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==The Spectrum of Acute Coronary Syndromes==
==The Spectrum of Acute Coronary Syndromes==


Unstable angina and non ST elevation MI are part of the spectrum of [[acute coronary syndrome]]s ([[ACS]]). [[ACS]] is a term that encompasses [[unstable angina]] ([[UA]]), [[non-ST-segment elevation myocardial infarction]] ([[NSTEMI]]) and [[ST-segment elevation myocardial infarction]] ([[STEMI]]).  All these underlying diseases result from an inadequate supply to meet the oxygen and metabolic demands of the [[myocardium]].  While all three usually result from [[atherosclerotic plaque rupture]] and subsequent [[thrombus|thrombus formation]] in one of the main epicardial coronary arteries, there are other possible etiologies of this imbalance such as coronary artery narrowing alone, coronary spasm, or coronary dissection. [[UA]], [[NSTEMI]] and [[STEMI]] are distinguished pathophysiologically as to whether or not the thrombus is occlusive (as in the case of [[STEMI]]) or non-occlusive (as in the case of [[UA]] and [[NSTEMI]]).  If an [[electrocardiogram]] ([[EKG]]) is performed at the time that an [[occlusive coronary artery thrombus]] is formed, it will usually show [[ST-segment elevation]] in the leads which correspond to the territory of [[myocardium]] in which blood supply has been disrupted (see [[STEMI]]).  If an EKG is performed at the time that a [[non-occlusive thrombus]] is formed, it may or may not show signs of [[ischemia]]. <ref name="Anderson"> Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE II, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non–ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction).'' Circulation 2007 116: e148 – e304. PMID 17679616</ref> <ref name="Anderson2"> Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE II, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS. Correction of ACC/AHA 2007 guidelines for the management of patients with unstable angina/non–ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction).'' J Am Coll Cardiol. 2008 Mar 4; 51(9): 974. PMID 17692738 </ref>  
Unstable angina and non ST elevation MI are part of the spectrum of [[acute coronary syndrome]]s ([[ACS]]). [[ACS]] is a term that encompasses [[unstable angina]] ([[UA]]), [[non-ST-segment elevation myocardial infarction]] ([[NSTEMI]]) and [[ST-segment elevation myocardial infarction]] ([[STEMI]]).  All these underlying diseases result from an inadequate supply to meet the oxygen and metabolic demands of the [[myocardium]].  While all three usually result from [[atherosclerotic plaque rupture]] and subsequent [[thrombus|thrombus formation]] in one of the main epicardial coronary arteries, there are other possible etiologies of this imbalance such as coronary artery narrowing alone, coronary spasm, or coronary dissection. [[UA]], [[NSTEMI]] and [[STEMI]] are distinguished pathophysiologically as to whether or not the thrombus is occlusive (as in the case of [[STEMI]]) or non-occlusive (as in the case of [[UA]] and [[NSTEMI]]).  If an [[electrocardiogram]] ([[EKG]]) is performed at the time that an [[occlusive coronary artery thrombus]] is formed, it will usually show [[ST-segment elevation]] in the leads which correspond to the territory of [[myocardium]] in which blood supply has been disrupted (see [[STEMI]]).  If an EKG is performed at the time that a [[non-occlusive thrombus]] is formed, it may or may not show signs of [[ischemia]]. Frequently, Unstable Angina and NSTEMI are indistinguishable on inital evaluation as these two conditions are at different spectrums of ischemia.  If the ischemia is significant to cause myocardial damage, there will be an elevation of Cardiac biomarkers ([[CK-MB]] or [[troponin]]) and would be classified as an NSTEMI.  Often, these may not be detected for up to 12 hours in the bloodstream, which emphasizes the need for thorough evaluation., <ref name="Anderson"> Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE II, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non–ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction).'' Circulation 2007 116: e148 – e304. PMID 17679616</ref> <ref name="Anderson2"> Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE II, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS. Correction of ACC/AHA 2007 guidelines for the management of patients with unstable angina/non–ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction).'' J Am Coll Cardiol. 2008 Mar 4; 51(9): 974. PMID 17692738 </ref>  


==Definition of Non ST Elevation MI==
==Definition of Non ST Elevation MI==

Revision as of 15:03, 20 August 2009

Unstable angina pectoris
Plaque rupture in a coronary artery at arrows yielding obstructive thrombus in red.
Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology
ICD-10 I20
ICD-9 413
DiseasesDB 8695
eMedicine med/133 
MeSH D000787

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Synonyms and related keywords: progressive angina, crescendo angina, accelerating angina, new-onset angina, pre-infarction angina, unstable angina pectoris, UAP, UA

