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Chapter 293. 294. 294
Non-ST Elevation Acute
Coronary Syndrom- NSTE ACS
Unstable Angina
Non-ST elevation MI
ST Elevation Myocardial Infarct
STMI...
Acute coronary syndrome is defined as
myocardial ischemia due to myocardial
infarction (NSTEMI or STEMI) or unstable angin...
Thrombus formation
Downstream embolization
Dynamic Obstruction (Spasm –f.e. Prinzmetal ‘s
Variant Angina
Invreased oxygen ...
Dx of acute coronary syndrome is based on history,
physical exam, ECG, cardiac enzymes
Patients can then be divided into s...
Severe chest discomfort
Occurs at rest
Lasting >10 min
Recent onset (up to 2 weeks)
Crescendo pattern
Plaque rupture and subsequent formation of thrombus
– this can be either occlusive or non-occlusive (STEMI,
NSTEMI, USA)
V...
Acute coronary syndromes can also be due to
secondary causes
Thyrotoxicosis
Anemia
Tachycardia
Hypotension
Hypoxemia
Ateri...
ECG
Echocardiography
Myocardial SPECT
Biomarkers – Troponin, CK-MB, Mioglobin
CCTA
Date of download: 9/30/2015
From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline Fro...
In the absence of abnormal findings on physical exam,
ECG, or enzymes, the pre-test probability of acute
coronary syndrome...
Aspirin is an antiplatelet agent that initiates the
irreversible inhibition of cyclooxygenase,
thereby preventing platelet...
Aspirin should be given in a dose of 75-325
mg/day to all patients with ACS unless there is a
contraindication (in which c...
Clopidogrel is a potent antiplatelet agent
It should be administered to all patients who
cannot take ASA
The CURE trial su...
Clopidogrel should be administered to patients who
cannot take ASA because of hypersensitivity or
gastrointestinal intoler...
Nitroglycerin is considered a cornerstone of anti-
anginal therapy, despite little objective evidence for its
benefit
Bene...
Beta Blockers reduce myocardial oxygen
demand by reducing heart rate, contractility,
and ventricular wall tension
Administ...
Intravenous beta blockers should be used
initially in all patients (without contraindication)
followed by oral beta blocke...
Heparin (unfractionated heparin or UFH) has
traditionally been the mainstay of therapy in
acute coronary syndromes as its ...
More recent studies indicate that low molecular
weight heparin is also effective in the reduction
of end points such as my...
All patients with acute coronary syndromes
should be treated with a combination of ASA
(325 mg/day) and heparin (bolus fol...
The best documented mechanism by which
these agents act is to reduce ventricular
remodeling over days to weeks after myoca...
ACE-I should be administered to all patients in
the first 24 hours of ACS provided hypotension
and other clear cut contrai...
Statins may be of benefit in ACS
Possible mechanisms include plaque
stabilization, reversal of endothelial
dysfunction, de...
Age >65 yrs
Daily ASA Therapy (>7 days prior to event)
Symptoms of Unstable Angina
Documented CAD (stenosis > 50%)
3 or mo...
Score of 3 or less = low risk
Score of 4-5 = intermediate risk (use IIBIIIA)
Score of 6-7 = high risk (use IIBIIIA)
In the setting of STEMI primary PCI is associated
with better outcomes than thrombolysis
Emergent PCI is also indicated in...
PAMI (PTCA vs. thrombolysis)
Netherlands Trials (PTCA vs. thrombolysis)
GUSTO IIB (PTCA vs. thrombolysis)
DANAMI-2 (stenti...
Primary PCI is indicated as an alternative to
thrombolysis when the following criteria are met:
STEMI or new LBBB
Can unde...
Good History and Physical (note time and
duration of symptoms)
Careful evaluation of ECG (compare to previous
when possibl...
ASA
NTG (consider MSO4 if pain not relieved)
Beta Blocker
Heparin/LMWH
ACE-I
+/- Statin
+/- Clopidogrel (don’t give if CAB...
