Advertisement

Predictive value of coronary artery stenoses and C-reactive protein levels in patients with stable coronary artery disease

      Abstract

      Introduction and aims

      Coronary occlusions resulting in acute events often occur at the site of non-severe stenoses. We sought to assess the prognostic value of non-obstructive coronary stenoses and C-reactive protein (CRP) levels in patients with chronic stable angina (CSA).

      Methods

      We studied 790 consecutive patients with CSA who underwent routine coronary arteriography. High sensitivity CRP and coronary angiograms were assessed at study entry. Angiographic coronary disease severity was graded using a “vessel score” (number of coronary arteries showing at least 50% reduction in lumen diameter) and extent of disease with an “extension score” (proportion of the coronary artery tree showing angiographically detectable atheroma). Patients were followed up for 1 year.

      Results

      Significant left main stem disease was present in 54 patients (6.8%). 368 patients (46.6%) underwent revascularization. 71 patients (9%) had at least one of the events comprised in the combined study end-point (unstable angina, myocardial infarction (AMI) and cardiac death). Patients who suffered cardiac adverse events had a significantly higher vessel score (n) (2.0 [2.0–3.0] vs. 2.0 [1.0–2.0], P < 0.001), extension score (%) (23.5 [17–34.5] vs. 16.0 [6.0–27.0], P < 0.001) and CRP levels (mg/L) (3.0 [1.8–7.2] vs. 2.3 [1.1–4.7], P = 0.001) compared to patients without events. Age, previous history of AMI, vessel score, extension score and CRP levels were significantly associated with the study end-point. Multivariate analysis showed extension score (OR 5.3 [2.8–10.3] CI 95%; P < 0.001), revascularization (OR 0.26 [0.14–0.48] CI 95%; P < 0.001) and CRP levels (OR 1.9 [1.1–3.2] CI 95%; P = 0.03), but not vessel score (P = 0.1), to be independent predictors of the combined end-point.

      Conclusions

      In patients with CSA, independently of revascularization, extension score and CRP levels predict cardiac adverse events, regardless of the presence or absence of flow limiting coronary lesions.

      Keywords

      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Atherosclerosis
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      References

        • Humphries JO.
        • Kuller L.
        • Ross RS.
        • Friesinger GC.
        • Page EE.
        Natural history of ischemic heart disease in relation to arteriographic findings: a twelve year study of 224 patients.
        Circulation. 1974; 49: 489-497
        • Falk E.
        • Shah PK.
        • Fuster V.
        Coronary plaque disruption.
        Circulation. 1995; 92: 657-671
        • Kaski JC.
        • Chester MR.
        • Chen L.
        • Katritsis D.
        Rapid angiographic progression of coronary artery disease in patients with angina pectoris The role of complex stenosis morphology.
        Circulation. 1995; 92: 2058-2065
        • Fuster V.
        • Badimon L.
        • Badimon JJ.
        • Chesebro JH.
        The pathogenesis of coronary artery disease and the acute coronary syndromes (1).
        N Engl J Med. 1992; 326: 242-250
        • Katritsis D.
        • Korovesis S.
        • Giazitzoglou E.
        • et al.
        C-Reactive protein concentrations and angiographic characteristics of coronary lesions.
        Clin Chem. 2001; 47: 882-886
        • Zouridakis E.
        • Avanzas P.
        • Arroyo-Espliguero R.
        • Fredericks S.
        • Kaski JC.
        Markers of inflammation and rapid coronary artery disease progression in patients with stable angina pectoris.
        Circulation. 2004; 110: 1747-1753
      1. Ischaemic heart disease registers. Report of the fifth Working Group convened by the Regional Office for Europe of the World Health Organization. Copenhagen, April 1971. Regional Office for Europe. Geneva: World Health Organization. 1971.

