Management of angina and acute coronary syndromes Flashcards Preview

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Myocardial ischaemia

Develops when blood supply to the myocardium is inadequate to meet the metabolic demands of the tissue
e.g. absolute reduction in blood flow at rest, supply ischaemia supply < demand
or relative reduction in face of increased muscle work, demand ischaemia demand > supply
In > 95% of cases, myocardial ischaemia is associated with a critical stenosis of one or more coronary arteries i.e. practically unknown in the absence of CAD


Myocardial oxygen supply-demand balance

Oxygen supply: coronary blood flow including collaterals, tissue oxygen extraction (75-95%)
Oxygen demand: pressure/ volume work, heart rate, wall tension/ wall stress, inotropy, ionic homeostasis etc.


Chronic stable angina

Underlying pathology
Critical stenosis (narrowing) of one or more epicardial coronary arteries due to atherosclerosis
Typical pattern of demand ischaemia in which anginal pain develops on exertion and is relieved by rest or nitrovasodilator e.g. GTN spray or buccal tablet


Goals of treatment in chronic stable angina

Chronic stable angina is a clinical syndrome which indicates established coronary artery disease
Principal goals of treatment are:
reduce and relieve symptoms, reduce frequency of attacks and improve exercise capacity, reduce risk of a major cardiovascular event


Lifestyle management

If not already done, risk factor management needs to be instigated urgently after diagnosis:
Smoking cessation
Blood pressure control
Weight loss supported by appropriate dietary changes


Pharmacological management

1. management of acute attacks, sublingual nitrates
2. long term anti-anginal prophylaxis (to prevent acute attacks)- calcium channel blockers, beta blockers, long acting nitrate formulations
3. risk factor modification- antiplatelet aspirin, statins, ACE inhibitors


Management of acute attacks

Buccal/ sublingual nitrates provide rapid and effective pain relief
Mechanism is principally rapid venodilatation and reduction in cardiac preload, leading to reduced cardiac work/ oxygen demand


Long term prophylaxis to prevent attacks

All patients should receive treatment with drugs which reduce cardiac oxygen demand in the longer term, minimising the frequency of acute attacks
First line drugs of choice are beta blockers and calcium channel blockers
Selection will depend on LV function (caution if LV systolic dysfunction/ CHF) and how well tolerated


Long term prophylaxis dosing

Step 1: either beta blocker of calcium channel blocker, if LV dysfunction start with low dose of beta blocker and do not use verapamil
Step 2: if inadequate response in step 1, beta blocker plus dihydropyridine calcium channel blocker
If no adequate response, or beta blocker or calcium channel blocker cannot be used or not tolerated, addition of long acting nitrate or ivabradine or nicorandil or ranolazine


Elective revascularisation

Patients with poorly controlled angina or worsening symptoms may be scheduled for elective revascularisation procedure
Either percutaneous coronary intervention (balloon angioplasty + stent) or coronary artery bypass graft surgery


Prevention of major cardiovascular events

Risk factor modification to prevent development of major cardiovascular events e.g. acute coronary syndrome
Statin treatment (whether plasma LDL cholesterol is high or normal)
Low dose aspirin (or clopidogre) to prevent thrombitoc events
ACE inhibitors e..g ramipril may decrease risk, especially if diabetes


Acute coronary syndromes

Underlying pathology
Rupture of unstable plaque in a major coronary artery leading to rapid coronary thrombosis
Thrombotic occlusion leads to severe supply ischaemia, unrelieved by rest or sublingual nitrate
Three forms of ACS dependent on severity or duration of treatment: STEMI, NSTEMI, unstable angina


Signs and symptoms of acute coronary syndrome

Crushing chest pain with or without referral to neck, face and arms
Nausea/ vomiting
Anxiety, panic or sense of impending death
Symptoms steadily worsen (crescendo angina), unrelieved by rest or nitrates
Always a medical emergency as may be at risk of sudden cardiac death


Diagnosis of acute coronary syndrome

Initially based on symptoms and risk factor profile
ECG changes
Serum markers (troponin)
STEMI: ST elevation, plasma Tn rise
NSTEMI: no ST elevation, plasma Tn rise
UA: no ST elevation, no plasma Tn rise


ECG changes

There may or may not be an early ST segment elevation (STEMI/NSTEMI)
Later development of Q wave is associated with established myocardial infarction


Serum markers

Provide biochemical diagnosis
Appearance in plasma of myocardial proteins are indicative of muscle damage


Diagnosis and risk stratification

Distinction between STEMI, NSTEMI and UA will b according to ECG changes and serum markers of myocardial damage
UA may precede or progress to MI within hours to months
STEMI is most likely to result in extensive necrosis
NSTEMI has less extensive necrosis
Both STEMI and NSTEMI may lead to chronic heart faliure


Goals of treatment in ACS

Reduce and relieve acute symptoms and distress
Prevent, or limit the extent of, myocardial necrosis
Reduce the risk of early death due to arrhythmia or acute heart failure
Reduce risk of recurrence
Limit the development o chronic ischaemic cardiomyopathy and heart failure


Primary management in acute phase

Immediate management, while awaiting exact diagnosis:
inhaled oxygen to relieve hypoxia
apsirin 300mg to reduce further thrombus formation
GTN IV to reduce cardiac preload and work/ oxygen demand
morphine IV to relieve pain and distress
anti-emetic e.g. cyclizine IV to relieve nausea/ vomiting


After exact diagnosis of STEMI, NSTEMI or UA:

For STEMI: reperfusion therpay, either fibrinolytic or emergency PCI or emergency CABG
For NSTEMI or UA: no evidence base or favourable risk/benefit ratio for fibrinolysis, but if high risk, PCI or CABG


Secondary management in acute phase

Parenteral anticoagulant e.g. heparin, LMW heparin, argartroban, bivalirudin) for 2-7 days to prevent further thrmobosis in hospital
Anti-arrhythmic therapy if necessary
Management of acute LV filure if necessary (as for decompensated heart failure)


Secondary dysfunction and management of LV dysfunction

Anti-platelet therapy e.g. low dose aspirin for life plus clopidogrel for 6-12 months
Statin, irrespective of plasma lipid profile
ACE inhibitor (dual action in preventing further major event and beneficial in LV dysfunction /CHF
Beta blocker
Aldosterone (MR) antagonist, eplerenone or spironolactone if LV dysfunction