ASA
NTG (consider MSO4 if pain not relieved)
Beta Blocker
Heparin/LMWH
ACE-I
+/-Clopidogrel (based on possibility of CABG)...
Medical Management of
Acute Coronary Syndrome
1. Evidence of myocardial necrosis: cardiac biomarker values (preferably
cardiac troponin [cTn]) and with at least one of ...
Criteria for Prior Myocardial l nfarction
Any one of the fol lowing criteria meets the diagnosis for prior
MI
. Pathologic...
Type 1: Sponta neous Myocardial lnfarction
Type 2: Myocardial l nfarction Secondary to an Ischemic Imbalance
Type 3: Myoca...
Date of download: 9/30/2015
From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline Fro...
Ventricular Disfunction
Hemodinamic Assessment
Hypovolemia
Cardiogenic shock
Arrhythmias, conduction disturbances
Pericard...
Complication
Type
Manifestations
Ischemic Angina, reinfarction, infarct extension
Mechanical Heart failure, cardiogenic sh...
Date of download: 9/30/2015
From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline Fro...
Syndrome Stenoses
Plaque
Disruption Plaque-Associated Thrombus
Stable angina >75% No No
Unstable angina Variable Frequent ...
Ischemic Heart Disease
Angina Pectoris
Chest discomfort = prolonged, recurrent, different qualities
Cause = transient myoc...
Transmural
Full thickness
Superimposed thrombus in
atherosclerosis
Focal damage
Sub-endocardial
Inner 1/3 to half of
ventr...
Ischemic Heart Disease
MI= Also called Heart attack
Incidence = disease of old
elderly (45% in 65 yrs. old)
young ( 10% in...
Ischemic Heart Disease
MI
Pathogenesis
Coronary vessel occlusion
Atherosclerosis with thrombus = MC cause ( 90% cases)
Oth...
Ischemic Heart Disease
TTC
Ischemic Heart Disease
MI -Morphology
light microscopy
First 12 hrs. after MI – no change
Up to 3 days = Coagulative necro...
One-day-old infarct
coagulative necrosis
wavy fibers
Up to 3 days duration
Neutrophilic infiltrate
1 -2 weeks
Granulation ...
Ischemic Heart Disease
MI –Reperfusion
Mechanisms
Intrinsic
Extrinsic =
Thrombolytic drugs = < 1hr. After onset of MI
PTCA...
Ischemic Heart Disease
Ischemic Heart Disease
MI = Clinical
Silent MI = DM, Elderly, Cardiac transplantation
recipients,
Typical features = Rapid...
Ischemic Heart Disease
MI –Complications
In 75% of Patients with MI
Poor prognosis in = elderly, females, DM, old case of ...
Ischemic Heart Disease
Sudden cardiac death = unexpected death in one hour due
to cardiac causes with or without clinical ...
Ischemic Heart Disease
Chronic IHD = also called ischemic cardiomyopathy
Patients = post heart transplant receipts, previo...
What is it?
What are these?
Date of download: 9/30/2015
From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline Fro...
Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.
From: 2014 AHA/ACC Guide...
Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.
From: 2014 AHA/ACC Guide...
Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.
From: 2014 AHA/ACC Guide...
Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.
From: 2014 AHA/ACC Guide...
