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Non ST elevation myocardial infarction pathophysiology

2009-09-09T16:41:58Z

NMGheewala: /* NSTEMI Background */

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==NSTEMI Background==
As alluded to in prior sections, Unstable Angina and NSTEMI are at different ends of the spectrum of the same disease. While there is no way to determine which patients presenting with Unstable Angina will ultimately progress to NSTEMI, the distinction between the two entities is clear. Often, for patients presenting prior to the four hour window before cardiac biomarkers are positive (namely CK-MB), the EKG in context of the patient's chest pain will be marker for whether patient has STEMI versus UA/NSTEMI and needs to urgently undergo percutaneous revascularization.

==Braunwald Classification==

==Plaque rupture, thrombus formation, and embolization underly the pathophysiology of NSTEMI==
[[Image:Plaque rupture and coronary thrombosis in the left anterior descending artery with distal embolization.gif]]

This video shows plaque rupture or disruption of the atherosclerotic plaque in the mid LAD. As is often the case, the plaque has torn at its edge, a location where the fibrous cap covering the atherosclerotic plaque is the thinnest. Clot has formed and it is embolizing downstream. The most common preceding pathophysiologic event in NSTEMI is the disruption of an [[Atherosclerosis|atherosclerotic]] [[Atheroma|plaque]] in an epicardial coronary artery such as that shown here. Exposure of the atherosclerotic plaque contents to the blood stream leads to activation of the [[clotting cascade]], local thrombus formation, and incomplete occlusion of the epicardial artery in NSTEMI. This artery is open, in NSTEMI unlike STEMI where the artery is closed. The downstream microvasculature is occluded by the clot that has embolized, and this accounts for the [[troponin]] elevation in this patient.

As opposed to the original hypothesis that acute coronary syndrome (ACS) is caused by gradual progression of coronary atherosclerosis to the point of a severe, fixed lesion, it has become clear that, in fact, ACS is usually caused by atherosclerotic plaque rupture at a site that previously had only mild to moderate stenosis.<ref>Martinez-Rumayor A, Januzzi JL Jr. Non-ST segment elevation acute coronary syndromes: A comprehensive review. South Med J. 2006 Oct;99(10):1103-10. PMID 17100031</ref> This plaque rupture exposes ligands (including collagen) for platelet adhesion which causes platelet aggregation and subsequent platelet activation. <ref>Patrono C, Renda G. Platelet activation and inhibition in unstable coronary syndromes. Am J Cardiol. 1997 Sep 4;80(5A):17E-20E. PMID 9296464 </ref> Platelets are activated by thrombin (found in blood clots), adenosine diphosphate (found in platelet granules), serotonin (also found in platelet granules) and thromboxane-A2. <ref>Patrono C, Renda G. Platelet activation and inhibition in unstable coronary syndromes. Am J Cardiol. 1997 Sep 4;80(5A):17E-20E. PMID 9296464 </ref> Upon activation, the glycoprotein IIb/IIIa receptor that in a non-active state is found in the cytosol is exteriorized and modified which enables additional platelet aggregation and cross-linking.<ref>Martinez-Rumayor A, Januzzi JL Jr. Non-ST segment elevation acute coronary syndromes: A comprehensive review. South Med J. 2006 Oct;99(10):1103-10. PMID 17100031</ref> The prothrombinase complex then binds to the activated platelet and starts to coagulation cascade.<ref>Martinez-Rumayor A, Januzzi JL Jr. Non-ST segment elevation acute coronary syndromes: A comprehensive review. South Med J. 2006 Oct;99(10):1103-10. PMID 17100031</ref> This entire process results in a thrombus which coalesces over the ruptured plaque.

Although less common, ACS may also occur by other mechanisms. These include

* coronary artery spasm as in Prinzmetal's angina,
* severe narrowing alone without plaque rupture, as in the case of restenosis after percutaneous coronary intervention (PCI) or as with progressive atherosclerosis,
* coronary artery dissection,
* secondary ischemia in cases in which there is either increased myocardial oxygen demand as in tachycardia from fever, anemia, hypoxemia, thyrotoxicosis, or in cases of decreased supply such as in hypotension or anemia from hemorrhage.

