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2007 ACC/AHA UA/NSTEMI Guideline Revision

NSTEMI

2014

Οξύ Έµφραγµα του Μυοκαρδίου χωρίς ανάσπαση του ST

ΘΩΜΑΣ ΜΠΕΛΕΒΕΣΛΗΣ Αρχίατρος – Επεµβατικός Καρδιολόγος


Acute Coronary Syndrome (ACS)

! Definition: The spectrum of acute ischemia related syndromes ranging from UA to MI with or without ST elevation that are secondary to acute plaque rupture or plaque erosion.

[----UA---------NSTEMI----------STEMI----]

2014


Decreased O2 Supply • Flow- limiting stenosis

• Anemia

• Plaque rupture/clot

Increased O2 Demand

O2 supply/demand mismatch→Ischemia

Myocardial ischemia→necrosis

Pathophysiology ACS

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Pathophysiology of Stable Angina and ACS

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2007 ACC/AHA UA/NSTEMI Guideline Revision 2014

Sudden Thrombus or Thromboembolism Ruptured

Fibrous CapSuperficial

Erosion

Modified from Libby P Circ 104:365,2001


No ST Elevation ST Elevation

Acute Coronary Syndrome

NQMI Qw MI

NSTEMI

Myocardial Infarction

Davies MJ Heart 83:361, 2000

Ischemic Discomfort Presentation

Working Dx

ECG

Biochem. Marker

Hamm Lancet 358:1533,2001

Unstable Angina Final Dx


Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS)

Acute Coronary Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMI† STEMI

1.24 million Admissions per year

.33 million Admissions per year

Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171. *Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.

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Placebo Event Rates in Recent Trials of UA and NSTEMI

!  PRISM1 7.1% !  PRISM-PLUS2 11.9% !  PURSUIT3 15.7% !  GUSTO-IV ACS4 8.0%

!  PARAGON A5 11.7%

Death/MI at 30 days

1. PRISM Study Investigators. N Engl J Med 1998;338:1498-1505. 2. PRISM-PLUS Study Investigators. N Engl J Med 1998;338:1488-1497. 3. Harrington RA. Am J Cardiol 1997;80:34B-38B. 4. The GUSTO IV-ACS Investigators. Lancet 2001;357:1915-1924. 5. The PARGON Investigators. Circulation 1998;97:2386-2395.

UA and NSTEMI

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Initial Evaluation and management of Non ST-elevation ACS

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Initial Evaluation and Management • History and Physical • ECG • Cardiac Biomarkers

Establish the Likelihood that Clinical Presentation Represents an ACS Secondary to CAD

Risk Stratify for Short-term Adverse Outcomes


Class I Patients with suspected ACS and high-risk

features such as 1.  continuing chest pain, 2.  severe dyspnea, 3.  syncope/presyncope, 4.  or palpitations should be referred immediately to the ED

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Initial Evaluation


Likelihood of ACS by Hx/PE

!  History/Examination "  Pain in Chest or Left Arm "  CP Radiation ○  Right Shoulder ○  Left Arm ○  Both Left & Right Arm

"  Diaphoresis "  3rd Heart Sound "  SBP < 80 mm Hg "  Pulmonary Crackles Panju AA. JAMA. 1998;280:1256.

Suggesting AMI LR 2.7 LR 2.9 (1.4-6.0) LR 2.3 (1.7-3.1) LR 7.1 (3.6-14.2) LR 2.0 (1.9-2.2) LR 3.2 (1.6-6.5) LR 3.1 (1.8-5.2) LR 2.1 (1.4-3.1)

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·∙ Nonischemic (e.g., aortic dissection, expanding aortic aneurysm, pericarditis, pulmonary embolism) ·∙ Noncardiovascular discomfort include: o Pulmonary causes (e.g., pneumonia, pleuritis, pneumothorax) o Gastrointestinal causes (e.g., gastroesophageal reflux, esophageal spasm, peptic ulcer, pancreatitis, biliary disease) o Musculoskeletal causes (e.g., costochondritis, cervical radiculopathy) o Psychiatric disorders o Other etiologies (e.g., sickle cell crisis, herpes zoster)

Differential diagnosis of NSTE-ACS

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Electrocardiogram

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Changes on ECG in patients with NSTE-ACS 1. ST depression, 2. transient ST elevation, or 3. new T-wave inversion

A normal ECG does not exclude ACS and occurs in 1% to 6% A normal ECG may also be associated with left circumflex or right coronary artery occlusions, which can be electrically silent (in which case posterior electrocardiographic leads [V7 to V9] may be helpful).


How Sensitive is the ECG Alone?

