Acute Coronary Syndrome – STEMI

Definition: clinical sx consistent w ACS w ECG features including any of:

1. Persistent ST-segment elevation of ≥1mm in 2 contiguous limb leads – limb leads (I, II, and III,AVR, AVL, and AVF)
2. ST segment elevation of ≥2mm in 2 contiguous chest leads OR
3. New LBBB (presumed new unless evidence otherwise; echo useful to detect regional wall contraction abnormalities)

Reperfusion Critera: 

• Chest pain >30 min and <12 hours
• ECG changes
  • Persistent ST-elevation ≥1 mm in 2 contiguous limb leads
  • persistent ST-elevation ≥2 mm in 2 contiguous chest leads
  •  or new or presumed new LBBB
• Myocardial infarct likely from history
• New Q Waves in STEMI Context

Qwaves

• Small ‘septal’ Q waves are typically seen in the left-sided leads (I, aVL, V5 and V6) 
• Q waves are considered pathological if:
  • > 40 ms (1 mm) wide 
  • > 2 mm deep
  • > 25% of depth of QRS complex
  • Seen in leads V1-3
• Q wave AMIs are transmural
• Q waves take several days to manifest. 
• Caused by total thrombotic occlusion. 
• Diagnosis is made retrospectively. Do not thrombolyse.

Area of Infarction

Type of Infarct	ECG Leads	Reciprocal ECG Changes	Heart Territory	Coronary Vessel
Inferior Infarct	II, III, aVF	I, aVL	Inferior wall of the left ventricle	Right Coronary Artery (RCA) or Left Circumflex (LCx)
Anterior Infarct	V1 to V4	None or rarely in inferior leads (II, III, aVF)	Anterior wall of the left ventricle	Left Anterior Descending Artery (LAD)
Septal Infarct	V1, V2	None or rarely in inferior leads (II, III, aVF)	Interventricular septum	Proximal Left Anterior Descending Artery (LAD)
Lateral Infarct	I, aVL, V5, V6	II, III, aVF	Lateral wall of the left ventricle	Left Circumflex Artery (LCx) or diagonal branches of LAD
Posterior Infarct	Reciprocal changes in V1-V3; direct leads V7, V8, V9	ST depression in V1-V3	Posterior wall of the left ventricle	RCA or LCx
Anterolateral Infarct	I, aVL, V3-V6	II, III, aVF	Anterior and lateral walls of the left ventricle	LAD, with possible involvement of LCx or diagonal branches
Inferolateral Infarct	II, III, aVF, V5, V6	I, aVL	Inferior and lateral walls of the left ventricle	RCA and/or LCx
Right Ventricular Infarct	V4R, V3R, V5R	None, but may affect adjacent leads	Right ventricle	RCA
Extensive Anterior/Anteroseptal Infarct	V1-V6, I, aVL	II, III, aVF	Extensive anterior wall including septal and lateral regions	LAD, often proximally occluded

Arterial Supply:

• RCA (Right Coronary Artery): primarily supplies the :
  • right atrium (RA)
  • right ventricle (RV)
  • inferior wall
  • parts of the posterior wall of the left ventricle.
  • SA Node:
    • Supplied by the
      • RCA in about 60% of people
      • left circumflex artery (LCx) in about 40% of cases.
  • AV Node: Typically supplied by the RCA.
• Posterior Descending Artery (PDA):
  • The RCA gives off the PDA in approximately 70-85% of people (right-dominant circulation).
    • The PDA supplies the inferior part of the ventricular septum and the posteromedial papillary muscle.
  • Left-Dominant Circulation: In 15-30% of people, the PDA originates from the LCx, which is considered left-dominant circulation

• LAD (Left Anterior Descending Artery):
  • Correctly noted to supply the anteroseptal and anteroapical regions. It also supplies a significant portion of the anterior wall and the anterolateral myocardium.
• LCx (Left Circumflex Artery):
  • Primarily supplies the anterolateral and posterolateral regions of the left ventricle. In left-dominant circulation, it may also supply a portion of the posterior wall and the AV node.

Inferior Infarcts

Inferior STEMI can result from occlusion of any of the three main coronary arteries:

• Dominant right coronary artery (RCA) in 80% of cases
  • Occlusion of the RCA, especially proximally, can also affect the right ventricle (RV) and posterior wall due to the RCA’s branches supplying these regions.
• Dominant left circumflex artery (LCx) in 18%
• Occasionally, a “type III” or “wraparound” left anterior descending artery (LAD), producing the unusual pattern of concomitant inferior and anterior ST elevation.

RCA occlusion is suggested by:	ST elevation in lead III > lead II Presence of reciprocal ST depression in lead I Signs of right ventricular infarction: STE in V1 and V4R
Circumflex occlusion is suggested by:	ST elevation in lead II = lead III Absence of reciprocal ST depression in lead I Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-6

Additional Features of Inferior STEMI

1. Posterior Wall Involvement:
   • Shared Blood Supply: The inferior and posterior walls of the left ventricle are commonly supplied by the right coronary artery (RCA) and, less frequently, by the left circumflex artery. Occlusion of these arteries during an inferior STEMI can extend the infarct to the posterior wall.
   • Clinical Implications: Involvement of the posterior wall suggests a larger myocardial infarct size, increasing the risk of complications such as left ventricular dysfunction, arrhythmias, and adverse clinical outcomes.
   • ECG Findings for Posterior MI: Posterior MI is indicated by reciprocal changes in the anteroseptal leads (V1-V3), such as horizontal ST depression, tall R waves, and upright T waves. The diagnosis is confirmed with posterior leads (V7-V9), showing ST elevation.
2. RV Infarcts:
   • RV Involvement in Inferior STEMI: Approximately 40% of inferior STEMIs involve the right ventricle due to proximal RCA occlusion. The RV’s shared blood supply with the inferior wall makes it particularly vulnerable in these cases.
   • Clinical Features: RV infarction commonly presents with hypotension, clear lung fields, distended neck veins, and Kussmaul’s sign (jugular venous distension increasing with inspiration).
   • ECG Findings for RV Infarcts: ST elevation in right-sided leads (V3R-V6R), particularly V4R, is highly indicative of RV infarction.
   • Management Considerations: Patients with RV infarction are preload-dependent; thus, nitrates and diuretics, which reduce preload, should be avoided. Careful fluid management is crucial to maintain RV filling without causing volume overload.
3. Bradycardia and AV Block in Inferior STEMI:
   • Incidence of Bradycardia and AV Block: Up to 20% of patients with inferior STEMI develop second- or third-degree AV block.
   • Mechanisms:
     • Ischemia of the AV Node: The AV node is often affected due to impaired blood flow from the AV nodal artery, which arises from the RCA in 80% of individuals.
     • Bezold-Jarisch Reflex: This reflex involves increased vagal tone secondary to myocardial ischemia, contributing to bradyarrhythmias.
   • Progression of Conduction Block: The conduction block can develop progressively (from first-degree AV block through Wenckebach to complete heart block) or appear abruptly as second- or third-degree heart block.
   • Sinus Node Dysfunction: Patients may also experience sinus bradycardia, sinus pauses, sinoatrial exit block, or sinus arrest, often due to ischemia of the SA node (supplied by the RCA in 60% of people) or increased vagal tone.
   • Management of Bradyarrhythmias: Bradyarrhythmias and AV blocks in inferior STEMI are usually transient (lasting hours to days), typically respond well to atropine, and rarely require permanent pacing.

Posterior Infarcts:

• Patients presenting with typical symptoms of acute coronary syndrome (chest pain, dyspnea, diaphoresis) but without obvious ST-elevation on a standard 12-lead ECG.
• This is often due to the fact that posterior changes are not directly visualized.
• Posterior MI often accompanies 15-20% of STEMIs
  • inferior STEMI
  • lateral STEMI
• Isolated posterior MI is less common, representing about 3-11% of all infarcts.
  • Isolated posterior MI requires emergent coronary reperfusion; however, the absence of obvious ST elevation means it can be easily missed.
• Always consider posterior involvement if ECG changes consistent with these infarctions
• presence of a posterior MI implies a greater extent of myocardial damage, increasing the risk of left ventricular dysfunction and mortality.

from LiFL = https://litfl.com/posterior-myocardial-infarction-ecg-library/: Acute Coronary Syndrome – STEMI

ECG Diagnosis:

Key ECG Changes in Leads V1-3 Suggesting Posterior MI:

• Horizontal ST depression – “Unexplained ST Depression in Leads V1-V3 is one of the hallmark reciprocal changes indicating a posterior MI.”
• Tall, broad R waves (>30 ms).
• Upright T waves.
• Dominant R wave (R/S ratio > 1) in lead V2.

The suspicion of posterior MI should be raised when these changes are present in patients with ischemic symptoms, especially if they already have an inferior or lateral STEMI.

Confirming Posterior MI with Posterior Leads (V7-9):

• Posterior leads are placed on the posterior chest wall:
  • V7: Left posterior axillary line, same horizontal plane as V6.
  • V8: At the tip of the left scapula, same horizontal plane as V6.
  • V9: Left paraspinal region, same horizontal plane as V6.
• ECG Features in Posterior Leads:
  • Confirmation of posterior MI is marked by ST elevation and Q waves in leads V7-9.
  • ST elevation in these leads is often subtle, and only 0.5 mm of ST elevation is sufficient to diagnose posterior MI.

Right Ventricular (RV) Infarction

• Common Association with Inferior STEMI: RVI is suspected in all patients with inferior STEMI and complicates up to 40% of these cases. Isolated RVI is rare.
• Additional Involvement in Anterior MIs: Cardiac MRI indicates that some anterior MIs also involve the RV, highlighting the broader impact of ischemia.

Pathophysiology:

• Primary Cause: Typically results from acute coronary syndrome involving the right coronary artery (RCA), especially proximal lesions.
• Unique Features of RV Ischemia:
  • The RV is more resistant to ischemia due to its thinner wall, rich collateral circulation, and perfusion during both systole and diastole.
  • The pulmonary circulation’s lower resistance means the RV needs less perfusion pressure compared to the LV.
  • The RV can be supported by collaterals from the left anterior descending artery, making significant RV infarctions less common.

Clinical Features:

• Classic signs include ischemic chest pain, bradycardia, hypotension, clear lung fields, and distended neck veins, sometimes with Kussmaul’s sign.
• Complications: Include ventricular septal rupture, right-to-left shunting, hypotension, AV block, and arrhythmias like ventricular tachycardia.

Investigations:

• ECG Findings:
  • ST elevation in V1 is specific for RV involvement, as V1 directly visualizes the RV.
  • ST elevation greater in lead III than in lead II suggests RV infarction.
  • ST elevation in right-sided leads (V3R-V6R), especially V4R, is a key diagnostic indicator.

Management:

• Acute Management: Includes calling Code STEMI, ensuring airway, breathing, and circulation (ABCs), providing oxygen, and giving analgesia.
• Avoid Nitrates and Diuretics: These can reduce preload, worsening RV failure.
• Fluids and Rate Control: IV fluids are used cautiously to maintain RV preload, and maintaining adequate heart rate and AV synchrony is important.
• Revascularization: Urgent revascularization (via cath lab or thrombolysis) is essential for improving outcomes.

Prognosis:

• RV involvement significantly increases mortality in inferior MI, with a mortality rate of 17% compared to 6.3% for inferior MI alone.
• Delayed revascularization leads to worse RV function and increased complications.

Early Repolarization and STEMI

Early Repolarization (ER) is a benign ECG pattern often seen in healthy individuals, characterized by specific changes in the ST segment and J-point. It is commonly observed in young adults, athletes, men, and individuals without any apparent heart disease. Although typically harmless, it has been historically associated with a low risk of arrhythmias in some rare cases.

Key Features of Early Repolarization

1. ECG Characteristics:
   • J-Point Elevation: The hallmark of early repolarization is the elevation of the J-point, which is the junction between the end of the QRS complex and the beginning of the ST segment. This elevation often appears as a notch or slur.
   • ST-Segment Elevation: The ST segment is typically concave (upward) and is most commonly observed in the lateral (V4-V6) and inferior leads (II, III, aVF). This ST elevation is usually mild and does not resemble the “tombstone” pattern seen in acute myocardial infarction.
   • Tall, Symmetrical T Waves: T waves are often large and upright, usually following the direction of the QRS complex.
   • Distribution: Commonly seen in precordial leads (V2-V5) and inferior or lateral leads.

Feature	Early Repolarization (ER)	ST-Elevation Myocardial Infarction (STEMI)
Definition	Benign ECG finding, often seen in healthy individuals.	Acute myocardial ischemia due to coronary artery occlusion.
ST Elevation	Concave (upward) ST-segment elevation, typically seen in precordial leads (V2-V5).	Convex (upward) or “tombstone” ST-segment elevation.
J-Point Elevation	Distinct upward notch or slur at the end of the QRS complex, often with a “fish-hook” appearance.	Present but lacks the benign features of ER.
T Waves	Large, upright, and symmetrical T waves.	Often hyperacute (tall and peaked) or inverted as infarction evolves.
Distribution	Commonly in inferior or lateral leads.	Corresponds to the infarcted myocardial territory (e.g., anterior, inferior).
Reciprocal Changes	Absent.	Often present in opposing leads, indicating myocardial injury.
Clinical Context	Typically asymptomatic, seen in young, healthy individuals without chest pain.	Associated with chest pain, diaphoresis, nausea, and other symptoms of ischemia.
Biomarkers	Normal cardiac biomarkers (e.g., troponin).	Elevated cardiac biomarkers (troponin, CK-MB) indicating myocardial damage.
Echocardiography	Normal findings without wall motion abnormalities.	Wall motion abnormalities consistent with infarcted area.
Response to Treatment	No treatment required as it is a benign condition.	Urgent reperfusion therapy required (e.g., PCI or thrombolytics).
Risk of Adverse Outcomes	Generally low risk, though slightly increased arrhythmia risk in rare cases.	High risk of severe complications, including heart failure and arrhythmias if untreated.

Acute Management

1. Seek help promptly for
   • chest discomfort at rest OR
   • for prolonged period (>10mins, not relieved by sublingual nitrates) OR
   • recurrent chest discomfort OR
   • ax w syncope or acute heart failure
2. Apply defibrillator to avoid cardiac death from reversible arrhythmias
3. ECG – 12 lead, V4R
4. Nb: pt’s w normal ECG + cardiac markers after an appropriate period of observation should, where practicable, undergo provocative testing (ie: stress testing) before discharge.
5. If not immediately available, provocative testing should be arranged at the earliest opportunity, optimally within 72hrs. 
6. Establish IV access and take blood tests.
7. CXR
8. Blood tests
   1. serum troponin (Lipid + glucose within 24hrs)
   2. Troponins are not useful for dx re-infarction, remain elevated 5-14d
9. Continuous Cardiac Monitoring

Key Door-to-Treatment Times in ACS Management

Door-to-ECG Time:

• Definition: The time from patient arrival at a healthcare facility to the acquisition of the first 12-lead ECG.
• Target Time: Within 10 minutes of arrival.
• Purpose: Early identification of ST-Elevation Myocardial Infarction (STEMI) or other cardiac conditions requiring urgent intervention. Rapid ECG acquisition is critical because it is the first diagnostic step in the pathway for reperfusion therapy.

Door-to-Balloon Time:

• Definition: The time from hospital arrival to the first balloon inflation during percutaneous coronary intervention (PCI).
• associated with lower mortality, reduced heart failure rates, and better long-term outcomes
• Target Time: Within 90 minutes of first medical contact, extended to 120 minutes if the patient requires transfer to a PCI-capable facility.
• Purpose: Early PCI is crucial for restoring coronary blood flow, minimizing infarct size, preserving myocardial function, and improving survival rates in STEMI patients.
• evidence:
  • National Cardiovascular Data Registry (NCDR)
  • DANAMI-2″ trial

Door-to-Needle Time:

• Definition: The time from arrival at a healthcare facility to the administration of fibrinolytic therapy.
• Target Time: Within 30 minutes of hospital arrival.
• Purpose: Fibrinolysis is used when PCI is not available within the ideal timeframe. Timely administration helps to restore blood flow, particularly in rural or remote settings without immediate access to PCI.
• This target is particularly relevant in rural or regional Australian settings where access to PCI-capable facilities may be limited.

Initial Management of ACS Patients

Oxygen Therapy

• Avoid routine use of oxygen therapy in patients with SaO2 > 93%.
• Use oxygen therapy when SaO2 is below 93% or if the patient is shocked (unless COPD or other reasons for a modified SaO2 target).

Analgesia

• Nitrates:
  • Sublingual glyceryl trinitrate:
    • 400 micrograms spray or 300 to 600 micrograms tablet.
    • Repeat every 5 minutes as needed, maximum of 3 doses (monitor for hypotension).
  • I.V.: INFUSION:
    • Commence at 5 microg/min, Increment dose by 5 microg/min 5 minutely until desired effect (i.e. no pain, target BP). SBP >100mmHg
    • Place 50mg ampoule into 490mL G 5% NaCl 0.9% glass bottle 100mcg=1mL
  • GTN contraindicated if RV infarct
• Opiates:
  • IV morphine: 2.5 to 5mg initial dose, titrate to effect every 5 to 10 minutes with further doses of 2.5 to 5mg.
  • In elderly or those with cardiorespiratory compromise: initial morphine dose less than 2.5mg, incremental doses of 0.5 to 1mg.
  • If contraindicated, consider IV fentanyl: 25 to 50 micrograms initial dose.

Anti-Emetic

• IV metoclopramide: 10 mg.
• IV prochlorperazine: 12.5 mg.

Antiplatelet Therapy

• Aspirin:
  • 300 mg orally initially, then 100-150 mg daily thereafter.
  • Continue indefinitely unless not tolerated or anticoagulation is indicated.
• P2Y12 Inhibitors:
  • Ticagrelor: 180 mg loading dose, followed by 90 mg twice daily.
  • Clopidogrel: 300-600 mg loading dose, then 75 mg daily if contraindications to ticagrelor or prasugrel exist. (Clopidogrel 300mg – lysis, Clopidogrel 600mg – PCI)

Anticoagulation

• Enoxaparin: 1 mg/kg SC (0.75 mg/kg SC in elderly or those with renal impairment).
• Heparin: Loading dose followed by infusion if urgent PCI is required.

Glycoprotein IIb/IIIa Inhibitors (tirofiban and eptifibatide)

• Consider IV glycoprotein IIb/IIIa inhibitors in combination with heparin at the time of PCI for high-risk patients.
• Agents: Abciximab, Eptifibatide, Tirofiban (specific agent determined by treating cardiologist).

Bivalirudin (Direct Thrombin Inhibitor)

• Consider 0.75 mg/kg IV bolus followed by 1.75 mg/kg/h infusion as an alternative to glycoprotein IIb/IIIa inhibitors and heparin in ACS patients undergoing PCI with increased bleeding risk.

Reperfusion Therapy

• Very High Risk NSTEACS: Angiography and revascularization within 2 hours.
• High Risk NSTEACS: Within 24 hours.
• Intermediate Risk NSTEACS: Within 72 hours.
• Low Risk NSTEACS: Selective invasive strategy guided by testing for inducible ischemia.

Further Secondary Prevention Medications

• Statins: Highest tolerated dose of an HMG-CoA reductase inhibitor indefinitely; target LDL < 1.8 mmol/L.
• Beta Blockers: Initiate in patients with left ventricular ejection fraction < 40% unless contraindicated.
• ACE Inhibitors/Angiotensin Receptor Blockers: Initiate in patients with heart failure, left ventricular systolic dysfunction, diabetes, anterior MI, or co-existent hypertension.

Fibrinolysis

Criteria for PCI vs. Fibrinolysis in Acute STEMI

1. Primary PCI (Preferred Reperfusion Strategy)

• Indication: PCI is the preferred treatment for STEMI if it can be performed promptly.
• Criteria for Choosing PCI:
  • Time Frame: PCI should be performed within 90 minutes of first medical contact (ideal) or within 120 minutes if transferring from a non-PCI-capable facility.
  • Availability of PCI Facility: A PCI-capable hospital is available, and skilled operators can perform the procedure promptly.
  • Contraindications to Fibrinolysis: Such as a high risk of bleeding, recent major surgery, intracranial hemorrhage, or known bleeding disorders.
  • Cardiogenic Shock or Severe Heart Failure: PCI is preferred for patients in cardiogenic shock or those with severe heart failure, as it is more effective than fibrinolysis in restoring blood flow and improving outcomes.
  • Late Presenters: Patients presenting 12-24 hours after symptom onset are still candidates for PCI if there is evidence of ongoing ischemia.

2. Fibrinolysis (Alternative When PCI is Unavailable)

• Indication: Fibrinolysis is an alternative when timely PCI cannot be performed, especially within 120 minutes from the first medical contact.
• Criteria for Choosing Fibrinolysis:
  • Time Frame: Fibrinolysis should be administered within 30 minutes of arrival at the hospital (door-to-needle time).
  • No Access to PCI: If PCI cannot be performed within 120 minutes, fibrinolysis is recommended to restore blood flow as quickly as possible.
  • Early Presentation: Best results are seen when administered within 12 hours of symptom onset, especially within the first 3 hours.
  • Absence of Contraindications: No absolute contraindications to fibrinolysis (e.g., recent stroke, active bleeding, severe uncontrolled hypertension).

Contraindications to Fibrinolysis:

Dose

1. Dose Tenecteplase: IV Bolus 0.5mg/kg (max 50mg) 
2. Also, if giving Heparin due to high bleeding risk or eGFR <30: 
3. Heparin is administered post thrombolytic, (max 4000 Units), slow I.V. push followed by infusion 12 units/kg/hour (max 1000 units/hr) Check APTT every 4‐6 hours.

Complication risks:

• Risk : ICH 1-2%, risk increase with age, HTN, previous stroke
• Rx: urgent CT, IV Tranexamic acid 1g, FFP 2 units, neurosurg, ICU consult
• Major bleeding: 5% 2 units FFP
• Reperfusion dysarrthymias – accelerated idioventricular rhythm

Failed reperfusion:

• Persistant ischemic symptoms, HD instability
• < %50 ST reduction at 90 ins post reperfusion🡪 need rescue PCI

Conduct ECG at 90min, 6hrs and 12hrs post lysis

Continue medications

1. Aspirin 75-300mg PO OD
2. Nitrates
3. UH 5000-7500IU S/C 12hourly in mobile patients
4. High risk DVT/PE TEDS + Increased UH
5. Beta blocker especially in LV dysfunction and ongoing ischaemia. Doses atenolol 25-100mg PO OD or metoprolol 25-100mg PO BD with SBP >95 and HR>55
6. ACEI improves the outcome.
   • Give within 24-48 hours in patients with
     • Previous AMI
     • DM
     • HT
     • Anterior infarct
     • HR >80
     • CXR showing LVF
     • LVEF <45% (especially good in patients with poor LV f(x))
   • Low risk patients can be stopped in 6/52
   • C/I include Hypotension (SBP<100) and haemodynamic instability
   • Must monitor BP and EUC on alternate days

7. Calcium Channel Blocker
   • Only used if C/I to Betablockers.
8. Statins

NSTEMI

Urgent PCI (within 2 hours) is indicated in very high-risk NSTEMI patients with instability or ongoing ischemia.

Early PCI (within 24 hours) is recommended for high-risk NSTEMI patients to reduce adverse outcomes.

Delayed PCI (within 72 hours) is safe for intermediate-risk, stable NSTEMI patients.

Selective PCI is suitable for low-risk NSTEMI patients, often guided by further testing.

Urgent PCI Indicated in NSTEMI

Urgent or immediate PCI is indicated in high-risk NSTEMI patients with any of the following conditions, usually requiring angiography and PCI within 2 hours:

1. Hemodynamic Instability or Cardiogenic Shock: Patients presenting with low blood pressure, shock, or other signs of circulatory collapse need urgent revascularization.
2. Refractory or Recurrent Chest Pain: Ongoing or recurrent chest pain despite optimal medical therapy suggests persistent ischemia, warranting urgent PCI.
3. Life-Threatening Arrhythmias: Ventricular tachycardia, ventricular fibrillation, or other arrhythmias that are life-threatening require immediate PCI.
4. Acute Heart Failure or Pulmonary Edema: NSTEMI associated with severe left ventricular dysfunction or heart failure symptoms (e.g., pulmonary edema) necessitates prompt intervention.
5. Mechanical Complications: Evidence of complications such as acute mitral regurgitation or ventricular septal rupture should prompt immediate PCI.

Timing of PCI in NSTEMI Based on Risk Stratification:

1. Very High-Risk NSTEMI:
   • PCI Timing: Within 2 hours of presentation.
   • Indications: Hemodynamic instability, ongoing chest pain, life-threatening arrhythmias, acute heart failure, or mechanical complications.
2. High-Risk NSTEMI:
   • PCI Timing: Within 24 hours of presentation.
   • Indications: Elevated troponins, dynamic ECG changes, diabetes, prior PCI or CABG, renal impairment, or GRACE score > 140.
   • Reasoning: Early intervention within 24 hours reduces the risk of major adverse cardiac events (MACE) without significant delay, especially in those with elevated troponin and ECG changes suggestive of ischemia.
3. Intermediate-Risk NSTEMI:
   • PCI Timing: Within 72 hours of presentation.
   • Indications: Stable patients with less severe presentations or moderate-risk features like prior MI, known coronary artery disease, or other risk factors but without ongoing ischemia.
   • Reasoning: Delayed intervention up to 72 hours can be safe in stable patients, focusing on optimizing medical therapy while awaiting angiography.
4. Low-Risk NSTEMI:
   • PCI Timing: Selective invasive strategy.
   • Indications: Low-risk patients may undergo non-invasive ischemia testing (stress testing) before deciding on PCI.
   • Reasoning: A conservative approach with medical management and risk stratification testing helps avoid unnecessary invasive procedures.

Evidence for Timing of PCI in NSTEMI:

• TIMACS Trial: Demonstrated that high-risk NSTEMI patients benefit from early PCI (within 24 hours), while lower-risk patients do not have improved outcomes with immediate intervention compared to delayed PCI.
• ACUITY and ICTUS Trials: Showed that very high-risk features (like ongoing pain or instability) warrant early PCI, while a delayed strategy is safe and effective in stable patients without urgent risk factors.

COMPLICATIONS OF ACUTE CORONARY SYNDROMES

• cardiac failure
  • Medication: ACE inhibitors/ARBs, beta-blockers, aldosterone antagonists, diuretics.
  • Lifestyle: Sodium restriction, weight monitoring, and fluid balance
• post-infarction ischaemia
  • Residual coronary artery disease leading to recurrent angina or silent ischaemia.
• ventricular free wall rupture
  • therapy: pericardiocentesis and repair
• ventricular septal rupture
  • therapy: IABP, inotropes, surgery
• acute mitral regurgitation
  • Papillary muscle dysfunction or ischemic changes affecting the mitral valv
  • therapy: afterload reduction, IABP, inotropes, surgery ASAP
• right ventricular infarction
  • therapy: IV fluids, inotropes, AV synchrony, IABP, reperfusion
• arrhythmias
  • therapy: correct hypoxia, acidosis, hypovolaemia, K+, Mg2+ (controversial)
• cardiogenic shock
  • therapy: must get revascularisation (PCI or CABG) within 24 hours
• thromboembolism
  • Stasis of blood or mural thrombus formation due to impaired heart function.
  • therapy: mural thrombus -> anticoagulate
• pericarditis and Dressler’s syndrome
  • Inflammation of the pericardium after MI; Dressler’s syndrome is immune-mediated and occurs weeks to months later.
• complications of therapy, e.g. haemorrhage, coronary artery dissection, stent thrombosis, surgical complications