Myocardial Infarction: NSTEMI Flashcards

1
Q

What is non-ST-elevation myocardial infarction (NSTEMI)?

A

Non-ST-elevation myocardial infarction (NSTEMI) is an acute ischaemic event causing myocyte necrosis.

NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion.

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2
Q

How does the pathology of NSTEMI and STEMI differ?

A

STEMI is complete occlusion (typically thrombosis or embolism) of a coronary artery.

NSTEMI is usually a result of a transient or near-complete occlusion of a coronary artery or acute factor that deprives myocardium of oxygen.

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3
Q

Briefly describe the pathophysiology of NSTEMI

A

Unstable plaques have soft, lipid-laden contents, with thin, often sclerotic fibrous caps infiltrated by macrophages (foam cells). Release of the lipid-rich atherogenic core causes adhesion, activation, and aggregation of platelets. This initiates the coagulation cascade. A superimposed thrombus forms, occluding the coronary blood flow and resulting in myocardial ischaemia

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4
Q

What are the risk factors for NSTEMI?

A
  • Diabetes
  • Hyperlipidaemia
  • Hypertension
  • Metabolic syndrome
  • Renal impairment
  • Peripheral arterial disease
  • A history of ischaemic heart disease and any previous treatment
  • Obesity
  • Advanced age
  • Smoking
  • Cocaine use
  • Physical inactivity
  • Family history of premature coronary artery disease (<60 years)
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5
Q

What are the signs of NSTEMI?

A
  • A new murmur
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6
Q

What are the symptoms of NSTEMI?

A
  • Chest pain (which may radiate to other areas such as the arms, back or jaw)
  • Nausea and vomiting
  • Marked sweating
  • Breathlessness
  • Palpitations
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7
Q

What investigations should be ordered for NSTEMI?

A
  • ECG
  • Troponin
  • CXR
  • FBC
  • U&Es and creatinine
  • LFTs
  • Blood glucose
  • CRP
  • Echocardiogram
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8
Q

Why investigate using ECG?

A

Record and interpret a resting 12-lead ECG within 10 minutes of the point of first medical contact in any patient with suspected cardiac chest pain.

Abnormal findings that suggest NSTEMI include:

  • ST depression; this indicates a worse prognosis
  • Transient ST elevation
  • T-wave changes
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9
Q

Why investigate troponins?

A

Troponins are proteins found in cardiac muscle. The specific type of troponin, the normal range and diagnostic criteria vary based on different laboratories (so check your policy). Diagnosis of ACS typically requires serial troponins (e.g. at baseline and 6 or 12 hours after onset of symptoms). A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle. They are non-specific, meaning that a raised troponin does not automatically mean ACS.

In NSTEMI there is a dynamic elevation.

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10
Q

What are the other causes of a rise in troponins?

A
  • Chronic renal failure
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
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11
Q

Which troponins are specific to cardiac muscle?

A

Troponin I and T.

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12
Q

Why investigate using CXR?

A

The National Institute for Health and Care Excellence (NICE) recommends ordering a chest x-ray only if you suspect other diagnoses or to rule out complications of ACS.

Other causes of acute chest pain, such as pneumothorax or a widened mediastinum in aortic dissection, or complications of ACS such as pulmonary oedema due to heart failure.

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13
Q

Why investigate FBC?

A

Check full blood count to evaluate:

  • Thrombocytopenia to estimate risk of bleeding; NSTEMI treatment increases the risk of bleeding
  • Possible secondary causes of NSTEMI (i.e., secondary blood loss, anaemia)
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14
Q

Why investigate U&Es and creatinine?

A

Determine serum creatinine and estimated glomerular filtration rate (eGFR); these are key elements in assessing the Global Registry of Acute Coronary Events (GRACE) risk score.

Determine the choice and dose of anticoagulant.

Prevent contrast-induced nephropathy if an invasive strategy is planned in a patient with renal impairment.

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15
Q

Why investigate LFTs?

A

Measure liver function to include in the assessment of bleeding risk before starting anticoagulation.

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16
Q

Why investigate blood glucose?

