Unstable angina non ST elevation myocardial infarction overview

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Overview

Classification

Pathophysiology

Unstable Angina
Non-ST Elevation Myocardial Infarction

Differentiating Unstable Angina/Non-ST Elevation Myocardial Infarction from other Disorders

Epidemiology and Demographics

Risk Stratification

Natural History, Complications and Prognosis

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Heart Failure and Cardiogenic Shock
Perioperative NSTE-ACS Related to Noncardiac Surgery
Stress (Takotsubo) Cardiomyopathy
Diabetes Mellitus
Post CABG Patients
Older Adults
Chronic Kidney Disease
Angiographically Normal Coronary Arteries
Variant (Prinzmetal's) Angina
Substance Abuse
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Additional Management Considerations for Antiplatelet and Anticoagulant Therapy

Risk Stratification Before Discharge for Patients With an Ischemia-Guided Strategy of NSTE-ACS

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Initial Conservative Versus Initial Invasive Strategies
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Complications of Bleeding and Transfusion

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Varun Kumar, M.B.B.S; Lakshmi Gopalakrishnan, M.B.B.S.; Cafer Zorkun, M.D., Ph.D. [2]; Neil Gheewala, M.D. [3]; Smita Kohli, M.D.

Overview

The Spectrum of Acute Coronary Syndromes

  • Unstable angina, 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).
  • 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 (see Biomarkers). Often, these may not be detected for up to 12 hours in the bloodstream, which emphasizes the need for thorough evaluation. [1] [2]

Definition

Unstable Angina (UA): 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 occurs at rest and may not improve with rest.

Unstable angina[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] is defined as new onset angina pectoris (or chest pain which is ischemic in origin) with the following features:

  • Occurs at rest or with lesser degrees of exertion than stable angina,
  • Lasts less than 30minutes,
  • Follows a crescendo pattern (i.e., occurs more frequently than previous)
  • There no sign of myocardial necrosis unlike in STEMI or NSTEMI, and there is no release of biomarkers of myonecrosis (CK or troponin).

Non-ST Elevation MI (NSTEMI):

Incidence

Pathophysiology

These conditions are characterized by an inadequate blood supply to meet the oxygen and metabolic demands of the myocardium.

  • 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.
  • 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).
  • A less common cause of UA is Prinzmetal angina where in a there is focal spasm of a segment of an epicardial coronary artery caused by smooth muscle hypercontractility and/or endothelial dysfunction resulting in dynamic obstruction.
  • Some patients with progressive atherosclerosis or with restenosis after a PCI can also cause UA by severe narrowing without spasm or thrombus.

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, ECG and cardiac biomarkers 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.

Unstable angina is associated with negative cardiac biomarkers whereas NSTEMI is associated with elevated cardiac biomarkers. Depending on the patient's symptoms and degree of suspicion for ACS, early coronary angiography can be performed to make a definitive diagnosis.

Risk Stratification

  • Patients with UA have lower short term mortality than NSTEMI or STEMI.
  • Early risk stratification is, therefore, 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 one of the three categories of low, intermediate or high likelihood. Patients with high risk score and/or hemodynamic instability should be managed in coronary care unit while those with intermediate to low risk score and hemodynamic stability can be managed in a step down unit.
  • A continuous ECG monitoring (telemetry) should be used to monitor for arrythmias.

Treatment

Immediate management is directed towards relief of chest pain.

  • Nitrates, ASA and morphine are recommended to control the symptoms from possible ACS.
  • Beta blockers, thienopyridines (like Clopidogrel and prasugrel) should be administered in the absence of contraindication to their use.
  • Based on the suspicion for likelihood of ACS, anticoagulants and GP IIb/IIIa inhibitors can be started early in the course of presentation.
  • Two strategies in the treatment are early invasive or conservative strategies. Most trials have shown benefit of early invasive therapy with cardiac catheterization and revascularisation procedures. Early invasive therapy is now recommended for patients with UA/NSTEMI and ST segment changes at presentation and/or positive troponins during first 24hrs of presentation.

Discharge Care

  • Discharge care after UA/NSTEMI must include a medication reconciliation of inpatient and discharge medications, life style modification counselling and instructions on smoking cessation, cardiac rehabilitation and arrangements for follow-up.
  • Patients with UA/NSTEMI diagnosis should be discharged home on an ASA, clopidogrel, beta blocker, nitrates, ACE inhibitors and statins, unless contraindicated.
  • Cardiac rehab has been shown to improve exercise tolerance, improve patient compliance and assist in lifestyle modification and all patient should be referred for this.
  • Both patient and family should be informed about the treatment plan and a what to do if symptoms recur.

Related Chapters

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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