++
There is a 2–3% incidence between 25 and 64 years.9
The history is the basis of diagnosis.
Angina is an oppressive discomfort rather than a pain, typically transient and lasting <10 mins.
It is mainly retrosternal: radiates to arms, jaw, throat, back.
It may be associated with shortness of breath, nausea, faintness and sweating.
It occurs during exercise, emotion, after meals or in cold.
It is relieved within a few minutes with rest.
Physical examination is usually not helpful, except during an attack.
Mitral valve prolapse, oesophageal spasm and dissecting aneurysm are important differential diagnoses.
The causes of angina are summarised in TABLE 40.7.
++
++
Note: Ensure that the patient is not anaemic or thyrotoxic. Fever and tachycardia also have to be excluded.
++
Stable angina. Pain occurs with exertion and is usually predictable with no symptom change during the past month.
Unstable angina (also referred to as crescendo angina, pre-infarct angina and acute coronary insufficiency). It is increasing angina (severity and duration) over a short period of time, precipitated by less effort and may come on at rest, especially at night. It may eventually lead to complete infarction, often with relief of symptoms. It is due to unstable plaque.
– Nocturnal angina. Pain occurs during the night. It is related to unstable angina.
– Decubitus angina. The pain occurs when lying flat and is relieved by sitting up.
– Variant angina or Prinzmetal angina or spasm angina.7 The pain occurs at rest and without apparent cause. It is associated with typical transient ECG changes of ST elevation (as compared with the classic changes of ST depression during effort angina). It can lead to infarction and cause arrhythmias. It is caused by coronary artery spasm.
++
This may be normal or show ischaemia or evidence of earlier infarction. During an attack it may be normal or show well-marked depression of the ST segment, symmetrical T-wave inversion (see FIG. 40.12) or tall upright T waves.
++
++
This is positive in about 75% of patients with severe coronary artery disease and should be performed if the diagnosis is in doubt, for prognostic reasons or to aid in the timing of additional investigations (e.g. coronary angiography). A normal stress test does not rule out coronary artery disease.
+++
Exercise thallium-201 scan
++
This test is helpful in some difficult circumstances such as in the presence of left branch bundle block (LBBB), old infarction and Wolff–Parkinson–White (WPW) syndrome (when exercise test is of little use) and with mitral valve prolapse, which gives high false positive tests. It helps determine the presence and extent of reversible myocardial ischaemia since thallium is only taken up by perfused tissue.
+++
Ambulatory ECG Holter monitoring
++
This may be useful in some patients.
+++
Gated blood pool nuclear scan
++
This test assesses the ejection fraction, which is a reliable index of ventricular function and thus aids assessment of patients for coronary artery bypass surgery.
++
This assesses global and regional wall motion abnormalities and assesses valvular dysfunction and pericardium status.
++
This test accurately outlines the extent and severity of coronary artery disease. It is usually used to determine the precise coronary artery anatomy prior to surgery.
++
The relationship between the degree of angina and coronary artery disease is not clear-cut. Some people with severe angina have normal coronary arteries.
++
Indications for coronary angiography are presented in TABLE 40.8.
++
++
‘Ultrafast CT’ may replace traditional angiography.
+++
Management of stable angina
++
This is especially important for those with a positive family history and an unsatisfactory lifestyle. Modification of risk factors:
++
+++
General advice for the stable angina patient
++
Reassure patient that angina has a reasonably good prognosis: 30% survive more than 10 years;10 spontaneous remission can occur.
Attend to any risk factors.
If inactive, take on an activity such as walking for 20 minutes a day.
Take regular exercise to the threshold of angina.
If tense and stressed, cultivate a more relaxed attitude to life—consider a stress management/relaxation course.
Avoid precipitating factors.
Don’t excessively restrict lifestyle.
