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An acute coronary syndrome is a spectrum of conditions involving myocardial ischemia (lack of oxygen to the heart muscle), which includes presentations from angina through to myocardial infarction with ST-segment changes

Acute coronary syndromes are classified based on the presenting ECG as either

  1. “ST-segment elevation myocardial infarction” (STEMI) or
  2. “Non–ST-segment elevation myocardial infarction” (NSTEMI).

Cardiac biomarkers allow determination of whether myocardial infarction has occurred.
Acute coronary syndromes represent a dynamic state in which patients frequently shift from one category to another, as new ST elevation can develop after the presentation and cardiac biomarkers can become abnormal with recurrent ischemic episodes

It is a  result of the rupture of atheromatous plaque in the coronary artery causing thrombus formation and, vessel occlusion locally or elsewhere in the heart.

Pathophysiology of Acute coronary syndrome

Atherosclerosis is the ongoing process of plaque formation that involves primarily the intima of large and medium-sized arteries; the condition progresses over time, before manifesting itself as an ACS.

The pathogenesis of ACS involves an interplay among the endothelium, the inflammatory cells, and the
thrombogenicity of the blood. After plaque rupture (or endothelial erosion), the subendothelial matrix (which is rich in tissue factor, a potent procoagulant) is exposed to the circulating blood; this exposure leads to platelet adhesion followed by platelet activation and aggregation and the subsequent formation of a thrombus.

Two types of thrombi can form: a platelet-rich clot (a white clot) that forms in areas of high shear stress and partially occludes the artery, or a fibrin-rich clot (a red clot) that is the result of an activated coagulation cascade and decreased flow in the artery

Types of acute coronary syndrome

The 3 acute coronary syndromes are:

  1. ST-elevation myocardial infarction (STEMI)

This is characterized by elevated troponin and ST elevation on ECG.

In practice, the ST elevation alone is sufficient to treat as the troponins take time to rise.

      2.Non-ST elevation MI (NSTEMI)

NSTEMI is characterized by elevated troponin and ischaemic symptoms or ECG changes.

      3.Unstable angina:

Unstable angina is characterized by prolonged, severe angina, usually at rest, possibly with ECG changes.

NSTEMI and unstable angina are often grouped together as non-ST elevation ACS (NSTEACS)

Types of myocardial infarction

Based on the causative mechanism, myocardial infarction can be classified into five types:

Type 1: This is the commonest type. It occurs due to a primary coronary event such as atherosclerotic plaque rupture, fissuring, coronary dissection or erosion.  It is also referred to as a spontaneous myocardial infarction.

Type 2: This occurs due to an imbalance in myocardial oxygen supply and demands. This can be a case of ischemia because of an increased oxygen demand like in hypertension or due to decreased oxygen supply like in an embolism, coronary artery spasm, hypotension(reduced blood pressure), arrhythmia, anemia or tachycardia (increased heart rate). It usually happens during surgery or illness.

Type 3: This type is related to sudden cardiac death with ischaemic features on an electrocardiogram, angiography, or autopsy but before troponin could be checked.

Type 4a: This is a myocardial infarction that is associated with percutaneous coronary intervention whereby there are signs and symptoms of myocardial infarction with cTn values more than 5 × 99th percentile URL.

Type 4b: This type is associated with a documented stent thrombosis

Type 5: It is a myocardial Infarction associated with coronary artery bypass grafting (CABG) with features of myocardial infarction with cTn values >10 × 99th percentile URL.

Signs and symptoms of acute coronary syndrome

Evaluate chest pain using SOCRATES:

  • Site: central.
  • Onset: usually sudden but can be more gradual.
  • Character: tight, crushing, but not sharp.
  • Radiation: left arm, neck, jaw. Less commonly right arm, epigastrium, back.
  • Associated symptoms: sweating, clamminess, SOB, dizziness, faint, angor animi (an impending sense of doom).
  • Timing: duration >15 minutes.
  • Exacerbating factors: Exertion, Emotion, Eating. Relieving factors: not ACS if relieved by GTN <5 mins.
  • Severity: high but can atypically be low.

Atypical presentations, more commonly seen in elderly or diabetic patients:

  • Little or no chest pain.
  • Shortness of breath
  • Sweating
  • Nausea and vomiting.
  • Sometimes no symptoms at all: 'silent MI'.
  • Signs:
  • HR and BP may be ↑ or ↓.
  • Pallor
  • S3 or S4 heart sounds (especially in STEMI).

Diagnosis and Investigations

An electrocardiogram should be done in the first ten minutes to help in differentiating the three.

Do immediately, and if negative repeat after 20 minutes if pain continues or suspicion is high.

