|
|
||||||||||
|
J Am Coll Cardiol, 1996; 28:597-603 © 1996 by the American College of Cardiology Foundation |
Department of Cardiological Sciences, St. George's Hospital Medical School, London, 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 > or = 20% diameter reduction or new total occlusion. RESULTS: At the first angiogram, 364 stenoses > or = 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 > or = 50% and 6 (29%) of 21 stenoses < 50% that progressed 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 stenoses 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 larger proportion of culprit complex stenoses progress in unstable angina than stable angina, and this is frequently associated with recurrence of coronary events.
This article has been cited by other articles:
![]() |
G. Rioufol, M. Gilard, G. Finet, I. Ginon, J. Boschat, and X. Andre-Fouet Evolution of Spontaneous Atherosclerotic Plaque Rupture With Medical Therapy: Long-Term Follow-Up With Intravascular Ultrasound Circulation, November 2, 2004; 110(18): 2875 - 2880. [Abstract] [Full Text] [PDF] |
||||
![]() |
D.D. Waters and K.K. Khush Management of the acute coronary syndrome patient Eur. Heart J. Suppl., July 1, 2004; 6(suppl_C): C49 - C57. [Abstract] [Full Text] [PDF] |
||||
![]() |
P J Sheridan and D C Crossman Critical review of unstable angina and non-ST elevation myocardial infarction Postgrad. Med. J., December 1, 2002; 78(926): 717 - 726. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. C. Sposito and M. J. Chapman Statin Therapy in Acute Coronary Syndromes: Mechanistic Insight Into Clinical Benefit Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1524 - 1534. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Rioufol, G. Finet, I. Ginon, X. Andre-Fouet, R. Rossi, E. Vialle, E. Desjoyaux, G. Convert, J.F. Huret, and A. Tabib Multiple Atherosclerotic Plaque Rupture in Acute Coronary Syndrome: A Three-Vessel Intravascular Ultrasound Study Circulation, August 13, 2002; 106(7): 804 - 808. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. A. Kerensky, M. Wade, P. Deedwania, W. E. Boden, C. J. Pepine, and Veterans Affairs Non-Q-Wave Infarction Strategies Revisiting the culprit lesion in non-Q-wave myocardial infarction: Results from the VANQWISH trial angiographic core laboratory J. Am. Coll. Cardiol., May 1, 2002; 39(9): 1456 - 1463. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. A. Goldstein Angiographic plaque complexity: the tip of the unstable plaque iceberg J. Am. Coll. Cardiol., May 1, 2002; 39(9): 1464 - 1467. [Full Text] [PDF] |
||||
![]() |
G. Pasterkamp, A. Vink, C. Borst, T. C. Wascher, A. deCampo, I. Schmoelzer, J. A. Goldstein, C. Grines, and W. W. O'Neill Multiple Complex Coronary Plaques in Patients with Acute Myocardial Infarction N. Engl. J. Med., February 15, 2001; 344(7): 527 - 528. [Full Text] [PDF] |
||||
![]() |
J. A. Goldstein, D. Demetriou, C. L. Grines, M. Pica, M. Shoukfeh, and W. W. O'Neill Multiple Complex Coronary Plaques in Patients with Acute Myocardial Infarction N. Engl. J. Med., September 28, 2000; 343(13): 915 - 922. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Tousoulis, G. Davies, C. Stefanadis, and P. Toutouzas Can angiography predict the vulnerable lesion that progresses to myocardial infarction? J. Am. Coll. Cardiol., January 1, 2000; 35(1): 261 - 262. [Full Text] [PDF] |
||||
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |