Progression and Regression of Coronary Stenosis in the Long-term Follow-up of Vasospastic Angina

Background Whether focal vasospasticity plays a pathogenic role in the progression or regression of coronary atherosclerosis is unknown. To determine whether evidence for such a role exists, we studied long-term changes in coronary luminal measurements in patients with vasospastic angina. Methods and Results Quantitative coronary angiography and repeated ergonovine provocation tests were performed 45±16 months apart in 30 patients. All patients had vasospastic anginal symptoms and coronary spasm on the initial provocation test. Of the 30 patients, 16 had persistent symptoms of vasospastic angina and showed coronary spasm at the same site on the follow-up angiogram (group 1), while the remaining 14 whose vasospastic anginal symptoms disappeared at follow-up demonstrated a negative response to ergonovine on the follow-up tests (group 2). There was no significant difference in patients’ baseline characteristics between the two groups. Long-term changes in minimal (MLD) and mean (MEAN) luminal diameter were measured (in millimeters) after administration of isosorbide dinitrate in 19 spastic and 93 nonspastic segments in group 1 and in 17 previously spastic and 81 nonspastic segments in group 2. Both MLD and MEAN were measured in 210 coronary segments of the 30 patients at baseline and after administration of ergonovine and isosorbide dinitrate by use of a computer-based quantitative coronary angiography system. Stenosis progression and regression of individual lesions were defined as a change in MLD of ≥0.40 mm. In group 1, both the MLD and MEAN of 19 spastic segments were significantly smaller (progression) at follow-up compared with the initial angiogram (MLD, 2.21±0.54 initially versus 1.95±0.65 at follow-up, P <.01; MEAN, 2.80±0.56 initially versus 2.56±0.58 at follow-up, P <.01), whereas the MLD and MEAN of 93 nonspastic segments in group 1 were not significantly different between the initial and follow-up angiograms (MLD, 2.47±0.67 initially versus 2.44±0.69 at follow-up, P =NS; MEAN, 2.96±0.69 initially versus 2.91±0.68 at follow-up, P =NS). In group 2, the MLD of the 17 previously spastic segments significantly improved (regression) at follow-up (MLD, 1.99±0.68 initially versus 2.24±0.54 at follow-up, P <.05); the MLD and MEAN of the 81 nonspastic segments were not significantly different (MLD, 2.36±0.59 initially versus 2.39±0.60 at follow-up, P =NS; MEAN, 2.81±0.58 initially versus 2.81±0.61 at follow-up, P =NS). In group 1, significant stenosis progression of individual lesions was observed more frequently at spastic than nonspastic segments (6 of 19 versus 10 of 93, P <.05), whereas stenosis regression was observed in no spastic and 3 nonspastic segments ( P =NS). In group 2, stenosis progression was observed at 1 previously spastic segment and 4 nonspastic segments ( P =NS), while significant stenosis regression of individual lesions was seen more commonly in previously spastic than nonspastic segments (6 of 17 versus 7 of 81, P <.01). Conclusions These results have demonstrated in patients an association between persistent vasospastic activity and progression of atherosclerosis and an association between cessation of vasospastic activity and regression of atherosclerosis.