(Circulation. 2001;103:3062.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Biological Profiles in Subjects With Recurrent Acute Coronary Events Compared With Subjects With Long-Standing Stable Angina
From the Quebec Heart Institute/Laval Hospital (P.B., P.P., S. Simard, L.B., G.R.D.), Laval University, Ste-Foy; and the Montreal General Hospital (S. Solymoss), McGill University, Montreal, Quebec, Canada.
Correspondence to Peter Bogaty, MD, Quebec Heart Institute/Laval Hospital, 2725 Chemin Ste-Foy, Ste-Foy, Quebec, Canada G1V 4G5. E-mail peter.Bogaty{at}med.ulaval.ca
Background—At one end of the clinical spectrum of coronary artery disease (CAD) are subjects who have had repeated acute ischemic events, and at the other end are those with long-standing angina who have never been unstable. This study tests the hypothesis that a specific biological profile can distinguish these 2 extreme groups and predict acute coronary events.
Methods and
Results—Blood levels of lipoprotein(a),
homocysteine, tissue plasminogen activator,
plasminogen activator inhibitor-1, C-reactive
protein (CRP), fibrinogen, and von Willebrand factor were
compared in 3 groups of 50 subjects each: (1) those with previous
multiple acute coronary events, (2) age-matched subjects with
3 years of stable angina and no prior acute coronary events,
and (3) matched controls without evidence of atherosclerotic disease
and a normal coronary angiogram. All subjects were followed for
4.0 years. Lipoprotein(a), homocysteine, tissue plasminogen
activator, and plasminogen activator
inhibitor-1 were similar in both CAD groups and
significantly higher than in the control group. However, compared with
subjects with long-standing stable angina, those with previous multiple
coronary events had higher values of CRP (5.7±5.4 versus
3.0±5.2 mg/L, P=0.012),
fibrinogen (3.38±0.75 versus 2.92±0.64 g/L,
P=0.001), and von
Willebrand factor (1.60±0.55 versus 1.25±0.36 U/mL,
P=0.0003). On follow-up,
myocardial infarction and unstable angina occurred in 42% of the group
with multiple events, 4% of the stable angina group
(P<0.0001), and none of the
control subjects. In the 100 patients with CAD, CRP was 4.9 mg/L in
those with and 1.8 mg/L in those without new instability
(P<0.0001). In a
multivariate analysis, only CRP distinguished
those with follow-up acute coronary events (adjusted odds ratio
5.9, 95% CI 2.0 to 17.9;
P=0.002). A baseline CRP >3.5
mg/L had a relative risk of 7.6 (2.6 to 21.7,
P=0.0002) for subsequent acute
events.
Conclusions—An inflammatory biological profile distinguished patients with previous multiple acute coronary events from those with long-standing stable angina and predicted acute coronary instability.
Key Words: myocardial infarction • angina • risk factors • coronary disease • inflammation
This article has been cited by other articles:
 |
|
 |
|
  C. W. Hamm, H. Möllmann, J.-P. Bassand, and F. van de Werf CHAPTER 16 Acute Coronary Syndromes ESC Textbook of Cardiovascular Medicine, January 1, 2009; 2(1): med-9780199566990-chapter - med-9780199566990-chapter. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Foglieni, F. Maisano, L. Dreas, A. Giazzon, G. Ruotolo, E. Ferrero, L. Li Volsi, S. Coli, G. Sinagra, B. Zingone, et al. Mild inflammatory activation of mammary arteries in patients with acute coronary syndromes Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2831 - H2837. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. O. Caymaz and G. Yuksel Fate of Incidental, Asymptomatic Lesions Discovered During Percutaneous Coronary Intervention Angiology, May 1, 2008; 59(2): 193 - 197. [Abstract] [PDF]
|
|
|
|
 |
|
 H. Loppnow, K. Werdan, and M. Buerke Invited review: Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms Innate Immunity, April 1, 2008; 14(2): 63 - 87. [Abstract] [PDF]
|
|
|
|
 |
|
 L. M. Reich, G. Heiss, L. L. Boland, A. T. Hirsch, K. Wu, and A. R. Folsom Ankle brachial index and hemostatic markers in the Atherosclerosis Risk in Communities (ARIC) study cohort Vascular Medicine, November 1, 2007; 12(4): 267 - 273. [Abstract] [PDF]
|
|
|
|
 |
|
 Authors/Task Force Members, J.-P. Bassand, C. W. Hamm, D. Ardissino, E. Boersma, A. Budaj, F. Fernandez-Aviles, K. A.A. Fox, D. Hasdai, E. M. Ohman, et al. Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology Eur. Heart J., July 1, 2007; 28(13): 1598 - 1660. [Full Text] [PDF]
