U12W3 MI/Angina Flashcards
What is triclegalor?
Class - anti-platelet, is a P2Y12 receptor antagonist that prevents ADP-mediated P2Y12 dependent platelet activation and aggregation.
Chem - derived from ATP
Pharmacology - is a competitive antagonist of ADP, may also bind allosterically to P2Y12
Clinical use - TIA and MI patients with a low risk of bleeding, prevention of atherotrhombotic events in ACS (combined with aspirin) or in history of MI.
What is QRISK3?
Calculates the risk of developing a stroke or a heart attack over the next ten years
Not used for patients who are already diagnosed with CHD, TIA or stroke.
Answer is the average risk of people presenting with the same risk factors as you
Patient must be aged between 25-84
What information about a patient does the QRISK3 score collect?
General =Age: 25 to 84 years, Sex, Ethnicity, post code
Clinical information =
Smoking status, diabetes status, angia/MI in first degree relative under 60, CKD stage 3+, Atrial fibrillation, on blood pressure treatment, migraine, RA, SLE, severe mental illness, atypical antipsychotic medication, on regular steroid tablets, diagnosis or treatment for erectile dysfunction
Data value: Cholesterol/HDL ratio, Systolic BP, SD of last two SBP reading, Height and weight to calculate BMI.
How is QRISK 3 used by the NHS?
To calculate a persons heart age and their risk of cardiovascular disease.
NICE recommends that use to assess CVD risk for primary prevention
Often used for patients between 25-84yrs old with an estimated increased risk of CVD and require a full formal risk assessment.
What is the most important lifestyle factor to encourage patients to change in order to reduce their risk of CVD?
Stop smoking.
Draw a diagram of the different coronary arteries and what region s of the heart they supply?
Describe the normal physiological process of blood flow into the coronary arteries.
How is this process relevant to the pathophysiology of angina?
Coronary blood flow only occurs during diastole
This means during increased cardiac work the perfusion to the myocardium decreases
Increased cardiac work can occur because of increased sympathetic tone - increasing heart rate, so smaller proportion of time is spent in diastole
- increasing contractility leading to vessel closure and force of muscle occludes coronary arteries
This loss of blood flow leads to decreased cardiac efficiency
This enable beta blockers to be used in angina (reduce HR and contractility) and explains why stable angina is mainly symptomatic during exercise or high stress (increase SANS tone).
What are the basic feature of atherosclerosis?
Atheroma formation
Can occlude vascular lumen or rupture to cause sudden thrombus formation and occlusion
Atheromatous plaques have soft friable lipid cores covered by fibrous caps.
Involve large and medium sized arteries.
What are the non-modifiable risk factors for atherosclerosis?
Genetic -
Family history - primary hyperlipidaemia
Age - tends to increase conc lipoproteins and susceptibility of arterial wall to injury
Sex - social factors around modifiable risks, andorgen inc conc of lipoproteins.
What are some modifiable risk factors for atherosclerosis?
Hyperlipidaemia - diet high in cholesterol and saturated fats, no exercise, obesity.
HTN - increase vulnerability of endothelial cells to injury
Smoking - increase conc of lipoprotein
DM - cause dyslipidemia, and increase vulnerability of vessel walls to damage due to hyperglycemia and hypertension.
Emotional factors - inc conc of lipoproteins, worsned by spike in adrenaline
Describe the core process by which an atheroma forms.
Response to injury hypothesis - chronic inflammatory response of arterial wall to endothelial injury
1. Vascular endothelium is exposed to chronic injury (smoking, HTN)
2. Dysfunction of the endothelium increases permeability and promotes leukocyte adhesion
3. Accumulation of lipoproteins (mainly oxidized LDL and cholesterol crystals) in the vessel wall
4. Monocyte and smooth muscle migrate into the intima with macrophage activation
5. Macrophage and smooth muscle cell uptake modified lipids, can form foam cells or further activate cells
6. Macrophages and damaged endothelium release cytokines and growth factors such as TGF-beta and PDGF.
6. Intima smooth muscle cell proliferation and ECM matrix (mainly collagen) form a well-developed plaque with a necrotic lipid centre and a fibrous cap.
What are the different stages in atherosclerotic plaque development?
Fatty streaks - focal lipoprotein deposition in intima and formation of foam cells
Transitional plaque - increased extraceullar lipid in endothelium
Rasied fibrolipid plaque - increased collagen production, smooth muscle proliferation and fibrous cap formation. Pathological intima thickening occurs and develops.
Complicated plaque - plaque slowly grows and obstructs lumen, or plaque ruptures and a resulting thrombosis causes obstruction
What are the different clinical presentations of atheroma formation?
