Cardio Flashcards
How does carotid USS differ from carotid CTA or MRA (or catheter angiography) in determining degree of carotid artery stenosis?
Carotid USS estimates the degree of stenosis based on elevations in blood flow velocity observed in the target vessel as opposed to the other modalities which undertake anatomic measurements of luminal narrowing (e.g. measure residual lumen diameter at the most stenotic portion of the vessel and compare this with the lumen diameter in the normal internal carotid artery distal to the stenosis)
Velocity criteria that correlate with angiography measurements have been developed that are categorical (rather than linear) ie 50-69% stenosis
What is the gold standard for diagnosing internal carotid artery stenosis?
Catheter cerebral аոgiοgrарhу BUT it is invasive, time consuming, assoc with stroke risk
What is the preferred diagnostic strategy in symptomatic (eg stroke/TIA) carotid artery disease?
Usually CT or MR head and neck angiogram (given usually performed in ED at time of stroke presentation)
What is the preferred diagnostic strategy for asymptomatic carotid artery disease?
Carotid duplex USS
If a carotid stenosis less than 50% is identified on initial imaging, what further evaluation needs to be done?
Usually none - effectively excludes haemodynamically significant CAD
Only exceptions:
- carotid stenosis that is unusually distal and beyond the field of insonation for CDUS
- short-segment stenosis in regions of heavily calcified plaque on СΤA in which adequate assessment of the residual lumen may be difficult
What further evaluation is indicated if a symptomatic carotid artery stenosis 50-99% is detected?
Confirmation with an alternative modality is generally advisable, as two separate noninvasive diagnostic modalities concordant for high-grade stenosis increase accuracy;
If concordant - proceed to revasc
If discordant - consider catheter angiogram
However some experts are happy with just one positive test
What further evaluation is indicated if an asymptomatic carotid artery stenosis 50-99% is detected?
Depends on if they are candidate for revascularisation
If not - serial carotid duplex USS
If they are - obtain alternative test + treat with statin and antiplatelet and aggressive risk factor modification
If a patient is found to have complete carotid artery occlusion on CTA can you trust it?
No, whilst CDUS and МRA are very accurate ; have to be suspicious of CTA because with increasing speed of image acquisition, can have “pseudo-occlusion” whereby image acquisition occurs before contrast bolus can fully opacify the affected vessel
Therefore if complete occlusion found on CTA suggest alternative study eg CDUS or MRA to confirm
What are the advantages of CT (head and neck) angiogram for the detection of carotid artery disease?
Quick (an important advantage in patients who are uncooperative or claustrophobic)
Can be useful in situations of difficult anatomy e.g. severe kinking
What are the disadvantages of CT (head and neck angiogram) for the detection of carotid artery disease?
Significant contrast bolus (same or higher dose than catheter angiogram) which poses risks to kidneys
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Radiation risk
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Pseudo-occlusion risk
What are the advantages and disadvantages of carotid duplex USS for evaluation of carotid artery disease?
Adv:
- noninvasive, safe, and inexpensive
- no claustrophobia
- no contrast
- can be easily repeated
- highly accurate
Disadv:
- operator dependent
- tends to overestimate the degree of stenosis
- less precise at identifying minimal stenoses (ie gets more accurate the higher the degree of stenosis)
- may be limited by features such as calcific carotid lesions, tortuous or kinked carotid arteries, and patient body habitus
- only a portion of the cervical internal carotid artery extending just past the carotid bifurcation can be evaluated (Fortunately, the vast majority of atherosclerotic stenoses occur within this region)
Is CDUS a good modality for detecting carotid artery dissection and why?
No - CDUS can only evaluate a portion of the cervical internal carotid artery extending just past the carotid bifurcation
However, carotid dissections often occur in the more distal portion of the cervical carotid artery and thus will not be accurately identified by СDUS
After carotid artery intervention (ie endarterectomy or stenting) what is the best imaging modality to evaluate for restenosis?
