Unstable angina non ST elevation myocardial infarction overview: Difference between revisions

Jump to navigation Jump to search
← Older editNewer edit →
VisualWikitext
Smitakohli (talk | contribs)
284 edits
No edit summary
Smitakohli (talk | contribs)
284 edits
No edit summary
Line 48: Line 48:
*Increasing angina-previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (i.e., increased by 1 or more CCS class to at least CCS class III severity)
*Increasing angina-previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (i.e., increased by 1 or more CCS class to at least CCS class III severity)


[[NSTEMI]] generally presents as prolonged, more intense rest angina or angina equivalent. Patients with suspected ACS must be evaluated rapidly. Evaluation should not be done over the phone but in person and in a place where a 12 lead ECG can be obtained. A focused history, examination and ECG are helpful to determine where the patient will be managed and whether the patient needs to be transferred or referred to a different hospital/setting.
[[NSTEMI]] generally presents as prolonged, more intense rest angina or angina equivalent. Patients with suspected ACS must be evaluated rapidly. Evaluation should not be done over the phone but in person and in a place where a 12 lead ECG can be obtained. A focused history, examination and ECG are helpful to determine where the patient will be managed and whether the patient needs to be transferred or referred to a different hospital/setting. Physical examination should focus on identifying the precipitating factors, comorbid conditions, rule out alternative diagnosis and assess hemodynamic status of the patient.


==Risk stratification==
==Risk stratification==
Early risk stratification is recommended and is based on the initial history, physical exam, ECG, assessment of renal function and cardiac biomarkers. Various models to calculate risk score and determine prognosis are available for example TIMI score, GRACE risk score etc. This evaluation is helpful in selecting the site of care and type of therapy.  
Early risk stratification is recommended and is based on the initial history, physical exam, ECG, assessment of renal function and cardiac biomarkers. Various models to calculate risk score and determine prognosis are available for example TIMI score, PURSUIT risk model, GRACE risk score etc. This evaluation is helpful in selecting the site of care and type of therapy. Physician should document their opinion of the likelihood of [[ACS]] in either low, intermediate or high likelihood.


==Treatment==
==Treatment==

Revision as of 16:31, 19 November 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

Template:Search infobox

Cardiology Network

Discuss Unstable angina non ST elevation myocardial infarction overview further in the WikiDoc Cardiology Network
Adult Congenital
Biomarkers
Cardiac Rehabilitation
Congestive Heart Failure
CT Angiography
Echocardiography
Electrophysiology
Cardiology General
Genetics
Health Economics
Hypertension
Interventional Cardiology
MRI
Nuclear Cardiology
Peripheral Arterial Disease
Prevention
Public Policy
Pulmonary Embolism
Stable Angina
Valvular Heart Disease
Vascular Medicine

Template:WikiDoc Cardiology News Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Associate Editor-In-Chief: Neil Gheewala, M.D. [3]

Please Join in Editing This Page and Apply to be an Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [4] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

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.

Pathophysiology

The most common cause of UA/NSTEMI is reduced myocardial perfusion that results from coronary artery narrowing caused by a thrombus that developed on a disrupted atherosclerotic plaque and is usually nonocclusive. The most common underlying molecular and cellular pathophysiology of disrupted atherosclerotic plaque is arterial inflammation which activates the macrophages and T lymphocytes located at the shoulder of a plaque increase the expression of enzymes such as metalloproteinases that cause thinning and disruption of the plaque, which in turn can lead to UA/NSTEMI. An occlusive thombus or plaque can also cause this syndrome in the presence of extensive collateral supply. Secondary UA can occur in conditions that increase myocardial oxygen requirements(such as fever, tachycardia or thyrotoxicosis), reduce coronary blood flow(such as hypotension) or reduce myocardial oxygen delivery(such as anemia or hypoxemia).

Presentation and Diagnosis

UA can have typical or atypical presentations. the 3 classic forms of presentation are

  • Rest angina(angina commencing when the patient is at rest)
  • New onset (less than 2 months) severe angina(at least CCS class II),or
  • Increasing angina-previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (i.e., increased by 1 or more CCS class to at least CCS class III severity)

NSTEMI generally presents as prolonged, more intense rest angina or angina equivalent. Patients with suspected ACS must be evaluated rapidly. Evaluation should not be done over the phone but in person and in a place where a 12 lead ECG can be obtained. A focused history, examination and ECG are helpful to determine where the patient will be managed and whether the patient needs to be transferred or referred to a different hospital/setting. Physical examination should focus on identifying the precipitating factors, comorbid conditions, rule out alternative diagnosis and assess hemodynamic status of the patient.