How is the pathology different?
Stable angina - slow growing plaque cause slowly narrowed lumen, pain predictable and stops with rest
Unstable angina - ruptured thrombuc cap forms a subtotal occlusive thrombus due to release of necrotic content
MI/STEMI - complete occlusion of the artery due to complete thrombosis formation after rupture of the fibrous cap.
Describe the link between atheroma and thrombosis.
Atherothrombosis is the term used to describe the formation of a thrombus associated with an atherosclerotic plaque.
This happens when plaques are eroded or ruptured.
This is due to the release of pro-thrombotic material contained within the plaque particularly is necrotic centre
This includes high levels of tissue factor and collagen.
How does the structure of a plaque influence its fate?
Thin cap and large necrotic core- plaque rupture and thrombosis - leads to sudden cardiac death as more likely to occlude whole diameter.
Thick cap with smaller necrotic centre and fewer inflam cells - erosion (superficial injury) and thrombosis - can lead to sudden cardiac death or critical stenosis as narrowing of the diameter is variable
Fibrotic plaques - may be via fibrocalcific plaque intermediate - leading to critical stenosis
What is some detail within atheroma formation?
Oxidised LDL in tunica intima - activate immune cells
Activate immune cells - produce ROS - convert immigrating LDL into oxidised LDL.
Foam cells - saturated with LDL, undergo cell death and release cell content.
Accumulating lipid and fragments of dead cells - soft lipid and necrotic core.
Calcium salts can accumulates in plaque - causing it to harden.
What is ischemic heart disease?
A reduced oxygen supply to the myocardium compared to metabolic oxygen demand.
Results in coagulative necrosis of myocardium.
Is the largest cause of death in many parts of the world (nn)
What are the common causes of ischemic heart disease?
Most common cause of reduced oxygen supply - coronary artery atheroma (fixed obstruction to coronary artery blood flow)
Other - thrombosis or spasm
Common causes of increased oxygen demand
Thyrotoxicosis or myocardial hypertrophy (complication of aortic stenosis or hypertension)
What ECG changes may indicate angina?
What causes pain in angina?
ST-T changes on the 12 lead ECG accompanied with cardiac ischaemic pain
Pain is caused by Ischaemic metabolites including adenosine stimulating nerve endings and producing pain.
What are the diagnostic criteria of classical angina?
1) Heavy, tight or gripping central or retrosternal pain which may radiate to the jaw and/or arms
2) Pain which occurs with emotional stress or exercise
3) Pain which eases rapidly with rest of GTN.
What are the different types of angina?
Atypical angina - 2/3 classical features
Non-angina chest pain - 1/3 classical features
Variant (Prinzmetal’s angina) - See card
Unstable - increased severity, at rest, recent in origin
Refractory - revasculatirsation is not possible and angina not controlled by medical therapy
Microvascular angina - positive exercise test and symptoms of angina but normal coronary arteries on angiogram,
What is variant or Prinzmetal angina?
Caused by coronary artery spasm.
Angina without provocation
Usually occurs at rest
ST segment elevation on ECG during pain
What is acute coronary syndrome?
Unstable angina that occurs with increases severity, at rest or is recent in origin (less than 24 hours)
What is microvascular angina?
Show symptoms of angina
Good prognosis but is difficult to treat
Have a positive exercise test
Normal coronary arteries on angiogram - hence though to be caused by functional abnormalities of the coronary microcirculation.
Intracoronary Ach may cause coronary spasm
Myocardial ischemia results from abnormal dilator responses of the coronary microvasculature to stress (most clear in women)
What is the most common aetiology of angina?
Coronary artery atheroma
Which results in fixed obstruction to coronary blood flow.
What investigations should be ordered when a patient presents with symptoms of angina?
FBC - Hb, hemoatocrit
THyroid function test - thyrotoxicosis inc oxygen demand in heart
Fasting glucose/HbA1c - diabetes risk factor
Fasting lipid - dyslipdaemia/hyperlipademia is a risk for atheroma
GFR - risk stratification, T2D, HTN, also drug titration.
Troponin - MI
12-ECG
Echocardiogram
CXR
Ambulatory ECG.
What are the ECG changes in acute anteroseptal myocardial infarction?
ST segment elevation and pathological Q waves in leads V1,2,3
ST segment depression in inferior leads may also be seen II, III, aVF.
What are the ECG changes seen in an acute inferior wall myocardial infarction?
Rasied ST segments and Q waves in inferior leads (II,III, aVF)
What ECG leads are affected in different types of STEMI?
Where are the different electrodes placed on a 12 lead ECG?