|
|
|
|
 |
|
 P. Poirier, T. D. Giles, G. A. Bray, Y. Hong, J. S. Stern, F. X. Pi-Sunyer, and R. H. Eckel Obesity and Cardiovascular Disease: Pathophysiology, Evaluation, and Effect of Weight Loss: An Update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease From the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism Circulation, February 14, 2006; 113(6): 898 - 918. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. K. Ray and C. P. Cannon The Potential Relevance of the Multiple Lipid-Independent (Pleiotropic) Effects of Statins in the Management of Acute Coronary Syndromes J. Am. Coll. Cardiol., October 18, 2005; 46(8): 1425 - 1433. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Bogaty, J. M. Brophy, L. Boyer, S. Simard, L. Joseph, F. Bertrand, and G. R. Dagenais Fluctuating Inflammatory Markers in Patients With Stable Ischemic Heart Disease Arch Intern Med, January 24, 2005; 165(2): 221 - 226. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Monaco, E. Rossi, D. Milazzo, F. Citterio, F. Ginnetti, G. D'Onofrio, D. Cianflone, F. Crea, L. M. Biasucci, and A. Maseri Persistent systemic inflammation in unstable angina is largely unrelated to the atherothrombotic burden J. Am. Coll. Cardiol., January 18, 2005; 45(2): 238 - 243. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Glaser, F. Selzer, D. P. Faxon, W. K. Laskey, H. A. Cohen, J. Slater, K. M. Detre, and R. L. Wilensky Clinical Progression of Incidental, Asymptomatic Lesions Discovered During Culprit Vessel Coronary Intervention Circulation, January 18, 2005; 111(2): 143 - 149. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Fichtlscherer, S. Breuer, and A. M. Zeiher Prognostic Value of Systemic Endothelial Dysfunction in Patients With Acute Coronary Syndromes: Further Evidence for the Existence of the "Vulnerable" Patient Circulation, October 5, 2004; 110(14): 1926 - 1932. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Bogaty, J. M. Brophy, M. Noel, L. Boyer, S. Simard, F. Bertrand, and G. R. Dagenais Impact of Prolonged Cyclooxygenase-2 Inhibition on Inflammatory Markers and Endothelial Function in Patients With Ischemic Heart Disease and Raised C-Reactive Protein: A Randomized Placebo-Controlled Study Circulation, August 24, 2004; 110(8): 934 - 939. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-J. Priebe Triggers of perioperative myocardial ischaemia and infarction Br. J. Anaesth., July 1, 2004; 93(1): 9 - 20. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Lombardo, L. M. Biasucci, G. A. Lanza, S. Coli, P. Silvestri, D. Cianflone, G. Liuzzo, F. Burzotta, F. Crea, and A. Maseri Inflammation as a Possible Link Between Coronary and Carotid Plaque Instability Circulation, June 29, 2004; 109(25): 3158 - 3163. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. W. Ketterer, G. Mahr, J. J. Cao, M. Hudson, S. Smith, and W. Knysz What's "Unstable" in Unstable Angina? Psychosomatics, June 1, 2004; 45(3): 185 - 196. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Luc, J.-M. Bard, I. Juhan-Vague, J. Ferrieres, A. Evans, P. Amouyel, D. Arveiler, J.-C. Fruchart, and P. Ducimetiere C-Reactive Protein, Interleukin-6, and Fibrinogen as Predictors of Coronary Heart Disease: The PRIME Study Arterioscler Thromb Vasc Biol, July 1, 2003; 23(7): 1255 - 1261. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Maseri and V. Fuster Is There a Vulnerable Plaque? Circulation, April 29, 2003; 107(16): 2068 - 2071. [Full Text] [PDF]
|
|
|
|
|
|
R. A. Hegele, M. E. Kraw, M. R. Ban, B. A. Miskie, M. W. Huff, and H. Cao Elevated Serum C-Reactive Protein and Free Fatty Acids Among Nondiabetic Carriers of Missense Mutations in the Gene Encoding Lamin A/C (LMNA) With Partial Lipodystrophy Arterioscler Thromb Vasc Biol, January 1, 2003; 23(1): 111 - 116. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. G. Hanratty, Y. Koyama, H. H. Rasmussen, G. I. C. Nelson, P. S. Hansen, and M. R. Ward Exaggeration of nonculprit stenosis severity during acute myocardial infarction: implications for immediate multivessel revascularization J. Am. Coll. Cardiol., September 4, 2002; 40(5): 911 - 916. [Abstract] [Full Text] [PDF]
|
|