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
What are the key initial tests to order for a patient with acute pericarditis?
ECG
Bloods incl FBC, Troponin, ESR, CRP, HIV and HCV
CXR
Echo
Consider:
- BC if febrile
- viral studies but yield is low/rarely alters management
- ANA (esp young women / history suggests underlying SLE)
- tuberculin skin test/interferon-gamma if suspect TB
- cardiac MRI - nondiagnostic echo, constrictive pericarditis, complicated course, suspicion of specific aetiology
- percardiocentesis - tamponade
What is an echocardiogram likely to show in acute pericarditis?
Often normal
May show associated pericardial effusion (which supports the diagnosis) - often small/without haemodynamic consequence
What does the CXR typically show in patients with acute pericarditis?
Normal
Rarely shows cardiomegaly - however acute pericarditis should be considered in the evaluation of a patient with new/otherwise unexplained cardiomegaly
What is the significance of finding elevated cardiac biomarkers in patient with acute pericarditis?
Indicates myopericarditis
What is the significance of raised inflammatory markers in patient with acute pericarditis?
Supports the diagnosis but is neither sensitive nor specific; also in hyperacute phase may remain normal
Their role is often more in determining optimal duration and approach to tapering of therapy
What are the typical findings of pericarditis on cardiac MRI and what other information can it provide?
Pericardial inflammation - bright and thickened pericardium on T2 weighted imaging + late gadolinium enhancement
+/- non-calcified pericardial thickening
May reveal concomitant myocarditis
May evaluate for concomitant pleuropulmonary diseases and lymphadenopathies eg TB, lung ca
Which patients should undergo pericardiocentesis?
Patients with symptomatic effusions and evidence of cardiac tamponade
Large effusions refractory to medical therapy
If pericardial effusion + specific aetiology suspected and diagnosis cannot be reached by other means (e.g. malignant or bacterial cause)
What are the diagnostic criteria for acute pericarditis?
Need 2 of 4:
1) Typical chest pain (sharp, pleuritic, improved sitting up and leaning forward)
2) Pericardial friction rub
3) Characteristic ECG changes
4) New or worsening pericardial efusion
What high-risk features indicate need for hospital admission in patients with acute pericarditis?
Fever
Subacute course over days to weeks
Cardiac tamponade
Moderate-to-large effusion (end-diastolic free space of >20mm)
Immunosuppression
Warfarin/DOAC therapy
Acute trauma
Failure to improve on 7 days of appropriate anti-inflammatory therapy
Elevated cardiac troponins
What approach should be taken to establishing a definite aetiology of acute pericarditis?
A specific non-viral/idiopathic cause of acute pericarditis is found in ~17%
Because of the relatively benign course associated with the common causes of реricаrditis, along with the relatively low yield of much of the diagnostic testing, it is not necessary to establish a definite etiology in all patients with acute реriϲаrditis. Initial efforts should focus on excluding a significant pericardial effusion or cardiac tamponade, and the identification of patients in whom a more comprehensive evaluation should be performed to exclude causes that require specific therapy (eg, malignancy, tսbеrϲսlοsis, or purulent реricаrditiѕ)
In addition, among patients at high risk of coronary disease, МΙ must be ruled out by appropriate studies
What are the non-viral/infective causes of pericarditis?
- Autoimmune eg SLE
- Neoplastic eg lung cancer, breast cancer, and lymphomas and leukemias
- Metabolic eg uraema
- Traumatic
- Post-AMI (Dressler syndrome)
- Iatrogenic secondary to immune checkpoint inhibitor therapy and COVID-19 vaccination
What is the classic triad of cardiac tamponade?
Soft heart sounds, elevated JVP, hypotension
In most patients (ie patients without specific cause) with pericarditis, what is the mainstay of treatment?
1) Restriction of exercise (until resolution of symptoms AND normalisation of biomarkers OR if competitive athlete = 3mths OR if competitive and myopericarditis present = 6mths)
2) Drug therapy with:
Colchicine (500mcg BD if wt >70kg for 3 months; once daily dose if wt<70kg)
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NSAIDs
(e.g. Aspirin 1g Q8H OR Ibuprofen 600mg Q8H for 1-2 weeks)
Usually wean NSAIDs over 1-2 weeks then stop after symptoms have resolved and normalisation of inflammatory markers
What is the role of oral steroids in acute pericarditis?
