Ischaemic Heart Disease Flashcards
Define
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.
ACS can be further subdivided into:
Unstable angina - chest pain at rest due to ischaemia but without cardiac injury
NSTEMI
STEMI - ST elevation with transmural infarction
NOTE: MI = cardiac muscle necrosis resulting from ischaemia
Causes
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
Endothelial injury leads to migration of monocytes into the subendothelial space
These monocytes differentiate into macrophages
Macrophages accumulate LDL lipids and become foam cells
These foam cells release growth factors that stimulate smooth muscle proliferation, production of collagen and proteoglycans
This leads to the formation of an atherosclerotic plaque
Risk factors
Male
Diabetes mellitus
Family history
Hypertension
Hyperlipidaemia
Smoking
Epidemiology
COMMON
Prevalence: > 2 %
More common in males
Annual incidence of MI in the UK ~ 5/1000
Symptoms
ACS
Acute-onset chest pain
Central, heavy, tight, crushing pain
Radiates to the arms, neck, jaw or epigastrium
Occurs at rest
More severe and frequent pain that previously occurring stable angina
Associated symptoms:
Breathlessness
Sweating
Nausea and vomiting
SILENT INFARCTS occur in the elderly and diabetics
Stable Angina
Chest pain brought on by exertion and relieved by rest
Signs
Stable Angina
Check for signs of risk factors
ACS
There may be NO CLINICAL SIGNS
Pale
Sweating
Restless
Low-grade pyrexia
Check both radial pulses to rule out aortic dissection
Arrhythmias
Disturbances of BP
New heart murmurs
Signs of complications (e.g. acute heart failure, cardiogenic shock)
Investigations
Bloods
FBC
U&Es
CRP
Glucose
Lipid profile
Cardiac enzymes (troponins and CK-MB)
Amylase (pancreatitis could mimic MI)
TFTs
AST and LDH (raised 24 and 48 hours post-MI, respectively)
ECG
Unstable Angina or NSTEMI:
May show ST depression or T wave inversion
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
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
CXR
Check for signs of heart failure
Exercise ECG
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
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
Radionuclide Myocardial Perfusion Imaging (rMPI)
Uses Technetium-99m sestamibi or tetrofosmin
Can be performed under stress or at rest
Stress testing shows low uptake in ischaemic myocardium
Echocardiogram
Measures left ventricular ejection fraction
Exercise or dobutamine stress echo may detect regional wall motion abnormalities
Pharmacological Stress Testing
This is used in patients who are unable to exercise
Pharmacological agents can be used to induce a tachycardia, such as:
Dipyridamole
Adenosine
Dobutamine
These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium
NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease
Cardiac Catheterisation/Angiography
Performed if ACS with positive troponin or if high risk on stress testing
Coronary Calcium Scoring
Uses specialised CT scan
May be useful in outpatients with atypical chest pain or in acute chest pain that isn’t clearly due to ischaemia
Management
STABLE ANGINA
- Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes)
- All patients should receive aspirin 75 mg/day unless contraindicated
- Immediate symptom relief (e.g. GTN spray)
Long-term management
-Beta-blockers Contraindicated in: Acute heart failure
Cardiogenic shock , Bradycardia , Heart block , Asthma , Calcium channel blockers , Nitrates
- Percutaneous coronary intervention (PCI) : Performed in patients with stable angina despite maximal tolerable medical therapy
- Coronary artery bypass graft (CABG)
Occurs in more severe cases (e.g. three-vessel disease)
UNSTABLE ANGINA/NSTEMI
Admit to coronary care unit
Oxygen, IV access, monitor vital signs and serial ECG
GTN
Morphine
Metoclopramide (to counteract the nausea caused by morphine)
Aspirin (300 mg initially, followed by 75 mg indefinitely)
Clopidogrel (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk)
LMWH (e.g. enoxaparin)
Beta-blocker (e.g. metoprolol)
Glucose-insulin infusion if blood glucose > 11 mmol/L
GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients:
Undergoing PCI
At high risk of further cardiac events
If little improvement, consider urgent angiography with/without revascularisation
NOTE: the acute management of ACS can be remembered using the mnemonic MONABASH
Morphine Oxygen Nitrates Antiplatelets (aspirin + clopidogrel) Beta-blockers ACE inhibitors Statins Heparin
:STEMI
Same as UAP/NSTEMI management except:
Secondary Prevention
Dual antiplatelet therapy (aspirin + clopidogrel)
Beta-blockers
ACE inhibitors
Statins
Control risk factors
Advice
No driving for 1 month following MI
CABG
Considered in patients with left main stem or three-vessel disease
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 (within 24-72 hrs)
Death
Cardiogenic shock
Heart failure
Ventricular arrythmias
Heart block
Pericarditis
Myocardial rupture
Thromboembolism
Late Complications
Ventricular wall rupture
Valvular regurgitation
Ventricular aneurysms
Tamponade
Dressler’s syndrome
Thromboembolism
MNEMONIC for Complications of MI
Death
Arrhythmias
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler’s syndrome
Embolism
Prognosis
TIMI score (0-7) can be used for risk stratification
NOTE: TIMI = thrombolysis in myocardial infarction
High scores are associated with high risk of cardiac events within 30 days of MI
Killip Classification of acute MI can also be used:
Class I: no evidence of heart failure
Class II: mild to moderate heart failure
Class III: over pulmonary oedema
Class IV: cardiogenic shock