A

Check blood glucose in any patient with known diabetes or hyperglycaemia on admission to hospital, regardless of a history of diabetes.

17
Q

Why investigate CRP?

A

CRP is commonly ordered to rule out other causes of acute chest pain (e.g., pneumonia).

18
Q

Why invetigate using echocardiography?

A

Organise urgent echocardiography for any patient with signs of acute heart failure or haemodynamic instability or who is in cardiac arrest.

May show damage following myocardial infarction (e.g. pulmonary oedema), regional wall motion abnormalities or alternative causes of chest pain such as acute aortic dissection, pericardial effusion, aortic valve stenosis, hypertrophic cardiomyopathy, or right ventricular dysfunction suggestive of acute pulmonary embolism.

19
Q

Briefly describe the acute treatment for NSTEMI

A

Beta blockers unless contraindicated.

Aspirin 300mg stat dose

Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative).

Morphine titrated to control pain.

Anticoagulant: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days).

Nitrates (e.g. GTN) to relieve coronary artery spasm.

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

20
Q

What scoring system is used to assess PCI for NSTEMI?

A

GRACE score.

21
Q

Briefly describe GRACE score used to assess if PCI is indicated in NSTEMI

A

This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:

  • <5% Low Risk
  • 5-10% Medium Risk
  • >10% High Risk

If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

22
Q

Briefly describe the secondary medical management of NSTEMI

A

Aspirin 75mg once daily.

Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months.

Atorvastatin 80mg once daily.

ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily).

Atenolol (or other beta blocker titrated as high as tolerated)

Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily).

23
Q

Briefly describe the secondary lifestyle prevention of NSTEMI

A
  • Stop smoking
  • Reduce alcohol consumption
  • Mediterranean diet
  • Cardiac rehabilitation (a specific exercise regime for patients post MI)
  • Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
24
Q

What are the complications of NSTEMI?

A
  • Death
  • Rupture of the heart septum or papillary muscles
  • Oedema (Heart Failure)
  • Arrhythmia and aneurysm
  • Dressler’s Syndrome
  • Cardiogenic shock
25
Q

What differentials should be considered for NSTEMI?

A
  1. STEMI
  2. Unstable angina
  3. Aortic dissection
  4. Pulmonary embolism
26
Q

How does NSTEMI and STEMI differ?

A

Differentiating signs and symptoms:

  • Clinical presentation may not differentiate

Differentiating investigations:

  • ECG will show ST-segment elevation
  • Cardiac biomarkers are elevated in both NSTEMI and STEMI
27
Q

How does NSTEMI and unstable angina differ?

A

Differentiating signs and symptoms:

  • Clinical presentation may not differentiate

Differentiating investigations:

  • ECG may show non-specific ST-segment and T-wave changes
  • Cardiac biomarkers are normal
28
Q

How does NSTEMI and aortic dissection differ?

A

Differentiating signs and symptoms:

  • Pain is described as a ‘tearing’ back pain. There may be blood pressure differential between upper and lower extremities
  • Aortic dissection often occurs in patients who have collagen vascular disease (i.e., Marfan syndrome)

Differentiating investigations:

  • Chest CT angiography with contrast or MR angiography may show the dissection or an intimal flap
  • CXR may reveal widened mediastinum
  • Transoesophageal echocardiography may show a dissection depending on the location
29
Q

How does NSTEMI and pulmonary embolism differ?

A

Differentiating signs and symptoms:

  • Patients often present with dyspnoea, pleuritic chest pain, cough, or haemoptysis
  • Hypoxia may be present
  • Lower limbs should be examined for deep vein thrombosis (enlarged, tender, erythematous calves)

Differentiating investigations:

  • For patients with a high probability of pulmonary embolism (PE) on clinical scoring (i.e., PE likely) or an abnormal D-dimer, imaging is required
  • CTPA scanning of the chest is the imaging study of choice for acute pulmonary embolism
  • For patients with renal insufficiency or iodinated contrast allergies, ventilation-perfusion scan ± peripheral venous doppler exam are recommended
  • Chest CT scan may show central filling defects within the vascular lumen, sharp cut-off of the artery, or a ‘tram track’ appearance of the artery in non-occlusive embolism