Ischaemic Heart Disease Flashcards
What are some of the causes of atherosclerotic coronary disease?
Chronic coronary insufficiency (results in angina), Unstable coronary disease (MI, sudden ischaemic coronary disease), Heart failure and Arrhythmias - Acute ischaemic or scar related.
What is the subendocardial region?
Water-shed area of perfusion and it is the first area to become ischaemic.
What are ways of imaging coronary arteries in life?
Coronary angiography, CT or MR imaging.
What are the risk factors for atherosclerotic coronary disease?
- Age
- Hypertension
- Hypercholesterolaemia
- Smoking
- Diabetes
- Obesity
- Physical inactivity
What are the three stages of atherosclerotic coronary artery disease?
- Fatty streak
- Fibro-fatty plaque
- Plaque disruption (rupture or erosion)
Describe the basic pathology of formation of fatty plaque
- Accumulation of lipids in intima due to impaired endothelial function
- Monocytes migrate and become macrophages which engulf oxidised LDL = foam cells.
- Smooth muscle cells migrate to surface of plaque and deposit collage and extracellular matrix. Now is mature
What are the symptoms of angina?
- Gripping central chest pain which can radiate to arm, jaw and bottom teeth.
- Clear relationship to exercise but stops after 2-10mins after discontinuation of exercise.
- Worse after food and when in cold
- NO autonomic features (nausea or sweating)
What is the cause of angina?
Sub-Endocardial ischaemia . Due to mismatch of blood supply to demand because of epicardial stenosis.
What appears on the ECG to show angina?
ST depression
Describe the basics of epicardial coronary stenosis
Atherosclerotic plaque limits the flow of coronary blood which means it cannot keep up with myocardial oxygen consumption. So the reserve of coronary flow is inadequate for MVO2
What are the two normal regulatory mechanisms for coronary circulation?
- Autoregulation
- Metabolic regulation
Describe the autoregulation mechanism for coronary blood flow?
it is the capacity of the heart to maintain steady myocardial perfusion across a range of perfusion pressures.
Describe the metabolic regulation for coronary blood flow
Hypothesised that adenosine causes vasodilation. Adenosine is product of breakdown of ATP so where more energy is being used (ATP being broken down) then the more vasodilation and blood supply to that area.
What is the coronary reserves?
The difference between autoregulation at rest and the changes by vasodilators
What are the determinants of myocardial oxygen consumption?
- Variables per unit mass - Tension development (LV pressure and volume), Contractility and HR.
- Fixed per unit mass of tissue - Basal activity.
- Mass of tissue
What occurs with a fixed coronary stenosis?
You can get variable angina. The change in coronary flow reserve determines the variability of angina therefore meaning sometimes patients will get angina with exercise but sometimes won’t.
Describe the investigations of chest pain
Do anatomical assessment - CT coronary angiography or invasive angiography.
Test inducible ischaemia - Exercise stress test, dobutamine stress echo, myocardial perfusion imaging with exercise/pharmacological stress and cMR.
Automic and functional - Invasive angiography and fractional flow reserve, cMR and Novel CT
What is the treatment of angina?
Reduce myocardial oxygen consumption via drugs. Improve coronary flow reserve via percutaneous coronary intervention, CABG or vasodilator drugs.
What vessels are most commonly used in CABG?
Saphenous vein or the left internal mammary artery (very successful)
What drugs are used in the treatment of angina?
- Beta adrenoceptor blockers (decrease HR and BP)
- Nitrates (vasodilators)
- Calcium channel blockers (reduce HR)
- Ikf channel inhibitors (Ivabradine - selective HR reduction by inhibiting channels in SA node)
Describe the clinical presentation of myocardial infarction
Chest pain - Severe crushing pain radiating to jaw and arm.
Associated with autonomic symptoms, so common to have nausea, sweating and terror. Also breathlessness.
What are the causes of myocardial infarction?
Most commonly is plaque rupture, then plaque erosion. Less common causes are coronary embolism, coronary artery spasm/drugs, coronary anomaly, spontaneous coronary dissection.
Describe the pathology of plaque rupture
There is an occlusive thrombus forming on an atherosclerotic plaque, along with platelet aggregation
Describe features of unstable plaques
Unstable plaque has thinner walls which can easily rupture and trigger thrombosis which can completely occlude the artery.
What events modify presentation of an acute myocardial infarction?
- Time of day,
- Inflammatory activity,
- Infection
- Elevation of BP
- Catecholamines.
Describe ways of classifying myocardial infarction
- Site of infarction (full thickness, transmural, subendocardial)
- By ECG ( ST elevation MI or Non-ST elevation MI)
- BY cause
Describe the relationship between anatomy and ECG presentation of MI
STEMI implies transmural MI (full thickness). NSTEMI included subendocardial infarction but doesn’t exclude transmural infarction from remote ECG regions.
How to diagnose myocardial infarctions
Clinical history with ECG changes (STEMI or NSTEMI) and raised cardiomyocyte markers in blood. such as Troponin T or I.
Describe management of a STEMI
Antiplatelet agents (Aspirin and clopidogrel or P2Y12 inhibitors) and immediate revascularisation
Describe the adjunctive therapy for STEMI
So after the anti-platelet agents and revascularisation you can give statins, ACE inhibitors or Beta blockers
WHAT ARE THE COMPLEICATIONS OF STEMI? (IMPORTANT TO KNOW)
Immediate - Ventricular arrhythmias and death or acute left heart failure.
Early (2-7days) - Myocardial rupture, mitral valve insufficiency, ventricular septal defect or mural thrombus and emboli.
Late (beyond day 7) - LV dilation and heart failure, arrhythmia, recurrent MI
What are NSTEMI caused by?
Threatened STEMI, small branch occlusion, occlusion of well collateralised vessels or lateral STEMI in territory not well seen by ECG
Decribe the treatment of NSTEMI
Similar to STEMI with use of Antiplatelet therapy, anti-ischaemics, statins, ACE inhibitors and coronary angiography and revascularisation but this can be delayed unless symptoms continue or troponin is raised.
