Author + information
- Received November 1, 1994
- Revision received April 8, 1996
- Accepted April 24, 1996
- Published online September 1, 1996.
- Lujia Chen, M.D.1,∗,
- Michael R. Chester, M.D.,
- Robert Crook, M.R.C.P.2 and
- Juan Carlos Kaski, M.D., F.A.C.C.∗
- ↵∗Address for correspondence: Dr. Juan Carlos Kaski, Department of Cardiological Sciences, St. George's Hospital Medical School, Crammer Terrace, London SW17 0RE, England, United Kingdom.
Objectives. This study sought to compare the evolution of complex culprit stenoses in patients with stable and those with unstable angina pectoris.
Background. Complex coronary stenoses are associated with adverse clinical and angiographic outcomes. However, it is not known whether the evolution of complex stenoses differs in unstable angina versus stable angina pectoris.
Methods. We prospectively assessed stenosis progression in 95 patients with unstable angina whose angina stabilized with medical therapy (Group 1) and 200 patients presenting with stable angina (Group 2). After diagnostic angiography, all patients were placed on a waiting list for coronary angioplasty and restudied at 8 ± 4 (mean ± SD) months later. In each patient the presumed culprit stenosis was identified and classified as complex (irregular borders, overhanging edges or thrombus) or smooth (absence of complex features). Stenosis progression, as assessed by computerized angiography, was defined as ⩾20% diameter reduction or new total occlusion.
Results. At the first angiogram, 364 stenoses ⩾50% and 383 stenoses <50% were identified. At restudy, 36 (15%) of 236 stenoses progressed in 29 Group 1 patients and 36 (7%) of 502 stenoses in 31 Group 2 patients (p = 0.001). Forty-five (88%) of 51 stenoses ⩾50% and 6 (29%) of 21 stenoses <50% that nitrogeressed developed to total coronary occlusion (p = 0.001). More culprit stenoses progressed in Group 1 than in Group 2 (p = 0.006), whereas progression of nonculprit stenoses was not significantly different in both groups. Culprit complex stenoses progressed more frequently in Group 1 than in Group 2 (p = 0.01). During follow-up, 3 patients died (myocardial infarction), and 51 had a nonfatal coronary event. Culprit steenoses progressed in 15 (54%) of the 28 patients with a nonfatal coronary event in Group 1 and in 9 (39%) of 23 patients in Group 2 (p = NS). Complex morphology (p < 0.001) and unstable angina at initial presentation (p < 0.01) were predictive factors for progression of culprit stenoses.
Conclusions. A larges proportion of culprit complex stenoses progress in unstable angina than stable angina, and this is frequently associated with recurrence of coronary events.
- Received November 1, 1994.
- Revision received April 8, 1996.
- Accepted April 24, 1996.