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Wellens’ syndrome

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Kaplan-Meier Estimates of Probability of Death Based on Admission Electrocardiogram

Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157


Biomarkers of Myocardial Necrosis


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3,4 3,7

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0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 9,0

Cardiac troponin I (ng/ml)

Mor

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42

Day

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831 174 148 134 50 67

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% %

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Risk Stratification by Troponin

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Non ACS causes of Troponin Elevation 1.  Trauma (including contusion; ablation; pacing; ICD firings,, endomyocardial biopsy, cardiac

surgery, after-interventional closure of ASDs) 2.  Congestive heart failure (acute and chronic) 3.  Aortic valve disease and HOCM with significant LVH 4.  Hypertension 5.  Hypotension, often with arrhythmias 6.  Noncardiac surgery 7.  Renal failure 8.  Critically ill patients, especially with diabetes, respiratory failure 9.  Drug toxicity (eg, adriamycin, 5 FU, herceptin, snake venoms) 10.  Hypothyroidism 11.  Coronary vasospasm, including apical ballooning syndrome 12.  Inflammatory diseases (eg, myocarditis, Kawasaki disease, smallpox vaccination, 13.  Post-PCI 14.  Pulmonary embolism, severe pulmonary hypertension 15.  Sepsis 16.  Burns, especially if TBSA greater than 30% 17.  Infiltrative diseases: amyloidosis, hemachromatosis, sarcoidosis, and scleroderma 18.  Acute neurologic disease, including CVA, subarchnoid bleeds 19.  Rhabdomyolysis with cardiac injury 20.  Transplant vasculopathy 21.  Vital exhaustion

Modified from Apple FS, et al Heart J. 2002;144:981-986.

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Combined Sensitivities for ACS

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Image

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Chest roentgenogram Transthoracic echocardiography Transesophageal echocardiography Computed tomography (CT) Coronary CT angiography Myocardial perfusion imaging


Risk Stratification

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Risk Assessment Dependent on Contingent Probabilities

!  Likelihood of obstructive CAD as cause of symptoms "  Dominated by acute

findings ○  Exam ○  Symptoms ○  Markers

"  Traditional risk factors are of limited utility

!  Does this patient have symptoms due to acute ischemia from obstructive CAD?

!  Risk of bad outcome "  Dominated by acute

findings ○  Older age very

important ○  Hemodynamic

abnormalities critical

○  ECG, markers !  What is the

likelihood of death, MI, heart failure?

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24h 3-4 days 6 months

Ris

k

Physiological monitoring Periodic physical exams Cardiac markers ECG

Time

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Unstable angina/NSTEMI cardiac care

! Evaluate for conservative vs. invasive strategy based upon: ○ Likelihood of actual ACS ○ Risk stratification by risk scores ○ ACS risk categories per AHA guidelines

Low Intermediate

High

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Risk Scores TIMI GRACE Future

History

Age Hypertension Diabetes Smoking ↑cholesterol Family history History of CAD

Age Continuous assessment

Presentation

Severe angina Aspirin within 7 days Elevated markers ST segment deviation

Heart rate Systolic BP Elevated markers Heart failure Cardiac arrest Elevated markers ST segment deviation

New markers Electronic health records

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TIMI Risk Score

Predicts risk of death, new/recurrent MI, need for urgent revascularization within 14 days

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Predicted 6-month mortality Risk of future adverse cardiovascular events

1.5% or below Lowest

> 1.5 to 3.0% Low

> 3.0 to 6.0% Intermediate

> 6.0 to 9.0% High

over 9.0% Highest

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TIMI Risk Score


Perform rapid determination of likelihood of ACS, including a 12-lead ECG within 10 min of arrival at an emergency facility, in patients whose symptoms suggest ACS

I C

Perform serial ECGs at 15- to 30-min intervals during the first hour in symptomatic patients with initial non diagnostic ECG

I C

Measure cardiac troponin (cTnI or cTnT) in all patients with symptoms consistent with ACS*

I A

Measure serial cardiac troponin I or T at presentation and 3–6 h after symptom onset* in all patients with symptoms consistent with ACS

I A

Use risk scores to assess prognosis in patients with NSTE-ACS I A Risk-stratification models can be useful in management IIa B Obtain supplemental electrocardiographic leads V7 to V9 in patients with initial nondiagnostic ECG at intermediate/high risk for ACS

IIa B

Continuous monitoring with 12-lead ECG may be a reasonable alternative with initial nondiagnostic ECG in patients at intermediate/high risk for ACS

IIb B

BNP or NT–pro-BNP may be considered to assess risk in patients with suspected ACS

IIb B

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Early Hospital Care

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! Anti-Ischemic Therapy ! Anti-Platelet Therapy ! Anticoagulant Therapy


Early Hospital Care Anti-Ischemic Therapy

!  Class I "  Bed/Chair rest and Telemetry "  Oxygen (maintain saturation >90%) "  Nitrates (SLx3 Oral/topical. IV for ongoing

iscemia, heart failure, hypertension) "  Oral B-blockers in First 24-hours if no

contraindications. (IV B-blockers class IIa indication)

