Ischaemic Heart Disease and its Consequences Flashcards
Epicardial
outer surface of heart
Endocardial
inner surface of heart
Subendocardial region
water-shed area of perfusion and first to become ischaemic
Coronary Artery Imaging in humans in life
- Coronary Angiography • CT
* MR imaging
Causes:
Chronic coronary insufficiency:
Angina
Unstable coronary disease:
Myocardial infarction
Sudden ischaemic coronary death
Heart Failure
Arrhythmia:
acute Ischaemia
Scar related
Atherosclerotic Coronary Artery Disease risk factors
Age Hypertension Hypercholesterolaemia Smoking Diabetes Obesity Physical inactivity
Atherosclerotic Coronary Artery Disease
Pathology- the three components
- fatty streak
- fibro-fatty plaque
- plaque disruption (plaque rupture or erosion)
symptoms of angina
– Gripping central chest pain
– Radiation to arm and jaw
– Clear and precise relationship to exercise
– Goes off in 2-10 mins after discontinuation of exercise – Worse after food. Worse in cold
– No autonomic features
– Flat of hand/fist to describe pain
cause of angina
– Sub-Endocardial ischaemia
how does angina present on an ECG
ST depression
angina mechanism
MISMATCH OF BLOOD SUPPLY TO DEMAND BECAUSE OF EPICARDIAL STENOSIS:
Supply = Coronary Blood Flow
Demand = Myocardial Oxygen Consumption
(MVO2 )
• Two regulatory systems with two control mechanisms
– Autoregulation (myogenic control)
– Metabolic regulation
determinants of myocardial oxygen consumption
- variable per unit mass of tissue: tension development – LV pressure and LV volume Contractility Heart rate - fixed per unit mass of tissue: basal activity (10-20%) - Mass of tissue
Identification of Coronary Disease as the cause: anatomical assessment
– CT coronary angiography
– Invasive angiography
Identification of Coronary Disease as the cause: Test of Inducible ischaemia
– Exercise stress test
– Dobutamine stress echo
– Myocardial perfusion imaging with either exercise or phamacological stress
– Cardiac magnetic resonance imaging (cMR)
Identification of Coronary Disease as the cause: anatomic and functional
– Invasive angiography and fractional flow reserve (FFR)
– cMR
– Novel CT
Angina Treatment - Reduce Myocardial Oxygen consumption.
drugs
Angina Treatment - improve coronary flow reserve
– Percutaneous Coronary Intervention (stents and balloons)
– Coronary Artery Bypass Grafting (CABG) – Drugs - Vasodilators
Drug treatment and Angina
- Reduction in myocardial oxygen consumption
2. Reduction in the variability of coronary flow reserve
Beta Adrenoceptor Blockers
– Reduce Heart Rate, Reduce Blood Pressure
– i.e. Reduce work of heart
• Nitrates(GTN)
– Venodilation → Reduced LV size → Wall tension. (reduces work) Small effect on epicardial stenosis dilation (improved supply)
• Calcium Channel blockers
– Reduce HR, some reduce Heart rate, small effect on from epicardial dilatation (mixed)
• Ikf Channel Inhibitors
– Selective heart rate reduction by inhibiting channels in SA node - Ivabridine
MYOCARDIAL INFARCTION – Clinical Presentation
- chest pain, severe, crushing radiating to jaw and arm
- associated ‘autonomic’ symptoms (nausea, sweating, terror)
- breathlessness
events modifying presentation of AMI
- time of day
- inflammatory activity
- infection esp. respiratory
- elevation of BP
- catecholamines
Classifications of Myocardial Infarction - by site of infarction, pathology
– Full thickness, transmural
– Sub endocardial
Classifications of Myocardial Infarction - By ECG - Clinical
– ST Elevation myocardial infarction (STEMI)
– Non-ST elevation myocardial infarction (non- STEMI)
Classifications of Myocardial Infarction - By cause
– Type 1-4
Relation between anatomy and ECG
- STEMI implies transmural myocardial infraction
* NSTEMI will include subendocardial infraction but does not exclude transmural infraction in regions remote from ECG
• A Clinical History with:
– ECGChanges,definingsub-classificationof:
- STEMI
* NSTEMI
ECG Changes, defining sub-classification of: And raised cardiomyocyte markers in blood
- Troponin T or I
- Creatine kinase MB isoform (CKMB)
- Creatine Phosphokinase (CPK)
- AST
- Myoglobin
STEMI Management
Antiplatelet agents:
Aspirin + Clopidogrel or other antiplatelet (P2Y12 inbibitor)
Immediate revascularisation:
Primary PCI
(Thrombolysis – clot busting)
Adjunctive Therapy for STEMI: • After anti-platelets agents and revascularisation
– Statin drugs (reduce cholesterol – plaque passivation)
– ACE inhibitors (usually a couple of days later to inhibit dilation of the left ventricle)
– Beta blockers (reduce myocardial infarction)
Complications of STEMI - immediate
– Ventricular Arrhythmia and death
– Acute Left Heart Failure
Complications of STEMI - Early (Day 2-7)
– Myocardial Rupture
– Mitral valve insufficiency
– Ventricular Septal defect
– Mural thrombus and emobolisation
Complications of STEMI Late (beyond day 7)
– LV dilatation and heart failure
– Arrhythmia
– Recurrent myocardial infarction
NSTEMI
• Getting more frequent (STEMI less common)
• More common in elderly
• Implies sub-endocardial ischaemia
• Caused by:
– Threatened STEMI
– Small branch occlusion
– Occlusion of well collateralised vessel
– Lateral STEMI in territory not well seen by ECG
Treatment of non-STEMI
• Anti platelet therapy (Aspirin and clopidogrel)
• Anti-ischaemics(beta blockers and nitrates)
• Statin drugs
• ACE inhibitors
• Coronary angiography and revascularisation
– Early if symptoms continue
– Early if Troponin raised
– Risk score (eg GRACE)
