Coronary Heart Disease and Acute Coronary Syndromes - Study Notes

Intended Learning Outcomes

• Describe the pathophysiology, epidemiology and typical presenting features of CHD (Coronary Heart Disease)

• Demonstrate understanding of evidence-based pharmacotherapy for CHD, including potential adverse effects, precautions and appropriate monitoring

ACS Guidelines Overview

• Management of Acute Coronary Syndromes (ACS) in Australia and New Zealand should align with Heart Foundation and Cardiac Society guidelines (original 2006; updated 2016 and 2025)

• Reference: Heart Foundation ACS guideline pages

ACS: Definition and Spectrum

• ACS described as a broad spectrum from ST-elevation MI (STEMI) to an accelerated pattern of angina without evidence of myonecrosis

• Numerous features help differentiate presentations within the spectrum

ACS: The Spectrum, Key Diagnoses

• STEMI (ST-elevation MI)

• NSTEMI (Non-ST-elevation MI)

• Unstable Angina (non-ST-elevation coronary syndromes; non-elevated troponin)

• ACOMI (AMI due to acute epicardial occlusion)

• MINOCA (MI with no acute coronary occlusion)

• Plaque rupture/erosion with thrombus is a common mechanism; SCAD, coronary embolism, vasospasm or microvascular dysfunction can also cause ACS

ACS: The Spectrum (Continued)

• AMI due to oxygen supply/demand mismatch without acute coronary occlusion present as ACS variants

• Elevated troponin distinguishes NSTEMI from unstable angina

ACS: Electrocardiography (ECG) in ACS

• ECG is fundamental for ACS diagnosis

• Each ECG point relates to a phase of the cardiac contraction cycle; certain changes (e.g., ST-elevation) are particularly important

ACS: MI, Myocardial Damage and ECG (Subendocardial and Transmural)

• Subendocardial infarction shows initial changes on ECG (ST depression) during early ischemia

• Transmural injury often presents with ST elevation in appropriate leads

• Normal ECG can occur early; serial ECGs and troponin testing are used to detect evolving injury

ACS: MI ECG Patterns and Criteria (Key patterns and notes)

• A) Regional STE with reciprocal STD (ST elevation with reciprocal changes)

• B) High lateral MI pattern (specific lead patterns)

• C) STEMI criteria (example):

  • STE ≥ 1 mm at the J-point in two contiguous limb leads (all leads except V2-4)

  • V2-4 STE: ≥ 1.5 mm in women; ≥ 2 mm in men ≥ 40 years; ≥ 2.5 mm in men < 40 years

• STEMI criteria also include STE in leads I and aVL with STD in inferior leads (and posterior/right-sided patterns in other scenarios)

• D) Posterior MI: posterior ST depression in V1-3 with confirmed posterior STE in V7-9

  • STE ≥ 0.5 mm in posterior leads; threshold adjustments for women/age

• E) De Winter pattern: J-point depression with upsloping ST segments and tall symmetric T waves in precordial leads, with STE ≥ 0.5 mm in aVR and absence of STE in precordial leads

• F) Modified Sgarbossa criteria (in LBBB or paced rhythm):

  • A) Concordant STE > 1 mm in leads with a positive QRS

  • B) Concordant STD ≥ 1 mm in V1-3

  • C) STE ≥ 1 mm in any lead at the J-point that is discordant to the S wave by > 25%

ACS: MI, Coronary Anatomy and Impact on Outcome

• Vessel location significantly influences outcome; larger vessels supply larger myocardial areas

• The left main coronary artery (LMCA) supplies > 2/3 of the left ventricle and branches into:

  • Left anterior descending (LAD): supplies the anterior wall

  • Left circumflex artery (LCx): supplies the lateral wall

• Occlusion of the LAD, especially high in the vessel, carries a particularly poor prognosis

ACS: Circadian Pattern of ACS Presentation

• ACS risk shows a circadian pattern: peak risk between 6:00 and 12:00

• Approximately 4-fold variation between highest (8–9 am) and lowest (12–1 am) risk hours

• Possible contributors: higher plaque rupture risk, increased platelet aggregation, elevated circulating catecholamines

• Many MIs are described as ACOMI when there is MI with acute occlusion

ACS: Peri-operative ACS and MINOCA

• ACS can occur peri-operatively (around 4% of patients with or at risk of cardiac disease)

• Contributing factors: tachycardia, hypotension, hypoperfusion, coagulation changes

• MINOCA: MI with no acute coronary occlusion

• In high-risk patients, surgical planning should consider ACS risk and timing

ACS: Recognition and Time-to-Treatment

• Critical issues: recognition by patients and health professionals; time to treatment

• Media campaigns (e.g., NHF) aim to raise awareness of warning signs

ACS: “Time is Heart” – Why Time Matters

• Ischemia causes symptoms; delay increases permanent myocardial damage

• Highest risk of death is in the first few hours after onset

• Priority: restore blood flow quickly to affected myocardium

ACS: Presentation and Symptoms

• Typical presentation: sudden chest or epigastric pain at rest, may radiate to neck/shoulder/arm/jaw

• Some patients feel discomfort, pressure or squeezing rather than pain

• Shortness of breath, nausea, vomiting, sweating and fatigue are common

• Atypical presentations more common in women, elderly, and people with diabetes; may lead to delayed help-seeking

ACS: First Steps on Presentation

• Call emergency number (e.g., 000 or 112 in Australia)

• Give aspirin 300 mg if not contraindicated

• Paramedics typically:

  • Perform 12-lead ECG

  • Establish IV access

  • Administer IV morphine or fentanyl

  • Administer GTN up to 3 doses if chest pain persists and no contraindications

  • Oxygen only if required; routine high-flow O2 is not advised and may be harmful unless hypoxaemic

• References: contemporary ACS guidelines and evidence on oxygen use

ACS: Tests to Guide Management

• ECG on arrival is essential

• Blood tests: cardiac enzymes (troponin), full blood count, serum creatinine and electrolytes, blood glucose

ACS: Cardiac Enzymes and Troponin

• Troponin (T and I) is the most useful cardiac enzyme for ACS diagnosis due to high sensitivity/specificity for cardiac injury

• High-sensitivity troponin (Hs-cTn) assays improve early detection

• Contemporary practice: repeat troponin 6 hours after onset to assess dynamic change

• Temporal pattern: troponin rises 3–6 hours after onset and may remain elevated for days

ACS: Troponin Change Criteria (two measurements, 6 hours apart)

• Two troponin levels are always obtained 6 hours apart to assess change and rule out false results

• Interpretation used in this context:

  • If the first level T1 < 50, then a ≥50% change in the second level (T2) relative to T1 is required: rac{T2 - T1}{T1} \ge 0.50

  • If the second level T2 > 50, then a ≥30% change relative to the second level is required: rac{T2 - T1}{T2} \ge 0.30

• Most patients with MI will have an elevated troponin 3–6 hours after onset

• An elevated troponin does not automatically confirm MI; clinical context is essential

Other Causes of Elevated Troponin

• Troponin can be elevated in conditions other than MI (e.g., renal failure, myocarditis, pulmonary embolism, sepsis)

• Correlate with symptoms, ECG, imaging and clinical context

ACS: STEMI Criteria (ST-Elevation MI)

• STEMI criteria include clinical ACS presentation plus ECG evidence:

  • Persistent ST-segment elevation ≥ 1 ext{ mm} in two contiguous limb leads

  • ST-segment elevation ≥ 2 ext{ mm} in two contiguous chest leads

  • New left bundle branch block (LBBB) pattern can also indicate STEMI

ACS: Acute Pharmacotherapy on Arrival

• In hospital, or on arrival, urgent management may include:

  • Glyceryl trinitrate (GTN) IV infusion

  • IV morphine or analgesia as needed

  • Oxygen if saturation < 90%

  • Anticoagulation (as indicated)

  • Antiplatelet therapy (aspirin plus a P2Y12 inhibitor)

  • Statin therapy

• Some therapies may have been given by paramedics; in-hospital care continues or escalates as needed

ACS: STEMI Reperfusion – PCI vs Fibrinolysis

• STEMI requires rapid reperfusion; priority is restoring coronary blood flow

• Two main reperfusion options:

  • Percutaneous coronary intervention (PCI)

  • Fibrinolysis (thrombolysis)

• PCI is preferred if it can be provided promptly, in suitably equipped facilities, by an experienced cardiology team

ACS: Reperfusion Algorithms and Pathways

• NHF/CSANZ algorithm guides acute management and subsequent reperfusion decisions

• Pathways prioritize timely PCI when feasible; fibrinolysis remains an option in remote settings or where PCI is not immediately available

PCI and Stenting – What is PCI?

• Performed in the Cardiac Catheter Laboratory

• Vascular access is commonly via the radial artery (preferred) rather than the femoral artery when possible

• Catheter is steered to the coronary circulation under fluoroscopic (X-ray) guidance with dye visualization

PCI and Stenting – PCI Steps

• Once the culprit artery is reached:

  • Angioplasty: inflate a balloon to compress plaque

  • Stent deployment to maintain patency

  • Atherectomy or other adjunctive interventions may be used

• Multiple stents may be deployed end-to-end or in different arteries

• PCI is preferred if feasible, but some plaque locations may preclude stenting

PCI: Primary vs Rescue PCI

• Primary PCI: treatment within 90 minutes of first medical contact

• Rescue PCI: used when primary PCI was not possible initially; patient is transferred to a PCI-capable facility