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293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
293. ischemic heart disease
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ischemic heart disease

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293. ischemic heart disease

  1. 1. Chapter 293. 294. 294
  2. 2. Non-ST Elevation Acute Coronary Syndrom- NSTE ACS Unstable Angina Non-ST elevation MI ST Elevation Myocardial Infarct STMI Stable Angina Class1 Class2 Class3 Class 4
  3. 3. Acute coronary syndrome is defined as myocardial ischemia due to myocardial infarction (NSTEMI or STEMI) or unstable angina Unstable angina is defined as angina at rest, new onset exertional angina (<2 months), recent acceleration of angina (<2 months), or post revascularization angina
  4. 4. Thrombus formation Downstream embolization Dynamic Obstruction (Spasm –f.e. Prinzmetal ‘s Variant Angina Invreased oxygen demand
  5. 5. Dx of acute coronary syndrome is based on history, physical exam, ECG, cardiac enzymes Patients can then be divided into several groups Non-cardiac chest pain (i.e., Gastrointestinal, musculoskeletal, pulmonary embolus) Stable angina Unstable angina Myocardial infarction (STEMI or NSTEMI) Other cardiac causes of chest pain (i.e., aortic dissection, pericarditis)
  6. 6. Severe chest discomfort Occurs at rest Lasting >10 min Recent onset (up to 2 weeks) Crescendo pattern
  7. 7. Plaque rupture and subsequent formation of thrombus – this can be either occlusive or non-occlusive (STEMI, NSTEMI, USA) Vasospasm such as that seen in Prinzmetal’s angina, cocaine use (STEMI, NSTEMI, USA) Progression of obstructive coronary atherosclerotic disease (USA) In-stent thrombosis (early post PCI) In-stent restenosis (late post PCI Poor surgical technique (post CABG)
  8. 8. Acute coronary syndromes can also be due to secondary causes Thyrotoxicosis Anemia Tachycardia Hypotension Hypoxemia Aterial inflammation (infection, arteritis)
  9. 9. ECG Echocardiography Myocardial SPECT Biomarkers – Troponin, CK-MB, Mioglobin CCTA
  10. 10. Date of download: 9/30/2015 From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010 Clinical Classification of Chest Pain Table Title: Copyright © American College of Physicians. All rights reserved.
  11. 11. In the absence of abnormal findings on physical exam, ECG, or enzymes, the pre-test probability of acute coronary syndrome must be determined by the clinician A good history is crucial (is the chest pain typical or atypical; what are the associated symptoms) Determination of risk factors is also crucial (male, age >55, smoking, DM, HTN, FamHx, hyperlipidemia, known CAD)
  12. 12. Aspirin is an antiplatelet agent that initiates the irreversible inhibition of cyclooxygenase, thereby preventing platelet production of thromboxane A2 and decreasing platelet aggregation Administration of ASA in ACS reduces cardiac endpoints
  13. 13. Aspirin should be given in a dose of 75-325 mg/day to all patients with ACS unless there is a contraindication (in which case, clopidogrel should be given)
  14. 14. Clopidogrel is a potent antiplatelet agent It should be administered to all patients who cannot take ASA The CURE trial suggests a benefit to adding Clopidogrel to ASA/Heparin in patients going for PCI Give 300 mg loading dose followed by 75 mg/day
  15. 15. Clopidogrel should be administered to patients who cannot take ASA because of hypersensitivity or gastrointestinal intolerance In hospitalized patients in whom an early, noninterventional approach is planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month and up to 9 months. Do not use clopidogrel if there is any possibility patient may be candidate for CABG
  16. 16. Nitroglycerin is considered a cornerstone of anti- anginal therapy, despite little objective evidence for its benefit Benefit is thought to occur via reduction in myocardial O2 demand secondary to venodilation induced reduction in preload as well as coronary vasodilation and afterload reduction Titrate to relief of chest pain; chest pain = death of myocardial cells No documented mortality benefit
  17. 17. Beta Blockers reduce myocardial oxygen demand by reducing heart rate, contractility, and ventricular wall tension Administration of beta blockers in ACS reduces cardiac endpoints
  18. 18. Intravenous beta blockers should be used initially in all patients (without contraindication) followed by oral beta blockers with the goal being decrease in heart rate to 60 beats per minute A combination of beta blockers and nitrates can be viewed as first line therapy in all patients with ACS
  19. 19. Heparin (unfractionated heparin or UFH) has traditionally been the mainstay of therapy in acute coronary syndromes as its efficacy has been documented in several large, randomized trials
