Pharmacological cardiac stress: when and how?

Pharmacological stress is vital to the modern nuclear cardiological laboratory. In clinical practice only adenosine, dipyridamole and dobutamine are used. Both adenosine (directly) and dipyridamole (indirectly) work via activation of alpha 2 receptors, which causes vasodilatation. Adenosine has a very short half-life and any adverse effects can be rapidly controlled. It is however more expensive and not yet commercially available in the UK when compared with dipyridamole, which has a prolonged 30-min half-life. Dobutamine is a beta-agonist which mimics exercise by raising the rate pressure product, and it also has a short half-life. Adenosine and dipyridamole share some contraindications which include asthma. Dobutamine has been shown to be safe in these patients. Exaggerated responses to adenosine are seen in sinoatrial disease and in patients taking maintenance dipyridamole treatment orally. The adenosine receptor antagonists must be avoided prior to the use of the vasodilators (caffeine 12 h, aminophylline/theophylline 24 h). There is no evidence to suggest any significant difference between pharmacological stress and maximal exercise for myocardial perfusion imaging, but pharmacological stress is necessary for patients who have no exercise capability. Studies which show that submaximal exercise reduces sensitivity suggest that pharmacological stress should also be used in patients whose exercise capacity is suboptimal. The addition of exercise to the vasodilator infusion has been shown to reduce non-cardiac side effects and improve imaging.