Risk stratification

Early risk stratification is recommended and is based on the initial history, physical exam, ECG, assessment of renal function and cardiac biomarkers. Various models to calculate risk score and determine prognosis are available for example TIMI score, PURSUIT risk model, GRACE risk score etc. This evaluation is helpful in selecting the site of care and type of therapy. Physician should document their opinion of the likelihood of ACS in either low, intermediate or high likelihood.

Treatment

Discharge care

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
  8. ↑ Braunwald E: Unstable angina: A classification. Circulation 1989; 80: 410-414. PMID 2752565
  9. ↑ Scirica BM, Cannon CP, McCabe CH, et al: Prognosis in the Thrombolysis in Myocardial Ischemia III Registry according to the Braunwald unstable angina pectoris classification. Am J Cardiol 2002; 90: 821-826.PMID 12372567
  10. ↑ Davies MJ: The composition of coronary-artery plaques. N Engl J Med 1997; 336:1312-1314. PMID 9113937
  11. ↑ Kennon S, Price CP, Mills PG, et al: The central role of platelet activation in determining the severity of acute coronary syndromes. Heart 2003; 89:1253-1254. PMID 12975438
  12. ↑ Kaski JC: Rapid coronary artery disease progression and angiographic stenosis morphology. Ital Heart J 2000; 1:21-25. PMID 10868918
  13. ↑ 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
  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
  17. ↑ Lindahl B, Diderholm E, Lagerqvist B, et al: Mechanisms behind the prognostic value of troponin T in unstable coronary artery disease: A FRISC II substudy. J Am Coll Cardiol 2001; 38:979-986. PMID 11583868
  18. ↑ Roffi M, Chew DP, Mukherjee D, et al: Platelet glycoprotein IIb/IIIa inhibitors reduce mortality in diabetic patients with non-ST-segment-elevation acute coronary syndromes. Circulation 2001; 104:2767-2771. PMID 11733392
  19. ↑ Westerhout CM, Fu Y, Lauer MS, et al: Short- and long-term risk stratification in acute coronary syndromes: The added value of quantitative ST-segment depression and multiple biomarkers. J Am Coll Cardiol 2006; 48:939-947. PMID 16949483
  20. ↑ Heeschen C, Hamm CW, Bruemmer J, Simoons ML, for the Chimeric c7E3 AntiPlatelet Therapy in Unstable angina REfractory to standard treatment trial (CAPTURE) Investigators : Predictive value of C-reactive protein and troponin T in patients with unstable angina: A comparative analysis. J Am Coll Cardiol 2000; 35:1535-1542. PMID 10807457
  21. ↑ Lindmark E, Diderholm E, Wallentin L, Siegbahn A: Relationship between interleukin 6 and mortality in patients with unstable coronary artery disease: Effects of an early invasive or noninvasive strategy. JAMA 2001; 286:2107-2113. PMID 11694151
  22. ↑ Sherman CT, Litvack F, Grundfest W, Lee M, Hickey A, Chaux A, Kass R, Blanche C, Matloff J, Morgenstern L, Ganz W, Swan HJC, Forrester J (1986) Coronary angioscopy in patients with unstable angina pectoris. PMID 3489893
  23. ↑ Zairis MN, Papadaki OA, Manousakis SJ, et al: C-reactive protein and multiple complex coronary artery plaques in patients with primary unstable angina. Atherosclerosis 2002; 164:355-359. PMID 12204808
  24. ↑ Mueller C, Neumann FJ, Roskamm H, et al: Women do have an improved long-term outcome after non-ST-elevation acute coronary syndromes treated very early and predominantly with percutaneous coronary intervention: A prospective study in 1450 consecutive patients. J Am Coll Cardiol 2002; 40:245-250. PMID 12106927
  25. ↑ Brennan ML, Penn MS, Van Lente F, et al: Prognostic value of myeloperoxidase in patients with chest pain. N Engl J Med 2003; 349:1595-1604. PMID 14573731
  26. ↑ Buffon A, Biasucci LM, Liuzzo G, et al: Widespread coronary inflammation in unstable angina. N Engl J Med 2002; 347:5-12. PMID 12097534
