**7.2 Calcium channel blockers for coronary vasospasm**

Coronary spasm results in transient functional occlusion of a coronary artery that is reversible with nitrate vasodilation. It occurs in the setting of coronary

stenosis. Variant angina results from reduced blood flow (a consequence of transient localized vasoconstriction) rather than increased O2 demand. Drug-induced causes (e.g., cocaine, amphetamines, sumatriptan, and related antimigraine drugs) should be excluded. CCBs are effective in about 90% of patients. These agents are considered first-line treatment and may be combined with nitrate. The effects of pharmacologic vasodilators on coronary flow reflect direct actions on vascular smooth muscle as well as secondary adjustments in resistance artery tone. All calcium channel blockers induce vascular smooth muscle relaxation and are to various degrees pharmacologic coronary vasodilators (**Figure 6**). In epicardial arteries, the vasodilator response is like nitroglycerin and is effective in preventing coronary vasospasm superimposed on coronary stenosis as well as in normal arteries of patients with variant angina. They also submaximally vasodilate coronary resistance vessels. In this regard, dihydropyridine derivatives such as nifedipine are particularly potent and can sometimes precipitate subendocardial ischemia in the presence of critical stenosis. This arises from a transmural redistribution of blood flow (coronary steal) as well as the tachycardia and hypotension that transiently occur with short half-life formulations of nifedipine. One study demonstrated that the use of calcium channel blocker therapy was an independent predictor of myocardial infarct-free survival in vasospastic angina patients.
