Acute Coronary Syndrome

ACS consists of the signs and symptoms that result from impaired cardiac perfusion at rest. It includes:

• STEMI - full-thickness infarction (complete occlusion)

• NSTEMI - mid-thickness infarction (partial occlusion)

• Unstable Angina - no infarction (partial occlusion)

Risk Factors:

• Non-modifiable - Age, Gender, Family hx

• Modifiable - Smoking, HTN, DM, Hyperlipidaemia, Obesity, Sedentary lifestyle

Presents with central, crushing chest pain that radiates to jaw/neck/left arm. This pain is worsened by exercise/exertion and may be improved by GTN. Associated symptoms include Nausea, Vomiting, Sweating, Clamminess, SOB.

N.B. Can present atypically as epigastric pain/no pain (Silent MI), especially in the elderly and diabetics.

Differentials include:

• Cardiac - Angina, Aortic dissection, Myocarditis, Pericarditis

• Pulmonary - PE, Pneumonia, PTX (pleuritic pain)

• GI - Oesophagitis, GORD, Peptic ulcer, Pancreatitis, Cholecystitis

• MSK - Costochondritis, Rib fracture

Types of MI

There are 6 types, but the main ones to remember are Type 1 and Type 2:

• Type 1 - Infarction secondary to ischaemia due to a primary coronary event e.g. plaque rupture, fissuring or dissection.

• Type 2 - Infarction secondary to ischaemia due to either increased oxygen demand or decreased supply e.g. in HF, AF, or septic patients.

Investigations

Immediate investigation:

• ECG! - Defines immediate management and, if it shows ST elevation, then troponin is essentially irrelevant and the patient will require immediate treatment

  • Hyperacute T waves (HATW) tend to be the first ECG changes seen that are indicative of an acute coronary occlusion, and is typically seen mins - hours after.

N.B. ST elevation is a sign of infarction, whereas ST depression is a sign of ischaemia.

Other investigations:

• Troponin!

• Bloods - FBC, U&Es, LFTs, Lipids, Glucose

• CXR - Check for pulmonary causes of chest pain

• Echo - Assess for functional damage

• CT Coronary Angiogram - Assess for obstruction and measure degree of perfusion using TIMI flow system

  • TIMI 0 - No flow

  • TIMI 1 - Faint flow w/incomplete filling of distal coronary bed

  • TIMI 2 - Delayed/slugglish flow w/complete filling of distal coronary bed

  • TIMI 3 - Normal flow

N.B. TIMI 0 - no. TIMI 3 - free.

Troponin is a protein released from damaged cardiac myocytes (typically raised 3 hours post-MI). However, this means it will also be raised in conditions that put strain on these cells e.g. Pericarditis, Myocarditis, Type A Aortic dissection, PE, CKD, Sepsis, and Prolonged strenuous exercise.

N.B. Myoglobin is the first biomarker raised after an MI.

N.B. If a patient, who has recently had a PCI w/stenting done, presents with new chest pain, you need to do a CK-MB as they’ve most likely re-stenosed the stent.

How to know the location of the MI with the ECG?

• ST elevation in Leads II, III, aVF - Inferior MI - This area is supplied by the Right coronary artery

• ST elevation in Leads I, aVL, V5-6 - Lateral MI - This area is supplied by the Left Circumflex coronary artery

• ST elevation in Leads V1-4 - Anteroseptal MI - This area is supplied by the Left Anterior Descending (LAD) coronary artery

  
  

• ST depression in reciprocal precordial leads (V1-4) - Posterior MI

  • One could always add on posterior leads (V7-8) to check for STE, but electricity conducts poorly through aerated lung, therefore any STE would be significantly reduced or absent.

Left Anterior Descending (LAD) Artery

In 90% of people, the proximal LAD supplies the Right bundle and Anterior fascicle of the Left bundle. Therefore, it's wise to say that any new-onset RBBB +/- ischaemic-sounding chest pain could be indicative of a proximal LAD occlusion and the need for urgent PCI. LAFB may also be seen.

STEMI

Diagnosis - Cardiac chest pain + ST-elevation/new LBBB¹ (no need for a troponin in this case). On the ECG, the ST elevation has to be 2mm in adjacent chest leads or >1mm in adjacent limb leads.

The mainstay of treatment here is PCI if presenting within 12 hours of onset, and should be given in under 120 mins. Fibrinolysis is an alternative if PCI isn't available.

Other immediate management includes:

• O2 (target sats > 90%)

• Loading dose of PO Aspirin 300mg

○ If eligible for PCI, add Prasugrel (if not on anti-coagulation) or Clopidogrel (if on anti-coagulation)

○ If not eligible for PCI, add Ticagrelor

• IV GTN infusion - for symptomatic relief

• IV Morphine/diamorphine - in addition to pain relief, this causes vasodilation, therefore reducing preload

NSTEMI

Diagnosis - Chest pain + abnormal/normal ECG (no ST elevation) + raised troponin

N.B. ST-depression as part of an NSTEMI is generally poorly localised, whereas a posterior STEMI will produce reciprocal, localised ST-depression in the anterior leads (V1-V3).

The first thing to do if suspected is to calculate the GRACE score, which gives an indication of the 6-month risk of mortality and cardiovascular events.

The mainstay of treatment here is treatment dose LMWH or Fondaparinux (if for immediate angiogram).

Other immediate management includes:

• O2 (target sats > 90%)

• Loading dose of PO Aspirin 300mg

              ○ Those with a higher GRACE score (6 month mortality risk) should be given Prasugrel or Ticagrelor instead

• IV GTN infusion - for symptomatic relief

• IV Morphine/diamorphine - in addition to pain relief, this causes vasodilation, therefore reducing preload

Unstable Angina

Diagnosis - Chest pain + abnormal/normal ECG + normal troponin.

Treatment here is very similar to that of an NSTEMI i.e. LMWH/Fondaparinux.

Post-MI Management

• Lifestyle changes - Smoking cessation, Reducing alcohol, Weight loss, Diet, Better diabetic/pressure control

• Start all patients on: BAAD

              ○ B-blocker (usually Bisoprolol)

              ○ ACEi (usually Ramipril)

              ○ Atorvastatin 80mg

              ○ Dual Antiplatelet therapy (Aspirin 75mg + Clopidogrel/Ticagrelor)

• Echo to assess systolic function and for evidence of heart failure

• Referred to cardiac rehabilitation

Aspirin vs Clopidogrel vs Ticagrelor

Aspirin (acetylsalicylic acid) inhibits platelets by permanently acetylating (adding acetyl group) COX-1, which is the enzymes involved in the synthesis of thromboxane A2; a potent platelet agonist. Thromboxane A2 is produced by activated platelets to stimulate the activation of new platelets and encourage platelet aggregation. Because it blocks platelets, its effects persist for the entire lifespan of a platelet, which is around 10 days.

Clopidogrel is a thienopyridines, which is an irreversible inhibitor of ADP/P2Y12 receptors (important in platelet aggregation). Before it can work, it undergoes hepatic metabolism to form the metabolites that work to inhibit these receptors. This is why you should avoid clopidogrel in those with hepatic impairment (won't be effective).

• In acute cases, such as an ACS, it's started as a loading dose of 300-600mg followed by a daily maintenance dose of 75 mg. The loading dose given is dependent on the clinical scenario and how quickly the maximum antiplatelet effect is desired. A 300mg loading dose will reach its maximum antiplatelet effect in 6-8 hours, whereas a 600mg loading dose will reach its maximum antiplatelet effect in 2-4 hours.

Ticagrelor is a new generation of reversible inhibitor of P2Y12 receptors (important in platelet aggregation). Unlike clopidogrel, ticagrelor does not require metabolic activation and achieves a faster, more potent and more predictable antiplatelet effect than clopidogrel. It therefore is safe to use in those with hepatic impairment.

Complications

• Cardiac Tamponade - Due to necrosis and rupture of ventricular free wall, presenting with cardiac arrest

• Acute Mitral Regurgitation - Due to rupture of papillary muscles (often the posterior muscle), presenting with a pan-systolic murmur and acute heart failure

• Heart Failure - Due to impairment of heart muscle function

• Arrhythmias - More common with an Inferior MI as the artery affected supplies the SA node

• Heart block - More common in Inferior MI as the artery affected supplies the SA node

• Acute pericarditis

• Dressler Syndrome - Pericarditis 2-3 weeks post-MI, presenting with pleuritic chest pain and a fever