The aim of treatment of stable angina is twofold: to control symptoms and to halt the progression of underlying coronary heart disease. Anti-anginals control symptoms and work by restoring the balance between myocardial O₂ demand and supply. Patients whose stable angina is refractory to pharmacological agents should be considered for revascularization with coronary artery angioplasty or bypass grafting. The treatment of variant angina is primarily directed at reversing coronary vasospasm.

Anti-Anginals

First line treatment for stable angina consists of either a β-adrenergic receptor blocker (β-blocker), or a calcium-channel blocker (CCB) together with a short-acting nitrate. If the patient’s symptoms are inadequately controlled on one sole agent, and if comorbidities permit, a combination may be used. If in spite of optimal doses of both β-blocker and CCB, the patient still reports anginal pain, other drugs could be added such as ivadrabine, nicorandil, ranolazine and a long-acting nitrate. The initial choice between a β-blocker or a CCB is influenced by coexisting conditions and contraindications. For example, a CCB is preferable if the patient has moderate or severe asthma or hypertension, and a β-blocker may be the choice if rate control is also required (i.e. if atrial fibrillation is also present). If the patient cannot tolerate either of these agents, then monotherapy with a long-acting nitrovasodilator should be commenced. Some patients need to take multiple classes of anti-anginal to control their symptoms.

β-Adrenergic Receptor Blockers

As Figure 41 illustrates, myocardial ischaemia creates a vicious cycle by activating the sympathetic nervous system and increasing ventricular end-diastolic pressure; both these effects then trigger ischaemia and anginal pain. β-Blockers help to block this cycle, thereby decreasing O₂ demand.They reduce O₂ demand by decreasing myocardial contractility and wall stress. The resting and exercising heart rate also falls. This increases the fraction of time the heart spends in diastole, thus enhancing perfusion of the coronary arteries, which occurs predominantly during diastole. The main therapeutic action of these drugs is on cardiac β₁-receptors, but both β₁-selective and (β₁/β₂) non-selective blockers are used.

Potential adverse effects of β-blockers include fatigue, reduced left ventricular function and severe bradycardia. Impotence may be a concern in men. β-Blockers can precipitate asthma by blocking β₂-receptors in the airways, and therefore even β₁-selective agents are contraindicated in this condition. Lipid-soluble β-blockers (e.g. propranolol) can enter the central nervous system and cause depression or nightmares. β-Blockers can also worsen insulin-induced hypoglycaemia in diabetics.

Ca²⁺-Channel Blockers (Also Ca²⁺ Antagonists)

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