Coronary Artery Disease Flashcards

1
Q

Angina — definition / criteria ?

A

left thoracic or retrosternal pain or tightness
associated with physical or psychological stress
completely reversible at rest or with nitroglycerine
1+: thoracic pain, 2+: atypical angina, 3+: typical angina

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2
Q

stable angina — MRI findings ?

A

stress perfusion defect

wall motion irregularities (at rest or at stress)

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3
Q

acute coronary syndrome (ACS) — definition and facts ?

A

STEMI — myocardial necrosis with specific ECG changes
NSTEMI — myocardial necrosis without specific ECG changes
unstable angina — myocardial ischemia without necrosis

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4
Q

acute coronary syndrome (ACS) — MRI findings ?

A

wall motion abnormality
perfusion defect
focal cardiac edema
subendocardial late gadolinium enhancement (LGE)

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5
Q

acute coronary syndrome (ACS) — role of MRI (detailed) ?

A
  • gold standard in assessment of global and regional LV function
  • detection of ischaema (perfusion defect)
  • detecting scar tissue / myocardial cell membrane destabilisation - LGE
  • myocardium at risk (mismatch edema/LGE)
  • prognosis / risk stratification (myocardial salvage, microvascular obstruction, haemorrhage)
  • exclusion of DDx eg. myocarditis or Takotsubo
  • discrepancy to clinical symptoms eg. spontaneous revascularisation, coronary vasospasm
    unstable angina, chest pain without ECG changes or elevated troponin
    I3 Indication: stress MRI in stable patients with low or intermediate risk
    NSTEMI
    I2 Indication: exclude DDx e.g. myocarditis
    U Indication: (TEI, area at risk, microvascular obstruction)
    STEMI
    I3 Indication: risk stratification in early phase (“myocardial salvage”, microvascular obstruction, myocardial haemorrhage)
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6
Q

acute coronary syndrome (ACS) — epidemiology ?

A

incidence 100-300/100000 per year
15% STEMI, 40% NSTEMI, 45% unstable angina
10-20% of all patients presenting with thoracic pain

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7
Q

acute coronary syndrome (ACS) — aetiology / pathophysiology ?

A

coronary arteriosclerosis — coronary plaque formation
imbalance between oxygen supply and demand -> ischaemia
plaque rupture -> coronary thrombosis / occlusion
coronary emboli
coronary vasospasm

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8
Q

acute coronary syndrome (ACS) — differential diagnosis (DDx) ?

A

cardiac origin — e.g. myocarditis, Takotsubo
non-cardiac vascular origin — aortic dissection, pulmonary embolism
pulmonary origin — pneumothorax, pneumonia
gastrointestinal origin — GERD, oesophageal rupture
musculoskeletal origin

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9
Q

coronary embolus / thrombosis — presentation ?

A

present as acute coronary syndrome (ACS) with elevated troponin
-> NSTEMI, STEMI

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10
Q

coronary thrombosis — aetiology ?

A
plaque rupture ~70%
coronary vasospasm
cocaine abuse
heparin induced thrombocytopenia 
antithrombin III deficiency
hormone therapy
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11
Q

coronary embolus — aetiology ?

A

atrial fibrillation
cardiomyopathy
valvular disease
septic or paradoxical emboli (rare)

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12
Q

coronary embolus — diagnosis ?

A

usually well defined (round) filling defect on ICA
usually no other arteriosclerotic changes
usually no causative lesion / plaque after thrombectomy
presence of risk factors

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13
Q

coronary embolus / thrombosis — role of MRI?

A

assessing consequences / outcome
volumes / function
LGE (TEI — transmural extent of infarction)
myocardial area at risk / myocardial salvage
microvascular obstruction, myocardial haemorrhage

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14
Q

coronary embolus / thrombosis — therapy ?

A
  • thrombectomy and stent placement

- surgery

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15
Q

coronary embolus — prognosis ?

A

acute mortality 3-6%
~10% repeated embolic events within 5 years
~27% other relevant cardiogenic or cerebrovascular complications
~28% of patients with cardiac embolus die within 5 years vs ~7.6% with MI of other origin

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16
Q

coronary thrombosis — prognosis ?

A

acute mortality 3-6%
after multifocal coronary thrombosis
~ 18% develop heart failure within 2 years
~ 4% develop an additional MI within 2 years

17
Q

coronary embolus / thrombosis — complications ?

A

cardiogenic shock

death

18
Q

coronary aneurysm — definition and facts ?

A

> 150% of normal lumen
<50% of vessel length otherwise coronary ectasia
true aneurysms include all three vascular layers
coronary pseudo-aneurysms are rare (include one or two layers)

19
Q

coronary aneurysms — aetiology ?

A

arteriosclerosis
congenital
infection
inflammation (Kawasaki syndrome)

20
Q

Kawasaki syndrome — definition and facts ?

A

coronary vasculitis of unknown origin leading to coronary aneurysms

21
Q

Stress CMR - advantages ?

A
  • really non-invasive
  • high spatial resolution (vs NM)
  • high temporal resolution (vs CT)
  • high contrast resolution (vs CT and NM)
  • less artefacts (vs NM)
  • structural and functional information
  • allows quantification
  • special issues: multi-vessel-disease (MVD), LBBB, women
22
Q

Ischaemia detection with stress CMR - evidence ?

A
  • IMPACT1 -> stress CMR > SPECT
  • IMPACT2 -> stress CMR > SPECT
  • CEMARK -> stress CMR > SPECT
  • CEMARK2 -> stress CMR > NICE guideline care
23
Q

Viability definition ?

A
  • preserved ED wall thickness
  • preserved contractile reserve
  • present but maybe reduced perfusion
  • preserved cell metabolism
  • functional intact (recovered) myocardium after revascularisation
24
Q

Stunned myocardium - definition ?

A
  • usually after acute ischaemic event
  • impaired function
  • preserved contractile reserve
  • preserved perfusion
  • preserved metabolism
  • no remodeling
25
Q

Hibernating myocardium - definition ?

A
  • usually in case of chronic ongoing ischaemia
  • impaired function (RWMA)
  • not fully preserved contractile reserve
  • present but reduced perfusion
  • normal metabolism
  • no remodeling
26
Q

Acute coronary syndrome - risk stratification ?

A
  • infarct size
  • transmurality (TEI)
  • peri-infarct zone (independent predictor)
  • microvascular obstruction (MVO) - associated with remodeling
  • haemorrhage - associated with remodeling
  • area at risk (AAR)
  • right ventricular infarction - worse prognosis
27
Q

Role of CMR in acute coronary syndrome (short) ?

A
  • detection / confirm diagnosis
  • age
  • stratifying risk (TEI, MVO, haemorrhage, RVI)
  • predicting response to therapy
  • detecting complications
  • differential diagnosis