Serial cardiac biomarkers such as Troponin T or I levels

Test on admission and 10-12 hours from symptom onset (or from the presentation if onset is unknown). Troponin peaks at 12-24 hours, then decline over 10 days.

Values >99th centile are diagnostic of acute MI. STEMI diagnosis is initially from the ECG alone so as not to delay treatment.

Other causes of elevated troponin that should be taken into consideration include;

Mnemonic (HEART DIES):

  • Heart Failure,
  • Embolus (pulmonary),
  • Atrial Fibrillation,
  • Renal failure (due to reduced clearance),
  • Thrombus (acute MI),
  • Dissection of the aorta,
  • Inflammation (myocarditis/pericarditis),
  • Exercise (very strenuous),
  • Sepsis.

Other investigations:

Full Blood Count: ↓Hemoglobin may exacerbate heart strain, and baseline Hb and PLT needed before anticoagulation.

Urea and Electrolytes: baseline before anticoagulants and ACEi, and screens for co-morbid renal disease from HTN.

Glucose levels: tight control improves outcomes.

Lipid levels: check on admission, as cholesterol can dip 24 hours post-MI.

Chest x-ray: rule out other causes and check for HF.

Exercise tolerance test: consider in ↓risk patients.

Management of acute coronary syndrome

Initial medical treatment entails:

  • Dual antiplatelet therapy: aspirin and P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel). Loading dose for both.
  • Analgesia PRN: morphine IV and/or nitrates (oral spray, sublingual tablet, or IV infusion in refractory chest pain).
  • Other therapies: oxygen if hypoxemic, β-blockers IV if tachycardic/hypertensive (but not if unstable).

Anticoagulation:

  • Unfractionated heparin or bivalirudin IV in those going for immediate or early angiography.
  • Glycoprotein IIb/IIIa inhibitor IV (eptifibatide, tirofiban, or abciximab) is sometimes added as an adjunctive antiplatelet, but not routinely.
  • Enoxaparin or fondaparinux SC for those without angiography planned.

Reperfusion

Indicated for STEMI presenting within 12 hours of onset:

  • Immediate (within 90-120 mins) primary PCI (percutaneous coronary intervention) i.e. dilation of an artery with balloon catheter ± stent placement.
  • If PCI not available within 120 mins, consider thrombolysis (alteplase, reteplase, or tenecteplase) and transfer to a PCI center.
  • Patients presenting beyond 12 hours are essentially managed like NSTEMI.

Non-ST-Elevation Acute Coronary Syndrome:

  • Angiography with or without revascularization within 48 hours ('early invasive strategy') if high risk as per TIMI or GRACE scores.
  • Revascularisation is usually PCI, but sometimes CABG if left main or triple vessel disease.
  • Immediate PCI if unstable, refractory chest pain, or acute severe heart failure.
  • Conservative management otherwise.

Further management

Start BAGS within 24 hours:

  • β-blocker PO e.g. metoprolol, atenolol. Started in the acute phase as it prevents recurrent ischemia and arrhythmias. May initially be given IV (see 'Initial medical treatment' above).
  • ACEi, especially if ↓LVEF, but even others benefit.
  • Maintain Glucose <11 mmol/L. May require insulin infusion.
  • Statin. Evidence of short-term benefit is unclear, but it will be needed for secondary prevention anyway.

Management of Other issues:

  • Anticoagulation is usually stopped post-PCI or continued until discharge in those managed without reperfusion. However, it is continued for 3 months in anterior MI.
  • Discharge on CVD secondary prevention medication and offer cardiac rehab.
  • Avoid nonsteroidal anti-inflammatory drugs, especially diclofenac.

Complications and prognosis

Short term complications

Third of myocardial infractions are fatal: 20% pre-hospital, and a further 10% within 30 days.

Electrical:

  • Heart block or sinus bradycardia following inferior MI (right coronary artery) as supply to the  AV and SA node is disrupted.
  • Bundle branch block following anterior MI (left anterior descending artery).
  • Ventricular fibrillation.

Structural:

  • Acute mitral regurgitation.
  • Papillary muscle rupture.
  • Ventricular free wall rupture leading to haemopericardium.
  • Ventricular septal rupture. Causes pan-systolic murmur. May lead to cardiogenic shock days later.
  • Ventricular aneurysm: blood pools under the dyskinetic, thin area of LV wall. Causes persistent (>6 weeks) ST elevation.

Inflammatory:

  • Peri-infarction pericarditis.
  • Dressler's syndrome: pericarditis weeks later.

Long term complications

Myocyte death + ↓stroke volume → ↓HR + ↓BP → sympathetic neurohumoral response + LV changes → HF.