CDUS is commonly used to conduct serial monitoring of the carotids over time to ensure patency of the vessel and evaluate for restenosis because it is:
low cost,
easy to use
accurately monitors changes
But structural changes to the carotid wall after endarterectomy or stenting may alter compliance of the vessel wall which in turn may impact the relationship between flow velocity and degree of stenosis such that standard velocity criteria may be inaccurate - note modified criteria have been developed to address this
Note the accuracy of CTA and especially MRA may be negatively impacted by stent artifact
What is the definition of symptomatic extracranial carotid atherosclerotic disease?
Neurologic symptoms (incl TIA, transient monocular blindness, stroke) that are sudden in onset and referable to the appropriate internal carotid artery distribution (ipsilateral to significant carotid atherosclerotic pathology)
Αthеrοѕϲlerоѕis of the internal carotid artery at the bifurcation accounts for what percentage of ischaemic strokes?
10-12%
What is the mechanism by which carotid artery disease may cause an ischaemic stroke?
Progressive atheromatous plaque at the carotid bifurcation results in luminal narrowing, often accompanied by ulceration
This may then lead to embolization, thrombosis, or reduced brain perfusion (more likely in the setting of bilateral disease)
What is the treatment of symptomatic carotid artery disease?
Intensive medical management +/- carotid artery revascularisation
What does intensive medical management of carotid artery disease entail?
1) Antithrombotic therapy
2) High-potency stаtiո therapy
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3) Risk factor modification, including blood pressure control, glucose control, weight control, and lifestyle modification with smoking cessation, exercise, and recommended dietary modifications
Which patients are most likely to benefit from carotid artery revascularisation?
Patients with recently symptomatic carotid stenosis of 70 to 99 percent who have a life expectancy of at least two years (ideally within 2 weeks of symptoms)
Patients with recently symptomatic carotid stenosis of 50 to 69 percent who have a life expectancy of at least three years, particularly if can be done within 2 weeks of symptoms (beyond 2 weeks - benefit is less certain overall, and females, in particular, may not benefit from revascularization beyond two weeks from symptom onset)
What is the preferred modality of carotid artery revascularisation?
Carotid endarterectomy rather than transfemoral carotid artery stenting when there is a surgically accessible carotid artery lesion; no clinically significant cardiac, pulmonary, or other disease that would greatly increase the risk of anaesthesia and surgery; and no prior ipsilateral endarterectomy
Which patients are unlikely to benefit from carotid artery revascularisation?
- Stenosis less than 50 percent.
- Severe comorbidity due to other surgical or medical illness.
- Strоkе associated with persistent, severe neurologic deficits and disability that precludes preservation of useful function.
- Near occlusion of the symptomatic ipsilateral internal carotid artery
- Total occlusion of carotid artery
What are the benefits of carotid artery revascularisation?
To prevent one event at five years for ipsilateral carotid territory ischemic ѕtrоke and operative strοke or death, the number needed to treat (NNT) was 6
Note whilst CEA and CAS have similar long-term benefits, CAS has higher rates of periprocedural complications and 30d death (note was transfemoral ?if transradial approach mitigates these risks somewhat)
In what circumstances may you consider carotid artery stenting over endarterectomy?
- A carotid lesion that is not suitable for surgical access
- Radiation-induced stenosis
- Carotid restenosis after endarterectomy
- Clinically significant cardiac, pulmonary, or other disease that greatly increases the risk of anaesthesia and surgery
- Unfavorable neck anatomy including contralateral vocal cord paralysis, open tracheostomy, or prior radical surgery
Which factors influence the benefit and risk of Carotid endarterectomy?
Baseline stroke risk - the higher the greater the benefit from CEA
Location of event: Hemispheric ischaemia rather than retinal ischaemia
Age: Older age (>70yo)
Gender: Males > females
Presence of contralateral carotid artery disease - if present, favour surgical revasc over medical mx (despite increased periprocedural risk)
Combined perioperative morbidity and mortality that exceeds 6 percent
Timing of revasc - best between 2 days and 2 weeks after event (ie stroke)
What is the definition of asymptomatic carotid atherosclerotic diease?
The presence of atherosclerotic narrowing of the extracranial internal carotid artery (significant = >50% stenosis) in individuals WITHOUT a history of ipsilateral carotid territory ischemic strokе or transient ischemic attack in the last six months
What is the annual stroke risk in patients with asymptomatic carotid artery disease?