=== Genetics ===
To date, there does not appear to be any single genetic marker predictive acute coronary syndrome (ACS).<ref>Anwaruddin S, Askari AT, Topol EJ. Redefining risk in acute coronary syndromes using molecular medicine. J Am Coll Cardiol. 2007 Jan 23;49(3):279-89. Epub 2007 Jan 4. PMID 17239708</ref> In a recent validation study of genetic variants associated with (which includes ST-elevation myocardial infarction (STEMI), NSTEMI and UA) none of the 85 genetic variants tested were shown to be correlated with ACS. The study chose the polymorphic genetic variants based on statistically significant findings of prior studies. <ref>Morgan TM, Krumholz HM, Lifton RP, Spertus JA.Nonvalidation of reported genetic risk factors for acute coronary syndrome in a large-scale replication study. JAMA. 2007 Apr 11;297(14):1551-61. PMID 17426274 Erratum in JAMA. 2007 Sep 5;298(9):973.</ref> Nonetheless, although no individual marker is likely to be predictive, in the future it is possible that a panel of markers may be used to assess risk.<ref>Anwaruddin S, Askari AT, Topol EJ. Redefining risk in acute coronary syndromes using molecular medicine. J Am Coll Cardiol. 2007 Jan 23;49(3):279-89. Epub 2007 Jan 4. PMID 17239708</ref> <ref>Wilcken DE. Overview of inherited metabolic disorders causing cardiovascular disease. J Inherit Metab Dis. 2003;26(2-3):245-57. PMID 12889664</ref>

==Complete List of (known) Underlying Mechanisms of NSTEMI==

* [[Coronary artery|Coronary artery vasoconstriction]]
* [[Infarct related artery|Culprit lesion morphology]]
* [[Embolism]] / [[microembolism]]
* [[Infection]]
:* [[Chlamydia pneumoniae]]
:* [[Cytomegalovirus ]]
:* [[Helicobacter pylori]]
* [[Inflammation]]
* [[Leukocyte]]s, [[platelet]]s
* Plaque disruption or plaque erosion
* [[Thrombosis]]

==List of Factors may Effect Development and Complications of NSTEMI==

(In alphabetical order)

* Blood lipid levels
* Catecholamine levels ([[smoking]], [[cocaine]], [[stress]])
* Degree of coronary vasoconstriction
* Endothelial function
* Extent of collaterals
* Extent of plaque rupture or erosion
* Inflammatory substrate
* Location of the culprit coronary lesion
* Microembolization and microvascular obstruction
* Stenosis morphology and severity
* Systemic factors
:* Heart rate and blood pressure
* Thrombotic factors
:* Blood viscosity
:* Intrinsic clotting activity
:* Leukocyte activation
:* Level of fibrinolytic activity
:* Plaque tissue factor levels
:* Platelet aggregability and reactivity

== References ==
{{Reflist|2}}

==See Also==

* [[The Living Guidelines: UA/NSTEMI]]

{{Electrocardiography}}
{{Circulatory system pathology}}
{{SIB}}

[[Category:Cardiology]]
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{{WikiDoc Sources}}

Non ST elevation myocardial infarction pathophysiology

2009-09-09T16:33:17Z

NMGheewala:

{{SI}}
{{WikiDoc Cardiology Network Infobox}}
{{CMG}}

{{Editor Help}}

==NSTEMI Background==
As alluded to in prior sections, Unstable Angina and NSTEMI are at different ends of the spectrum of the same disease. While there is no way to determine which patients presenting with Unstable Angina will ultimately progress to NSTEMI, the distinction between the two entities is clear. Often, for patients presenting prior to the four hour window before cardiac biomarkers (namely CK-MB), the EKG in context of the patient's chest pain will be marker for whether patient has STEMI versus UA/NSTEMI and needs to urgently undergo percutaneous revascularization.