  27. ↑ Gibson CM, Pinto DS, Murphy SA, et al: Association of creatinine and creatinine clearance on presentation in acute myocardial infarction with subsequent mortality. J Am Coll Cardiol 2003; 42:1535-1543. PMID 14607434
  28. ↑ Boersma E, Pieper KS, Steyerberg EW, et al: Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. Circulation 2000; 101:2557-2567. PMID 10840005
  29. ↑ 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; 284:835-842. PMID 10938172
  30. ↑ Granger CB, Goldberg RJ, Dabbous O, et al: Predictors of hospital mortality in the global registry of acute coronary events. Arch Intern Med 2003; 163:2345-2353. PMID 14581255
  31. ↑ Gottlieb SO, Weisfeldt ML, Ouyang P, et al: Effect of the addition of propranolol to therapy with nifedipine for unstable angina: A randomized, double-blind, placebo-controlled trial. Circulation 1986; 73:331-337. PMID 3510764
  32. ↑ The Holland Interuniversity Nifedipine/Metoprolol Trial (HINT) Research Group : Early treatment of unstable angina in the coronary care unit: A randomised, double blind, placebo controlled comparison of recurrent ischaemia in patients treated with nifedipine or metoprolol or both. Br Heart J 1986; 56:400-413. PMID 2878675
  33. ↑ Theroux P, Ouimet H, McCans J, et al: Aspirin, heparin or both to treat unstable angina. N Engl J Med 1988; 319: 1105-1111.1998 PMID 3050522
  34. ↑ Topol EJ, Easton D, Harrington RA, et al: Randomized, double-blind, placebo-controlled, international trial of the oral IIb/IIIa antagonist lotrafiban in coronary and cerebrovascular disease. Circulation 2003; 108:` 399-406. PMID 12874182
  35. ↑ Peters RJ, Mehta SR, Fox KA, et al: Effects of aspirin dose when used alone or in combination with clopidogrel in patients with acute coronary syndromes: Observations from the Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) study. Circulation 2003; 108:1682-1687. PMID 14504182
  36. ↑ Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial Investigators : Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001; 345:494-502. PMID 11519503
  37. ↑ Yusuf S, Mehta SR, Zhao F, et al: Early and late effects of clopidogrel in patients with acute coronary syndromes. Circulation 2003; 107:966-972. PMID 12600908
  38. ↑ Montalescot G, Sideris G, Meuleman C, et al: A randomized comparison of high clopidogrel loading doses in patients with non-ST-segment elevation acute coronary syndromes: The ALBION (Assessment of the Best Loading Dose of Clopidogrel to Blunt Platelet Activation, Inflammation, and Ongoing Necrosis) trial. J Am Coll Cardiol 2006; 48:931-938. PMID 16949482
  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
  40. ↑ Patti G, Colonna G, Pasceri V, et al: Randomized trial of high loading dose of clopidogrel for reduction of periprocedural myocardial infarction in patients undergoing coronary intervention: Results from the ARMYDA-2 (Antiplatelet therapy for Reduction of MYocardial Damage during Angioplasty) study. Circulation 2005; 111:2099-2106. PMID 15750189
  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
  42. ↑ Giugliano RP, Newby LK, Harrington RA, et al: The early glycoprotein IIb/IIIa inhibition in non-ST-segment elevation acute coronary syndrome (EARLY ACS) trial: A randomized placebo-controlled trial evaluating the clinical benefits of early front-loaded eptifibatide in the treatment of patients with non-ST-segment elevation acute coronary syndrome—study design and rationale. Am Heart J 2005; 149:994-1002. PMID 15976780
  43. ↑ Eikelboom JW, Anand SS, Malmberg K, et al: Unfractionated heparin and low-molecular-weight heparin in acute coronary syndrome without ST elevation: A meta-analysis. Lancet 2000; 355:1936-1942. PMID 10859038