0.5 to 1.0 percent annually
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Also a marker for MI and vascular death
Does an isolated unilateral carotid stenosis cause vertigo, diplopia, lightheadedness or syncope?
No
What is the preferred treatment approach for asymptomatic extracranial carotid artery disease?
Intensive medical management
Revascularisation is controversial given periprocedural risks and low absolute risk reduction assoc with revasc ie 2.9% risk of periprocedural stroke or death vs 1% absolute risk reduction; NNT = 33
Controversial but some evidence of equivalence between intensive medical tx and CEA in asymptomatic px ie risk of stroke similar
Others would argue still benefit for CEA in asymptomatic 70-99%
SPACE-2 trial suggested nil significant differences in 30d death, cumulative stroke or ipsilateral stroke out to 5 years between intensive medical mx, CEA + medical mx, CAS + medical mx but limitations incl stopped early due to slow recruitment and low event rates
What are the four key manifestations of acute pericarditis?
1) Chest pain
2) Pericardial friction rub
3) ECG changes
4) Pericardial effusion
What are the typical features of chest pain in acute pericarditis?
Sudden onset
Anterior chest
Sharp and pleuritic + worse with coughing
Better sitting up and leaning forward
May radiate to trapezius ridge
Chest pain may be minimal or absent in patients with pericarditis due to which aetiologies?
Uraemia
Rheumatologic disorder eg SLE
What are the key features of the pericardial friction rub?
Classically triphasic (but may have only one or two phases)
Superficial scratchy or squeaking quality
Often intermittent/waxes and wanes
Best heard with diaphragm of stethoscope over LLSE with patient leaning forward and suspending breath (intensifies in this position)
What are the four stages of ECG changes in acute pericarditis
Stage 1 - (hours to days) - widespread concave-up ST elevation with reciprocal ST depression in aVR and V1 with PR depression in leads (except elevation in aVR) - ie PR and ST segments change in different directions
Stage 2 - (first week) - normalisation of ST and PR segments
Stage 3 - (weeks to ?months) - diffuse T wave inversion after ST segments have become isoelectric
Stage 4 - normalisation of ECG
Why might some patients not experience classical ECG changes with acute pericarditis?
If the parietal pericardium is more involved than epicardial pericardium as parietal pericardium is electrially inert
E.g. uraemic pericarditis
What ECG features may distinguish acute pericarditis from STEMI in patients with chest pain and troponin elevation?
1) STE in acute pericarditis begins at J-point, rarely exceeds 5mm and retains its normal concave experience
whereas STEMI typically convex (dome-shaped) and may be >5mm (also begins at J-point)
2) STEMI typically involves STE in anatomical groupings of leads that corresponds to vascular area of infarct (e.g. inferior leads) whereas acute pericarditis STE more generalised/most leads (as pericardium envelops the heart)
3) STEMI often associated with reciprocal ST segment changes whereas pericarditis is not (except for aVR/V1)
4) Concurrent STE and TWI do not generally occur simultaneously in pericarditis WHEREAS they commonly do in STEMI
5) Widespread PR depression (with PR elevation in aVR) is often seen in pericarditis but rarely in STEMI
6) Hyperacute T waves, new pathologic Q waves and QTc prolongation are all rare in pericarditis but common in acute MI
How might acute pericarditis ECG be differentiated from a benign early repolarisation ECG?
1 - Acute pericarditis, STE in both limb and precordial leads whereas half the time BER patients have no STE in limb leads
2 - PR changes strongly favour pericarditis and are not seen in BER
3 - ratio of STE to T wave amplitude in V6 >0.24 favours pericarditis
What are the two main forms of pericarditis in advanced chronic kidney disease and how might they be differentiated?
Uraemic pericarditis - pericarditis beginning withing 8 weeks of dialysis initiation
Dialysis-associated pericarditis - pericarditis arising any time after 8 weeks of dialysis
- complex pathogenesis
- less response to increasing the frequency/intensity of dialysis
- more likely to be associated with haemodynamic instability and serosanguinous pericardial effusion
Does the absence of a pericardial effusion exclude pericarditis?
No
