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

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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).
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==
==Presentation and Diagnosis==
[[UA]] can have typical or atypical presentations. the 3 classic forms of presentation are  
[[UA]] can have typical or atypical presentations. the 3 classic forms of presentation are  
*Rest angina(angina commencing when the patient is at rest)
*Rest angina(angina commencing when the patient is at rest)
Line 50: Line 50:
[[NSTEMI]] generally presents as prolonged, more intense rest angina or angina equivalent.
[[NSTEMI]] generally presents as prolonged, more intense rest angina or angina equivalent.


==Diagnosis==
==Risk stratification==
==Risk stratification==
==Treatment==
==Treatment==

Revision as of 14:33, 16 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

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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.

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.

Risk stratification

Treatment

Discharge care

References

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  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
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  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

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