==Braunwald Classification==

==Plaque rupture, thrombus formation, and embolization underly the pathophysiology of NSTEMI==
[[Image:Plaque rupture and coronary thrombosis in the left anterior descending artery with distal embolization.gif]]

This video shows plaque rupture or disruption of the atherosclerotic plaque in the mid LAD. As is often the case, the plaque has torn at its edge, a location where the fibrous cap covering the atherosclerotic plaque is the thinnest. Clot has formed and it is embolizing downstream. The most common preceding pathophysiologic event in NSTEMI is the disruption of an [[Atherosclerosis|atherosclerotic]] [[Atheroma|plaque]] in an epicardial coronary artery such as that shown here. Exposure of the atherosclerotic plaque contents to the blood stream leads to activation of the [[clotting cascade]], local thrombus formation, and incomplete occlusion of the epicardial artery in NSTEMI. This artery is open, in NSTEMI unlike STEMI where the artery is closed. The downstream microvasculature is occluded by the clot that has embolized, and this accounts for the [[troponin]] elevation in this patient.

As opposed to the original hypothesis that acute coronary syndrome (ACS) is caused by gradual progression of coronary atherosclerosis to the point of a severe, fixed lesion, it has become clear that, in fact, ACS is usually caused by atherosclerotic plaque rupture at a site that previously had only mild to moderate stenosis.<ref>Martinez-Rumayor A, Januzzi JL Jr. Non-ST segment elevation acute coronary syndromes: A comprehensive review. South Med J. 2006 Oct;99(10):1103-10. PMID 17100031</ref> This plaque rupture exposes ligands (including collagen) for platelet adhesion which causes platelet aggregation and subsequent platelet activation. <ref>Patrono C, Renda G. Platelet activation and inhibition in unstable coronary syndromes. Am J Cardiol. 1997 Sep 4;80(5A):17E-20E. PMID 9296464 </ref> Platelets are activated by thrombin (found in blood clots), adenosine diphosphate (found in platelet granules), serotonin (also found in platelet granules) and thromboxane-A2. <ref>Patrono C, Renda G. Platelet activation and inhibition in unstable coronary syndromes. Am J Cardiol. 1997 Sep 4;80(5A):17E-20E. PMID 9296464 </ref> Upon activation, the glycoprotein IIb/IIIa receptor that in a non-active state is found in the cytosol is exteriorized and modified which enables additional platelet aggregation and cross-linking.<ref>Martinez-Rumayor A, Januzzi JL Jr. Non-ST segment elevation acute coronary syndromes: A comprehensive review. South Med J. 2006 Oct;99(10):1103-10. PMID 17100031</ref> The prothrombinase complex then binds to the activated platelet and starts to coagulation cascade.<ref>Martinez-Rumayor A, Januzzi JL Jr. Non-ST segment elevation acute coronary syndromes: A comprehensive review. South Med J. 2006 Oct;99(10):1103-10. PMID 17100031</ref> This entire process results in a thrombus which coalesces over the ruptured plaque.

Although less common, ACS may also occur by other mechanisms. These include

* coronary artery spasm as in Prinzmetal's angina,
* severe narrowing alone without plaque rupture, as in the case of restenosis after percutaneous coronary intervention (PCI) or as with progressive atherosclerosis,
* coronary artery dissection,
* secondary ischemia in cases in which there is either increased myocardial oxygen demand as in tachycardia from fever, anemia, hypoxemia, thyrotoxicosis, or in cases of decreased supply such as in hypotension or anemia from hemorrhage.