  20. 20. More recent studies indicate that low molecular weight heparin is also effective in the reduction of end points such as myocardial infarction or death Some studies report that LMWH, when used in combination with ASA, may be superior to continuous infusion of Heparin
  21. 21. All patients with acute coronary syndromes should be treated with a combination of ASA (325 mg/day) and heparin (bolus followed by continuous infusion with goal of PTT 1-2.5X control) or ASA and low molecular weight heparin unless one of the drugs is contraindicated
  22. 22. The best documented mechanism by which these agents act is to reduce ventricular remodeling over days to weeks after myocardial damage. However, there is data that a mortality benefit exists when these agents are used early in the course of ACS Administration of ACE-I in ACS reduces cardiac endpoints
  23. 23. ACE-I should be administered to all patients in the first 24 hours of ACS provided hypotension and other clear cut contraindications are absent
  24. 24. Statins may be of benefit in ACS Possible mechanisms include plaque stabilization, reversal of endothelial dysfunction, decreased thrombogenicity, and reduction of inflammation
  25. 25. Age >65 yrs Daily ASA Therapy (>7 days prior to event) Symptoms of Unstable Angina Documented CAD (stenosis > 50%) 3 or more traditional cardiac risk factors Elevated cardiac enzymes ECG changes
  26. 26. Score of 3 or less = low risk Score of 4-5 = intermediate risk (use IIBIIIA) Score of 6-7 = high risk (use IIBIIIA)
  27. 27. In the setting of STEMI primary PCI is associated with better outcomes than thrombolysis Emergent PCI is also indicated in the setting of a new LBBB
  28. 28. PAMI (PTCA vs. thrombolysis) Netherlands Trials (PTCA vs. thrombolysis) GUSTO IIB (PTCA vs. thrombolysis) DANAMI-2 (stenting vs. thrombolysis) STAT (stenting vs. thrombolysis)
  29. 29. Primary PCI is indicated as an alternative to thrombolysis when the following criteria are met: STEMI or new LBBB Can undergo PCI within 12 hours of the onset of symptoms The MD doing the intervention does more than 75 PCI’s/yr The procedure is done in a center that does more than 200 PCI’s/yr and has surgical backup
  30. 30. Good History and Physical (note time and duration of symptoms) Careful evaluation of ECG (compare to previous when possible) Check Cardiac Enzymes Monitor on Telemetry Oxygen
  31. 31. ASA NTG (consider MSO4 if pain not relieved) Beta Blocker Heparin/LMWH ACE-I +/- Statin +/- Clopidogrel (don’t give if CABG is a possibility) +/- IIBIIIA inhibitors (based on TIMI risk score)
  32. 32. ASA NTG (consider MSO4 if pain not relieved) Beta Blocker Heparin/LMWH ACE-I +/-Clopidogrel (based on possibility of CABG) IIBIIIA +/- Statin Activate the Cath Lab!!!
  33. 33. Medical Management of Acute Coronary Syndrome
  34. 34. 1. Evidence of myocardial necrosis: cardiac biomarker values (preferably cardiac troponin [cTn]) and with at least one of the following . Symptoms of ischemia . New or presumed new significant ST-T changes or new LBBB . Development of pathologic Q waves on ECG . Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality . Identification of an intracoronary thrombus by angiography or autopsy . Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes of new LBBB, but death occurred before cardiac biomarkers were obtained or before cardiac biomarker values would be increased . Percutaneous coronary intervention (PCI)-related MI is arbitrarily de有 ned by elevation of cTn val ues (>5 x 99th percentile U RL) in patients with nor mal 七as巳line val ues (王99th percentile URL) or a rise of cTn val ues
  35. 35. Criteria for Prior Myocardial l nfarction Any one of the fol lowing criteria meets the diagnosis for prior MI . Pathologic Q waves with or without 5ym仁tom5 in the ab5巳 nce of nonischemlc caU5巴5 . I maging evidence of a region of 1055 of viable myocardium that i5 thinned and fails to contract, in the absence of a noni5chemic cause. . Pathologic 有ndings of a prior M
  36. 36. Type 1: Sponta neous Myocardial lnfarction Type 2: Myocardial l nfarction Secondary to an Ischemic Imbalance Type 3: Myocardial l nfarction Resulting in Death When Biomarker Values Are Unavailable Type 4a: Myocardia川 nfarction Related to Percutaneous Coronary Intervention (PCI) Type 4b: Myocardial lnfarction Related to Stent Thrombosis Type 5: Myocardial l nfarction Related to Coronary Artery Bypass Grafting (CABG)
  37. 37. Date of download: 9/30/2015 From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010 Pretest Likelihood of Coronary Artery Disease in Symptomatic Patients According to Age and Sex Copyright © American College of Physicians. All rights reserved.
