Myocardial infarction

An acute myocardial infarction (MI) is the death of the myocardium as a result of a profound imbalance in the oxygen supply vs demand of the myocardium due to a lack of blood being supplied to the tissue.

Let’s recap our anatomy of the coronary arteries briefly:

We have 2 main coronary arteries which come off of our aortic sinus:

1. Left coronary artery - comes off the left aortic sinus to give off 2 main branches:
1. Left anterior descending (LAD)/anterior interventricular artery - found in the anterior interventricular sulcus. It supplies the right ventricle, left ventricle and anterior 2/3rds of the interventricular septum.
2. Left circumflex (LCx) - travels in the coronary sulcus towards the base of the heart. It supplies the left atrium and left ventricle. It also gives off the left marginal branch.
1. Left marginal artery - travels along the obtuse margin of the heart and supplies the left ventricle.

2. Right coronary artery - comes off the right aortic sinus also travelling in the coronary sulcus towards the diaphragmatic surface (base of the heart). It itself has 4 main branches:
1. Atrial branch - found in between the right auricle and ascending aorta. It gives rise to the SA nodal branch.
1. SA nodal branch - supplies SA node.
2. Right marginal artery - travels from the acute margin to the apex, supplying the right ventricle.
3. Atrioventricular branch - a small branch for the AV node.
4. Posterior interventricular artery/posterior descending artery (PDA) - it is found in the posterior interventricular sulcus, travelling to the base of the heart also. It supplies the posterior 1/3rd of the interventricular septum.

ECG

🥇 ECG is the first-line investigation. It is needed to distinguish between a STEMI, and NSTEMI/UA:

	ECG changes	Coronary artery affected
Anterior	V1-v4	LAD
Inferior	II, III, aVF	Right coronary
Lateral	I, V5-V6, aVL	Left circumflex

Pathophysiology

ACS usually results from a thrombus due to an atherosclerotic plaque that ruptures to occlude a coronary artery.

Atherosclerotic plaques rupture/erode to form a thrombosis. Arteries are platelet-rich, therefore the thrombus is a platelet rich thrombus (white thrombus), as opposed to RBC rich thrombi in veins (red thrombi). The thrombus then occludes the coronary artery → ischaemia/infarction of the myocardium → myocardial death. Depending on the extent of damage as well as the ECG presentation, it is classified as a STEMI, NSTEMI, unstable angina.

Depending on the level of occlusion, MI can be broken down into 2 main conditions:

1. ST elevation MI - when there is a complete occlusion of the artery by an atherothrombotic lesion.
2. Non-ST elevation MI - when there is a near-complete occlusion of the coronary artery.

As their names imply, the key difference is the presence of ST elevation on an ECG reading. The leads in which the ST elevation is identified corresponds with the portion of the myocardium that has been affected. This is why it is crucial to refer to the table above and be aware of which leads correspond with which artery and which part of the heart.

Simply put let’s look at some examples:

1. LAD occlusion - will cause an anterior infarction. This is the most common occlusion (50%) and is known as the artery of sudden death. It can be detected on leads V1-V4.
2. LCx occlusion - causes a lateral infarction. It can be detected on lead I, aVL, V5-V6. Makes up 30% of MIs.
3. RCA occlusion - causes an inferior infarction. It is detectable on lead II, III, aVF. Makes up 20% of MIs.

😷 Presentation

Any ACS should be suspected in a patient who presents with chest pain radiating to other areas (such as arms, back, or jaw) and has associated breathlessness, diaphoresis, nausea and vomiting.

• ⭐️ Chest pain - this is the classical, most notable symptom. It is typically on the left side of the chest and may radiate to the left arm, jaw, or back. It is described as a crushing chest pain as if there was a heavy pressure sitting on the chest. However, this presentation differs sometimes. Pain is also reported in the neck and shoulder blades or even the epigastric area. It may occur at rest or with activity. It may be constant or it may be intermittent.
• Palpitations
• Dizziness
• Dyspnoea
• Nausea and vomiting
• Sweating (diaphoresis)

On examination, we may notice changes to the , blood pressure, temperature and SpO2. However, these are often normal.

⚠️ Risk factors

🔍 Investigations

🥇 ECG:

Needs to be performed within 10 minutes of first medical contact.

STEMI:

To diagnose a STEMI, we need to see a new/increased and persistent (20 minutes or more) ST-segment elevation in at least 2 contiguous leads of >1mm in all leads except V2-V3.

The following cut off points apply for V2-V3:

• >2.5mm in men <40 years old
• >2mm in men >40 years old
• >1.5mm in women, regardless of age
• OR new LBBB in 2 contiguous leads.

Contiguous leads are leads that are looking at anatomically neighbouring areas.

• Hyperacute T-waves
• New onset LBBB

NSTEMI:

Look for changes in T-wave (e.g T-wave inversion), transient ST elevation, or ST depression (suggests a worse prognosis)

After diagnosing STEMI, we should order the following:

1. Coronary angiography - if the patient is indicated for PCI that can be done within 120 minutes of the time when fibrinolysis could have been given and has presented within 12 hours of symptom onset.
2. Blood glucose - check for uncontrolled hyperglycaemia due to stress (infarction is one of the 6 Is)
3. FBC - anaemia may affect the duration of dual anti-platelet therapy.
4. U&Es & creatinine - to prevent bradyarrhythmias and tachyarrhythmias in the peri-infarct interval.
5. eGFR - to assess how much nephrotoxic contrast may be tolerated with angiography.
6. Serum lipids - to assess risk of recurrence.
7. CRP - to assess for infection.

