Calcium antagonists and coronary artery disease: an opportunity missed?

Why are calcium antagonists not used clinically in myocardial protection to prevent sudden death despite evidence from animal experiments that such activity may exist? The reason is that calcium antagonists are relatively vascular-selective and, at the sub-vasodilatory doses which have been tested clinically, do not inhibit the slow inward current in the myocardium. As a result a belief has grown in the fallacious concept that calcium antagonist activity in the myocardium is not a protective mechanism. Animal studies suggest that the opposite is the case. In my view, in the 20 years since the cardioprotective actions of verapamil were first demonstrated, an opportunity for drug development has been wasted. To rectify this, new drug development should begin with the objective of designing calcium antagonists with inbuilt site-selectivity for ischaemic tissue.