+++
The acute attack and episodic angina
++
Nitrates:
glyceryl trinitrate 300–600 mcg tab sublingually, max 1800 mcg
or
glyceryl trinitrate SL 400 mcg metered dose spray: 1 spray; repeat after 5 minutes if pain persists (maximum three doses)
or
isosorbide dinitrate 5 mg sublingually; repeat every 5 minutes if pain persists (maximum 3 tablets)
or
nifedipine 5 mg capsule (suck or chew) if intolerant of nitrates
Aspirin 150 mg (o)
Tips about glyceryl trinitrate tablets:
if pain persists for longer than 10 minutes despite two doses of nitrates, take a third dose and call for an ambulance
warn patient about headache and other side effects
sit down to take the tablet
take ½ (initially) or 1 tablet every 5 minutes
take a maximum of 3 tablets in 15 minutes
tablets must be fresh
discard the bottle after being opened for 3 months or after 2 days if carried on the person
keep tablets out of light and heat
if pain relieved quickly, spit out residual tablet
advise patient to get medical advice if no relief after 3 tablets
++
Note: avoid nitrates if patient has taken sildenafil or vardenafil in the previous 24 hours or tadalafil in the previous 5 days.
+++
Moderate stable angina
++
Regular predictable attacks precipitated by moderate exertion. For prevention:
++
add to aspirin (if not contraindicated) beta blocker, e.g. atenolol 25–100 mg (o) once daily
or
metoprolol 25–100 mg (o) twice daily plus nitrates
glyceryl trinitrate (transdermal: ointment or patches) daily (use for 14 hours only)
or
isosorbide mononitrate 30 mg (o) SR tablet mane, increasing to 120 mg if required
Note: Aim for a daily nitrate-free interval.
++
Not prevented by beta blocker:
++
add
a dihydropyridine calcium-channel blocker (CCB) nifedipine CR 30–60 mg (o) once daily
or
amlodipine 2.5–10 mg (o) once daily plus nitrates
If beta blocker contraindicated (use a non-dihydropyridine calcium-channel blocker):
diltiazem 30–90 mg (o) tds or CR 180–360 mg (o) daily
or
verapamil (according to directions)
+++
Refractory stable angina
++
Consider adding nicorandil 5 mg (o) bd, increasing after a week to 10–20 mg bd or replacing the CCB with perhexiline
++
++
Includes onset of angina at rest, abrupt worsening of angina and angina following acute myocardial infarction.
++
Should be hospitalised for stabilisation and further evaluation. May need IV nitrate therapy.
The objectives are to optimise therapy and consider coronary angiography with a view to a corrective procedure.
++
For variant angina (spasm) use nitrates and calcium antagonist (avoid beta blockers).
As a rule, avoid the combination of verapamil and a beta blocker (risk of tachycardia and heart block).
Do not combine a dihydropyridine CCB with a non-dihydropyridine CCB.
Tolerance to nitrate use is a problem, so 24-hour coverage with long-acting preparations is not recommended.
Consider using the potassium channel opening vasodilator nicorandil 5 mg (o) bd to 10–20 mg (o) bd (after 1 week). Can use as alternative to long-acting nitrates. The new agent ivabradine can be considered.
Nitrates can be used prophylactically prior to any exertion that is likely to provoke angina (e.g. glyceryl trinitrate spray or tablet or isosorbide dinitrate 5 mg tablet)
Avoid nitrates if the patient has used a 5 phosphodiesterase inhibitor in the past 1–5 days.
+++
Non-medical treatment5
+++
Percutaneous intervention (PCI) and coronary angioplasty (the gold standard)
++
One current technique is dilating coronary atheromatous obstructions by inflating a balloon against the obstruction—percutaneous transluminal coronary angioplasty (PTCA) (see FIG. 40.13) and maintaining patency with intracoronary stent devices.
++
++
Two complications of the balloon inflation angioplasty are acute coronary occlusion (2–4%) and restenosis, which occurs in 30% in the first 6 months after angioplasty.10
+++
Intra-coronary stents
++
PTCA followed by stenting is now the most favoured procedure to maintain patency of the obstructed coronary vessel (see FIG. 40.14). Modern drug eluting stents, which include drugs such as primolimus, sirolimus or paclitaxel, can be used as well as the bare metal stent. Stent patients require long-term antiplatelet agents (e.g. aspirin plus clopidogrel) (specialist advice is required).
++
+++
Coronary artery surgery
++
The main surgical techniques in current use are coronary artery bypass grafting (CABG) using either a vein (usually the saphenous) (see FIG. 40.15) or internal mammary arterial implantation (see FIG. 40.16) or both and endarterectomy.
