title: Nifedipine and angina pectoris. Short-term changes in quantitative coronary angiography with nifedipine and clinical response to treatment in effort-induced, mixed, and spontaneous angina pectoris.
abstract: Changes induced by nifedipine (10 mg sublingually) in the residual luminal diameter of significant (greater than 50 percent) coronary lesions were assessed angiographically in 69 patients with effort-induced angina (group 1), in 22 patients with mixed angina (group 2), and in 14 patients with Prinzmetal's angina (group 3). These changes were related to the clinical response to treatment with the same drug, as evaluated through diary records and Holter monitoring in the mixed (spontaneous component) and Prinzmetal forms and through exercise testing in effort-induced and mixed (effort-associated component) angina. In groups 1 and 2, segments of stenotic vessels showed either an increase or decrease or no change in diameter with the calcium antagonist; in group 3, the majority of the lesions had compliant portions which invariably responded with dilatation. Nifedipine failed to improve cases with exertional (20 percent [14/69] unchanged; 19 percent [13/69] worsened) and mixed (41 percent [9/22] exacerbated) forms; 100 percent of the 14 patients with the Prinzmetal form had relief of the anginal episodes. In group 1, the response to exercise tests was dissociated from the short-term vasomotor pattern, and the pressure-rate product failed to explain the clinical results. Forty-five percent (ten) of the patients in group 2 showed significant short-term widening of critical stenoses, as well as obvious improvement; patients who did worse with treatment in this group had reacted to nifedipine with narrowing of critical stenoses. These data suggest that the response to nifedipine of classic effort-induced angina is probably the net result of an interaction of changes in myocardial oxygen consumption and supply; coronary vasomotion has a role in mixed angina, and influences of nifedipine may be either favorable or unfavorable; stenotic lesions in the Prinzmetal form are quite sensitive to the relaxant action of calcium blockade, and this probably represents a background to the highly positive clinical response to treatment.
authors.affiliation: Istituto di Cardiologia, University of Milan, Italy.
authors.forename: N
authors.initials: N
authors.lastname: De Cesare
authors.forename: A
authors.initials: A
authors.lastname: Bartorelli
authors.forename: F
authors.initials: F
authors.lastname: Fabbiocchi
authors.forename: A
authors.initials: A
authors.lastname: Loaldi
authors.forename: P
authors.initials: P
authors.lastname: Montorsi
authors.forename: A
authors.initials: A
authors.lastname: Polese
authors.forename: M D
authors.initials: MD
authors.lastname: Guazzi
mesh_terms: D000787:Angina Pectoris / Q000000981:diagnostic imaging / Q000188:drug therapy*; D000788:Angina Pectoris, Variant / Q000000981:diagnostic imaging / Q000188:drug therapy*; D002932:Cineangiography; D002986:Clinical Trials as Topic / Q000379:methods; D017023:Coronary Angiography; D003331:Coronary Vessels / Q000187:drug effects*; D004359:Drug Therapy, Combination; D004562:Electrocardiography; D005080:Exercise Test; D006801:Humans; D008991:Monitoring, Physiologic; D009543:Nifedipine / Q000627:therapeutic use*; D005082:Physical Exertion; D013997:Time Factors
chemical_list: D009543:Nifedipine