"  Non-dihydropyridine Ca-channel blockers for those with contraindication fo B-blockers

"  ACE inhibitors in first 24-hours for heart failure or EF<40% (Class IIa for all other pts) (ARBs for those intolerant)

"  Statins

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Early Hospital Care Anti-Platelet Therapy

! Class I "  Aspirin (162-325 mg), non enteric coated "  P2Y12 inhibitors Clopidogrel or Ticagrelor " GI prophylaxis if a Hx of GI bleed " GP IIb/IIIa inhibitors should be evaluated based on

whether an invasive or conservative strategy is used

" GP IIb/IIIa inhibitors recommended for all diabetics and all patient in early invasive arm

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Early Hospital Care Anticoagulant Therapy

! Class I " Unfractionated Heparin "  Enoxaparin "  Bivalarudin "  Fondaparinux " Argatroban

" Relative choice depends on invasive vs conservative strategy and bleeding risk

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Early Hospital Care Statin Therapy

! In patients recently hospitalized within 10 days for an acute coronary syndrome:

•  “Intensive” high-dose LDL-C lowering (median LDL-C 62 mg/dL) compared to “moderate” standard-dose lipid-lowering therapy (median LDL-C 95 mg/dL) reduced the risk of all cause mortality or major cardiac events by 16% (p=0.005)

• Benefits emerged within 30 days post ACS with continued benefit observed throughout the 2.5 years of follow-up

• Benefits were consistent across all cardiovascular endpoints, except stroke, and most clinical subgroups

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Invasive or Conservative Strategy

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Invasive vs Conservative Strategy Clinical Trials

TIMI IIIB (94)

Conservative Strategy Favored

N=920

Invasive Strategy Favored

N=7,018

VANQWISH (98)

MATE

FRISC II (99)

TACTICS- TIMI 18 (01)

VINO

RITA-3 (02)

TRUCS

ISAR- COOL

ICTUS (05)

No difference N=2,874

Weight of the evidence

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Invasive Strategies

FRISC-II trial ICTUS RITA-3 trial

Absolute reductions of 2.0% to 3.8% in cardiovascular death or MI in the low- and intermediate-risk and an 11.1% absolute risk reduction in the highest-risk patients. The invasive strategy demons t ra ted i t s g rea tes t advantage in the highest-risk stratum of patients with no significant benefit on mortality over the noninvasive approach in moderate- and low-risk patients

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Diagnosis of UA/NSTEMI is Likely or Definite

Ischaimia – Guided strategy

Early inasive strategy

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Immediate invasive (within 2 h)

Refractory angina Signs or symptoms of HF or new or worsening mitral regurgitation Hemodynamic instability Recurrent angina or ischemia at rest or with low-level activities despite intensive medical therapy

Sustained VT or VF Ischemia-guided strategy

Low-risk score (e.g., TIMI [0 or 1], GRACE [<109]) Low-risk Tn-negative female patients Patient or clinician preference in the absence of high-risk features

Early invasive (within 24 h)

None of the above, but GRACE risk score >140 Temporal change in Tn (Section 3.4) New or presumably new ST depression

Delayed invasive (within 25-72 h)

None of the above but diabetes mellitus Renal insufficiency (GFR <60 mL/min/1.73 m²) Reduced LV systolic function (EF <0.40) Early postinfarction angina PCI within 6 mo Prior CABG GRACE risk score 109–140; TIMI score ≥2

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Early Invasive Strategy or Ischemia-Guided Strategy in Patients With NSTE-ACS


NSTE-ACS : Definite or Likely

Ishemia-Guided Strategy Early Invasive Strategy

Initiate DAPT and Anticoagulant Therapy 1.  ASA 2.  P2Y12 inhibitor (in addition to

ASA) Clopidogrel or Ticagrelor 3.  Anticoagulant : UFH Enoxaparin Fondaparinux

Initiate DAPT and Anticoagulant Therary 1.  ASA 2.  P2Y12 inhibitor (in addition to ASA) Clopidogrel or Ticagrelor 3.  Anticoagulant : UFH Enoxaparin Fondaparinux Bivalirudin

Can consider GPI in addition to ASA and P2Y12 inhibitor in high-risk (e.g., troponine positive) pts Eptifibatide Tirofiban

Medical therapy chosen based on cath findings

Therapy ineffective Therapy effective

PCI CABG

(Continued) Stress tests


Therapy effective Therapy ineffective

PCI With Stenting Initiate/ continue antiplatelet and anticoagulant

therapy 1.  ASA 2.  P2Y12 inhibitor (in addition to ASA0 Cloprdogrel Prasugrel Ticagrelor 3.  GPI (if not treated with bivalirudin at time of PCI High-risk features, not adequately pretreated with clopidogrel (Class I) High-risk features adequately pretreated with clopidogrel (class Iia) 4.  Anticoagulant : UFH Enoxaparin Bivalirudin Fondaparinux class III as the sole anticoagulant