++
++
++
Symptomatic patients with significant left main coronary obstruction should undergo bypass surgery, and those with two or three vessel obstruction and good ventricular function are often considered for angioplasty or surgery. A significant improvement in the quantity and quality of life can be expected.
+++
Myocardial infarction
+++
Clinical guidelines11
++
Variable pain; may be mistaken for indigestion
Similar to angina but more oppressive
So severe, patient may fear imminent death— angor animi
About 20% have no pain. These have a high mortality rate
‘Silent infarcts’ in diabetics, hypertensives, females and elderly; one report (European Heart Journal, 14 February 2006, online) reported that 40% of infarcts were silent and undetected in older patients
60% of those who die do so before reaching hospital, within 2 hours of the onset of symptoms
Hospital mortality is 8–10%10
Like CVA, seems to peak at 6–10 am
++
Diagnosis is based on 2 out of 3 criteria: history of prolonged ischaemic pain, typical ECG appearance, and rise and fall of cardiac enzymes.
++
++
++
no abnormal signs
pale/grey, clammy, dyspnoeic
restless and apprehensive
variable BP with pain ↓ heart pump failure
variable pulse: watch for bradyarrhythmias
mild cardiac failure: third or fourth heart sound, basal crackles
++
ECG. The ECG is valuable with characteristic changes in a full thickness infarction. The typical features (see FIG. 40.17) are:
the Q wave: broad (>1 mm) and deep >25% length R wave
– occurs normally in leads AVR and V1; III (sometimes)
– abnormal if in other leads
– occurs also with WPW and ventricular tachycardia (VT)
– usually permanent feature after full thickness AMI
T wave and ST segment:
The typical progression is shown in FIGURE 40.18. Note:
Q waves do not develop in subendocardial infarction.
The strategies for management of AMI are based on the distinction between Q wave (transmural) or non-Q wave (subendocardial) infarction.
Q wave infarction has been proved to benefit from thrombolytic therapy, but non-Q wave infarction has not.
If new LBBB think AMI (in LBBB no Q wave).
A normal ECG, especially early, does not exclude AMI. Q waves may take days to develop.
Cardiac enzymes. The typical enzyme patterns are presented in FIGURE 40.19. As a rule, large infarcts tend to produce high serum enzyme levels. The elevated enzymes can help time the infarct:
troponin I or T:
– starts rising at 3–12 hours, peaks at 24 hours and persists for about 5–14 days
– now the preferred test
– positive in unstable angina
– raised in aortic dissection and kidney impairment
– may have to wait until 10 hours before recording a negative result
– not useful for repeat MI
– both proteins, I and T, provide same information
– reference interval <0.1 μg/L
creatinine kinase (CK):
– after delay of 6–8 hours from the onset of pain it peaks at 20–24 hours and usually returns to normal by 48 hours
– CK–MB: myocardial necrosis is present if >15% of total CK; unlike CK, it is not affected by intramuscular injections
Technetium pyrophosphate scanning
It is performed from 24 hours to 14 days after onset.
It scans for ‘hot spots’, especially when a posterolateral AMI is suspected and ECG is unhelpful because of pre-existing LBBB.
Echocardiography. This is used to assist diagnosis when other tests are not diagnostic.
++
++
++
++
Note: The clinical diagnosis may be the most reliable, as the ECG and enzymes may be negative.
+++
Management of acute coronary syndromes
+++
General principles11,12
++
Aim for immediate attendance if suspected.
Pre-hospital: make diagnosis, assess risk, ensure stability. A 12-lead ECG should be arranged ASAP.
Call a mobile coronary care unit.
Achieve coronary perfusion and minimise infarct size.
Prevent and treat cardiac arrest; have a defibrillator available to treat ventricular fibrillation.
Optimal treatment is in a modern coronary care unit (if possible) with continuous ECG monitoring (first 48 hours) and a peripheral IV line (consider intranasal oxygen only if hypoxaemic <94% saturation).
Pay careful attention to relief of pain and apprehension.
Establish a caring empathy with the patient.