  44. ↑ Rich JD, Maraganore JM, Young E, et al: Heparin resistance in acute coronary syndromes. J Thromb Thrombolysis 2007; 23:93-100. PMID 17221324
  45. ↑ Warkentin TE, Kelton JG: Temporal aspects of heparin-induced thrombocytopenia. N Engl J Med 2001; 344:1286-1292 PMID 11320387
  46. ↑ Petersen JL, Mahaffey KW, Hasselblad V, et al: Efficacy and bleeding complications among patients randomized to enoxaparin or unfractionated heparin for antithrombin therapy in non-ST-segment elevation acute coronary syndromes: A systematic overview. JAMA 2004; 292:89-96. PMID 15238596
  47. ↑ Ferguson JJ, Califf RM, Antman EM, et al: Enoxaparin vs unfractionated heparin in high-risk patients with non-ST-segment elevation acute coronary syndromes managed with an intended early invasive strategy: Primary results of the SYNERGY randomized trial. JAMA 2004; 292:45-54. PMID 15238590
  48. ↑ Michalis LK, Katsouras CS, Papamichael N, et al: Enoxaparin versus tinzaparin in non-ST-segment elevation acute coronary syndromes: The EVET trial. Am Heart J 2003; 146:304-310. PMID 12891200
  49. ↑ Yusuf S, Mehta SR, Chrolavicius S, et al: Comparison of fondaparinux and enoxaparin in acute coronary syndromes. N Engl J Med 2006; 354:1464-1476. PMID 16537663
  50. ↑ Stone GW, McLaurin BT, Cox DA, et al: Bivalirudin for patients with acute coronary syndromes. N Engl J Med 2006; 355:2203-2216. PMID 17124018
  51. ↑ FRagmin and Fast Revascularisation during InStability in Coronary artery disease Investigators : Invasive compared with non-invasive treatment in unstable coronary artery disease: FRISC II prospective randomised multicentre study. Lancet 1999; 354:708-715. PMID 10475181
  52. ↑ Fox KA, Goodman SG, Klein W, et al: Management of acute coronary syndromes. Variations in practice and outcome; findings from the Global Registry of Acute Coronary Events (GRACE). Eur Heart J 2002; 23:1177-1189. PMID 12127920
  53. ↑ Lagerqvist B, Husted S, Kontny F, et al: 5-year outcomes in the FRISC-II randomised trial of an invasive versus a non-invasive strategy in non-ST-elevation acute coronary syndrome: A follow-up study. Lancet 2006; 368:998-1004 PMID 16980115
  54. ↑ Mahoney EM, Jurkovitz CT, Chu H, et al: Cost and cost-effectiveness of an early invasive versus conservative strategy for the treatment of unstable angina and non-ST elevation myocardial infarction. JAMA 2002; 288:1851-1858. PMID 12377083
  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
  69. ↑ Suzuki H, Kawai S, Aizawa T, et al: Histological evaluation of coronary plaque in patients with variant angina: relationship between vasospasm and neointimal hyperplasia in primary coronary lesions. J Am Coll Cardiol 1999; 33:198-205. PMID 9935030
  70. ↑ Sakata K, Miura F, Sugino H, et al: Assessment of regional sympathetic nerve activity in vasospastic angina: Analysis of iodine 123-labeled metaiodobenzylguanidine scintigraphy. Am Heart J 1997; 133:484-489. PMID 9124179
  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
  72. ↑ Hung MJ, Cheng CW, Yang NI, et al: E. Coronary vasospasm-induced acute coronary syndrome complicated by life-threatening cardia arrhythmias in patients without hemodynamically significant coronary artery disease. Int J Cardiol 2007; 117:37-44. PMID 16844245
  73. ↑ Yuksel UD, Celik T, Iyisoy A, et al:. Polymorphic ventricular tachycardia induced by coronary vasospasm: A malignant case of variant angina. Int J Cardiol, 2006. E-pubahead of print, Nov. 22, 2006. PMID 17125857
  74. ↑ Kawano H, Motoyama T, Yasue H, et al: Endothelial function fluctuates with diurnal variation in the frequency of ischemic episodes in patients with variant angina. J Am Coll Cardiol 2002; 40:266-270. PMID 12106930