CABG Initiate / continue ASA therapy and

discontinue P2Y12 and / or GPI therapy

1.  ASA 2.  Discontinue clopidogrel/ticagrelor 5

d before, and prasugrel at least 7 d before elective CABG

3.  Discontinue clopidogrel/ticagrelor up to 24h before urgent CABG. May perfotm urgent CABG< 5 d after clopidogrel/ticagrelor and < 7 d after prasugrel discontinued

4.  Discontinue eptifibatide/ tirofiban at least 2-4h before, and abciximab ≥ 12h before CABG

Late Hospital / Possthospital Care 1.  ASA 2.  P2Y12 inhibitor (clopidogrel or ticagrelor), in

addition to ASA, up to 12 mo if medically treated

3.  P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor), in addition to ASA, at least 12 mo if treated with coronary stenting

PCI CABG

Stress tests


Risk Stratification Before Discharge for Patients With an Ischemia-Guided Strategy of NSTE-ACS: recommendations Class I 1.  Noninvasive stress testing is recommended in low- and intermediate-risk

patients who have been free of ischemia at rest or with low-level activity for a minimum of 12 to 24 hours. (Level of Evidence: B)

2. Treadmill exercise testing is useful in patients able to exercise in whom the ECG is free of resting ST changes that may interfere with interpretation (Level of Evidence: C) 3. Stress testing with an imaging modality should be used in patients who are able to exercise but have ST changes on resting ECG that may interfere with interpretation. In patients undergoing a low-level exercise test, an imaging modality can add prognostic information (Level of Evidence: B) 4. Pharmacological stress testing with imaging is recommended when physical limitations preclude adequate exercise stress. (Level of Evidence:C)

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Therapy effective Therapy ineffective

PCI With Stenting Initiate/ continue antiplatelet and anticoagulant

therapy 1.  ASA 2.  P2Y12 inhibitor (in addition to ASA0 Cloprdogrel Prasugrel Ticagrelor 3.  GPI (if not treated with bivalirudin at time of PCI High-risk features, not adequately pretreated with clopidogrel (Class I) High-risk features adequately pretreated with clopidogrel (class Iia) 4.  Anticoagulant : UFH Enoxaparin Bivalirudin Fondaparinux class III as the sole anticoagulant

CABG Initiate / continue ASA therapy and

discontinue P2Y12 and / or GPI therapy

1.  ASA 2.  Discontinue clopidogrel/ticagrelor 5

d before, and prasugrel at least 7 d before elective CABG

3.  Discontinue clopidogrel/ticagrelor up to 24h before urgent CABG. May perfotm urgent CABG< 5 d after clopidogrel/ticagrelor and < 7 d after prasugrel discontinued

4.  Discontinue eptifibatide/ tirofiban at least 2-4h before, and abciximab ≥ 12h before CABG

Late Hospital / Possthospital Care 1.  ASA 2.  P2Y12 inhibitor (clopidogrel or ticagrelor), in

addition to ASA, up to 12 mo if medically treated

3.  P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor), in addition to ASA, at least 12 mo if treated with coronary stenting

PCI CABG

Stress tests


PCI—General Considerations:

Recommendation Class IIb

A strategy of multivessel PCI, in contrast to culprit lesion-only PCI, may be reasonable in patients undergoing coronary revascularization as part of treatment for NSTE-ACS (Level of Evidence: B)

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ACS With Normal Coronary Arteries

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Class IIb 1. If coronary angiography reveals normal coronary arteries and endothelial dysfunction is suspected, invasive physiological assessment such as coronary flow reserve measurement may be considered). (Level of Evidence: B)

Stress (Takotsubo) Cardiomyopathy Class I 1. Stress (Takotsubo) cardiomyopathy should be considered in patients who present with apparent ACS and nonobstructive CAD at angiography. (Level of Evidence: C) 2. Imaging with ventriculography, echocardiography, or magnetic resonance imaging should be performed to confirm or exclude the diagnosis of stress (Takotsubo) cardiomyopathy. (Level of Evidence: B)


Preparation for Discharge After UA/NSTEMI !  Beta Blocker !  ACEI / ARB

–  Especially if DM, HF, EF <40%, HTN !  Statin

–  LDL <100 mg/dL (ideally <70 mg/dL) !  Secondary Prevention Measures

–  Smoking Cessation –  BP <140/90 mm HG or <130/80 mm HG for DM or chronic kidney

disease –  HbA1C <7% –  BMI 18.5-24.9 –  Physical Exercise 30-60 min at least 5 days/wk

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