Give aspirin as early as possible (if no contraindications): 300 mg chewed or dissolved sublingually.
Prescribe a beta blocker and an ACE inhibitor early (if no contraindications).
++
Note: For a STEMI it is important to re-establish flow as soon as possible, usually by either thrombolytic therapy or primary angioplasty (preferably with stenting). Rescue angioplasty is usually used when large infarcts have not perfused at 60–90 minutes.5
+++
Hospital management5,11
++
As for first-line management.
Confirm ECG diagnosis: STEMI or NSTEACS.
Take blood for cardiac enzymes, particularly troponin levels, urea and electrolytes.
Organise an urgent cardiology consultation for risk stratification and a decision whether to proceed to coronary angiography and coronary reperfusion with PCI (or CABG) or with thrombolysis.
+++
Management of STEMI12
++
The optimal first-line treatment for the patient with a STEMI is urgent referral to a coronary catheter laboratory ideally within 60 minutes (the golden hour) of the onset of pain for assessment after coronary angiography for percutaneous transluminal coronary angioplasty (PTCA). If available and performed by an interventional cardiologist it has the best outcomes (level I evidence).
++
The principle is to achieve rapid reperfusion via primary angioplasty with a stent (optimal stent status currently under evaluation).
++
Adjunct therapy will include dual antiplatelet therapy—aspirin and a P2Y12 inhibitor (clopidogrel, ticagrelor or prasugrel) and anticoagulation with low molecular weight heparin or unfractionated heparin, a statin and an ACE inhibitor.
+++
Urgent reperfusion guidelines
++
Within 60 minutes of symptom onset STEMI: PCI (optimal)
Within 90 minutes of onset STEMI: PCI (acceptable)
If these targets are not reached: fibrinolysis within 30 minutes of arrival
++
First-line management (e.g. outside hospital)
Perform an ECG and classify ACS into STEMI or NSTEACS, and notify the medical facility that will receive the patient (discuss over the telephone). The ECG is the sole test required to select patients for emergency perfusion
Oxygen 4–6 L/min only if hypoxaemic (aim to keep PaO2 >90%)
Secure an IV line (withdraw blood for tests especially troponin levels)
Glyceryl trinitrate (nitroglycerine) 300 mcg (½ tab) SL or spray 400 mcg (every 5 minutes as necessary to maximum of three doses). Beware of sildenafil (Viagra) and related drugs use and bradycardia—correct with atropine
Aspirin 300 mg
Morphine 2.5 mg IV statim bolus: then 1 mg/min every 5–10 mins until pain relief (up to 15 mg) (If feasible, it is preferable to give IV morphine 1 mg/min until relief of pain; this titration is easier in hospital.)
+++
Management of NSTEACS
++
NSTEACS can progress to a STEMI; therefore all patients with NSTEACS should have ongoing monitoring in hospital and their risk stratified to direct management decisions.
+++
Reperfusion therapy13,14
++
All patients with acute myocardial infarction should be considered for admission to a coronary care unit for monitoring and expert care. The decision of reperfusion therapy by PCI or fibrinolytic therapy will be determined by unit policy based on availability of PCI.
++
If angioplasty is unachievable either through timing or the unavailability of the service (such as in rural locations), thrombolysis is an indication for STEMI and the sooner the better, but preferably within 12 hours of the commencement of chest pain.5,12 The decision should be made by an experienced consultant, especially as PCI is not usually possible once fibrinolytic therapy has been given.
++
Second-generation fibrin-specific agents (reteplase, alteplase or tenecteplase) are the agents of choice. Streptokinase can be used but it is inappropriate for use in Indigenous people and those who have received it on a previous occasion. There are several other contraindications for the use of fibrinolytic agents.
++
Further management strategies include:
++
Full heparinisation for 24–36 hours (after rt-PA—not after streptokinase), especially for large anterior transmural infarction with risk of embolisation, supplemented by warfarin.
Use LMW heparin (e.g. enoxaparin 1 mg/kg SC bd or unfractionated heparin 5000–7500 units SC 12-hourly).
