Ischaemic heart disease (IHD), also known as coronary heart disease (CHD) or coronary artery disease (CAD), is one of the leading cause of morbidity and mortality worldwide.
It is defined as a reduced blood flow to the myocardium. Depending on the degree of this ischaemia, it may be asymptomatic or it can result in life threatening complications.
Pathophysiology
In elderly patients with the associated risk factors, IHD has the same pathophysiology as ACS, that being atherosclerotic plaque build up and rupture → reduced blood flow to the myocardium.
It can range from being asymptomatic, if an insignificant occlusion is present), to life threatening. Such complications include:
- Myocardial infarction
- Ischaemic cardiomyopathy
- Sudden cardiac death
- Angina pectoris
Younger patients or those without risk factors may also have IHD due to vasospasm. This is known as vasospastic angina (or prinzmetal angina or variant angina). In these cases, the coronary arteries spasm sporadically → vasoconstriction → transient ischaemia to the myocardium until the arteries spontaneously relax.
Other potential causes in these patients could be:
- Endothelial or microvascular dysfunction
- Spontaneous thrombosis/embolism
- Coronary artery dissection
- Compression
- Vasculitis/arteritis
- Radiation damage
⚠️ Risk factors
- Smoking
- Hypertension
- Hyperlipidaemia
- Isolated low HDL
- Diabetes mellitus
- Physical inactivity
- Obesity
- Family history
- Male sex
- Illicit drug use - such as cocaine.
😷 Presentation
In chronic stable angina it is typically asymptomatic.
In angina pectoris (exertional angina) there is:
- ⭐️ Chest pain upon exertion - this pain comes on with exercise or increased stress and is relieved with rest or GTN. This is the hallmark symptom of angina.
Other symptoms may include:
- Jaw pain, epigastric or shoulder pain
- Dyspnoea
- Palpitations
- Diaphoresis and fatigue
Low-risk unstable angina patients may also present with chest pain upon exertion for <20 minutes. The pain usually is not rapidly increasing and there is often a normal ECG along with it.
🔍 Investigations
There are a multitude of tests that can be done and it may differ according to local policies, however, NICE does recommend:
- CT coronary angiography
- ECG
An ECG is beneficial for all patients with IHD. It gives us a baseline that we can compare new ECGs to in the future.
Signs of ischaemia on an ECG may include:
- T-wave flattening or inversion - it must be present in 2 contiguous leads and at least 1mm deep. T-wave inversion is normal in aVR and V1 and sometimes lead III.
- ST depression - must be >1mm deep. Typically found in leads I, II, V5, V6
Other investigations we can perform include:
- Haemoglobin - to rule out anaemia as a cause of chest pain as anaemia can increase the cardiac workload leading to angina signs with absence of occlusion.
- Lipid profile - as hyperlipidaemia, particularly high LDL, is a risk factor.
- HbA1c - as diabetes mellitus is also a risk factor.
- Stress testing - which can precipitate angina.
🧰 Management
- Lifestyle modification + anti-platelet therapy + statin is first-line.
- Lifestyle modification - weight management, increased exercise, dietary modifications, reduced lipid intake, smoking cessation.
- Anti-platelet therapy
- Aspirin - 75mg OD indefinitely.
- Clopidogrel - 75mg OD indefinitely.
- Statin
- Atorvostatin
- If they are not benefiting from a statin, they can consider using ezetimibe which reduces cholesterol delivery to the liver.
- 😖 IHD patients with anginal symptoms:
- Sublingual GTN - 0.3-0.6mg sublingually every 5 minutes when required (maximum of 3 doses).
- Adverse effects: headaches, dizziness, flushing.
- B-blocker - metoprolol/bisoprolol/carvedilol/timolol/nadolol
- Adverse effects: orthostatic hypotension, GI upset, dizziness.
- CCB
- Dihydropyridine CCBs - nifedipine/amlodipine are more effective but have worse adverse effect profile.
- Adverse effects: flushing, ankle swelling and headaches.
- Non-DHP CCBs - diltiazem
The other first-line addition is a B-blocker and/or CCB and/or long acting nitrate.
If they do not respond to initial treatment then we should increase it to the maximum tolerated dosage, however, if they are still symptomatic add either a ß-blocker or CCB depending on what is used for monotherapy.
If a CCB is used first-line, diltiazem or verapamil is preferred for monotherapy.
If a ß-blocker is used first-line and we need to add dual therapy, a DHP CCB can be used, such as amlodipine or nifedipine.
- For a patient with symptomatic stable angina on a CCB but with a contraindication to a ß-blocker (eg asthma, COPD), the next line treatment should be long-acting nitrate, ivabradine or nicorandil or ranolazine.
- Nicorandil can cause GI ulceration.
- If the patient is also taking a rate-limiting (non-dihydropiridine) CCB (eg. verapamil), so even if he did not have asthma, beta-blockers would still be contraindicated as they should not be co-prescribed due to the risk of severe heart block, bradycardia, and heart failure.
Consider revascularisation such as coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) for people with stable angina whose symptoms are not satisfactorily controlled with optimal medical treatment.
If a patient is taking both a beta-blocker and a calcium-channel blocker, they should only add a third drug while they are waiting to be assessed for either percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG).
Offer CABG to people with stable angina and suitable coronary anatomy when:
- Symptoms are not satisfactorily controlled with optimal medical treatment and
- Revascularisation is considered appropriate and
- PCI is not appropriate.
Offer PCI to people with stable angina and suitable coronary anatomy when:
- Symptoms are not satisfactorily controlled with optimal medical treatment and
- Revascularisation is considered appropriate and
- CABG is not appropriate.