The Spectrum of Acute Coronary Syndromes

Unstable angina and non ST elevation MI are part of the spectrum of acute coronary syndromes (ACS). ACS is a term that encompasses unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). All these underlying diseases result from an inadequate supply to meet the oxygen and metabolic demands of the myocardium. While all three usually result from atherosclerotic plaque rupture and subsequent thrombus formation in one of the main epicardial coronary arteries, there are other possible etiologies of this imbalance such as coronary artery narrowing alone, coronary spasm, or coronary dissection. UA, NSTEMI and STEMI are distinguished pathophysiologically as to whether or not the thrombus is occlusive (as in the case of STEMI) or non-occlusive (as in the case of UA and NSTEMI). If an electrocardiogram (EKG) is performed at the time that an occlusive coronary artery thrombus is formed, it will usually show ST-segment elevation in the leads which correspond to the territory of myocardium in which blood supply has been disrupted (see STEMI). If an EKG is performed at the time that a non-occlusive thrombus is formed, it may or may not show signs of ischemia. Frequently, Unstable Angina and NSTEMI are indistinguishable on inital evaluation as these two conditions are at different spectrums of ischemia. If the ischemia is significant to cause myocardial damage, there will be an elevation of Cardiac biomarkers (CK-MB or troponin) and would be classified as an NSTEMI. Often, these may not be detected for up to 12 hours in the bloodstream, which emphasizes the need for thorough evaluation., [1] [2]

Definition of Non ST Elevation MI

UA and NSTEMI are differentiated from each other based upon whether there are elevated serum levels of cardiac biomarkers (i.e., creatine kinase (CK), MB isoenzyme of CK (CK-MB) and Troponins I and T). Elevated cardiac biomarkers are present in NSTEMI but not in UA. However, it is important to note that although troponins are fairly sensitive and specific for myocardial necrosis, the diagnosis of NSTEMI should not be made based on laboratory findings alone, as there are other possible etiologies for elevated troponins. [1] [2] For the diagnosis of non ST elevation MI to be made, the troponin elevation must occur in the context of ischemic chest pain.

Definition of Unstable Angina Pectoris

Unstable angina pectoris is chest pain which is ischemic in origin and either occurrs more frequently, lasts longer, and/or manifests with lesser degrees of exertion than stable angina. It can occur at rest and/or at night. Unlike ST elevation MI (STEMI) or non ST elevation MI (NSTEMI), there no sign of myocardial necrosis and there is no release of biomarkers of myonecrosis (CK or troponin) in unstable angina pectoris. [3] [4] [5] [6] [7] [8] [9] [10] [11] [1] [2] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32] [33] [34] [35] [36] [37] [38] [39] [40] [41] [42] [43] [44] [45] [46] [47] [48] [49] [50] [51] [52] [53] [54] [55] [56] [57] [58] [59] [60] [61] [62] [63] [64] [65] [66] [67] [68] [69] [70] [71] [72] [73] [74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86] [87] [88] [89] [90] [91] [92] [93] [94] Angina pectoris is classified as stable when its characteristics are unchanged for 60 days. Stable angina pectoris usually responds to sublingual nitroglycerin or rest. Unstable angina may occur at rest and may be unrelieved by rest.

