Stable Angina and Acute Coronary Syndromes Flashcards
Learning outcomes
- Briefly review risk factors for, & consequences of, ischaemic heart disease
- Review control of coronary blood flow & the mechanisms of ischaemia
- Describe the symptoms & diagnosis of stable ischaemic heart disease / chronic coronary syndromes (brief comment on investigation)
- Recognise the aims of antianginal drug therapy & revascularisation
- Link the pathophysiology of abnormal myocardial perfusion with potential therapeutic strategies, & briefly introduce pharmacological strategies for relief of acute attacks of stable angina & long-term prevention
- Recognise the importance of lifestyle changes & drugs including anti-hypertensive agents, low-dose aspirin and statins in stable angina patients
- Review the pathophysiology of coronary artery occlusion & consequent myocardial ischaemia and infarction
- Recognise the symptoms of an acute coronary syndrome & distinguish between unstable angina, NSTEMI and STEMI
- Explain the interpretation of ECG recordings & cardiac troponin values in clinical investigation of acute coronary syndromes
Myocardial blood supply
- Pump function requires energy and oxygen
- These are delivered by the coronary arteries- first arteries arising off aorta coming off LV- R and L coronary artery- left divides into Left anterior descending (LAD) and Left Circumflex (LCX)
- Oxygen extraction is high at rest
- Coronary arteries are essentially end arteries
•The heart is therefore relatively susceptible to ischaemia- end arteries, do not anastamose well
Ischaemic heart disease- what is it, risk factors
•Nearly always due to coronary atheroma
•Obstructive disease of epicardial arteries
•Multiple risk factors: some most common are
Modifiable- HT, diabetes mellitus, hyperlipidaemia, cigarette smoking
Non- modifiable- age, gender, genetic (older you get, south asians/ afro-caribbean)
•Results in angina, MI and their consequences
Atheromatous coronary artery disease
-Endothelial injury
•‘Fatty steak’ formation
•Role of LDL cholesterol : foam cells (oxidised LDL)
•Macrophage accumulation and inflammation
•Smooth muscle migration
•Progressive narrowing of lumen with reduction in blood delivery
•Microcirculatory compensation to try normalise blood flow to myocardium after obstruction in larger arteries
Myocardial blood flow and ischaemia- factors that influence supply and demand
Supply- Oxygen carrying capacity •Driving pressure •Coronary tone -vasodilatory factors -vasoconstricting factors -metabolic factors
Demand- •Cardiac work heart rate blood pressure •Cardiac mass •Inotropic status: strength of cardiac contraction, high inotropic status leads to higher oxygen demand
Testing for angina/ IHD
Treadmill test- oxygen demand increases and ECG monitored for ischaemia, to see if angina occurs upon exertion
Myocardial perfusion scan using radioactive tracer- maps coronary blood flow : these are both functional tests
Anatomy test- look at arteries themselves on CT cardioangiogram
Angina pectoris: characteristics
-Pain related to myocardial ischaemia
- Chronic coronary syndrome
-•Character- dull, crushing, tight chest pain
•Location- usually central or left side of chest
•Precipitant- exercise, stress- increased myocardial oxygen demand eg tachycardia
•Relief- remove precipitant, resting, GTN spray (vasodilation)
•Association- nausea, sweating but not overly prominent in angina: moreso in MI
Radiation- often into neck, sometimes epigastric, commonly down left arm (referal)
Clinical assessment and therapeutic goals
Chest pain history (and associated symptoms)
•Prior cardiac history
•Presence of risk factors
•Other conditions- acid reflux, some muscular problems
•Medication
•Full cardiovascular examination including HR, BP, JVP, praecordium, lungs, pulses
•12 lead ECG
• Disease modification - atheroma • Treat risk factors -lifestyle • Reduce myocardial ischaemia -improve oxygen delivery -reduce oxygen demand
• Thereby improve symptoms, outcomes
Disease modifying drugs/ secondary outcomes
- Anti platelet agents to prevent thrombosis
- Usually aspirin 75mg daily
- Alternatives including clopidogrel
- Dual antiplatelet treatment after ACS
- Cholesterol reduction (esp. LDL)
- Generally HMGCoA Reductase-inhibitors ‘statins’ (e.g atorvastatin) (HMGCoAR: rate limiting step of cholestrol synthesis in liver, inhibitors inhibit chol. synth)
- Alternatives including ezetimibe (high cholestrol), fibrates, PSCK9-inhibitors (LDL proteins)
Balancing blood flow- how to improve supply and reduce demand
Improving supply
Nitrates
Calcium antagonists
Nicorandil
Reducing demand
- Beta blockers
- Diltiazem/verapamilI
- vabradine
Medical therapy NICE guidelines: first and second line for stable angina
1st line:-Offer either a beta blocker or a calcium channel blocker as first-line treatment for stable angina, based on comorbidities, contraindications and the person’s preference.
- If the person cannot tolerate the beta blocker or calcium channel blocker, consider switching to the other option (calcium channel blocker or beta blocker). -If the person’s symptoms are not satisfactorily controlled on a beta blocker or a calcium channel blocker, consider either switching to the other option or using a combination of the two.
( Offer GTN for acute symptomatic relief)
2nd: For people on beta blocker or calcium channel blocker monotherapy whose symptoms are not controlled and the other option (calcium channel blocker or beta blocker) is contraindicated or not tolerated, consider one of the following as an additional drug: a long-acting nitrate (Vasodilation) or ivabradine (reduce HR) or nicorandil or ranolazine.
Revascularisation
Consider revascularisation (coronary artery bypass graft [CABG] or percutaneous coronary intervention [PCI]) for people with stable angina whose symptoms are not satisfactorily controlled with optimal medical treatment.
Offer coronary angiography to guide treatment strategy for people with stable angina whose symptoms are not satisfactorily controlled with optimal medical treatment. Additional non-invasive or invasive functional testing may be required to evaluate angiographic findings and guide treatment decisions: either CA stenting (PCI) : fine wire and balloon inflated to crack plaque, widen artery and stent tube holds open artery
or CABG: bypass sown into aorta and after narrowing (angina refractory to medical treatment)
Myocardial infarction
Ischaemia
•Reversible/transient reduction in blood supply
•Acidosis, tissue hypoxia
•Results in CCS
Infarction
•Complete cessation of blood flow
•Tissue necrosis with loss of myocytes
•Results in ACS
Acute coronary syndrome
Episode of acute myocardial ischaemia in one of the following patterns
Unstable angina:
•Accelerating symptoms
•Sometimes rest pain
•Variable ECG changes
•No cardiac injury/damage
•No rise in cTn ( cardiac troponin: biomarker of cardiac injury)
Myocardial infarction •Often rest symptoms •Usually ECG changes •Cardiac injury/damage •cTn elevated
Clinical diagnosis of MI
- denotes presence of acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischaemia
- Myocardial injury demonstrated by rise and fall in cTn
- Evidence of acute myocardial ischaemia, usually from symptoms and ECG
- Additionally, ECG sub classifies
