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2025 PACUPrep BCCCP Preparatory Course Acute Coronary Syndromes Risk Stratification and Timing of Invasive Strategy in Acute Coronary Syndromes

Lesson 9, Topic 2

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Risk Stratification and Timing of Invasive Strategy in Acute Coronary Syndromes

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Diagnosis, Risk Stratification, and Initial Management Planning in Acute Coronary Syndromes

Learning Objective

Apply diagnostic and classification criteria to assess ACS and guide initial management.

I. Clinical Manifestations & Presentation

Acute myocardial ischemia manifests with chest discomfort and associated symptoms; atypical or silent presentations are common in women, elderly and diabetics.

Typical chest pain:

Quality: pressure, tightness, heaviness
Location: substernal; may radiate to jaw, left arm or shoulder
Duration: >20 minutes, constant
Triggers: exertion or emotional stress; not reliably relieved by rest or nitrates

Associated symptoms:

Diaphoresis, dyspnea, nausea/vomiting, palpitations, syncope

Atypical presentations:

Epigastric discomfort, indigestion, profound fatigue

High-risk groups for silent or atypical ACS:

Diabetes, older age, female sex

Key Pearl: Suspect ACS in Specific Populations

Always suspect ACS in diabetics or elderly with unexplained dyspnea or fatigue, even without classic chest pain.

II. Diagnostic Modalities

Rapid integration of ECG, biomarkers and echocardiography confirms myocardial ischemia and guides urgency of care.

A. Electrocardiography

Obtain 12-lead ECG within 10 minutes of presentation
STEMI criteria:
- New ST elevation ≥1 mm in ≥2 contiguous leads (V2–V3 criteria higher in men/women)
- New or presumed new LBBB in appropriate context
NSTEMI/UA patterns: ST depression ≥0.5 mm, T-wave inversion, transient changes
Serial ECGs every 15–30 min if initial tracing is nondiagnostic and suspicion persists

Key Pearl: Importance of Serial ECGs

Early and repeat ECGs detect evolving ischemia—don’t rely on a single normal tracing.

B. Cardiac Biomarkers

High-sensitivity troponin I/T (hs-cTn): rise and/or fall above the 99th percentile confirms MI
- Serial sampling at 0 and 1–2 hours accelerates rule-in/rule-out
- Δ change (20–50% relative increase) supports acute event over chronic elevation
CK-MB: useful for detecting reinfarction; less sensitive/specific than troponin
Pitfalls: chronic troponin elevation in CKD or structural heart disease; always correlate with clinical/ECG data

Key Pearl: Interpreting Troponin Levels

A single normal troponin early after symptom onset does not exclude MI—always perform serial assays.

C. Echocardiography

Identify new regional wall motion abnormalities (RWMA) as markers of acute ischemia
Assess left ventricular ejection fraction and mechanical complications (MR, VSD)
Differentiate ACS from myocarditis or stress cardiomyopathy via RWMA patterns

Key Pearl: Value of Portable TTE

Portable TTE is invaluable when ECG or biomarkers are inconclusive or alternate diagnoses are considered.

III. Risk Stratification Tools

TIMI and GRACE scores quantify ischemic risk and guide the timing of invasive evaluation.

A. TIMI Score for NSTE-ACS

Seven 1-point criteria:

Age ≥65 years
≥3 CAD risk factors (HTN, hyperlipidemia, DM, smoking, family history)
Known CAD (≥50% stenosis)
Aspirin use in past 7 days
≥2 anginal events in prior 24 h
ST deviation ≥0.5 mm
Elevated cardiac markers

Score: 0–2 low risk; 3–4 intermediate; 5–7 high risk

Limitation: underestimates risk in elderly or renal-impaired patients

Key Pearl: TIMI Score and Invasive Strategy

TIMI ≥3 supports early invasive strategy in NSTE-ACS.

B. GRACE Score

Variables: age, HR, SBP, creatinine, Killip class, cardiac arrest at admission, ST deviation, elevated enzymes

Provides in-hospital and 6-month mortality risk (continuous scale)

GRACE >140 signifies high risk—favors immediate/early cath

Key Pearl: GRACE Score Superiority

GRACE outperforms TIMI for mortality prediction in complex patient populations.

Comparison Table: TIMI vs GRACE

Comparison of TIMI and GRACE Risk Scores
Feature	TIMI Score	GRACE Score
Variables	7 binary	8 continuous & categorical
Risk estimates	14-day composite (death/MI)	In-hospital & 6-month mortality
Ease of use	Bedside calculation	Online calculator
Strength	Simplicity	Superior discrimination
Limitation	Less accurate in high-risk	Requires more data inputs

IV. Mortality Prediction & Clinical Application

Mortality models inform invasive versus conservative management and prognosis.

In-hospital vs 6-month models guide short-term and mid-term risk discussions
High-risk features driving urgent invasive management:
- Ongoing chest pain, hemodynamic instability, life-threatening arrhythmias
- GRACE >140 or Killip class ≥II
STEMI: immediate reperfusion is indicated regardless of score
NSTEMI/UA: use scores to decide timing of angiography and resource allocation

Key Pearl: Consistent Application of Risk Scores

Failure to apply risk scores consistently can delay necessary invasive interventions in high-risk ACS.

