Ischaemic heart disease Flashcards
So, heart disease is bad yeah?
Yeah, leading cause of death bro
What are some causes of atherosclerotic coronary diseases?
Chronic coronary insufficiency
Angina
Unstable coronary disease
Myocardial infarction
Sudden ischaemic coronary death
Heart Failure
Arrhythmia
Acute ischaemic
Scar related
Describe the layers used when discussing the anatomy of the coronary artery
- Epicardial–outer surface of heart
- Endocardial–inner surface of heart
- Subendocardialregion is water-shed area of perfusion and first to become ischaemic
Name the epicardial coronary arteries
Circumflex coronary
Left anterior descending
Posterior descending artery
Right ventricular branch
What can be used to image coronary arteries
Coronary angiography
CT
MRI
Discuss what factors increase risk for atherosclerotic coronary artery disease
Age Hypertension Hypercholesterolaemia Smoking Diabetes Obesity Physical inactivity
Discuss the pathology found in atherosclerotic coronary artery disease
Fatty streak
Fibro-fatty palque
Plaque disruption Plaque rupture Plaque erosion
What will occur in the coronary arteries in response to total occlusion of the left anterior descending artery?
The supply will be filled by collaterals from the RCA
Discuss the symptoms, cause and ECG indications of angina
• SYMPTOMS – 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
– Sub-Endocardial ischaemia
• ECG
– ST depression
What mechanisms are at play in angina in relation to basic physiology?
MISMATCH OF BLOOD SUPPLY TO DEMAND BECAUSE OF EPICARDIAL STENOSIS
Discuss the cause of angina pectoris
Mismatch of supply and demand
Supply = Coronary Blood Flow
Demand = Myocardial Oxygen Consumption
(MVO2 )
What are the two regulatory systems of the normal control of the coronary circulation?
– Autoregulation (myogenic control) – Metabolic regulation
Discuss exercise and myocardial blood flow
CBF can rise up to five fold (400 ml/min/100g) to accommodate a 20 fold increase in total body O2 consumption.
Little change in a near maximal O2 extraction.
A rise in heart rate where per beat CBF is constant can account for 1/3 of the increase seen.
What are the 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
Discuss investigation of chest pain to identify CAD as the cause
• Anatomical assessment
– CT coronary angiography
– Invasive angiography
• Test of Inducible ischaemia
– Exercise stress test
– Dobutamine stress echo
– Myocardial perfusion imaging with either exercise or phamacological stress
– Cardiac magnetic resonance imaging (cMR)
• Anatomic and functional
– Invasive angiography and fractional flow reserve (FFR)
– cMR
– Novel CT
Discuss angina treatment
• Reduce Myocardial Oxygen consumption. – Drugs
• Improve coronary flow reserve.
– Percutaneous Coronary Intervention (stents and balloons)
– Coronary Artery Bypass Grafting (CABG) – Drugs - Vasodilators
CABG bitches
Coronary artery bypass graft is bae, great saphenous vein grafted to RCA and left internal mammary artery grafted to LAD
What are the principles of drug treatment and angina
- Reduction in myocardial oxygen consumption
2. Reduction in the variability of coronary flow reserve
Discuss the action of drugs in angina
• 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
What are the stats on myocardial infarction (heart attack)
• 15-20 % do not make it to hospital • In hospital Mortality ~ 6 -15%
What is the clinical presentation of a myocardial infarction
- Chest Pain – severe – crushing radiating to jaw and arm
- Associated “Autonomic symptoms (nausea, sweating, terror)
- Breathlessness
What are the causes of a myocardial infarction
- Plaque rupture – 70 – 75%
- Plaque erosion – 25 – 30%
- Coronary embolism
- Coronary artery spasm / drugs
- Coronary anomaly
- Spontaneous coronary dissection
What events modify the presentation of AMI?
Time of day
Inflammatory activity
Infection esp. Respiratory
Elevation of blood pressure
Catacholamines
How do we classify myocardial infarctions
• By site of infarction - pathology
– Full thickness, transmural
– Sub endocardial
• By ECG - Clinical
– ST Elevation myocardial infarction (STEMI)
– Non-ST elevation myocardial infarction (non- STEMI)
• By cause
– Type 1-4
Discuss the relation between anatomy and ECG in AMI
- STEMI implies transmural myocardial infraction
* NSTEMI will include subendocardial infraction but does not exclude transmural infraction in regions remote from ECG
What are the type categories of myocardial infarction
Type 1 - spontaneous MI related to schema due to primary coronary event like plaque erosion +/or rupture, fissuring or dissection
Type 2 - MI secondary to ischaemia due to either increased O2 demand or decreased supply
Type 3 - Sudden unexpected cardiac death often with symptoms suggestive of myocardial ischaemia
Type 4 - MI associated with percutaneous coronary intervention (4a) or stent thrombosis (4b)
Type 5 - Myocardial infarction associated w cardiac surgery
How does one diagnose myocardial infarction
• A Clinical History with:
– ECG Changes, defining sub-classification of:
• STEMI
• NSTEMI
- And raised cardiomyocyte markers in blood
- Troponin T or I
- Creatine kinase MB isoform (CKMB)
- Creatine Phosphokinase (CPK)
- AST
- Myoglobin
Discuss STEMI management
Antiplatelet agents
Aspirin + Clopidogrel or other antiplatelet (P2Y12 inbibitor)
Immediate revascularisation
Primary PCI (percutaneous coronary intervention)
(Thrombolysis – clot busting)
What is 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)
What are the complications of a STEMI
• Immediate
Complications of STEMI
– Ventricular Arrhythmia and death
– Acute Left Heart Failure
• Early (Day 2-7) – Myocardial Rupture – Mitral valve insufficiency – Ventricular Septal defect – Mural thrombus and emobolisation
• Late (beyond day 7)
– LV dilatation and heart failure
– Arrhythmia
– Recurrent myocardial infarction
Discuss the causes of NSTEMI
• 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
Discuss treatment of non-STEMI
- Antiplatelet 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)