Once we have ruled out a STEMI, we may consider NSTEMI with the following investigations:

• FBC - look for thrombocytopenia or anaemia as NSTEMI management increases bleeding risk.
• U&E’s & creatinine - to calculate GRACE score.
• LFTs and coagulation profile
• Blood glucose
• CRP

💯 Scoring

GRACE risk assessment

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It predicts 6-month mortality using:

1. Age
2. Heart rate and BP
3. Cardiac function (Killip classification) and renal function (serum creatinine)
4. Cardiac arrest on presentation
5. ECG findings
6. Troponin levels

It can be calculated online with a predicted risk outcome:

HEART score

Predicts 6-week risk of major adverse cardiac event.

It considers 5 aspects:

1. History
2. ECG
3. Age
4. Risk factors
5. Troponin

🧰 Management

When we have identified ACS we need to primarily focus on 3 aspects with management:

1. Pain relief
2. Preventing deterioration
3. Revascularisation

NICE divides ACS into 2 groups for management:

1. STEMI
2. NSTEMI

Let’s look at the common management of all ACS patients then we will look at the management of these 2 groups specifically:

• We then need to do an ECG to determine the subtype of ACS that the patient has

STEMI management:

If the patient does not meet the criteria for reperfusion therapies, dual antiplatelet therapy with aspirin and ticagrelor is recommended. If the bleeding risk is high then consider clopidogrel.

If the patient meets the criteria for STEMI (to be discussed in the MI CCC) then we need to assess their eligibility for percutaneous coronary intervention or fibrinolysis, both are which are types of coronary reperfusion therapies.

1. Percutaneous coronary intervention

This entails coronary angioplasty along with stenting. It is performed through catheterisation via the radial artery (although femoral access may be used).

Stenting is done using drug-eluding stents. They are covered in drugs such as sirolimus or paclitaxel as these inhibit cell proliferation and restenosis.

PCI is offered if the patient is presenting within <12 hours of symptom onset and the PCI can be delivered within 2 hours of the time when fibrinolysis could have been given.

It is considered if the patient presents after 12 hours with signs of ongoing coronary ischaemia.

• Prior to PCI:
1. Angiography
2. Dual anti-platelet therapy

→ Aspirin

→ Prasugrel (P2Y12 inhibitor) if they are taking an oral anticoagulant or clopidogrel if they are already taking an oral anticoagulant or have a high risk of bleeding.

• During PCI:
1. IV anticoagulants (alongside dual-platelet therpay)

If they are undergoing PCI with radial access → unfractionated heparin (UFH) with bailout glycoprotein IIb/IIIa inhibitor (tirofiban and eptifibatide) which are used in case of any complications that may arise during PCI.

If they are undergoing PCI with femoral access → bivalirudin (a direct thrombin inhibitor) along with bailout GPI.

2. Fibrinolysis

Fibrinolytic agents such as streptokinase, alteplase, urokinase. These promote plasminogen conversion into plasmin. As we know, plasmin is a fibrinolytic enzyme which breaks down fibrin into fibrin degradation products.

It needs to be offered within 12 hours of symptom onset if PCI cannot be delivered within these 120 minutes (for example if they need to be transferred to a larger hospital from a district hospital). However, if the ECG taken 90 minutes after does not show resolution, then PCI will be considered again.

1. During fibrinolysis:

We need to give an antithrombin agent such as enoxaparin, fondaparinux, or UFH.

2. After fibrinolysis:

Give dual antiplatelet therapy with ticagrelor if not treated with PCI. We give clopidogrel if the bleeding risk is high but the P2Y12 inhibitor of choice depends on the bleeding risk ultimately.

If an ECG done 90 minutes after fibrinolysis still shows STEMI → offer immediate coronary angiography and consider PCI.
3. Treat the hyperglycaemia if present. This is a common finding in patients after having an acute MI.

NSTEMI/unstable angina management:

Once diagnosis of NSTEMI or UA is made:

1. Aspirin - 300mg loading dose and continue on 75mg OD lifelong.
2. Antithrombin therapy
1. Fondaparinux - unless patient has high risk of bleeding or is going for immediate coronary angiography.
2. Enoxaparin - if the patient has renal impairment (creatinine >265umol/L).
3. GRACE risk assessment - to formally assess risk of future CVS event.

GRACE risk assessment:

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It predicts 6-month mortality using:

1. Age
2. Heart rate and BP
3. Cardiac function (Killip classification) and renal function (serum creatinine)
4. Cardiac arrest on presentation
5. ECG findings
6. Troponin levels

It can be calculated online with a predicted risk outcome:

Predicted 6-month mortality	Risk of future CVS events
<1.5%	Lowest
1.5% - 3%	Low
3% - 6%	Intermediate
6% - 9%	High
9%	Highest

Low risk patients:

• Conservative management without coronary angiography - this involves dual antiplatelet therapy.

Intermediate - highest risk patients:

• If clinically unstable:
• Coronary angiography ± revascularisation within 72 hours
• Dual antiplatelet therapy
• Anticoagulant (heparin)
• ACEI or ARB
• If clinically stable:
• Immediate coronary angiogrpahy + revascularisation with PCI or CABG
• Dual antiplatelet therapy
• Anticoagulant (heparin)

🚨 Complications

• Acute mitral regurgitation - acute mitral regurgitation is commonly seen 2-10 days post myocardial infarction and can be seen with both anterior and inferior MIs. A rapid rise of pressure in a non-dilated and non-compliant left atrium and subsequent lack of forward flow causes hypotension and tachycardia. It is a medical emergency and needs mitral valve repair or replacement.
• Rupture of the interventricular septum - occlusion of the left anterior descending artery creates risk of rupture of the interventricular septum due to infarction of the septal area. The rupture usually leads to haemodynamic instability, with hypotension and biventricular failure (often largely right-sided). On auscultation, a harsh and pansystolic (holosystolic) murmur may be heard.
• Cardiogenic shock - has a poor prognosis.