=== Genetics ===
To date, there does not appear to be any single genetic marker predictive acute coronary syndrome (ACS).<ref>Anwaruddin S, Askari AT, Topol EJ. Redefining risk in acute coronary syndromes using molecular medicine. J Am Coll Cardiol. 2007 Jan 23;49(3):279-89. Epub 2007 Jan 4. PMID 17239708</ref> In a recent validation study of genetic variants associated with (which includes ST-elevation myocardial infarction (STEMI), NSTEMI and UA) none of the 85 genetic variants tested were shown to be correlated with ACS. The study chose the polymorphic genetic variants based on statistically significant findings of prior studies. <ref>Morgan TM, Krumholz HM, Lifton RP, Spertus JA.Nonvalidation of reported genetic risk factors for acute coronary syndrome in a large-scale replication study. JAMA. 2007 Apr 11;297(14):1551-61. PMID 17426274 Erratum in JAMA. 2007 Sep 5;298(9):973.</ref> Nonetheless, although no individual marker is likely to be predictive, in the future it is possible that a panel of markers may be used to assess risk.<ref>Anwaruddin S, Askari AT, Topol EJ. Redefining risk in acute coronary syndromes using molecular medicine. J Am Coll Cardiol. 2007 Jan 23;49(3):279-89. Epub 2007 Jan 4. PMID 17239708</ref> <ref>Wilcken DE. Overview of inherited metabolic disorders causing cardiovascular disease. J Inherit Metab Dis. 2003;26(2-3):245-57. PMID 12889664</ref>

==Complete List of (known) Underlying Mechanisms of NSTEMI==

* [[Coronary artery|Coronary artery vasoconstriction]]
* [[Infarct related artery|Culprit lesion morphology]]
* [[Embolism]] / [[microembolism]]
* [[Infection]]
:* [[Chlamydia pneumoniae]]
:* [[Cytomegalovirus ]]
:* [[Helicobacter pylori]]
* [[Inflammation]]
* [[Leukocyte]]s, [[platelet]]s
* Plaque disruption or plaque erosion
* [[Thrombosis]]

==List of Factors may Effect Development and Complications of NSTEMI==

(In alphabetical order)

* Blood lipid levels
* Catecholamine levels ([[smoking]], [[cocaine]], [[stress]])
* Degree of coronary vasoconstriction
* Endothelial function
* Extent of collaterals
* Extent of plaque rupture or erosion
* Inflammatory substrate
* Location of the culprit coronary lesion
* Microembolization and microvascular obstruction
* Stenosis morphology and severity
* Systemic factors
:* Heart rate and blood pressure
* Thrombotic factors
:* Blood viscosity
:* Intrinsic clotting activity
:* Leukocyte activation
:* Level of fibrinolytic activity
:* Plaque tissue factor levels
:* Platelet aggregability and reactivity

== References ==
{{Reflist|2}}

==See Also==

* [[The Living Guidelines: UA/NSTEMI]]

{{Electrocardiography}}
{{Circulatory system pathology}}
{{SIB}}

[[Category:Cardiology]]
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Unstable angina non ST elevation myocardial infarction overview

2009-08-20T15:03:43Z

NMGheewala:

{{Infobox_Disease
| Name = Unstable angina pectoris
| Image = Coronary thrombosis 3.jpg
| Caption = Plaque rupture in a coronary artery at arrows yielding obstructive thrombus in red. <br> <small> [http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] </small>
| DiseasesDB = 8695
| ICD10 = {{ICD10|I|20||i|20}}
| ICD9 = {{ICD9|413}}
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj = med
| eMedicineTopic = 133
| MeshID = D000787
}}
{{Search infobox}}
{{WikiDoc Cardiology Network Infobox}}
{{WikiDoc Cardiology News}}
{{CMG}}
__NOTOC__
'''Associate Editor-In-Chief:''' {{CZ}}

