediate symptom relief (e.g. GTN spray)
o Long-term management · Beta-blockers § Contraindicated in: · Acute heart failure · Cardiogenic shock · Bradycardia · Heart block · Asthma · Calcium channel blockers · Nitrates
o Percutaneous coronary intervention (PCI)
· Performed in patients with stable angina despite maximal tolerable medical therapy
o Coronary artery bypass graft (CABG)
· Occurs in more severe cases (e.g. three-vessel disease)
Management plan (unstable angina/NSTEMI)
o Admit to coronary care unit
o Oxygen, IV access, monitor vital signs and serial ECG
o GTN
o Morphine
o Metoclopramide (to counteract the nausea caused by morphine)
o Aspirin (300 mg initially, followed by 75 mg indefinitely)
o Clopidogrel (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk)
o LMWH (e.g. enoxaparin)
o Beta-blocker (e.g. metoprolol)
o Glucose-insulin infusion if blood glucose > 11 mmol/L
o GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients:
· Undergoing PCI
· At high risk of further cardiac events
o If little improvement, consider urgent angiography with/without revascularisation
o NOTE: the acute management of ACS can be remembered using the mnemonic MONABASH · Morphine · Oxygen · Nitrates · Anticoagulants (aspirin + clopidogrel) · Beta-blockers · ACE inhibitors · Statins · Heparin
Management plan (STEMI)
o Same as UAP/NSTEMI management except:
· Clopidogrel
§ 600 mg if patient is going to PCI
§ 300 mg if undergoing thrombolysis and < 75 yrs
§ 75 mg if undergoing thrombolysis and > 75 yrs
§ MAINTENANCE: 75 mg daily for at least 1 year
· If undergoing primary PCI:
§ IV heparin (plus GlpIIb/IIIa inhibitor)
§ Bivalirudin (antithrombin)
o Primary PCI
· Goal < 90 min if available
o Thrombolysis
· Uses fibrinolytics such as streptokinase and tissue plasminogen activator (e.g. alteplase)
· Only considered if within 12 hours of chest pain with ECG changes and not contraindicated
· Rescue PCI may be performed if continued chest pain or ST elevation after thrombolysis
o Secondary Prevention · Dual antiplatelet therapy (aspirin + clopidogrel) · Beta-blockers · ACE inhibitors · Statins · Control risk factors
o Advice
· No driving for 1 month following MI
o CABG
· Considered in patients with left main stem or three-vessel disease
Possible complications
· Increased risk of MI and other vascular disease (e.g. stroke, PVD)
· Cardiac injury from an MI can lead to heart failure and arrhythmias
Early complications
o Death o Cardiogenic shock o Heart failure o Ventricular arrythmias o Heart block o Pericarditis o Myocardial rupture o Thromboembolism