PCI/Stenting – Stent-Related Issues

• Stents are foreign bodies and can trigger thrombosis; careful antithrombotic management is essential

• Restenosis: tissue growth around the stent over time can narrow the lumen

PCI: Types of Stents

• Drug-eluting stents (DES): release cytotoxic drugs, slow tissue regrowth, reduce restenosis risk

  • Example: everolimus (mTOR inhibitor)

  • DES may prolong the period during which clots can form; longer antiplatelet therapy is often needed

• Bare-metal stents (BMS): higher restenosis risk; historically used when DES contraindicated

• Contemporary data suggest DES associated with lower all-cause death, MI, or revascularisation compared with BMS in some settings

Drug Therapy in PCI/Stenting – Antiplatelet Therapy

• Typical initial strategy: aspirin plus a P2Y12 inhibitor

  • Options: Ticagrelor, Prasugrel, Clopidogrel

  • In anticoagulated patients (e.g., AF), clopidogrel is often preferred due to lower bleeding risk

• One of Ticagrelor or Prasugrel is generally preferred over clopidogrel due to superior efficacy

Drug Therapy in PCI/Stenting – Antithrombin Therapy

• Options include low-molecular-weight heparin (LMWH, e.g., enoxaparin), fondaparinux, or bivalirudin

• Enoxaparin is commonly used at therapeutic dosing to reduce re-occlusion and VTE risk

• Additional agents (e.g., parenteral glycoprotein IIb/IIIa inhibitors like tirofiban) may be used in high-risk thrombotic scenarios

Fibrinolysis (Thrombolysis) in ACS

• Fibrinolysis dissolves clots using thrombolytic drugs; two classifications:

  • Fibrin-selective: Tenecteplase, Reteplase, Alteplase

  • Non-fibrin selective: Streptokinase (less used in ACS in Australia)

• Not suitable for everyone; contraindications exist due to bleeding risk

Fibrinolysis – Practical Considerations

• PCI/stenting is generally preferred where available; fibrinolysis remains valuable in remote settings without PCI access

• In some areas, paramedics can administer fibrinolytics as part of pre-hospital care

• Rescue PCI may be performed after initial fibrinolysis if reperfusion is incomplete or unsuitable

Major Complications of ACS

• Arrhythmias (including reperfusion arrhythmias)

• Heart failure and left ventricular dysfunction

• Ventricular thrombus, pulmonary embolism

• Infarct extension; risk highest in STEMI

NSTEACS (Non-ST Elevation ACS)

• NSTEACS includes NSTEMI and Unstable Angina (UA)

• Management is aimed at diagnosis, risk stratification, and determining the need for PCI or CABG

• High-risk features include: persistent chest pain, elevated enzymes, SBP < 90 mmHg, prior CABG/PCI, sustained VT

• Management pathways may involve PCI or CABG, or medical therapy similar to STEMI

Post-ACS Therapy – Core Long-Term Strategy (Fab Four, Fab Five)

• Fab Four for many patients with LVEF ≤ 40%: Antiplatelets, Statin, ACE inhibitor (ACEi) or ARB, Beta-blocker

• Newer guidelines consider adding colchicine 0.5 mg (if not contraindicated) suggesting a potential Fab Five

• Goals: reduce mortality, prevent recurrent events, improve quality of life; adherence is critical

Post-ACS – Dual Antiplatelet Therapy (DAPT)

• To mitigate recurrent thrombotic events, DAPT (aspirin plus a P2Y12 inhibitor) is common

• Options to add to aspirin in DAPT:

  • Clopidogrel, Prasugrel, Ticagrelor

• Among these, Ticagrelor or Prasugrel are generally preferred over Clopidogrel for many ACS patients due to superior efficacy

Post-ACS – Clopidogrel Details

• Clopidogrel (Plavix®, Iscover®) is a prodrug activated via CYP2C19

• Suboptimal responses can occur in individuals with certain CYP2C19 genotypes or when taking CYP2C19 inhibitors (e.g., some proton pump inhibitors)

• If necessary for GI protection due to bleeding risk with DAPT, a PPI should be used judiciously; evidence supports continuing PPI if needed

• Standard dosing: 75 mg daily; loading dose up to 600 mg STAT with PCI

Post-ACS – Ticagrelor and Prasugrel

• Ticagrelor: non-thienopyridine, reversible P2Y12 blocker; metabolized by CYP3A4; fewer CV events vs clopidogrel; slight bleeding risk increase but not necessarily severe

• Prasugrel: more potent P2Y12 blocker; superior efficacy vs clopidogrel but higher bleeding risk; stroke signals reported in trials

  • Australian guidelines: avoid prasugrel in patients with age > 75 years, body weight < 65 kg, or history of TIA/stroke