++
Further management of STEMI (? myocardial infarction)
++
Antiplatelet therapy: aspirin + clopidogrel
Beta blocker (if no thrombolytic therapy or contraindications) as soon as possible: atenolol 25–100 mg (o) daily
or
metoprolol 25–100 mg (o) twice daily
Consider glyceryl trinitrate IV infusion if pain recurs
Start early introduction of ACE inhibitors (within 24–48 hours) in those with significant left ventricular (LV) dysfunction (and other indications)
Statin therapy to lower cholesterol
Treat hypokalaemia
Consider magnesium sulphate (after thrombolysis)
Consider frusemide
+++
Post-AMI drug management
++
++
beta blockers—within 12 hours
ACE inhibitors—within 24 hours
aspirin 75–150 mg and clopidogrel 75 mg (o) daily or both (alternatives to clopidogrel: ticagrelor or prasugrel)
lipid-lowering drugs (e.g. statins)
warfarin
Targets:
BP <140/90; TC <4 mmol/L; LDLC <2 mmol/L; TG <2 mmol/L
++
Education and counselling
Bed rest 24–48 hours
Continuing ECG monitoring
Check serum potassium and magnesium
Early mobilisation to full activity over 7–12 days
Light diet
Sedation
Beta blocker (o): atenolol or metoprolol
Anticoagulation where indicated (certainly if evidence of thrombus with echocardiography)
ACE inhibitors for left ventricular failure and to prevent remodelling
monitor psychological issues (e.g. anxiety)
++
Rehabilitation program
Continued education and counselling
No smoking
Reduce weight
Encourage consumption of omega-3 fatty acids
Regular exercise, especially walking
Exercise test (to be considered)
Continue beta blockers for 2 years
Continue ACE inhibitors
Aspirin 100–300 mg daily and clopidogrel 75 mg daily
Anticoagulation where indicated (at least 3 months)
Statin therapy
+++
Special management issues
+++
Indications for coronary angiography
++
+++
Management of the extensive infarction
++
ACE inhibitors (even if no CCF)
Radionuclide studies (to assess left ventricular function)
Beta blockers (proven value in severe infarction) if no contraindications or LV dysfunction
Anticoagulation
+++
Treating and recognising complications of STEMI
+++
Acute left ventricular failure
++
Signs: basal crackles, extra (third or fourth) heart sounds, X-ray changes
Treatment (according to severity) (refer to CHAPTER 88):
– oxygen
– diuretic (e.g. frusemide)
– morphine IV
– glyceryl trinitrate: IV, SL, (o) or topical
– ACE inhibitors
+++
Cardiogenic shock (a major hospital management procedure)
++
Requires early specialist intervention which may include:
++
adrenaline—titrated to BP
treat hypotension with inotropes
intra-aortic balloon pump
urgent angiography ± angioplasty/surgery
++
This occurs in first few days after AMI (usually anterior AMI), with onset of sharp pain.
++
Signs: pericardial friction rub
Treatment:9 anti-inflammatory medication (e.g. aspirin, indomethacin or ibuprofen for pain) with caution
++
Note: Avoid anticoagulants.
+++
Post-AMI syndrome (Dressler syndrome)
++
This occurs weeks or months later, usually around 6 weeks.
++
Features: pericarditis, fever, pericardial effusion (an autoimmune response)
Treatment: as for pericarditis
+++
Left ventricular aneurysm
++
This is a late complication.
++
Clinical: cardiac failure
Features: arrhythmias, embolisation
Signs: double ventricular impulse, fourth heart sound, visible bulge on X-ray
Diagnosis: 2D electrocardiography
Treatment:
+++
Right ventricular infarction
++
This may accompany inferior MI and is life-threatening.
+++
Ventricular septal rupture and mitral valve papillary rupture
++
This presents with severe cardiac failure and a loud pansystolic murmur. Both have a poor prognosis and early surgical intervention may be appropriate.
++
All types are common with STEMI and require treatment according to guidelines in CHAPTER 70. Methods may include defibrillation, cardioversion and pacemaking. Past infarct prophylaxis with IV lignocaine is not indicated.5,15
+++
Anxiety and depression
++
Patients require anticipatory guidance and support including education, reassurance and counselling. If necessary, anxiolytic agents and antidepressants may help recovery.