[Dynamics of critical stenosis in patients with unstable angina pectoris]

In 28 patients with unstable angina pectoris biplane coronary angiography was performed in the acute stage. Arteriography of the ischemia-related vessel was subsequently repeated in 14 patients after intracoronary infusion of 0.2 mg nifedipine and ten minutes later after 10 mg sublingual nifedipine (group I) and in 14 patients after intracoronary infusion of 0.4 mg 3-N-morpholinosyndnonimine (SIN-1) (group II). 17 patients were on intravenous nitroglycerin and 11 patients on high-dose oral isosorbide dinitrate therapy at the time of angiography. Pre- and postintervention, the degree of coronary stenosis of the ischemia-related vessel was determined by three morphometric methods: rmin, minimal diameter of the stenosis, Amin, planimetered area under the stenosis and minimal diameter ratio (min diam ratio), ratio of the minimal diameter of the stenosis and the pre- and poststenotic diameter. An increase in lumen was considered to be significant when two of the three parameters increased by more than 5%. Nifedipine application resulted in an increase in lumen in 13 patients of group I. After i.c. nifedipine the lumen increased by 16% and after s.l. nifedipine by an additional 9%. Combined i.c. and s.l. nifedipine increased the lumen of the critical stenosis by 24 +/- 6.8%. In 10 patients of group II, SIN-1 application was successful and resulted in a luminal increase of 28 +/- 2.6%. In more than 80% of our patients with unstable angina pectoris application of nifedipine and SIN-1 resulted in an increase of the lumen. Thus, coronary vasoconstriction seems to be the predominant mechanism next to organic stenosis in unstable angina.