  75. ↑ Matsuguchi T, Araki H, Nakamura N, et al: Prevention of vasospastic angina by alcohol ingestion: Report of 2 cases. Angiology 1988; 39:394-400. PMID 3364807
  76. ↑ Raxwal V, Gupta K: Images in cardiovascular medicine. Coronary artery spasm. Circulation 2006; 113:e689-e690. PMID 16606795
  77. ↑ Chen HS, Pinto DS: Images in clinical medicine. Prinzmetal's angina. N Engl J Med 2003; 349:e1. PMID 12840104
  78. ↑ Wang K, Asinger RW, Marriott HJ: ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003; 349:2128-2135. PMID 14645641
  79. ↑ Unverdorben M, Haag M, Fuerste T, et al: Vasospasm in smooth coronary arteries as a cause of asystole and syncope. Cathet Cardiovasc Diagn 1997; 41:430-434. PMID 9258492
  80. ↑ Lip GY, Gupta J, Khan MM, Singh SP: Recurrent myocardial infarction with angina and normal coronary arteries. Int J Cardiol 1995; 51:65-71. PMID 8522399
  81. ↑ Pepine CJ, el-Tamimi H, Lambert CR: Prinzmetal's angina (variant angina). Heart Dis Stroke 1992; 1:281-286. PMID 1344118
  82. ↑ Crea F: Variant angina in patients without obstructive coronary atherosclerosis: a benign form of spasm. Eur Heart J 1996; 17:980-982. PMID 8809510
  83. ↑ Hirano Y, Ueharfa H, Nakamura H, et al: Diagnosis of vasospastic angina: Comparison of hyperventilation and cold-pressor stress echocardiography, and coronary angiography with intracoronary injection of acetylcholine. Int J Cardiol 2007; 116:331-337. PMID 16890307
  84. ↑ Nakao K, Ohgushi M, Yoshimura M, et al: Hyperventilation as a specific test for diagnosis of coronary artery spasm. Am J Cardiol 1997; 80:545-549. PMID 9294979
  85. ↑ Antman E, Muller J, Goldberg S, et al: Nifedepine therapy for coronary artery spasm. Experience in 127 patients. N Engl J Med 1980; 302:1269-1273. PMID 6767986
  86. ↑ De Cesare N, Cozzi S, Apostolo A, et al: Facilitation of coronary spasm by propranolol in Prinzmetal's angina: Fact or unproven extrapolation?. Coron Artery Dis 1994; 5:323-330. PMID 8044344
  87. ↑ Tzivoni D, Keren A, Benhorin J, et al: Prazosin therapy for refractory variant angina.Am Heart J 1983; 105:262-266. PMID 6823808
  88. ↑ Kaski JC: Management of vasospastic angina—role of nicorandil. Cardiovasc Drugs Ther 9 Suppl 1995; 2:221-227. PMID 7647026
  89. ↑ Kawano H, Motoyama T, Hirai N, et al: Estradiol supplementation suppresses hyperventilation-induced attacks in postmenopausal women with variant angina. J Am Coll Cardiol 2001; 37:735-740. PMID 11693745
  90. ↑ Tanabe Y, Itoh E, Suzuki K, et al: Limited role of coronary angioplasty and stenting in coronary spastic angina with organic stenosis. J Am Coll Cardiol 2002; 39:1120-1126. PMID 11923034
  91. ↑ Meisel SR, Mazur A, Chetboun I, et al: Usefulness of implantable cardioverter-defibrillators in refractory variant angina pectoris complicated by ventricular fibrillation in patients with angiographically normal coronary arteries. Am J Cardiol 2002; 89:1114-1116. PMID 11988204
  92. ↑ Bory M, Pierron F, Panagides D, et al: Coronary artery spasm in patients with normal or near normal coronary arteries. Long-term follow-up of 277 patients. Eur Heart J 1996; 17:1015-1021. PMID 8809518
  93. ↑ Shimokawa H, Nagasawa K, Irie T, et al: Clinical characteristics and long-term prognosis of patients with variant angina. A comparative study between western and Japanese populations. Int J Cardiol 1998; 18:331-349. PMID 3129375
  94. ↑ Tashiro H, Shimokawa H, Koyanagi S, Takeshita A: Clinical characteristics of patients with spontaneous remission of variant angina. Jpn Circ J 1993; 57:117-122. PMID 8450595

See Also

Template:SIB


Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=Unstable_angina_non_ST_elevation_myocardial_infarction_overview&oldid=561794"