        • Braunwald E.
        Unstable angina a classification.
        Circulation. 1989; 80: 410-414
        • Avanzas P.
        • Arroyo-Espliguero R.
        • Cosin-Sales J.
        • et al.
        Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes.
        Heart. 2004; 90: 847-852
        • Avanzas P.
        • Arroyo-Espliguero R.
        • Quiles J.
        • Roy D.
        • Kaski J.C.
        Elevated serum neopterin predicts future adverse cardiac events in patients with chronic stable angina pectoris.
        Eur Heart J. 2005; 26: 457-463
        • Sullivan D.R.
        • Marwick T.H.
        • Freedman S.B.
        A new method of scoring coronary angiograms to reflect extent of coronary atherosclerosis and improve correlation with major risk factors.
        Am Heart J. 1990; 119: 1262-1267
        • Davies MJ.
        Stability and instability: two faces of coronary atherosclerosis The Paul Dudley White Lecture 1995.
        Circulation. 1996; 94: 2013-2020
        • Yokoya K.
        • Takatsu H.
        • Suzuki T.
        • et al.
        Process of progression of coronary artery lesions from mild or moderate stenosis to moderate or severe stenosis: a study based on four serial coronary arteriograms per year.
        Circulation. 1999; 100: 903-909
        • Bigi R.
        • Cortigiani L.
        • Colombo P.
        • et al.
        Prognostic and clinical correlates of angiographically diffuse non-obstructive coronary lesions.
        Heart. 2003; 89: 1009-1013
        • Zebrack J.S.
        • Muhlestein J.B.
        • Horne B.D.
        • Anderson J.L.
        C-reactive protein and angiographic coronary artery disease: independent and additive predictors of risk in subjects with angina.
        J Am Coll Cardiol. 2002; 39: 632-637
        • Arroyo-Espliguero R.
        • Avanzas P.
        • Cosin-Sales J.
        • et al.
        C-reactive protein elevation and disease activity in patients with coronary artery disease.
        Eur Heart J. 2004; 25: 401-408
        • Palmerini T.
        • Marzocchi A.
        • Marrozzini C.
        • et al.
        Preoperative C-reactive protein levels predict 9-month mortality after coronary artery bypass grafting surgery for the treatment of left main coronary artery stenosis.
        Eur J Cardiothorac Surg. 2007; 31: 685-690
        • Bucher H.C.
        • Hengstler P.
        • Schindler C.
        • Guyatt G.H.
        Percutaneous transluminal coronary angioplasty versus medical treatment for non-acute coronary heart disease: meta-analysis of randomised controlled trials.
        BMJ. 2000; 321: 73-77
      2. RITA-2 trial participants. Coronary angioplasty versus medical therapy for angina: the second Randomised Intervention Treatment of Angina (RITA-2) trial. Lancet 1997; 350(9076):461–68.

        • Henderson RA.
        • Pocock SJ.
        • Clayton TC.
        • et al.
        Seven-year outcome in the RITA-2 trial: coronary angioplasty versus medical therapy.
        J Am Coll Cardiol. 2003; 42: 1161-1170
        • Hueb W.
        • Soares PR.
        • Gersh BJ.
        • et al.
        The medicine, angioplasty, or surgery study (MASS-II): a randomized, controlled clinical trial of three therapeutic strategies for multivessel coronary artery disease: one-year results.
        J Am Coll Cardiol. 2004; 43: 1743-1751
        • Cutlip DE.
        • Chhabra AG.
        • Baim DS.
        • et al.
        Beyond restenosis: five-year clinical outcomes from second-generation coronary stent trials.
        Circulation. 2004; 110: 1226-1230
        • Boden WE.
        • O’Rourke RA.
        • Teo KK.
        • et al.
        Optimal medical therapy with or without PCI for stable coronary disease.
        N Engl J Med. 2007; 356: 1503-1516
        • Ridker PM.
        • Cannon CP.
        • Morrow D.
        • et al.
        C-reactive protein levels and outcomes after statin therapy.
        N Engl J Med. 2005; 352: 20-28
        • Nissen SE.
        • Nicholls SJ.
        • Sipahi I.
        • et al.
        Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial.
        JAMA. 2006; 295: 1556-1565
        • Ridker PM.
        • Morrow DA.
        • Rose LM.
        • et al.
        Relative efficacy of atorvastatin 80 mg and pravastatin 40 mg in achieving the dual goals of low-density lipoprotein cholesterol <70 mg/dl and C-reactive protein <2 mg/l: an analysis of the PROVE-IT TIMI-22 trial.
        J Am Coll Cardiol. 2005; 45: 1644-1648
        • Wiviott SD.
        • Cannon CP.
        • Morrow DA.
        • et al.
        Can low-density lipoprotein be too low? The safety and efficacy of achieving very low low-density lipoprotein with intensive statin therapy: a PROVE IT-TIMI 22 substudy.
        J Am Coll Cardiol. 2005; 46: 1411-1416