Classification of unstable angina and non-ST elevation myocardial infarction
- Michael Simons, MD
Michael Simons, MD
- Robert W Berliner Professor of Medicine
- Yale University School of Medicine
The non-ST elevation acute coronary syndromes (ACS; unstable angina [UA] and non-ST elevation [non-Q wave] myocardial infarction [NSTEMI]) occur in a variety of clinical settings. The definitions of and classification systems for UA and NSTEMI and their use to assess risk will be reviewed here. Issues related to the evaluation, treatment, and risk stratification of patients with non-ST elevation ACS are discussed separately. (See "Overview of the acute management of non-ST elevation acute coronary syndromes" and "Risk stratification after non-ST elevation acute coronary syndrome".)
Both UA and NSTEMI, as well as ST elevation MI, are associated with unstable coronary lesions and plaque rupture. (See "The role of the vulnerable plaque in acute coronary syndromes".)
Unstable angina (UA) and non-ST elevation (non-Q wave) myocardial infarction (NSTEMI) differ primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury. Unstable angina is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponin, with or without ECG changes indicative of ischemia (eg, ST segment depression or transient elevation or new T wave inversion). Since an elevation in troponin may not be detectable for up to 12 hours after presentation, UA and NSTEMI are frequently indistinguishable at initial evaluation. ST segment and/or T wave changes are often persistent in NSTEMI while, if they occur in UA, they are usually transient. (See "Troponin testing: Clinical use".)
It should be kept in mind that the sensitivity of the biomarker test (usually troponin) used to evaluate patients with ACS determines whether a patient is labeled as having UA or NSTEMI. With the development of increasingly more sensitive troponins, it can be anticipated that the percent of patient with UA will decrease and the percent with NSTEMI will increase .
The 2012 joint task force of the European Society of Cardiology (ESC), American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), and the World Health Federation (WHF) defined MI (in pathologic terms) as myocardial cell death due to prolonged ischemia . (See "Criteria for the diagnosis of acute myocardial infarction", section on 'Third universal definition of MI'.)To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
- Braunwald E, Morrow DA. Unstable angina: is it time for a requiem? Circulation 2013; 127:2452.
- Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circulation 2012; 126:2020.
- Braunwald E. Unstable angina. A classification. Circulation 1989; 80:410.
- Patel DJ, Gomma AH, Knight CJ, et al. Why is recurrent myocardial ischaemia a predictor of adverse outcome in unstable angina? An observational study of myocardial ischaemia and its relation to coronary anatomy. Eur Heart J 2001; 22:1991.
- Bosch X, Théroux P, Waters DD, et al. Early postinfarction ischemia: clinical, angiographic, and prognostic significance. Circulation 1987; 75:988.
- Schuster EH, Bulkley BH. Early post-infarction angina. Ischemia at a distance and ischemia in the infarct zone. N Engl J Med 1981; 305:1101.
- GISSI-3 APPI Study Group. Early and six-month outcome in patients with angina pectoris early after acute myocardial infarction (the GISSI-3 APPI [angina precoce post-infarto] study). Am J Cardiol 1996; 78:1191.
- Armstrong PW, Fu Y, Chang WC, et al. Acute coronary syndromes in the GUSTO-IIb trial: prognostic insights and impact of recurrent ischemia. The GUSTO-IIb Investigators. Circulation 1998; 98:1860.
- Betriu A, Califf RM, Bosch X, et al. Recurrent ischemia after thrombolysis: importance of associated clinical findings. GUSTO-I Investigators. Global Utilization of Streptokinase and t-PA [tissue-plasminogen activator] for Occluded Coronary Arteries. J Am Coll Cardiol 1998; 31:94.
- Robbins MA, Marso SP, Wolski K, et al. Chest pain--a strong predictor of adverse cardiac events following precutaneous intervention (from the Evaluation of Platelet IIb/IIIa Inhibitor for Stenting Trial [EPISENT])]. Am J Cardiol 1999; 84:1350.
- Kini AS, Lee P, Mitre CA, et al. Postprocedure chest pain after coronary stenting: implications on clinical restenosis. J Am Coll Cardiol 2003; 41:33.
- Jeremias A, Kutscher S, Haude M, et al. Nonischemic chest pain induced by coronary interventions: a prospective study comparing coronary angioplasty and stent implantation. Circulation 1998; 98:2656.
- Labinaz M, Kilaru R, Pieper K, et al. Outcomes of patients with acute coronary syndromes and prior coronary artery bypass grafting: results from the platelet glycoprotein IIb/IIIa in unstable angina: receptor suppression using integrilin therapy (PURSUIT) trial. Circulation 2002; 105:322.
- Kleiman NS, Anderson HV, Rogers WJ, et al. Comparison of outcome of patients with unstable angina and non-Q-wave acute myocardial infarction with and without prior coronary artery bypass grafting (Thrombolysis in Myocardial Ischemia III Registry). Am J Cardiol 1996; 77:227.
- Chen L, Théroux P, Lespérance J, et al. Angiographic features of vein grafts versus ungrafted coronary arteries in patients with unstable angina and previous bypass surgery. J Am Coll Cardiol 1996; 28:1493.
- Chandrasekar B, Bourassa MG. Incidence and risk factors predictive of unstable angina resulting from restenosis after percutaneous angioplasty of saphenous vein grafts. Am Heart J 2000; 140:827.