• DAPT duration with DES or BMS varies; common practice has been DES for longer durations (e.g., 12 months) to reduce restenosis risk

Post-ACS – Duration of DAPT

• Traditional approach depended on stent type and trial data:

  • BMS: typically 1 month DAPT, then aspirin monotherapy

  • DES: commonly 12 months DAPT, then aspirin monotherapy

• More recent guidelines individualize duration based on bleeding risk, stent type, and ischemic risk

Post-ACS – Statins

• Statins improve outcomes after ACS beyond LDL lowering: plaque stabilization and anti-inflammatory effects

• Benefit of statins even when LDL-C is not markedly elevated

• Historical landmark: 4S trial (simvastatin 20–40 mg post-MI) reduced all-cause mortality and coronary death; newer guidelines favor higher-potency statins in many patients

Post-ACS – Beta-Blockers

• Indicated in patients with reduced LV systolic function (LVEF ≤ 40%), or continued in those already taking beta-blockers for other indications (e.g., angina, atrial fibrillation)

• Meta-analyses show long-term beta-blocker use post-MI reduces all-cause mortality (~23%) and non-fatal reinfarction (~26%)

Post-ACS – ACE Inhibitors (ACEi) / ARBs

• ACE inhibitors particularly justified in heart failure, LVEF ≤ 40%, diabetes, anterior MI, or coexisting hypertension

• Trials show ACEi reduce mortality, heart failure admissions, and reinfarction

• Start with a low dose and titrate; ARBs as an alternative if ACEi not tolerated

Post-ACS – Mineralocorticoid Receptor Antagonists (MRA)

• Eplerenone (Inspra) shown to reduce morbidity/mortality in certain post-MI patients with early signs of heart failure (LVEF < 40%) when started within 3–14 days of MI, in addition to standard therapy

• Start at 25 mg/day, titrate to 50 mg/day within 4 weeks

• Monitor potassium, especially with concurrent ACEi/ARB

• Spironolactone may be used in some settings; data on direct comparisons are limited

Post-ACS Rehabilitation

• All patients should be referred to Cardiac Rehabilitation (CR) programs

• CR covers drug therapy optimization, diet, exercise, smoking cessation, and mental health support

• Evidence: CR associated with ~26% reduction in cardiac mortality and ~20% reduction in all-cause mortality

CHD Summary and Practical Implications

• CHD remains a major burden; risk-factor modification and prevention are critical

• Early recognition of warning signs and urgent specialist treatment improve outcomes

• Acute management approaches are evolving with ongoing integration of PCI/stenting, pharmacotherapy, and secondary prevention

• Adherence and persistence with evidence-based therapies are essential for maximizing long-term benefit

Practical Takeaways for Exam Preparation

• Be able to classify ACS presentations (STEMI, NSTEMI, UA) and identify when to activate reperfusion pathways

• Memorize STEMI ECG criteria and the major alternative ECG patterns (De Winter, Sgarbossa) and their clinical implications

• Understand the sequence of ACS management: pre-hospital steps, hospital diagnostics, initiation of therapy, and reperfusion strategy

• Know the roles of PCI/stenting, DES vs BMS, and the concept of DAPT including agent choices and duration guidelines

• Recall post-ACS secondary prevention: Fab Four (and potential Fab Five), statin, beta-blocker, ACEi/ARB, and MRA; Rationale for each

• Recognize key risk factors and practical considerations: circadian pattern, MINOCA, and perioperative ACS

• Be able to express key numerical/threshold values in LaTeX format, e.g., STEMI thresholds, troponin change criteria, and lesion/ischemia associations

Key Formulas and Thresholds (LaTeX)

• STEMI ECG criteria (example):
  STE \,\ge \,1\text{ mm} \text{at the J-point in two contiguous limb leads}
  STE \,\ge \,2\text{ mm} \text{in two contiguous chest leads}

• Troponin dynamic criteria (6-hour interval):
  T1 < 50 \Rightarrow \frac{T2 - T1}{T1} \ge 0.50
  T2 > 50 \Rightarrow \frac{T2 - T1}{T2} \ge 0.30

• De Winter pattern: explicit criteria involve J-point depression with upsloping ST and STE in aVR ≥ 0.5 mm with no STE in precordial leads

• Sgarbossa criteria (concordant/discordant patterns):

  • A) Concordant STE > 1 mm in leads with positive QRS

  • B) Concordant STD ≥ 1 mm in V1–V3

  • C) STE ≥ 1 mm in one or more leads with S wave discordant by > 25%

If you want, I can tailor these notes to a specific sub-topic (e.g., ECG patterns, PCI vs fibrinolysis decision-making, or post-ACS pharmacotherapy) or add more real-world clinical examples to help you study for the exam.