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In 30 consecutive patients with Prinzmetal's angina pectoris, the antiischemic effect of felodipine, a new long-acting vasoselective calcium antagonist, administered at doses of 10 and 20 mg once daily was compared with that of the well-established therapeutic regimen with nifedipine administered at a dose of 20 mg 4 times daily. Twenty-four-hour Holter monitoring was performed during a 2-day placebo run-in and at the end of each of 3 consecutive 6-day periods during which the 3 active treatments were administered in randomized sequence. Three patients withdrew, whereas 27 completed the study. The therapeutic regimens tested proved to be similarly effective; primary end points (ischemic episodes recorded by Holter monitoring, and anginal attacks reported on diary cards) occured in 5 patients (19%) during nifedipine treatment, and in 7 (26%) and 3 (11%) during felodipine treatment with 10 and 20 mg, respectively (p = not significant). The distribution of residual ischemic episodes demonstrated that treatment with felodipine once daily provides 24-hour antiischemic protection. Twenty-six patients were followed up with 20 mg of felodipine once daily for a mean of 6 [+ or -] 5 months, and 21 of them (81%) remained free of symptoms and Holter-recorded ischemic attacks. It is concluded that for Prinzmetal's angina pectoris, 24-hour antiischemic protection may be achieved with administration of felodipine once daily. The availability of a simplified therapeutic approach may constitute a real advantage in terms of patient compliance and improving the quality of life. (Am J Cardiol 1991;68:1587-1592)

To verify that myocardial ischemia occurring during either the overbreathing or recovery phase of the hyperventilation test is based on different pathogenetic mechanisms, 2 consecutive series of patients, selected on the basis of their response to a run-in hyperventilation test, were studied. Group I comprised 15 patients who developed ST-segment depression early during overbreathing, whereas group II consisted of 12 patients showing ST-segment depression late during the recovery phase. A single oral dose of felodipine 10 mg or of placebo was administered on 2 consecutive days according to a randomized, double-blind, crossover design, and the hyperventilation test was repeated, on both days of the study, 3 to 5 hours after drug intake. In group I, ST-segment depression occurred after placebo in all patients during overbreathing, with an increase in rate pressure product (from 112 [+ or -] 31 at baseline to 168 [+ or -] 55 mm Hg X beats/min/100 at the onset of ST-segment depression; p [is less than]0.01). After felodipine, 13 patients continued to show ST-segment depression during overbreathing, together with an increase in rate pressure product (from 107 [+ or -] 24 at baseline to 158 [+ or -] 46 mm Hg X beats/min/100 at the onset of electrocardiographic changes; p [is less than]0.01). In group II, all 12 patients showed ST-segment depression during recovery after placebo, with a rate pressure product comparable to baseline conditions (112 [+ or -] 35 at baseline vs 102 [+ or -] 27 mm Hg X beats/min/100 at the onset of ST-segment depression; difference not significant). After felodipine, no patient developed ST-segment depression or chest pain. These findings confirm that early hyperventilation-induced ST-segment depression is related to increased oxygen consumption, which cannot be prevented by felodipine. On the other hand, felodipine is highly effective in preventing delayed ischemia, which is due to a primary reduction in coronary blood flow. (Ann J Cardiol 1990;66:1304-1308), Coronary artery disease (CAD) is a progressive condition in which the blood vessels supplying the heart are partially or completely occluded, resulting in diminished blood flow to that organ. Ischemia, or decreased blood flow to the heart, can be experimentally induced in patients with CAD by having them hyperventilate (breathe deeply and rapidly). The ischemia that results from this process can occur immediately or during the recovery phase. It has been hypothesized that immediate ischemia is mediated by increased oxygen demand by the heart (in the face of poor coronary reserve), while ischemia during recovery is mediated by constriction of the coronary vessels. This hypothesis was tested by using the selective calcium antagonist felodipine, which inhibits coronary vasoconstriction, but has no appreciable effect on cardiac oxygen consumption. Ninety-seven patients with a history of angina pectoris (chest pain) and CAD were evaluated. Following administration of either felodipine or a placebo, patients were asked to hyperventilate for five minutes. Measurements were made of cardiac oxygen consumption during hyperventilation and 10 minutes into the recovery phase. Hyperventilation caused cardiac ischemia in all patients; in those who experienced ischemia occurred during hyperventilation, no effect of felodipine was observed. In patients with recovery-phase ischemia, prior administration of felodipine blocked the induction of ischemia. This indicates that two different mechanisms are, in fact, responsible for hyperventilation-induced ischemia. (Consumer Summary produced by Reliance Medical Information, Inc.)

It is well known that constriction of the coronary arteries, the vessels that deliver blood to the heart muscle itself, can cause angina, a painful and potentially dangerous heart condition. Measurement of coronary artery constriction in patients suffering from chest pain, however, relies on invasive tests such as angiography that carry a certain risk. The hyperventilation test, in which patients breathe deeply and rapidly for five minutes while the electrical activity of the heart and blood pressure are recorded, is proposed as an alternative to invasive methods for estimating the extent of blood vessel constriction. To test this possibility, 83 patients hospitalized for chest pain or for narrowing of one or more coronary arteries underwent hyperventilation and exercise stress testing. Changes in their electrocardiograms that reflect coronary artery constriction were noted. Patients who showed such changes (Group I) returned the next day and were tested in the same way after receiving a calcium antagonist drug, which reduces blood pressure and oxygen demand by the heart. An equal number of patients whose electrocardiograms had not been affected by hyperventilation served as a control group (Group II). Fifteen out of 16 Group I patients had a more normal electrocardiogram after medication, while there was no change for Group II patients. In addition, exercise duration increased for Group I patients, but not for Group II members. These results suggest that the outcome of the hyperventilation test can serve as a screening measure for patients with stable exertional angina and vasoconstriction to help determine who will benefit from treatment with calcium blockers. (Consumer Summary produced by Reliance Medical Information, Inc.)