- Bugiardini R, Manfrini O, De Ferrari GM. Unanswered questions for management of acute coronary syndrome: risk stratification of patients with minimal disease or normal findings on coronary angiography. Arch Intern Med 2006; 166:1391.
- Diver DJ, Bier JD, Ferreira PE, et al. Clinical and arteriographic characterization of patients with unstable angina without critical coronary arterial narrowing (from the TIMI-IIIA Trial). Am J Cardiol 1994; 74:531.
- Roe MT, Harrington RA, Prosper DM, et al. Clinical and therapeutic profile of patients presenting with acute coronary syndromes who do not have significant coronary artery disease.The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) Trial Investigators. Circulation 2000; 102:1101.
- Invasive compared with non-invasive treatment in unstable coronary-artery disease: FRISC II prospective randomised multicentre study. FRagmin and Fast Revascularisation during InStability in Coronary artery disease Investigators. Lancet 1999; 354:708.
- Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med 2001; 344:1879.
- Glaser R, Herrmann HC, Murphy SA, et al. Benefit of an early invasive management strategy in women with acute coronary syndromes. JAMA 2002; 288:3124.
- Patel MR, Chen AY, Peterson ED, et al. Prevalence, predictors, and outcomes of patients with non-ST-segment elevation myocardial infarction and insignificant coronary artery disease: results from the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA Guidelines (CRUSADE) initiative. Am Heart J 2006; 152:641.
- Hamm CW, Braunwald E. A classification of unstable angina revisited. Circulation 2000; 102:118.
- Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA 2000; 284:835.
- Diderholm E, Andrén B, Frostfeldt G, et al. The prognostic and therapeutic implications of increased troponin T levels and ST depression in unstable coronary artery disease: the FRISC II invasive troponin T electrocardiogram substudy. Am Heart J 2002; 143:760.
- Califf RM, Abdelmeguid AE, Kuntz RE, et al. Myonecrosis after revascularization procedures. J Am Coll Cardiol 1998; 31:241.
- Cutlip DE, Leon MB, Ho KK, et al. Acute and nine-month clinical outcomes after "suboptimal" coronary stenting: results from the STent Anti-thrombotic Regimen Study (STARS) registry. J Am Coll Cardiol 1999; 34:698.
- Steinhubl SR, Lauer MS, Mukherjee DP, et al. The duration of pretreatment with ticlopidine prior to stenting is associated with the risk of procedure-related non-Q-wave myocardial infarctions. J Am Coll Cardiol 1998; 32:1366.
- Mehran R, Dangas G, Mintz GS, et al. Atherosclerotic plaque burden and CK-MB enzyme elevation after coronary interventions : intravascular ultrasound study of 2256 patients. Circulation 2000; 101:604.
- Shyu KG, Kuan PL, Cheng JJ, Hung CR. Cardiac troponin T, creatine kinase, and its isoform release after successful percutaneous transluminal coronary angioplasty with or without stenting. Am Heart J 1998; 135:862.
- Fuchs S, Kornowski R, Mehran R, et al. Prognostic value of cardiac troponin-I levels following catheter-based coronary interventions. Am J Cardiol 2000; 85:1077.
- Akkerhuis KM, Alexander JH, Tardiff BE, et al. Minor myocardial damage and prognosis: are spontaneous and percutaneous coronary intervention-related events different? Circulation 2002; 105:554.
- Ricciardi MJ, Wu E, Davidson CJ, et al. Visualization of discrete microinfarction after percutaneous coronary intervention associated with mild creatine kinase-MB elevation. Circulation 2001; 103:2780.
- Gibson CM, Murphy SA, Marble SJ, et al. Relationship of creatine kinase-myocardial band release to Thrombolysis in Myocardial Infarction perfusion grade after intracoronary stent placement: an ESPRIT substudy. Am Heart J 2002; 143:106.
- Brener SJ, Lytle BW, Schneider JP, et al. Association between CK-MB elevation after percutaneous or surgical revascularization and three-year mortality. J Am Coll Cardiol 2002; 40:1961.
- Ahmed WH, Bittl JA, Braunwald E. Relation between clinical presentation and angiographic findings in unstable angina pectoris, and comparison with that in stable angina. Am J Cardiol 1993; 72:544.
- De Servi S, Arbustini E, Marsico F, et al. Correlation between clinical and morphologic findings in unstable angina. Am J Cardiol 1996; 77:128.
- Dangas G, Mehran R, Wallenstein S, et al. Correlation of angiographic morphology and clinical presentation in unstable angina. J Am Coll Cardiol 1997; 29:519.
- van Miltenburg-van Zijl AJ, Simoons ML, Veerhoek RJ, Bossuyt PM. Incidence and follow-up of Braunwald subgroups in unstable angina pectoris. J Am Coll Cardiol 1995; 25:1286.
- Calvin JE, Klein LW, VandenBerg BJ, et al. Risk stratification in unstable angina. Prospective validation of the Braunwald classification. JAMA 1995; 273:136.
- Heeschen C, van Den Brand MJ, Hamm CW, Simoons ML. Angiographic findings in patients with refractory unstable angina according to troponin T status. Circulation 1999; 100:1509.
- CLASSIFICATION OF UNSTABLE ANGINA
- New onset angina
- Rest angina
- Early post-MI angina
- Postrevascularization angina
- - Periprocedural
- - Late
- Absence of significant coronary disease
- CLASSIFICATION OF NSTEMI
- ST segment changes
- After PCI
- After CABG
- PROGNOSIS ACCORDING TO TYPE
- INFORMATION FOR PATIENTS