'''Associate Editor-In-Chief:''' {{NMG}}

{{Editor Join}}

'''''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 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==
UA and NSTEMI are differentiated from each other based upon whether there are elevated serum levels of [[cardiac biomarker]]s (i.e., [[creatine kinase]] ([[CK]]), [[MB]] isoenzyme of CK ([[CK-MB]]) and [[Troponin]]s I and T). Elevated [[cardiac biomarker]]s are present in [[NSTEMI]] but not in [[UA]]. However, it is important to note that although [[troponin]]s 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 [[troponin]]s. <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> 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. <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>Braunwald E: Unstable angina: A classification. Circulation 1989; 80: 410-414. PMID 2752565</ref> <ref>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</ref> <ref>Davies MJ: The composition of coronary-artery plaques. N Engl J Med 1997; 336:1312-1314. PMID 9113937</ref> <ref>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</ref> <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> <ref>Kaski JC: Rapid coronary artery disease progression and angiographic stenosis morphology. Ital Heart J 2000; 1:21-25. PMID 10868918</ref> <ref>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</ref> <ref>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</ref> <ref>Prinzmetal M, Kennamer R, Merliss R, et al: A variant form of angina pectoris. Am J Med 1959; 27:375. PMID 14434946</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>Buffon A, Biasucci LM, Liuzzo G, et al: Widespread coronary inflammation in unstable angina. ''N Engl J Med'' 2002; 347:5-12. PMID 12097534</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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 </ref> <ref>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 </ref> <ref>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</ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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 </ref> <ref>Rich JD, Maraganore JM, Young E, et al: Heparin resistance in acute coronary syndromes. ''J Thromb Thrombolysis'' 2007; 23:93-100. PMID 17221324</ref> <ref>Warkentin TE, Kelton JG: Temporal aspects of heparin-induced thrombocytopenia. ''N Engl J Med'' 2001; 344:1286-1292 PMID 11320387</ref> <ref>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 </ref> <ref>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 </ref> <ref>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</ref> <ref>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 </ref> <ref>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 </ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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 </ref> <ref>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 </ref> <ref>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</ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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 </ref> <ref>Mayer S, Hillis LD: Prinzmetal's variant angina. ''Clin Cardiol'' 1998; 21:243-246. PMID 9562933 </ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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</ref> <ref>Raxwal V, Gupta K: Images in cardiovascular medicine. Coronary artery spasm. ''Circulation'' 2006; 113:e689-e690. PMID 16606795</ref> <ref>Chen HS, Pinto DS: Images in clinical medicine. Prinzmetal's angina. ''N Engl J Med'' 2003; 349:e1. PMID 12840104</ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>Pepine CJ, el-Tamimi H, Lambert CR: Prinzmetal's angina (variant angina). ''Heart Dis Stroke'' 1992; 1:281-286. PMID 1344118</ref> <ref>Crea F: Variant angina in patients without obstructive coronary atherosclerosis: a benign form of spasm. ''Eur Heart J'' 1996; 17:980-982. PMID 8809510</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>Tzivoni D, Keren A, Benhorin J, et al: Prazosin therapy for refractory variant angina.''Am Heart J'' 1983; 105:262-266. PMID 6823808 </ref> <ref>Kaski JC: Management of vasospastic angina—role of nicorandil. ''Cardiovasc Drugs Ther 9 Suppl'' 1995; 2:221-227. PMID 7647026</ref> <ref>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</ref> <ref>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 </ref> <ref>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</ref> <ref>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</ref> <ref>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</ref> <ref>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 </ref> 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==
{{Reflist|2}}

==See Also==

* [[The Living Guidelines: UA/NSTEMI]]
* [[Chronic stable angina]]
* [[Non ST Elevation Myocardial Infarction]]
* [[ST Elevation Myocardial Infarction]]

{{Circulatory system pathology}}
{{SIB}}

[[Category:Cardiology]]
[[Category:Emergency medicine]]
[[Category:Signs and symptoms]]

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Template:NMG

2009-08-18T16:19:41Z

NMGheewala: New page: Neil Gheewala, M.D. [mailto:nmgheewala@wikidoc.org]

[[User:NMGheewala|Neil Gheewala, M.D.]] [mailto:nmgheewala@wikidoc.org]

Unstable angina non ST elevation myocardial infarction

2009-08-18T16:08:39Z

NMGheewala:

[[Image:Plaque rupture and coronary thrombosis in the left anterior descending artery with distal embolization.gif|right|130pix]]

''''{{Infobox_Disease
| Name = Unstable angina pectoris
| Image =
| Caption =
| DiseasesDB = 8695
| ICD10 = {{ICD10|I|20||i|20}}
| ICD9 = {{ICD9|413}}
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj = med
| eMedicineTopic = 133
| MeshID = D000787
}}
{{Search infobox}}

