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