  38. 38. Ventricular Disfunction Hemodinamic Assessment Hypovolemia Cardiogenic shock Arrhythmias, conduction disturbances Pericarditis Aneurism
  39. 39. Complication Type Manifestations Ischemic Angina, reinfarction, infarct extension Mechanical Heart failure, cardiogenic shock, mitral valve dysfunction, aneurysms, cardiac rupture Arrhythmic Atrial or ventricular arrhythmias, sinus or atrioventricular node dysfunction Embolic Central nervous system or peripheral embolization Inflammatory Pericarditis
  40. 40. Date of download: 9/30/2015 From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010 Comparing Pretest Likelihoods of Coronary Artery Disease in Low-Risk Symptomatic Patients and High-Risk Symptomatic Patients Table Title: Copyright © American College of Physicians. All rights reserved.
  41. 41. Syndrome Stenoses Plaque Disruption Plaque-Associated Thrombus Stable angina >75% No No Unstable angina Variable Frequent Non-occlusive Transmural MI Variable Frequent Occlusive Subendocardial MI Variable Variable Widely variable Sudden death severe Frequent Often small
  42. 42. Ischemic Heart Disease Angina Pectoris Chest discomfort = prolonged, recurrent, different qualities Cause = transient myocardial ischemia( seconds to minutes) Patterns Stable = 75% vessel block, transient ( <15 minutes), aggravated by exertion, relived by rest & Nitroglycerin (VD) Prinzmetal = coronary spasm, episodic, Typical EKG change – ST elevation, Relived by VD but not rest Unstable = 90% vessel block or Acute plaque change ( superimposed thrombus), prolonged ( >15 min.), not relived by rest, VD, Pre-infarction Angina
  43. 43. Transmural Full thickness Superimposed thrombus in atherosclerosis Focal damage Sub-endocardial Inner 1/3 to half of ventricular wall Decreased circulating blood volume( shock, Hypotension, Lysed thrombus) Circumferential
  44. 44. Ischemic Heart Disease MI= Also called Heart attack Incidence = disease of old elderly (45% in 65 yrs. old) young ( 10% in 40yrs. Old), Sex = Male > Female Ethnic = same in African & American Risk factors Major modifiable- DM, HTN, Smoking, Hypercholesterolemia HRT for Postmenopausal females – will not protect the heart
  45. 45. Ischemic Heart Disease MI Pathogenesis Coronary vessel occlusion Atherosclerosis with thrombus = MC cause ( 90% cases) Others = vasospasm (10%) Most important mechanism = dynamic changes in the plaque (rather than plaque size), Plaque disruption PLTS aggregation thrombus and VC (happens in minutes) Irreversible changes = after 30 minutes of ischemia ATP < 10% of normal Mechanism of cell death = necrosis ( Coagulative)
  46. 46. Ischemic Heart Disease TTC
  47. 47. Ischemic Heart Disease MI -Morphology light microscopy First 12 hrs. after MI – no change Up to 3 days = Coagulative necrosis, neutrophils 1-2 weeks = Granulation tissue ≥ 3 weeks = fine scar ≥ 2 months = dense scar EM – membrane disruption and Mitochondrial densities Special stain = TTC ( Triphenyl Tetrazolium chloride), Detects and stains Mahogany brown with Lactate dehydrogenase Unstained area = infarction Mahogany brown = viable White, glistening= scar Most common and nonspecific change in ischemia = sub- endocardial myocyte vacuolization
  48. 48. One-day-old infarct coagulative necrosis wavy fibers Up to 3 days duration Neutrophilic infiltrate 1 -2 weeks Granulation tissue Scar >3 weeks
  49. 49. Ischemic Heart Disease MI –Reperfusion Mechanisms Intrinsic Extrinsic = Thrombolytic drugs = < 1hr. After onset of MI PTCA/CABG = > 1hr. After onset of MI Target = clot lysis and restoration of blood flow Post- reperfusion changes = Contraction bands = hyper contracting myocytes, Stunned myocardium = transient, protective dysfunction Reperfusion damage = mostly apoptosis by free radicals ( unlike MI)