{{CMG}}
__NOTOC__
'''Associate Editor-In-Chief:''' {{CZ}}

'''Associate Editor-In-Chief:''' {{NMG}}

{{Editor Join}}

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

==Overview==

===[[Unstable angina / non ST elevation myocardial infarction overview | Overview]]===

===[[Unstable angina / non ST elevation myocardial infarction epidemiology and demographics | Epidemiology and Demographics]]===

==Pathophysiology and Etiology==

===[[Unstable angina pathophysiology & etiology|Pathophysiology and Etiology (UA)]]===

===[[Non ST elevation myocardial infarction pathophysiology & etiology|Pathophysiology and Etiology (NSTEMI)]]===

==[[Unstable angina diagnosis| Diagnosis]]==

===[[Unstable angina / non ST elevation myocardial infarction symptoms | Symptoms]]===

===[[Chest pain|Differential diagnosis of chest pain]]===

===[[Unstable angina / non ST elevation myocardial infarction physical examination | Physical Examination]]===

==[[Unstable angina risk stratification and prognosis| Risk Stratification and Prognosis]]==

==[[Unstable angina treatment| Treatment]]==

===[[Unstable angina / non ST elevation myocardial infarction immediate management | Immediate Management]]===

===[[Unstable angina / non ST elevation myocardial infarction initial therapy | Initial Therapy]]===

[[Unstable angina / non ST elevation myocardial infarction antiplatelet therapy| Antiplatelet Therapy]] | [[Unstable angina / non ST elevation myocardial infarction anticoagulant therapy | Anticoagulant Therapy]] | [[Unstable angina / non ST elevation myocardial infarction additional management considerations for antiplatelet and anticoagulant therapy | Additional Management Considerations for Antiplatelet and Anticoagulant Therapy]]

'''Mechanical Reperfusion''' | [[Unstable angina / non ST elevation myocardial infarction initial conservative versus initial invasive strategies | Initial Conservative Versus Initial Invasive Strategies]] | [[Unstable angina / non ST elevation myocardial infarction recommendations for PCI‎ | PCI]] | [[Unstable angina / non ST elevation myocardial infarction recommendations for CABG | CABG]]

==Discharge Care==
===[[Unstable angina / non ST elevation myocardial infarction medical regimen and use of medications | Medical Regimen]]===
===[[Unstable angina / non ST elevation myocardial infarction long-term medical therapy and secondary prevention | Long-Term Medical Therapy and Secondary Prevention]]===
===[[Unstable angina / non ST elevation myocardial infarction post-discharge follow-up | Post-Discharge Follow-Up]]===
===[[Unstable angina / non ST elevation myocardial infarction cardiac rehabilitation | Cardiac Rehabilitation]]===

==Special Groups==
[[Unstable angina / non ST elevation myocardial infarction women | Women]] | [[Unstable angina / non ST elevation myocardial infarction diabetic patients | Diabetic Patients]] | [[Unstable angina / non ST elevation myocardial infarction post CABG patients | Post CABG Patients]] | [[Unstable angina / non ST elevation myocardial infarction elderly | Elderly]] | [[Unstable angina / non ST elevation myocardial infarction chronic kidney disease | Chronic Kidney Disease]] | [[Unstable angina / non ST elevation myocardial infarction drug and substance abusers | Drug and Substance Abusers]] | [[Unstable angina / non ST elevation myocardial infarction prinzmetal's angina | Prinzmetal's Angina]] | [[Unstable angina / non ST elevation myocardial infarction cardiovascular syndrome x | Cardiovascular Syndrome X]]

==[[Unstable angina and complications of bleeding and transfusion|Complications of Bleeding and Transfusion]]==

==See Also==
* [[The Living Guidelines: UA/NSTEMI | The UA / NSTEMI Living Guidelines: Vote on current recommendations and suggest revisions to the guidelines]]
* [[Chronic stable angina]]
* [[Non ST Elevation Myocardial Infarction]]
* [[ST Elevation Myocardial Infarction]]