References

  1. ↑ 1.0 1.1 1.2 Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE II, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non–ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction). Circulation 2007 116: e148 – e304. PMID 17679616
  2. ↑ 2.0 2.1 2.2 Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE II, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS. Correction of ACC/AHA 2007 guidelines for the management of patients with unstable angina/non–ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction). J Am Coll Cardiol. 2008 Mar 4; 51(9): 974. PMID 17692738
  3. ↑ Ambrose JA, Winters SL, Stern A, et al: Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol 1985 Mar; 5(3): 609-16. PMID 3973257
  4. ↑ Crea F, Biasucci LM, Buffon A, Liuzzo G, Monaco C, Caligiuri G, et al. Role of inflammation in the pathogenesis of unstable coronary artery disease. Am J Cardiol 1997; 80: 10-6E. PMID 9296463
  5. ↑ Biasucci LM, Colizzi C, Rizzello V, Vitrella G, Crea F, Liuzzo G. Role of inflammation in the pathogenesis of unstable coronary artery diseases. Scand J Clin Lab Invest Suppl 1999; 230: 12-22 PMID 10389197
  6. ↑ Asher CR, Topol EJ, Moliterno DJ, et al: Insights into the pathophysiology of atherosclerosis and prognosis of black Americans with acute coronary syndromes. Am Heart J 1999 Dec; 138(6 Pt 1): 1073-81 PMID 10577437
  7. ↑ Fuster V, Moreno PR, Fayad ZA, Corti R, Badimon JJ. Atherothrombosis and high-risk plaque: part I: evolving concepts. J Am Coll Cardiol. 2005 Sep 20;46(6):937-54. PMID 16168274
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  14. ↑ Ryan JW, Peterson ED, Chen AY, et al: Optimal timing of intervention in non-ST-segment elevation acute coronary syndromes: Insights from the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines) Registry. Circulation 2005; 112:3049-3057. PMID 16275863
  15. ↑ Prinzmetal M, Kennamer R, Merliss R, et al: A variant form of angina pectoris. Am J Med 1959; 27:375. PMID 14434946
  16. ↑ 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; 102:1101-1106. PMID 10973837
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  39. ↑ Neumann FJ, Kastrati A, Pogatsa-Murray G, et al: Evaluation of prolonged antithrombotic pretreatment (“cooling-off” strategy) before intervention in patients with unstable coronary syndromes: A randomized controlled trial. JAMA 2003; 290:1593-1599. PMID 14506118
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  41. ↑ Wiviott SD, Antman EM, Gibson CM, et al: Evaluation of prasugrel compared with clopidogrel in patients with acute coronary syndromes: Design and rationale for the TRial to assess Improvement in Therapeutic Outcomes by optimizing platelet InhibitioN with prasugrel Thrombolysis In Myocardial Infarction 38 (TRITON-TIMI 38). Am Heart J 2006; 152:627-635. PMID 16996826
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  55. ↑ Fox KA, Poole-Wilson PA, Henderson RA, et al: Interventional versus conservative treatment for patients with unstable angina or non-ST-elevation myocardial infarction: The British Heart Foundation RITA 3 randomised trial. Randomized Intervention Trial of unstable Angina. Lancet 2002; 360:743-751. PMID 12241831
  56. ↑ Fox KAA, Poole-Wilson P, Clayton TC, et al: 5-Year outcome of an interventional strategy in non-ST-elevation acute coronary syndrome: The British Heart Foundation RITA 3 randomised trial. Lancet 2005; 366:914-920. PMID 16154018
  57. ↑ van't Hof AW, de Vries ST, Dambrink JH, et al: A comparison of two invasive strategies in patients with non-ST elevation acute coronary syndromes: Results of the Early or Late Intervention in unStable Angina (ELISA) pilot study. 2b/3a upstream therapy and acute coronary syndromes. Eur Heart J 2003; 24:1401-1405. PMID 12909068
  58. ↑ McCullough PA, Gibson CM, DiBattiste PM, et al: Timing of angiography and revascularization in acute coronary syndromes: An analysis from the TACTICS-TIMI 18 trial. J Interv Cardiol 2004;81-86. PMID 15104769
  59. ↑ Ryan JW, Peterson ED, Chen AY, et al: Optimal timing of intervention in non-ST-segment elevation acute coronary syndromes: Insights from the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines) Registry. Circulation 2005; 112:3049-3057. PMID 16275863
  60. ↑ Tonkin AM, Colquhoun D, Emberson J, et al: Effects of pravastatin in 3260 patients with unstable angina: Results from the LIPID study. Lancet 2000; 356: 1871-1875. PMID 11130382
  61. ↑ Scirica BM, Cannon CP, Gibson CM, et al: Assessing the effect of publication of clinical guidelines on the management of unstable angina and non-ST-elevation myocardial infarction in the TIMI III (1990-93) and the GUARANTEE (1995-96) registries. Crit Path Cardiol 2002; 1:151-160. PMID 18340298
  62. ↑ Giugliano RP, Lloyd-Jones DM, Camargo Jr. CA, et al: Association of unstable angina guideline care with improved survival. Arch Intern Med 2000; 160:1775-1780. PMID 10871970
  63. ↑ Roe MT, Peterson ED, Newby LK, et al: The influence of risk status on guideline adherence for patients with non-ST-segment elevation acute coronary syndromes. Am Heart J 2006; 151:1205-1213. PMID 16781220
  64. ↑ Sueda S, Kohno H, Fukuda H, Uraoka T: Did the widespread use of long-acting calcium antagonists decrease the occurrence of variant angina?. Chest 2003; 124:2074-2078. PMID 14665482
  65. ↑ Mayer S, Hillis LD: Prinzmetal's variant angina. Clin Cardiol 1998; 21:243-246. PMID 9562933
  66. ↑ Okumura K, Osanai T, Kosugi T, et al: Enhanced phospholipase C activity in the cultured skin fibroblast obtained from patients with coronary spastic angina: Possible role for enhanced vasoconstrictor response. J Am Coll Cardiol 2000; 36:1847-1852. PMID 11092655
  67. ↑ Hung MJ, Cherng WJ, Yang NI, et al: Relation of high-sensitivity C-reactive protein level with coronary vasospastic angina pectoris in patients without hemodynamically significant coronary artery disease. Am J Cardiol 2005; 96:1484-1490. PMID 16310426
  68. ↑ Park JS, Zhang SY, Jo SH, et al: Common adrenergic receptor polymorphisms as novel risk factors for vasospastic angina. Am Heart J 2006; 151:864-869 PMID 16569551
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  71. ↑ Onaka H, Hirota Y, Shimada S, et al: Clinical observation of spontaneous anginal attacks and multivessel spasm in variant angina pectoris with normal coronary arteries: Evaluation by 24-hour 12-lead electrocardiography with computer analysis. J Am Coll Cardiol 1996; 27:38-44. PMID 8522708
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