Clinical and Therapeutic Profile of Patients Presenting With Acute Coronary Syndromes Who Do Not Have Significant Coronary Artery Disease

BackgroundA proportion of patients who present with suspected acute coronary syndrome (ACS) are found to have insignificant coronary artery disease (CAD) during coronary angiography, but these patients have not been well characterized. Methods and ResultsOf the 5767 patients with non–ST-segment elevation ACS who were enrolled in the Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin (Eptifibatide) Therapy (PURSUIT) trial and who underwent in-hospital angiography, 88% had significant CAD (any stenosis >50%), 6% had mild CAD (any stenosis >0% to ≤50%), and 6% had no CAD (no stenosis identified). The frequency of death or nonfatal myocardial infarction at 30 days was reduced with eptifibatide treatment in patients with significant CAD (18.3% versus 15.6% for placebo, P =0.006) but not in those with mild CAD (6.6% versus 5.4%, P =0.62) and with no CAD (3.0% versus 1.2%, P =0.28). We identified independent baseline predictors of insignificant CAD (mild or no CAD) and used them to develop a simple predictive nomogram of the probability of insignificant CAD for use at hospital presentation. This nomogram was validated in a separate population of patients with non–ST-segment elevation ACS. ConclusionsPatients with suspected ACS found to have insignificant CAD have a low risk of adverse outcomes, do not appear to benefit from treatment with eptifibatide, and can be predicted with a simple nomogram drawn from baseline characteristics. Because patients with significant CAD appear to have an enhanced benefit from eptifibatide treatment, the predictive nomogram developed can be used to determine indications for glycoprotein IIb/IIIa blockade.

[1]  H. White,et al.  Troponin concentrations for stratification of patients with acute coronary syndromes in relation to therapeutic efficacy of tirofiban , 1999, The Lancet.

[2]  C. Heeschen,et al.  Angiographic findings in patients with refractory unstable angina according to troponin T status. , 1999, Circulation.

[3]  R. Califf,et al.  Clinical significance of thrombocytopenia during a non-ST-elevation acute coronary syndrome. The platelet glycoprotein IIb/IIIa in unstable angina: receptor suppression using integrilin therapy (PURSUIT) trial experience. , 1999, Circulation.

[4]  C. Heeschen,et al.  Benefit of abciximab in patients with refractory unstable angina in relation to serum troponin T levels. c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) Study Investigators. , 1999, The New England journal of medicine.

[5]  Corrections: Benefit of Abciximab in Patients with Refractory Unstable Angina in Relation to Serum Troponin T Levels. , 1999, The New England journal of medicine.

[6]  S. Higano,et al.  Prevalence of coronary blood flow reserve abnormalities among patients with nonobstructive coronary artery disease and chest pain. , 1998, Mayo Clinic proceedings.

[7]  Inhibition of platelet glycoprotein IIb/IIIa with eptifibatide in patients with acute coronary syndromes. , 1998, The New England journal of medicine.

[8]  R. Harrington,et al.  Design and methodology of the PURSUIT trial: evaluating eptifibatide for acute ischemic coronary syndromes. Platelet Glycoprotein IIb-IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy. , 1997, The American journal of cardiology.

[9]  C. Cannon,et al.  The electrocardiogram predicts one-year outcome of patients with unstable angina and non-Q wave myocardial infarction: results of the TIMI III Registry ECG Ancillary Study. Thrombolysis in Myocardial Ischemia. , 1997, Journal of the American College of Cardiology.

[10]  S Wallenstein,et al.  Correlation of angiographic morphology and clinical presentation in unstable angina. , 1997, Journal of the American College of Cardiology.

[11]  M. Simoons A comparison of recombinant hirudin with heparin for the treatment of acute coronary syndromes. , 1996, The New England journal of medicine.

[12]  B. Nafe,et al.  Clinical predictors of unstable coronary lesion morphology. , 1995, European heart journal.

[13]  J. Kaski,et al.  Angiographic stenosis progression and coronary events in patients with 'stabilized' unstable angina. , 1995, Circulation.

[14]  E. Braunwald,et al.  Clinical and arteriographic characterization of patients with unstable angina without critical coronary arterial narrowing (from the TIMI-IIIA Trial). , 1994, The American journal of cardiology.

[15]  E. Braunwald,et al.  Relation between clinical presentation and angiographic findings in unstable angina pectoris, and comparison with that in stable angina. , 1993, The American journal of cardiology.

[16]  A. Takeshita,et al.  Evidence of impaired endothelium-dependent coronary vasodilatation in patients with angina pectoris and normal coronary angiograms. , 1993, The New England journal of medicine.

[17]  R. Califf,et al.  Answers to complex questions cannot be derived from “simple” trials , 1992, British heart journal.

[18]  K. Mizuno,et al.  Angioscopic evaluation of coronary-artery thrombi in acute coronary syndromes. , 1992, The New England journal of medicine.

[19]  V. Fuster,et al.  The pathogenesis of coronary artery disease and the acute coronary syndromes (2). , 1992, The New England journal of medicine.

[20]  P. Puddu,et al.  Angiographic morphology in unstable angina and its relation to transient myocardial ischemia and hospital outcome. , 1991, The American journal of cardiology.

[21]  P. Armstrong,et al.  Intracoronary thrombus and complex morphology in unstable angina. Relation to timing of angiography and in-hospital cardiac events. , 1989, Circulation.

[22]  P. Armstrong,et al.  Angiographic morphology in unstable angina pectoris. , 1988, The American journal of cardiology.

[23]  S. Ellis,et al.  Presentation and late outcome of myocardial infarction in the absence of angiographically significant coronary artery disease. , 1988, The American journal of cardiology.

[24]  A. Jaffe,et al.  Thrombolysis in myocardial infarction (TIMI) trial—Phase I: Hemorrhagic manifestations and changes in plasma fibrinogen and the fibrinolytic system in patients treated with recombinant tissue plasminogen activator and streptokinase , 1988 .

[25]  V. Fuster,et al.  Angiographic evolution of coronary artery morphology in unstable angina. , 1986, Journal of the American College of Cardiology.