==Sources==
*The ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction <ref name="pmid17692738">{{cite journal |author=Anderson JL, Adams CD, Antman EM, ''et al'' |title=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) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine |journal=JACC |volume=50 |issue=7 |pages=e1–e157 |year=2007 |month=August |pmid=17692738 |doi:10.1016/j.jacc.2007.02.013 |url=}}</ref>

==References==
{{Reflist|2}}

==External links==
* [http://www.themdtv.org The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research]
* [http://www.clinicaltrialresults.org Clinical Trial Results: An up to date resource of Cardiovascular Research]
* [http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=pub Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack] - based on information of the [[Framingham Heart Study]], from the United States [[National Heart, Lung and Blood Institute]]
* [http://www.nlm.nih.gov/medlineplus/heartattack.html Heart Attack] - overview of resources from [[MedlinePlus]].
* [http://ww2.heartandstroke.ca/Page.asp?PageID=1975&ArticleID=5288 Heart Attack Warning Signals] from the Heart and Stroke Foundation of Canada
* [http://www.regionalpci-stemi.org/index.html Regional PCI for STEMI Resource Center] - Evidence based online resource center for the development of regional PCI networks for acute STEMI
* [http://www.stemisystems.org/ STEMI Systems] - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
* [http://d2b.acc.org/ American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.]
*[http://www.americanheart.org/heartattack American Heart Association's Heart Attack web site] - Information and resources for preventing, recognizing and treating heart attack.

{{Circulatory system pathology}}
{{Electrocardiography}}
{{SIB}}

[[Category:Cardiology]]
[[Category:Emergency medicine]]
[[Category:Signs and symptoms]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Unstable angina non ST elevation myocardial infarction

2009-08-18T16:04:08Z

NMGheewala:

[[Image:Plaque rupture and coronary thrombosis in the left anterior descending artery with distal embolization.gif|right|130pix]]

''''{{Infobox_Disease
| Name = Unstable angina pectoris
| Image =
| Caption =
| DiseasesDB = 8695
| ICD10 = {{ICD10|I|20||i|20}}
| ICD9 = {{ICD9|413}}
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj = med
| eMedicineTopic = 133
| MeshID = D000787
}}
{{Search infobox}}

{{CMG}}
__NOTOC__
'''Associate Editor-In-Chief:''' {{CZ}}
'''Associate Editor-In-Chief:''' {{NMG}}

{{Editor Join}}

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

==Overview==

===[[Unstable angina / non ST elevation myocardial infarction overview | Overview]]===

===[[Unstable angina / non ST elevation myocardial infarction epidemiology and demographics | Epidemiology and Demographics]]===

==Pathophysiology and Etiology==

===[[Unstable angina pathophysiology & etiology|Pathophysiology and Etiology (UA)]]===

===[[Non ST elevation myocardial infarction pathophysiology & etiology|Pathophysiology and Etiology (NSTEMI)]]===

==[[Unstable angina diagnosis| Diagnosis]]==

===[[Unstable angina / non ST elevation myocardial infarction symptoms | Symptoms]]===

===[[Chest pain|Differential diagnosis of chest pain]]===

===[[Unstable angina / non ST elevation myocardial infarction physical examination | Physical Examination]]===

==[[Unstable angina risk stratification and prognosis| Risk Stratification and Prognosis]]==

==[[Unstable angina treatment| Treatment]]==

===[[Unstable angina / non ST elevation myocardial infarction immediate management | Immediate Management]]===

===[[Unstable angina / non ST elevation myocardial infarction initial therapy | Initial Therapy]]===

[[Unstable angina / non ST elevation myocardial infarction antiplatelet therapy| Antiplatelet Therapy]] | [[Unstable angina / non ST elevation myocardial infarction anticoagulant therapy | Anticoagulant Therapy]] | [[Unstable angina / non ST elevation myocardial infarction additional management considerations for antiplatelet and anticoagulant therapy | Additional Management Considerations for Antiplatelet and Anticoagulant Therapy]]

'''Mechanical Reperfusion''' | [[Unstable angina / non ST elevation myocardial infarction initial conservative versus initial invasive strategies | Initial Conservative Versus Initial Invasive Strategies]] | [[Unstable angina / non ST elevation myocardial infarction recommendations for PCI‎ | PCI]] | [[Unstable angina / non ST elevation myocardial infarction recommendations for CABG | CABG]]

