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(Circulation. 1995;92:2446-2456.)
© 1995 American Heart Association, Inc.
Articles |
Progression and Regression of Coronary Stenosis in the Long-term Follow-up of Vasospastic Angina
From the Catheterization Laboratory, Department of Interventional Cardiology, Thoraxcenter, Erasmus University, Rotterdam, the Netherlands.
Correspondence to Patrick W. Serruys, MD, PhD, FESC, FACC, Professor of Interventional Cardiology, Thoraxcenter, Erasmus University, PO Box 1738, 3000 DR Rotterdam, Netherlands.
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.
Key Words: atherosclerosis • vasospasm • angina • coronary spasm • tests • angiography
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