  50. 50. Ischemic Heart Disease
  51. 51. Ischemic Heart Disease MI = Clinical Silent MI = DM, Elderly, Cardiac transplantation recipients, Typical features = Rapid, weak pulse and sweating profusely (diaphoretic), Dyspnea, chest pain Lab= Diagnostic Best markers = Troponins ( T & I), both sensitive and cardio – specific Next best – CK-MB Predictive CRP- >3mg/l – highest risk
  52. 52. Ischemic Heart Disease MI –Complications In 75% of Patients with MI Poor prognosis in = elderly, females, DM, old case of MI, Anterior wall infarct – worst, posterior –worse, Inferior wall – best 1. Arrhythmia = Ventr. Fibrillation – MC arrhythmia lead to sudden death in MI patients, before they reach hospital 2. pump failure – LVF, cariogenic shock, if >LV wall infarcts, lead to death ( 70% of hospitalized MI patients) 3.Ventricular rupture = Free or lateral LV wall – MC site, later cause false aneurysm, 4.True aneurysm = rupture is very rare 5.Pericarditis = Dressler’s syndrome ( Late MI complication) 6.Recurrence
  53. 53. Ischemic Heart Disease Sudden cardiac death = unexpected death in one hour due to cardiac causes with or without clinical symptoms Cause – Atherosclerosis ( 90%), others (10%) Romano- Ward syndrome – Long Q-T syndrome ( K+, Na+ channel defects) Mechanism- Most likely due to arrhythmias ( VF) Patients – young athletes, with Pul. HTN, IHD Morphology Prominent finding – increased heart mass Vacuolations in Sub – endocardial myocardium
  54. 54. Ischemic Heart Disease Chronic IHD = also called ischemic cardiomyopathy Patients = post heart transplant receipts, previous MI or CABG pts Cause =compromised ventricular function Morphology =vacuoles, Myocyte Hypertrophy Diagnosis= by exclusion
  55. 55. What is it?
  56. 56. What are these?
  57. 57. Date of download: 9/30/2015 From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010 Alternative Diagnoses to Angina for Patients With Chest Pain Table Title: Copyright © American College of Physicians. All rights reserved.
  58. 58. Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved. From: 2014 AHA/ACC Guideline for the Management of Patients With Non– ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017
  59. 59. Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved. From: 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017 Global Registry of Acute Coronary Events Risk Calculator for In-Hospital Mortality for Acute Coronary Syndrome
  60. 60. Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved. From: 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017 Algorithm for Management of Patients With Definite or Likely NSTE-ACS* *See corresponding full-sentence recommendations and their explanatory footnotes. †In patients who have been treated with fondaparinux (as upfront therapy) who are undergoing PCI, an additional anticoagulant with anti-IIa activity should be administered at the time of PCI because of the risk of catheter thrombosis. ASA indicates aspirin; CABG, coronary artery bypass graft; cath, catheter; COR, Class of Recommendation; DAPT, dual antiplatelet therapy; GPI, glycoprotein IIb/IIIa inhibitor; LOE, Level of Evidence; NSTE-ACS, non–ST-elevation acute coronary syndrome; PCI, percutaneous coronary intervention; pts, patients; and UFH, unfractionated heparin. Figure Legend:
  61. 61. Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved. From: 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017 Stepped-Care Approach to Pharmacological Therapy for Musculoskeletal Symptoms in Patients With Known Cardiovascular Disease or Risk Factors for Ischemic Heart Disease ASA indicates aspirin; COX-2, cyclooxygenase-2; GI, gastrointestinal; NSAIDs, nonsteroidal anti-inflammatory drugs; and PPI, proton-pump inhibitor. Figure Legend:
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