Guidelines for treatment of Angina

The diagnosis is based on obtaining an accurate history. Virtually all cases are caused by coronary artery disease, but aortic valve disease and hypertrophic cardiomyopathy are sometimes responsible. Anaemia, especially in the elderly may be a contributing factor.

The resting ECG is often normal. Most patients should have exercise testing in order to objectively assess limitations and for risk stratification.

Risk factor identification and modification is an integral part of treatment.

Medication 

  1. Sub-lingual GTN, a GTN spray or buccal GTN should be given to each patient for prompt symtomatic relief and for prophylactic use when angina is anticipated. Choice should be on patient preference. The spray is preferable for patients who use GTN infrequently but is expensive.

  2. Anti-platelet treatment with aspirin 75mg daily unless contraindicated. 

  3. Anti-anginal medication.

a) A cardio-selective beta blocker (atenolol, metoprolol) should be prescribed unless contraindicated. This will reduce cardiac work by decreasing blood pressure and heart rate. 

b) A calcium channel antagonist - Nifedipine increases heart rate and may be preferred in patients with a resting bradycardia or those taking a beta blocker. The short acting formulations should be avoided. Amlodipine is (relatively) neutral with respect to heart rate. Verapamil and diltiazem decrease the heart rate and may thus be especially useful in patients with a high resting rate. Verapamil and diltiazem should be co-prescribed with a beta blocker only with caution and in the knowledge that severe bradycardia or heart block may occasionally occur. Both are negatively inotropic and should not be prescribed to patients with heart failure and with caution in those with impaired left ventricular function.

c) A nitrate. Isosorbide mononitrate gives predictable blood levels and can be prescribed once daily . Nitrate tolerance is a well documented clinical entity, it can be avoided by allowing a six to eight hour nitrate free interval in each 24 hour period, or if using a nitrate patch, by removing it at night.  

d) Nicorandil belongs to new group of anti-anginal drugs which are called potassium-channel activators. It is a mixed arteriolar and venodilator and thus has similar side effects to calcium channel antagonists. Currently, it is used as an add-on treatment with other anti-anginals. 

Most patients receive a beta blocker or a long-acting nitrate together with a calcium channel antagonist. All patients should be prescribed a short-acting nitrate. 

Potential candidates for intervention (coronary artery surgery or angioplasty) should be referred for cardiological assessment. 

Non-ST segment elevation acute coronary syndrome

This term encompasses the spectrum of acute coronary syndromes from unstable angina through minimal myocardial necrosis to myocardial infarction without ST elevation. The condition is accompanied by a heightened risk of recurrent myocardial ischaemia or infarction are elevation of the Troponin T 12 hours after the onset of symptoms and ST segment depression on the electrocardiogram. A heightened risk of death is predicted by greater age, the magnitude of the rise in troponin and by evidence of left ventricular impairment - either pre-existing or during ischaemia. Patients with a normal troponin and either a normal ECG or T-wave inversion are at a relatively low risk in the short term.

The pathophysiology is similar to that of ST segment elevation myocardial infarction - rupture or erosion of the endothelium overlying an atheromatous plaque with consequent thrombus formation resulting in an acute reduction of the arterial lumen and distal embolism causing myocardial ischaemia and necrosis. However, unlike the fibrin-rich occlusive thrombus that causes ST elevation myocardial infarction, the thrombus in non-ST segment acute coronary syndromes consists predominately of aggregated platelets.

Patients present with new onset of severe effort angina (class III-IV), an abrupt increase in the severity of previous angina with attacks of pain being prolonged and less responsive to nitrates, or with angina at rest.

Because of the risk of complications, patients should be admitted to hospital. The principles of management are to stabilise the patient with anti-thrombotic and anti-ischaemic therapy and regularly to review the risk as the condition evolves. Initial treatment should be bed-rest (to minimise myocardial oxgen consumption), anti-thrombotic treatment with enoxaparin (1mg/kg body weight BD), aspirin and clopidogrel. All patients should receive a beta-blocker unless contr-indicated and regular nitrates; the nitrate should be given intravenouslyfor those with recurrent or refractory ischaemia. If a beta-blocker is contra-indicated, a rate-limiting calcium channel blocker (verapamil or diltiazem) should be prescribed. The enoxaparin should be withdrawn 48 hours after the last episode of ischaemia or earlier if the troponin T is not elevated. Early coronary angiography is indicated for patients with recurrent ischaemia or other evidence of moderate or high risk because myocardial revascularisation (surgery or PCI) relieves symptoms and, in certain circumstances, improves prognosis.