Coronary Heart Disease
Coronary Heart Disease
Stable angina
Ischaemia due to fixed atheromatous stenosis of one or more coronary arteries
Unstable angina
Ischaemia caused by dynamic obstruction of a coronary artery due to plaque rupture or erosion with superimposed thrombosis
Myocardial infarction
Myocardial necrosis caused by acute occlusion of a coronary artery due to plaque rupture or erosion with superimposed thrombosis
Heart failure
Myocardial dysfunction due to infarction or ischaemia
Arrhythmia
Altered conduction due to ischaemia or infarction
Sudden death
Ventricular arrhythmia, asystole or massive MI
Stable Angina
· Symptom complex caused by transient myocardial ischaemia
· Occurs whenever there is imbalance between myocardial oxygen supply and demand
· Causes
o Coronary atheroma – commonest cause
o Aortic valve disease
o Hypertrophic cardiomyopathy
· Precipitating factors (activities)
o Physical exertion
o Cold exposure
o Heavy meals
o Intense emotion
o Lying flat (decubitus angina)
o Vivid dreams (nocturnal angina)
Clinical Features
Symptoms
· Central chest pain/ discomfort
· Breathlessness
(Precipitated by exertion/ other forms of stress; relieved by rest)
*Warm-up angina – discomfort when start walking à does not return despite greater effort
Signs
· Evidence of valve disease (esp aortic)
· Risk factors – HT, DM
· Left ventricular dysfunction – cardiomegaly, gallop rhythm
· Manifestations of arterial disease – carotid bruits, peripheral vascular disease
· Exacerbating factors – anemia, thyrotoxicosis
Investigations
· ECG
o Resting ECG
§ Normal
§ Evidence of previous MI
§ T wave flattening/ inversion (non-specific evidence of myocardial ischemia/ damage)
§ ST segment depression/ elevation
o Exercise ECG – using treadmill/ bicycle ergometer
§ Planar/ down-sloping ST segment depression of >1mm – ischemia
§ Up-sloping ST segment depression – normal
False positives - digoxin therapy, left ventricular hypertrophy, bundle branch block or WPW syndrome
· Myocardial perfusion scanning – IV radioactive isotope such as 99technetium tetrofosmin given; perfusion defect during stress but not at rest gives evidence of reversible myocardial ischemia
· Stress echocardiography - uses transthoracic echocardiography to identify ischaemic segments of myocardium and areas of infarction
· Coronary arteriography – to provide detailed anatomical information about the extent and nature of coronary artery disease; done in view to CABG surgery/ PCI
Treatment
· Non-pharmacological
o Advice
§ Do not smoke
§ Ideal body weight
§ Regular exercise (But not beyond the point of chest discomfort)
§ Avoid severe unaccustomed exertion, vigorous exercise after heavy meal/ very cold weather
§ Take sublingual GTN before undertaking exertion that may induce angina
o Reassurance – psychological factors
· Pharmacological
o Antiplatelet therapy
§ Low dose (75mg) aspirin daily
§ Clopidogrel (75mg) daily
o Anti-anginal therapy
§ Nitrates – produce venous and arteriolar dilatation à reduce myocardial oxygen demand (lower preload, afterload), increase in myocardial oxygen supply (coronary vasodilation)
· Glyceryl trinate (GTN)
o Sublingual - from a metered-dose aerosol (400ug per spray)/ as a tablet (300/ 500ug) – relieves attack in 2-3 minutes
o Transcutaneously – patch (5-10mg daily),
· Isosorbide dinitrate (10-20mg 8 hourly)
· Isosorbide mononitrate (20-60mg once/ twice a day)
· Long-acting nitrates – for nocturnal angina
§ Beta-blockers (Cardioselective) – lower myocardial oxygen demand by reducing HR, BP, myocardial contractility
· SR metoprolol 50-200mg daily
· Bisoprolol 5-15mg daily
(Beta blocker withdrawal syndrome – rebound effect – arrhythmias, worsening angina, MI)
§ Calcium channel antagonists – lower myocardial oxygen demand by reducing BP, myocardial contractility
· Verapamil 40-80mg 8 hourly, diltiazem 60-120mg 8 hourly – for patients unsuitable for B-blocker (eg airway obstruction)
· Nifedipine – cause reflex tachycardia, hence used in combination with a B-blocker
§ Potassium channel activators
· Nicorandil 10-30mg 12 hourly orally – arterial and venous dilating properties, but no tolerance as with nitrates
§ If channel antagonist
· Ivabradine – induces bradycardia
o Control of risk factors
§ Statin
· Invasive treatment
o Percutaneous coronary intervention (PCI) – for single/ two-vessel disease
§ Performed by passing a fine guidewire across a coronary stenosis under radiographic control and using it to position a balloon which is then inflated to dilate the stenosis
§ Palliative therapy for patients with recurrent angina after CABG
§ Complications
· Occlusion of the target vessel or a side branch by thrombus or a loose flap of intima (coronary artery dissection) à myocardial damage
· Restenosis – reduced by stenting
· Recurrent angina requiring further PCI or bypass grafting
§ Adjunctive therapy – potent platelet inhibitors (clopidogrel, gpIIb/IIIa receptor antagonists), aspirin, heparin
o Coronary artery bypass graft – for three-vessel (LAD, CX, RCA)/ left main stem/ 2 vessel disease involving proximal LAD
§ Arteries – internal mammary arteries, radial arteries, reversed segment of saphenous vein
§ Complications
· Recurrent angina
o Early – graft failure
o Late – progressive disease, graft degeneration
· Perioperative stroke
· Diffuse myocardial damage
· Infection (chest, wound)
· Wound pain
§ Adjunctive therapy – aspirin, clopidogrel, intensive lipid-lowering therapy
Angina with normal coronary arteries
· F > M
Coronary artery spasm (variant angina/ Prinzmetal’s angina)
· Occur without angiographically detectable atheroma
· ECG – spontaneous, transient ST elevation
· Treatment
o CCB
o Nitrates
o Other coronary vasodilators
Syndrome X
· Typical angina on effort
· Objective evidence of myocardial ischaemia on stress testing
· Angiographically normal coronary arteries
- Stable angina
- ACS
o Unstable angina – no elevation of cardiac enzymes
o MI – elevation of cardiac enzymes
§ STEMI
§ NSTEMI