Management of angina and acute coronary syndromes Flashcards
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
- management of acute attacks, sublingual nitrates
- long term anti-anginal prophylaxis (to prevent acute attacks)- calcium channel blockers, beta blockers, long acting nitrate formulations
- 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
Dyspnoea
Nausea/ vomiting
Sweating
Palpitations
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