==Discharge Care==
===[[Unstable angina / non ST elevation myocardial infarction medical regimen and use of medications | Medical Regimen]]===
===[[Unstable angina / non ST elevation myocardial infarction long-term medical therapy and secondary prevention | Long-Term Medical Therapy and Secondary Prevention]]===
===[[Unstable angina / non ST elevation myocardial infarction post-discharge follow-up | Post-Discharge Follow-Up]]===
===[[Unstable angina / non ST elevation myocardial infarction cardiac rehabilitation | Cardiac Rehabilitation]]===

==Special Groups==
[[Unstable angina / non ST elevation myocardial infarction women | Women]] | [[Unstable angina / non ST elevation myocardial infarction diabetic patients | Diabetic Patients]] | [[Unstable angina / non ST elevation myocardial infarction post CABG patients | Post CABG Patients]] | [[Unstable angina / non ST elevation myocardial infarction elderly | Elderly]] | [[Unstable angina / non ST elevation myocardial infarction chronic kidney disease | Chronic Kidney Disease]] | [[Unstable angina / non ST elevation myocardial infarction drug and substance abusers | Drug and Substance Abusers]] | [[Unstable angina / non ST elevation myocardial infarction prinzmetal's angina | Prinzmetal's Angina]] | [[Unstable angina / non ST elevation myocardial infarction cardiovascular syndrome x | Cardiovascular Syndrome X]]

==[[Unstable angina and complications of bleeding and transfusion|Complications of Bleeding and Transfusion]]==

==See Also==
* [[The Living Guidelines: UA/NSTEMI | The UA / NSTEMI Living Guidelines: Vote on current recommendations and suggest revisions to the guidelines]]
* [[Chronic stable angina]]
* [[Non ST Elevation Myocardial Infarction]]
* [[ST Elevation Myocardial Infarction]]

==Sources==
*The ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction <ref name="pmid17692738">{{cite journal |author=Anderson JL, Adams CD, Antman EM, ''et al'' |title=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) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine |journal=JACC |volume=50 |issue=7 |pages=e1–e157 |year=2007 |month=August |pmid=17692738 |doi:10.1016/j.jacc.2007.02.013 |url=}}</ref>

==References==
{{Reflist|2}}

==External links==
* [http://www.themdtv.org The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research]
* [http://www.clinicaltrialresults.org Clinical Trial Results: An up to date resource of Cardiovascular Research]
* [http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=pub Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack] - based on information of the [[Framingham Heart Study]], from the United States [[National Heart, Lung and Blood Institute]]
* [http://www.nlm.nih.gov/medlineplus/heartattack.html Heart Attack] - overview of resources from [[MedlinePlus]].
* [http://ww2.heartandstroke.ca/Page.asp?PageID=1975&ArticleID=5288 Heart Attack Warning Signals] from the Heart and Stroke Foundation of Canada
* [http://www.regionalpci-stemi.org/index.html Regional PCI for STEMI Resource Center] - Evidence based online resource center for the development of regional PCI networks for acute STEMI
* [http://www.stemisystems.org/ STEMI Systems] - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
* [http://d2b.acc.org/ American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.]
*[http://www.americanheart.org/heartattack American Heart Association's Heart Attack web site] - Information and resources for preventing, recognizing and treating heart attack.

{{Circulatory system pathology}}
{{Electrocardiography}}
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Neil's test page

2009-08-18T15:51:52Z

NMGheewala: New page: Image:sigcollateralsLAD3.avi

[[Image:sigcollateralsLAD3.avi]]

File:Mitral stenosis, gross pathology 20G0015 lores.jpg

2009-08-18T15:34:20Z

NMGheewala: uploaded a new version of "Image:Mitral stenosis, gross pathology 20G0015 lores.jpg"

[[User:C Michael Gibson|Chief WikiDoc]] 16:51, 10 February 2008 (EST)