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Ischaemic Heart Disease

Imbalance between oxygen supply to cardiac muscle and myocardial
Most common cause coronary artery atheroma (coronary artery
o Causes fixed obstruction to coronary blood flow.
Less common cause coronary artery thrombosis, spasm or, rarely,
arteritis (e.g. polyarteritis).
Thyrotoxicosis or myocardial hypertrophy (e.g. aortic stenosis or
hypertension) Increase oxygen demand due to increased cardiac
Coronary artery disease (CAD)
Single largest cause of death.
Atheroma atherosclerotic plaques (accumulation of lipid,
macrophages and smooth muscle cells in intima).
Risk factors contributes to development of atheroma through
o Vascular endothelial dysfunction
o Biochemical abnormalities
o Immunological factors
o Inflammation
Risk factors:
Gender (men > premenopausal women. Similar incidence after
menopause; probably due to loss of oestrogen protective effect.)
Family history positive family history first-degree relative has
developed ischaemic heart disease before 50 years old.
Hyperlipidaemia risk of CAD directly related to serum cholesterol
level; inversely proportional to HDLs. Lowering serum cholesterol slows
coronary atherosclerosis progression and causes regression of disease.
Cigarette smoking risk declines to almost normal after 10 years of
Metabolic factors

o DM, lack of exercise, obesity

Diets high in fats (especially saturated fat) and low antioxidant intake
(fruit and vegetables)
Other risk factors
o Lack of exercise, psychosocial factors (e.g. depression, etc),
elevated serum C- reactive protein, high alcohol intake and
coagulation factors (high levels of fibrinogen, factor VII and
Angina Pectoris
Chest pain arising from the heart due to myocardial ischaemia.
Description central, crushing, retrosternal chest pain. Comes on with
exertion and relieved by rest.
Exacerbated by cold weather, anger and excitement.
Frequently radiates to the arms and neck.
Associated symptoms dyspnoea, nausea, sweatiness, faintness.
Decubitus angina occurs on lying down.
Nocturnal angina at night and may waken the patient from sleep.
Variant (Prinzmetals) angina caused by coronary artery spasm; occur
without provocation/ at rest.
Unstable angina rapid increase in severity, occurs at rest, or is of
recent onset (less than 1 month).
Cardiac syndrome X angina symptoms + positive exercise test +
normal coronary arteries on angiogram.
o Due to functional abnormalities of coronary microcirculation.
o Resting ST depression, T-wave flattening or inversion during
attack. Normal between attacks.
o Exercise positive in most people with CAD; normal test doesnt
exclude diagnosis. ST depression (>1mm) at low workload
(within 6 mins) or paradoxical fall in blood pressure with
exercise severe CAD; indication for coronary angiography.
If cant exercise/ have baseline ECG abnormalities (i.e. interfere with

Other testing protocols (pharmacological stress testing with myocardian

perfusion imaging or stress echocardiography).
Coronary angiography
o When diagnosis of angina is uncertain.
o Commonly delineate exact coronary anatomy before coronary
o CT coronary angiography and cardiovascular MR coronary
Identify and treat risk factors for CAD; offer secondary prevention.
Symptomatic treatment of angina.
Secondary prevention:
Patients with angina high risk of subsequent cardiovascular events
(MI, stroke and sudden death).
Modify risk factors
+ Aspirin and statin
o Aspirin (75mg daily). If not tolerated/contraindicated clopidogrel.
o Statin given to patients to achieve cholesterol level of < 5 mmol/L.
Used unless triglycerides are above 3.5 mmol/L; fibrate is
Symptomatic treatment:
Acute attacks sublingual GTN tablet or spray.
o Encouraged to use before exertion.
o Main S/Es severe headache. Relieved by inactivating tablet
swallowing or spitting it out.
Prophylactic therapies:
B blockers (e.g. atenolol)
o Decrease Ionotropic and chronotropic effects; reduce myocardial
oxygen demand.
Calcium antagonists (e.g. diltiazem)
o Block calcium influx into cell and utilisation of calcium within the
o Relax coronary arteries and reduce force of left ventricular
contraction; reducing oxygen demand.
o S/Es systemic vasodilation (postural dizziness, headache, ankle
o High dose nifedipine increases mortality! Should be avoided.

