Different coronary vasomotor effects of nifedipine and therapeutic correlates in angina with spontaneous and effort components versus Prinzmetal angina

Alessandro Loaldi, Franco Fabbiocchi, Piero Montorsi, Nicoletta De Cesare, Antonio Bartorelli, Alvise Polese, Maurizio D. Guazzi

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Flow impedance, probably of vasomotor origin, superimposed on severe coronary stenosis has been considered a trigger for the spontaneous component of angina occurring both on effort and at rest. To investigate more thoroughly this pathophysiologic aspect we evaluated (by means of quantitative coronary angiography) the acute vasomotor reaction to nifedipine (10 mg sublingually) of significant (>50%) stenotic lesions in 22 patients with double-component angina. We also correlated this reaction with the clinical response (dally number of ischemic episodes evaluated by means of 48-hour Holter ambulatory monitoring) to treatment with nifedipine (20 mg four times a day); calcium channel blockade, in fact, is considered a specific remedy in cases of altered coronary vasomotility. Patients with Prinzmetal angina, who were known to have homogeneous coronary vasodilating reactions and favorable clinical responses to nifedipine, were studied by means of the same methods and served as the control group (14 patients). In double-component angina the residual lumen diameter of significant lesions was unchanged in two patients, enhanced in 10, and reduced in 10 after sublingual nifedipine; lumen variations from baseline values ranged from +1.29 to -1.56 mm. Acute changes in stenosis correlated closely with results obtained with oral treatment. In the group with Prinzmetal angina, coronary stenoses invariably responded with dilatation (the residual coronary lumen increased by an average of 69% of baseline); 100% of the patients in this group responded favorably to treatment. These observations indicate that there is a relationship between the short-term angiographic and the therapeutic responses to nifedipine in spontaneous angina, in both the double-component and Prinzmetal forms. In the latter nifedipine causes dilatation of compliant stenotic lesions and invariably promotes clinical improvement. In the former the clinical condition may become worse in some instances; this pattern appears to be at least partially related to a paradoxical vasoconstrictor effect of nifedipine.

Original languageEnglish
Pages (from-to)315-322
Number of pages8
JournalAmerican Heart Journal
Issue number2
Publication statusPublished - 1989

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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