V. Timing of Invasive Strategy

Angiography timing is stratified as immediate (<2 h), early (<24 h) or delayed (>24 h) based on risk and clinical features.

Immediate (<2 h): refractory angina, cardiogenic shock, dynamic ECG changes, mechanical complications
Early (<24 h): intermediate/high-risk NSTE-ACS (TIMI ≥3, GRACE >140)
Delayed (>24 h): low-risk NSTE-ACS after stabilization and noninvasive testing
Consider institutional resources, bleeding risk and comorbidities when scheduling

Key Pearl: Reducing Door-to-Cath Times

Predefined activation criteria and checklists reduce door-to-cath times and improve outcomes.

ISCHEMIA Trial Implications

In stable patients with moderate-severe ischemia, a conservative strategy was non-inferior to routine early invasive management for major events
High-risk ACS patients were excluded—findings do not apply to STEMI or unstable high-risk NSTEMI
Ongoing debate persists for intermediate-risk NSTE-ACS; tailor decisions via multidisciplinary discussion

Key Pearl: ISCHEMIA Trial Context

ISCHEMIA supports selective invasive strategy in stable moderate-risk patients but does not change the need for immediate intervention in high-risk ACS.

VI. Integration into Initial Management Plan

Synthesize presentation, ECG, biomarkers and risk scores to develop a rapid, protocolized care pathway; pharmacists ensure safe and timely pharmacotherapy and coordination.

A. Diagnostic-to-Treatment Pathway

Figure 1: ACS Diagnostic and Treatment Pathway

1. Suspected ACS

↓

2. ECG within 10 min

↓

3. STEMI?

Yes

↓

Activate Cath Lab + Immediate Antithrombotic Therapy

↓

hs-Troponin (0 & 1-2h) + Serial ECG

↓

4. NSTEMI/UA Confirmed?

↓

Calculate TIMI/GRACE → Determine Invasive Timing

↓

5. Initiate Guideline-Directed Drugs (pending angiography)

B. Initial Pharmacotherapy

Initial Pharmacotherapy for Acute Coronary Syndromes
Class	Agent(s)	Mechanism	Loading/Maintenance	Monitoring & Pitfalls
Aspirin	Aspirin	COX-1 inhibitor; ↓TXA₂	162–325 mg chew once, then 81–162 mg/day	GI bleeding; hypersensitivity
P2Y₁₂ inhibitors	Clopidogrel, Ticagrelor, Prasugrel	ADP receptor blockade	Clop 600 mg/75 mg; Tica 180 mg/90 mg BID; Pras 60 mg/10 mg daily	Bleeding; ticagrelor dyspnea; prasugrel contraindicated in stroke/TIA
Anticoagulants	UFH, Enoxaparin, Bivalirudin	Thrombin/Xa inhibition	UFH: bolus 60 U/kg + infusion; Enox 1 mg/kg q12h; Bivi 0.75 mg/kg + 1.75 mg/kg/h	Monitor aPTT (UFH), anti-Xa (Enox), renal dosing; bleeding risk
Nitrates	Nitroglycerin	NO-mediated vasodilation	SL 0.4 mg q5 min ×3; IV 5–200 µg/min	Hypotension; right-ventricular infarct caution
Analgesics	Morphine	Opioid analgesic; venodilation	2–4 mg IV q5–15 min PRN	Hypotension; respiratory depression; may ↓P2Y₁₂ absorption

Key Pearl: Pharmacotherapy Sequencing and Adjustments

Give aspirin before P2Y₁₂ inhibitors; adjust anticoagulants for renal function and bleeding risk.

C. Multidisciplinary Communication

Pharmacists verify doses, check interactions and monitor labs
Standardized order sets and checklists align timing across pharmacy, cardiology and ICU teams
Regular multidisciplinary rounds promote real-time adjustments and prevent delays

Clinical Vignette

A 68-year-old diabetic woman presents with dyspnea and mild chest discomfort. ECG shows ST depression in V4–V6; hs-troponin rises from 22 to 90 ng/L at 2 h. Her GRACE score is 158. Initiate DAPT (aspirin + ticagrelor), UFH infusion, and plan early (<24 h) angiography. Pharmacist adjusts enoxaparin for CrCl 45 mL/min and confirms SL nitrates for symptom relief.

References

Rao SV, O’Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the management of patients with acute coronary syndromes. Circulation. 2025;151:e771–e862.
Thomas JJ, Brady WJ. Acute Coronary Syndrome. In: Medicine and Surgery, Section Three Cardiac System. Elsevier; 2018:891–928.
O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. Circulation. 2013;127:e362–e425.
Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol. 2012;60(16):1581–1598.
Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. Circulation. 2014;130:e344–e426.
Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR guideline for the evaluation and diagnosis of chest pain. Circulation. 2021;144:e368–e454.
Pope JH, Selker HP. Diagnosis of acute cardiac ischemia. Emerg Med Clin North Am. 2003;21(1):27–59.

2025 PACUPrep BCCCP Preparatory Course

Pulmonary

Participants 432