o Reduce venous and intracardiac diastolic pressure, reduce

impedance to the emptying of the left ventricle, and dilate
coronary arteries.
o Major S/Es headache; tends to diminish with continued use.
Other treatments
For those with contraindications or inadequate response to other treatments.
o Nicorandil
Combines nitrate-like activity with potassium channel
Arterial and venous dilating properties.
o Ranolazine
Interacts with Na channels and can improve exercise
tolerance; causes QT prolongation.
o Ivabradine
Inhibits cardiac pacemaker If current and lowers heart rate.
Used in those with contraindications or intolerance of B
If still persists or worsen, consider:
Percutaneous Coronary Intervention (PCI)
Small inflatable balloons dilate localised atheromatous lesions.
Stent placement reduces risk of acute vessel closure and restenosis
Applied for angina resulting from isolated, proximal, non-calcified
atheromatous plaques.
Complications death, acute MI, need for urgent CABG and
Dual antiplatelet therapy with aspirin and clopidogrel is routinely given.
Drug-eluting stents release antiproliferative agents (sirolimus,
paclitaxel) reduce restenosis rates; risk of late stent thrombosis.
Coronary Artery Bypass Grafting (CABG)
Left/ right Internal mammary artery is used to bypass stenosis in left
anterior decending or right coronary artery respectively.
Less common saphenous vein is anastomosed between the proximal
aorta and coronary artery distal to obstruction.
Successfully relieves angina in about 90% of cases.
Operative mortality rate - <1%.
Most patients angina recurs because of accelerated atherosclerosis in
the graft (particularly vein grafts); can be treated by stenting.

Acute Coronary Syndromes (ACS)

Spectrum of unstable CAD.
Common mechanism of all ACS:
Rupture or erosion of the fibrous cap of a coronary artery
atheromatous plaque with subsequent formation of a platelet-rich clot
and vasoconstriction produced by platelet release of serotonin and
thromboxane A2.
ACS includes unstable angina, NSTEMI, STEMI.
Unstable Angina
Occluding thrombus not sufficient to
cause damage and elevation of
serum markers.

Occluding thrombus can cause
myocardial damage and an elevation
in myocardial injury serum markers
(troponin and creatinine kinase).
ECG may be normal or show evidence of ischaemia with T wave inversion
and/or ST segment depression.
May be complicated by MI with ST segment elevation; if treatment is
Complete occlusion of coronary artery by thrombus with usually more
severe symptoms.
Typical ECG changes of MI, and elevated troponin and creatine kinase.
Patients with known angina and worsening pain on minimal
exertion, chest pain at rest, or chest pain unrelieved in the usual
time by nitrates or rest.
In some chest pain absent ; present with collapse, arrhythmia or new
onset of heart failure.
Patients without previous angina may also present for the first time with
Acute central chest pain; >20 mins, often associated with nausea,
sweatiness, dyspnoea, palpitations.
If without chest pain (in elderly or diabetics) syncope, pulmonary
oedema, epigastric pain and vomiting, post-operative hypotension or
oliguria, acute confusional state, stroke, diabetic hyperglycaemic states.
Distress, anxiety, pallor, sweatiness, increased/ pulse,
! Other causes of chest pain must be considered e.g. aortic dissection,
musculoskeletal pain, GORD.

In those presenting with symptoms suggestive of ACS,
Serum troponin should be measured on arrival and at 12 hours after
onset of symptoms.
Normal serum troponin at 12 hours unstable angina, rather than MI.
Immediate management of ACS

Antiplatelet therapy
If no contraindications, aspirin (300 mg initially, then 75 mg daily) in all
Reduce risk of subsequent vascular events and deaths; continued
Clopidogrel (300 mg initially, then 75 mg daily) is also given and
continued for 12 months.

Platelet glycoprotein IIb/IIIa receptor inhibitors are added to high-risk

Heparin interferes with thrombus formation at the site of plaque rupture
and reduces risk of ischaemic events and death.
o Low molecular weight heparin (e.g. enoxaparin 1mg/kg twice
daily) has better efficacy.
o Treatment given for at least 48 hours.
Synthetic pentasaccharide (fondaparinux) inhibits facot Xa of
coagulation cascade.
o Lower risk of bleeding than heparin.
Anti-ischaemia agents
Nitrates given sublingually or by IV infusion with continuing pain for 2448 hours.
B blockers (e.g. metoprolol) are first line oral anti-anginal secondary
preventative effects in CAD.
Plaque stabilisation
Statin and an ACE inhibitor are continued long term and reduce future
cardiovascular events.
! Oral medication is continued indefinitely after hospital discharge. EXCEPT
clopidogrel, which is stopped after 12 months.
Risk stratification
Thrombolysis in Myocardial Infarction (TIMI)
Predict subsequent risk of STEMI and death in patients with unstable
angina/NSTEMI; provide basis for therapeutic decision-making.

Intermediate/high risk
early coronary angiography with a view to surgery or PCI
Coronary stenting may stabilize disrupted coronary plaque and reduces
angriographic restenosis rates, compared to angioplasty alone.
Low risk
cardiac stress test (e.g. exercise ECG).
ST Segment Elevation Myocardial Infarction (STEMI)
Most common cause of death in developed countries.
Associated Conditions: