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Acute Cardiac Syndrome

title: Acute cardiac syndrome tags: #FFICM #Oh #cardiac #ACS notebook: 🌑-FFICM type: anki

[@Oh, Chapter 20]

Definition of ACS: "A spectrum of clinical conditions characterised by acute chest pain or myocardial ischaemia" [@Oh, Chapter 20]

Epidemiology

  • 1 / 5 of all deaths in over 40's is due to MI [@Oh, Chapter 20]

Outcomes

  • 1 / 20 die early (in hospital)
  • 60% of these deaths are within 1st hour (VF arrest)
  • British Cardiac Society has a 13% mortality for ACS with clinical MI at 30 days [@Oh, Chapter 20]
  • Somewhere between one in 5 and one in 20 die within 12 months [@Oh, Chapter 20]

Flashcard type:basic
What's the average mortality of patients with clinical MI at 30 days? 13%

Outcome Predictions

Use the STEMI-TIMI (TIMI = thrombolysis in myocardial infarction) score [@Oh, Chapter 20]

Flashcard type:basic
What scoring system can be used to predict ACS outcomes? STEMI-TIMI score

Killip Classification (Severity and Outcomes in MI)

Classifying severity of outcome of MI, and corrolation with mortality. [@Oh, Chapter 20]

Developed in 1960s. [@Oh, Chapter 20]

  1. No Failure - ~5% inpatient mortality
  2. Mild to Mod Failure (Rales 50%- lung fields) - ~15% inpatient mortality
  3. Severe Heart Failure (Ralse 50%+ lung fields) - ~40% inpatient mortality
  4. Cardiogenic Shock - ~80% inpatient mortality [@Oh, Chapter 20]

Flashcard type:cloze_reference
The classification scoring system for {{c1::MI with Heart Failure::disease}} is called the {{c2::Killip Classification::name}}.
The options are:
1. {{c3::No Failure}} - Inpatient Mortality {{c4::~5%}}
2. {{c3::Mild to Mod Failure (Rales -50% lung fields)}} - Inpatient Mortality {{c4::~15%}}
{{c3::Severe Heart Failure (Rales 50%+ Lung Fields)}} - Inpatient Mortality {{c4::40%}}
{{c3::Cardiogenic Shock}} - Inpatient Mortality {{c4::80%}}		 Oh ICM - ACS

Classification

Classification of ACS

  • MI
  • STEMI
  • NSTEMI
    • Either non occluding thrombus or occlusion with collateral flow
  • Unstable Angina [@Oh, Chapter 20]

Classification of MI

  • Type 1 - Spontaneous - Plaque Rupture or Erosion
  • Type 2 - Ischaemic Imbalance - Oxygen Demand Is Greater Than Supply Due To Something Else than CAD
  • Type 3 - Death without any biomarker results (no troponins)
  • Type 4a - Due To PCI
  • Type 4b - Due To Stent Thrombosis
  • Type 5 - Due to CABG Problems [@Oh, Chapter 20]

Flashcard type:cloze_reference
The 5 Types of MI are:
Type 1 - {{c1::Spontaneous Plaque Rupture}}
Type 2 - {{c2::Ischaemic Imbalance}}
Type 3 - {{c3::Death Prior to biomarker results}}
Type 4a - {{c4::MI due to PCI}}
Type 4b - {{c4::MI due to stent thrombosis}}
Type 5 - {{c5::Due to CABG}}		 Oh ICM - ACS

Presentation

  • Chest Pain
  • Syncope
  • Palpitations
  • Shortness of Breath
  • Fatigue
  • Cardiac Arrest
  • LV Failure and Shock
  • Murmurs - Mitral Regurg - Papillary Muscle Rupture/LV Dilatation [@Oh, Chapter 20]

Flashcard type:basic
Why might you get murmurs following MI? Papillary Muscle Rupture = MR
VSD

Atypical Presentations

  • 1 in 4 (25%) of STEMIs have atypical or no symptoms
  • Almost half (45%) of NSTEMIs have atypical or no symptoms
  • You are more likely to have an atypical if you are a woman or elderly or comorbid [@Oh, Chapter 20]

Flashcard type:reference ...
What percentage of STEMI patients are atypical / no symptoms? 25% Oh ICM - ACS
What percentage of NSTEMI patients are atypical / no symptoms? 45% Oh ICM - ACS
Which patients with ACS are more likely to be atypical/asymptomatic? Women
Elderly
Comorbid		 Oh ICM - ACS

Differential For Same Symptoms

  • Pericarditis
  • Aortic Dissection (About 1% occur at same time with STEMIs)
  • Massive PE
  • Takotsubo

Takotsubo

Japanese octopus pot

Also called Apical Ballooning Syndrome (ABS)

Caused by stresses in 70% of cases

Not sure why it happens, but may be high levels endogenous catecholamines (adrenaline)

Can represent up to 1-2% of STEMI like presentations [@Oh, Chapter 20]

  • 90% of cases are post menopausal women
  • So 10% of ACS in post menopausal women may be ABS

Will have ST elevation in 30% of cases

Acute mortality up to 5% [@Oh, Chapter 20]

Flashcard type:cloze_reference
The other name for {{c1::Takotsubo}} is {{c2::Apical Ballooning Syndrome}} Oh ICM - ACS
A small percentage of {{c2::STEMI-like}} presentations ({{c1::1% each}}) are actually {{c3::Takotsubo}} or {{c3::Aortic Dissection}} Oh ICM - ACS
An echo of {{c1::Takotsubo}} shows:
{{c2::Apical + Mid LV Ballooning}}
{{c2::LVOT Obstruction}}
{{c2::Hypokinetic Apex}}
{{c2::Hypercontractile Base}}		 Oh ICM - ACS

On echo you see:

  • apical ballooning with preserved basal contraction
  • hypercontractile base of heart
  • LV outflow tract obstruction
  • hypokinetic apical
  • mid-LV ballooning [@Oh, Chapter 20]

It can cause:

  • Hypotension
  • Heart Failure
  • Cardiogenic Shock
  • arrhythmias
  • LV thrombus
  • mitral Regurg [@Oh, Chapter 20]

Treat with fluids, don't know which inotropes, maybe needs mechanical support

Complications

  • arrhythmias
  • Angina
  • reinfarction
  • cardiogenic shock/cardiac failure - SBP less than 90mmHg or Cardiac Index less than 1.8L/min/m2
  • 15% of ACS
  • Mechanical
  • Free wall rupture - happens in 0.5% of MI - causing catastrophic tamponade
  • acute VSD - super rare, 0.2% of MI
  • acute MR - functional MR common transient after MI
  • RV infarction
  • cardiogenic shock
  • Emboli - after mural LV thrombus - rare post PCI era
  • Post Myocardial Infarction Injury Syndrome (Dresslers) and Pericarditis
  • Dresslers is 2-3 weeks afterwards [@Oh, Chapter 20]

Flashcard type:basic
How likely is Cardiogenic Shock after MI? ~15%
How likely is Free Wall Rupture after MI? ~0.5%
How likely is VSD after MI? ~0.2%
What are the five big potential complications after MI? Cardiogenic Shock
Free Wall Rupture
VSD
MR
Dresslers Syndrome
What is dresslers syndrome? Post Myocardial Infarction Injury Syndrome

Aetiology

  • First there are atheroma deposits in coronary artery walls
  • These come from vessel wall injury (could happen as early as childhood)
  • Deposits come from fatty macrophages (foam cells) and T lympohcytes getting into arterial intima
  • These increase an inflammatory process in there
  • These fat deposits then get a scab like "fibromuscular cap", the "fibrous plaque"
  • Eventually either the plaque ruptures or gets eroded
  • This exploses fat to blood, and the fat is very thrombogenic, activating platelets
  • This activates the clotting cascade, platelet glycoprotein IIb/IIIa receptor is activated
  • Resulting in platelets clump in "white thrombus" with fibrinogen
  • Then thrombin is activated and red cells clumps in "red thrombus" [@Oh, Chapter 20]

Flashcard type:basic
Which are the two main immune cells involved in formation of atheroma deposits in vascular disease? Fatty Macrophages (foam cells)
T Lymphocytes
Why is the clotting cascade activated by atheroma in vascular disease? Rupture of plaque exposes fat. Fat is thrombogenic
How does fat activate clotting cascade in vascular disease? Activates platelets and their glycoprotein IIb/IIIa receptor

Investigations

ECG

  • Number of leads involved roughly reflects extent of myocardium
  • Height of ST elevation is modestly related to degree of ischaemia
  • Resolution of ST elevation correlates well with reperfusion [@Oh, Chapter 20]

ECG changes - STEMI

  • Hyperacute - First 20 mins - Tall T waves, elevation of ST segments
  • Acute - First Few Hours - Persistent more flat ST segments with loss of R wave, with inverted T waves
  • Early - First Few Days - Development of Q waves, return of ST segments, persistent T wave inversion
  • Indeterminate - First Few Weeks - Pathological Q waves with T wave inversion. ST segments normal.
  • Old - First Few Months - Persisting deep Q waves with normal ST segments and T waves. [@Oh, Chapter 20]

Flashcard type:basic
What are the hyperacute ECG changes in STEMI? Tall T waves
ST Elevation
What are the acute ECG changes in STEMI? Persistent ST Elevation
Loss of R Wave
Inverted T Waves
What are the early ECG changes in STEMI? Q Wave Formation
Normal ST Segments
Inverted T Waves
What are the indeterminate ECG changes in STEMI? Pathological Q Waves
Inverted T Waves
Normal ST segments
What are the old ECG changes in STEMI? Persisting Q Waves
Normal ST and T waves
What is the timescale for hyperacute ECG changes in STEMI? 20 mins
What is the timescale for acute ECG changes in STEMI? First few hours
What is the timescale for early ECG changes in STEMI? First few days
What is the timescale for indeterminate ECG changes in STEMI? First few weeks
What is the timescale for old ECG changes in STEMI? First few months
What do you call the ECG changes seen in STEMI in/after the first 20 mins? Hyperacute
What do you call the ECG changes seen in STEMI in/after the first few hours? Acute
What do you call the ECG changes seen in STEMI in/after the first few days? Early
What do you call the ECG changes seen in STEMI in/after the first few weeks? Indeterminate
What do you call the ECG changes seen in STEMI in/after the first few months? Old

Sgarbossa criteria are specific but low sensitivity [@Oh, Chapter 20]

LBBB

It used to be that LBBB meant STEMI, and it pretty much still does. But really only 1/3 patients with LBBB have STEMI, 1/3 have non acs cardiac disease, and 1/3 have non-cardiac illness [@Oh, Chapter 20]

Flashcard type:basic
What is the distribution of patient pathology when you see new LBBB? 1/3 STEMI
1/3 Non ACS Cardiac Disease
1/3 Non Cardiac Disease

ECG Changes - NSTEMI

  • ST segment depression
  • ST elevation but not enough to meet criteria
  • T wave inversion [@Oh, Chapter 20]

ECG Localisation

ECG Location Location on Heart Culprit Lesion
V1 - V6 + aVL Anterolateral LAD Occlusion
V1 - V3 Septal LAD-septal branches
V2 - V5 Anterior Diagonal (For ant LV wall)
V5 - V6 Lateral Distal LAD
II, III, aVF Inferior RCA (sometimes circumflex)
I, aVL, V5, V6 plus inferior leads Inferolateral RCA (sometimes circumflex)
V7 - V9, ST Depression V1, V2, plus inferior leads Inferoposterior RCA (sometimes circumflex)
V1, V3, V4 Right Ventricle RCA
V7-V9 Posterior RCA

[@Oh, Chapter 20]

Flashcard type:basic
What is the name for ECG changes seen in leads V1 - V6 + aVL Anterolateral changes
What is the name for ECG changes seen in leads V1 - V3 Septal changes
What is the name for ECG changes seen in leads V2 - V5 Anterior changes
What is the name for ECG changes seen in leads V5 - V6 Lateral changes
What is the name for ECG changes seen in leads II, III, aVF Inferior changes
What is the name for ECG changes seen in leads I, aVL, V5, V6 plus inferior leads Inferolateral changes
What is the name for ECG changes seen in leads V7 - V9, ST Depression V1, V2, plus inferior leads Inferoposterior changes
What is the name for ECG changes seen in leads V1, V3, V4 Right Ventricle changes
What is the name for ECG changes seen in leads V7-V9 Posterior changes
What ECG leads would change when there is Anterolateral ischaemia V1 - V6 + aVL
What ECG leads would change when there is Septal ischaemia V1 - V3
What ECG leads would change when there is Anterior ischaemia V2 - V5
What ECG leads would change when there is Lateral ischaemia V5 - V6
What ECG leads would change when there is Inferior ischaemia II, III, aVF
What ECG leads would change when there is Inferolateral ischaemia I, aVL, V5, V6 plus inferior leads
What ECG leads would change when there is Inferoposterior ischaemia V7 - V9, ST Depression V1, V2, plus inferior leads
What ECG leads would change when there is Right Ventricle ischaemia V1, V3, V4
What ECG leads would change when there is Posterior ischaemia V7-V9
When there are Anterolateral changes seen on ECG, what artery is affected? LAD Occlusion
When there are Septal changes seen on ECG, what artery is affected? LAD-septal branches
When there are Anterior changes seen on ECG, what artery is affected? Diagonal (For ant LV wall)
When there are Lateral changes seen on ECG, what artery is affected? Distal LAD
When there are Inferior changes seen on ECG, what artery is affected? RCA (sometimes circumflex)
When there are Inferolateral changes seen on ECG, what artery is affected? RCA (sometimes circumflex)
When there are Inferoposterior changes seen on ECG, what artery is affected? RCA (sometimes circumflex)
When there are Right Ventricle changes seen on ECG, what artery is affected? RCA
When there are Posterior changes seen on ECG, what artery is affected? RCA

Bloods

Troponin

It's cardiac troponins, which are cTnT and cTnI [@Oh, Chapter 20]

Newer tests you can take on admission Older tests are positive 4-6 hrs post MI Peak 18-24hrs Back to normal after 1-2weeks [@Oh, Chapter 20]

  • In general ICU, cTN may be elevated in 40-50% or all patients!
  • Post major surgery, 12% had a raised trop by day 3
  • Mortality is worse in these patients, between 4 and 16x worse than those with normal trop. The higher the trop the worse the outcomes. [@Oh, Chapter 20]

That may be due to Type 2 MI, or it may not even be that, maybe a myocardial injury.

Other markers

These ones are probably more research tests

  • cardiac myosin binding protein C (cMyC)
  • vascular cell adhesion molecule-1
  • interleukin-6 [@Oh, Chapter 20]

Echo

  • Regional wall motion abnormalities
  • Global abnormalities
  • Loss of wall thickening during contraction
  • differential diagnoses like pericardial effn or aortic Dissection
  • complications like MR, papillar muscle rupture, effusion, VSD
  • or mural thrombus [@Oh, Chapter 20]

Treatment

Flashcard type:basic
How does aspirin work? Antiplatelet that blocks Thromboxane A2 Synthesis
How does clopidogrel work? Antiplatelet that blocks ADP receptors
"P2Y12 inhibitor"
How does ticagrelor work? Antiplatelet that blocks ADP receptors
"P2Y12 inhibitor"
How does tirofiban work? Antiplatelet
Glycoprotein IIb/IIIa inhibitor
How do heparins work in general? Limit Thrombin Activation
How effective is aspirin in ACS? Reduces total mortality by ~2.5%
Which drug blocks Thromboxane A2 synthesis? Aspirin
Which are the two main drugs that are P2Y12 inhibitors? Clopidogrel and Ticagrelor

  • Aspirin - Blocks Thromboxane A2 Synthesis
  • Loading dose of ~300mg
  • Daily Dose of 150mg/day
  • Reduces absolute mortality by 2.4%
  • Should be life long
    • Benefit has been shown at 10 years [@Oh, Chapter 20]
  • Clopidogrel - Blocks ADP receptors (Adenosine Diphosphonate, a receptor on platelets that activates them) - P2Y12 inhibitors
  • Clopidogrel has slow onset (6+ hours)
  • Ticagrelor has fastor action
  • As Dual Anti Platelet Therapy in Primary PCI
    • DAPT for 12 months
  • glycoprotein IIb/IIIa inhibitors - older than P2Y12 inhibitors
  • Like tirofiban
    • Have a role for complex lesions

  • Heparins - Limit Thrombin Activation [@Oh, Chapter 20]

  • GTN for relief of chest pain

  • Analgesia - Morphine (1-2mg) / Fentanyl (20-40microg) boluses
  • May need CPAP if pulm oedema
  • B Blockers as soon as able when CV stable (usually around time of PCI)
  • Maybe less useful in the post thrombolysis era than they were before
  • Start in first 24hours if not shocked or in heart block
  • Reduces recurrent MI/VF risk, increases risk of CS
  • Should continue long term (although much less evidence for those with good LV function)
  • RAAS (Renin Angiotensin Aldosterone System) Inhibitors
  • ACEis and ARBs
  • Reduces 30day mortality
  • Should be long term in those with HF, may be of benefit for those without, may not be
  • Lipid lowering agents
  • HMG COa reductase inhibitors - Statins
  • Benefits are seen at 1 year [@Oh, Chapter 20]

Flashcard type:basic
When should you start a B Blocker after ACS? When CV stable
When should you start a B Blocker in the first 24hrs after ACS? If CV stable and not in heart block
What is the risk of starting a B Blocker after ACS? Increases risk of cardiogenic shock
What broader category of drugs does an ACEi fit into? Renin Angiotensin Aldosterone System Inhibitor (RAAS)
What broader category of drugs does an ARB fit into? Renin Angiotensin Aldosterone System Inhibitor (RAAS)
What does RAAS mean? Renin Angiotensin Aldosterone System
Which are the two main group of drugs that fit under defn of RAAS inhibitors? ACEis
ARBs
How do statins work? HMG COa reductase inhibitors
When do you see mortality benefit from statins in ACS? After one year
When do you see mortality benefit from ACEis in ACS? In first month

Reperfusion (PCI/Thrombolysis)

PCI:

  • less than 12 hours with ACS, not relieved by gtn
  • new st segment elevation in two or more leads with
    • 2mV+ (small boxes) in men, 1.5mV+ in women in V2-V3
    • 1mV+ in other leads
  • new onset LBBB
  • posterior infarction
  • 12-24hrs with continuing pain and evolving infarction
  • Up to 36hrs if cardiogenic shock
  • When uncertain diagnosis and angiography during PCI may get us answers [@Oh, Chapter 20]

Flashcard type:cloze
PCI is indicated for MI in patients in the {{c1::first 12 hours::time scale}} when there is {{c2::ST elevation::ONE}}, {{c2::LBBB::TWO}}, or {{c2::posterior infarction::THREE}}. It is indicated in {{c3::up to 24 hours::}} if there is {{c4::worsening signs of infarction::indication}}. It is indicated in {{c5::up to 36 hours::time scale}} if there is {{c6::cardiogenic shock::indication}}. It can also be done {{c7::as an investigation to help get diagnosis if uncertain::indication}}.

PCI is better than thrombolysis (short term 5% mortality vs 7% mortality). Thrombolyse when cant do PCI within 2 hours Thrombolysis has a number needed to harm of 50 for stroke Thrombolysis has somewhere between 1-4% risk of early cerebral haemorrhage = NNH 25 - 100 Thrombolysis has somewhere between 4-13% risk of non cerebral major bleeds = NNH 8 - 20 PCI has a number needed to harm of 100 for stroke Thrombolysis has a NNT of around 25 to avoid a death PCI has a NNT of around 16-20 to avoid a death [@Oh, Chapter 20]

Flashcard type:basic
When should you thrombolyse ACS instead of PCI? If you cant PCI within 2 hours
What are the short term mortalities in ACS for Thrombolysis and PCI? 7% and 5%
What is the NNH for Stroke after Thrombolysis and PCI for ACS? Thrombolysis = NNH 50 for Stroke
PCI = NNH 100 for Stroke
What is the NNT for avoiding death with Thrombolysis and PCI for ACS? Thrombolysis = NNT 25 to avoid a death
PCI = NNT of 15-20 to avoid a death
How likely is Thrombolysis for MI going to cause major cerebral bleeds? ~1-4%
How likely is Thrombolysis for MI going to cause major non-cerebral bleeds? ~4-12%

Should do PCI when can get to it within 2 hrs. Else it should be thrombolysis. [@Oh, Chapter 20]

PCI could be:

  • Primary PCI
  • Rescue PCI
  • Pharmaco-Invasive PCI (thrombolysis then PCI) [@Oh, Chapter 20]

Flashcard type:basic
What are the three types of PCI for MI? Primary
Rescue
Pharmaco-Invasive

PCI is angiography followed by balloon dilatation and stent placement. [@Oh, Chapter 20]

Stents may be either bare metal, or now more commonly are drug eluting. Stents can thrombose when antiplatelets are stopped! [@Oh, Chapter 20]

Thrombolysis could be:

  • Streptokinase - These are the non fibrin specific agents
  • Alteplase, Reteplase, Tenecteplase - These are the fibrin specific agents [@Oh, Chapter 20]

Streptokinase works by reacting with plasminogen, releasing the protease plasmin, which lyses coronary thrombus. [@Oh, Chapter 20]

Flashcard type:basic
How do thrombolytic agents work? Increases plasmin levels (by reacting with plaminogen). Plasmin lyses thrombus
What is the difference between Streptokinase and newer thrombolytic drugs? Newer drugs work more specifically on thrombus. Streptokinase works on fibrin everywhere in body.
What is the disadvantage of Streptokinase in comparison to newer thrombolytic drugs Works on everywhere in body rather than specifically thrombus, higher bleeding risk elsewhere
What is the advantage of Streptokinase in comparison to newer thrombolytic drugs Works longer in body, have longer until needing to start heparin
Give three names of newer thrombolytic drugs Alteplase
Tenecteplase
Reteplase

The other agents are more localised, working more on the coronary artery thrombus, rather than fibrin everywhere. But they do last for less time so you may need to start heparin sooner. [@Oh, Chapter 20]

Contraindications

Absolute contraindications to thrombolysis in MI would be:

  • Previous haemorrhagic stroke at any point
  • Other strokes in last 6 months
  • Intracranial cancers
  • Active internal bleeding in last 2 Weeks
  • Aortic Dissection [@Oh, Chapter 20]

Flashcard type:cloze
Absolute contraindications to thrombolysis in MI would be things that really up your bleeding risk (particularly bleeding in head):
{{c1::haemorrhagic stroke ever}} ,
{{c1::any stroke in last 6 months}},
{{c1::internal bleeding in last two weeks}},
{{c1::aortic dissection}},
{{c1::intracranial cancers}}
Everything else is just relative contraindication.
Heparin can be reversed with {{c1::protamine}}

Relative contraindications to thrombolysis in MI would be:

  • Severe hypertension on presentation (180+ systolic)
  • Oral anticoagulants with tendency to bleeding
  • Trauma/Surgery/Head Trauma in last month
  • Allergy
  • CPR
  • Peptic Ulcer Disease
  • Pregnancy
  • Recent thrombolysis with Streptokinase as less effective second time around cos of antibodies
  • previous CVA
  • hypertension [@Oh, Chapter 20]

You shouldn't PCI early all thrombolysis patients as the bleeding risk is too high, but should for failed thrombolysis, or cardiogenic shock.

Anticoagulants

Treating Bleeding Complications

Flashcard type:basic
What can you use for reversing antiplatelets? Platelets
FFP
Recombinant Factor VIIa
Desmopressin
What can you use for reversing heparin? Protamine
What can you use for reversing dabigatran? Idarucizumab
What can you use for reversing fibrinolytics? FFP
Cryoprecipitate
TXA
What is idarucizumab for? Reversing Dabigatran
What is protamine for? Reversing heparin

No specific drugs for antiplatelet reversal. Can give platelets, FFP, recombinant factor VIIa, desmopressin.

Unfractionated heparin can be reversed with protamine.

Dabigatran can be rebersed with idarucizumab

Dealing with bleeding in fibrinolysis, FFP, Cryoprocipitate, Tranexamic acid. [@Oh, Chapter 20]

Misc

You need revascularisation if cardiogenic shock here, it's the only thing with proven survival benefit. Fibrinolysis if you can't get PCI in time. [@devices_critical_care]

SHOCK trial for cardiogenic shock. Early revascularisation was no use in 30 day mortality but did improve 6 months. [@devices_critical_care]

If there are multiple vessels diseased should you revascularise all or just the culprit lesion. CULPRIT-SHOCK trial said better survival if just the cuprit at the time (reduces mortality by 10% in short term. At one year mortality much the same but less readmissions in the culprit only group). [@devices_critical_care]

Flashcard type:basic
What is the name of the trial looking at use of PCI in Cardiogenic Shock? SHOCK Trial
What did the SHOCK Trial show? In patients with cardiogenic shock from ACS, early revascularisation improved 6 month mortality
What is the name of the trial looking at single vessel vs multi vessel PCI in ACS? CULPRIT-SHOCK trial
What did the CULPRIT-SHOCK trial show? In patients with ACS, if you just do early revascularisation of culprit lesion and leave the rest for the time being, mortality reduction of about 10%