Can provide relief but are associated with usual complications of long-term corticosteroid therapy AND recurrence is common after stopping therapy
THEREFORE should only be considered if NSAIDS are contraindicated or ineffective or for some immune-mediated causes
Are there any alternative drug therapies for resistant or recurrent cases of pericarditis?
Yes - IL-1 inhibitors (anakinra) is showing promising but is not currently approved by TGA
What does failure to respond to aspirin/NSAID therapy within 7 days (ie persistence of fever/pleuritic chest pain/new pericardial effusion/worsening general illness) indicate?
Suggests cause other than idiopathic/viral pericarditis is present OR aspirin resistance present OR constrictive pericarditis
NSAIDs alone effective in reducing inflammation and pain relief in 70-80%; no evidence they alter natural history of acute pericarditis
Which NSAIDs must be used in Dressler’s syndrome?
Aspirin (+ Colchicine)
Avoid others since anti-inflammatory therapy may impair scar formation
What are the risks/issues with using NSAID therapy in acute pericarditis?
Theoretical risk that the antiplatelet activity may promote the development of a haemorrhagic pericardial effusion - however has not been convincingly established
GI toxicity (eg gastritis, ulcers) - caution in px >65yo, hx of PUD, concurrent steroids/anticoagulant use
Interaction with other medications especially warfarin (NSAIDs alter metabolism of VKA thus enhancing anticoagulant effect)
Which patients with pericarditis benefit from colchicine and which don’t/should avoid?
Benefit
- idiopathic or viral pericarditis
- autoimmune disease
- post-cardiac injury syndromes/Dressler’s
Not benefit
- bacterial pericarditis (may impair clearance of infectious agent)
- malignancy-related
- pericardial effusion
What is the role/benefit of colchicine in patients with pericarditis?
Reduces symptoms
Decreases the rate of recurrent pericarditis (HR 0.40)
What are the side effects/risks of colchicine therapy?
Common = GI eg diarrhoea, nausea, vomiting
Uncommon = bone marrow suppression, hepatotoxicity, myotoxicity
- CKD seems to be major risk factor for these + drug-interactions/altered metablism
If oral steroids are used for acute pericarditis, what is the optimal dose and guidelines around tapering?
0.2 to 0.5 mg/kg/day of prednisolone
- usually begin tapering at 2-4 weeks after resolution of symptoms and CRP normalisation
- more rapid tapering increases risk of treatment failure/recurrence
Are there any adjunctive therapies that can be used in pericarditis?
For patients with elevated HR (>70bpm) - with nil evidence of tamponade but persistent symptoms, can trial beta-blockers if nil c/i
How do you treat acute pericarditis in patients with advanced chronic kidney disease?
Uraemic pericarditis - commence dialysis )if not already)
Dialysis-associated pericarditis - intensify dialysis regime
+ selective medical therapy with NSAIDs, colchicine, corticosteroids
What are the risks of acute pericarditis?
Rare to get tamponade (usually only if malignancy/TB/purulent pericarditis)
1% risk of constrictive pericarditis
15-30% risk of recurrence/incessant disease if NOT treated with colchicine (approx halved by colchicine use); women at higher risk
What is the key challenge in managing myopericarditis?
Excluding ACS
How?
coronary angiography (either invasive of CTCA) if intermediate or high risk for ACS
(ie if:
- hx of prior CAD
- non-classical ECG findings
- markedly elevated trop
- high GRACE or TIMI score
- unstable arrhythmias
- persistent symptoms
What is the difference between myopericarditis and perimyocarditis?
Often used interchangeably but technically two different disease processes with different approach to diagnosis and treatment
Myopericarditis = confirmed acute pericarditis with elevated troponin but without LV systolic dysfunction
Perimyocarditis = acute pericarditis + elevated troponin + LVEF <55% (approach same as myocarditis)
What clinical features increase the likelihood of myopericarditis over isolated acute pericarditis?
Younger age
Male sex
Recent febrile illness
ST elevation
Ventricular arrhythmias
Presence of pericardial effusion decreases likelihood of myopericarditis (ie raises chance of isolated acute pericarditis)
What are the key tests to order in patients with myopericaditis?
Cardiac MRI with late gadolinium enhancement (within 2 weeks of symptom onset)
How do you treat myopericarditis?
Exclude ACS/myocarditis/perimyocarditis
Exercise restriction
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NSAIDs + colchicine (as per pericarditis tx)
How do you treat Vaccinia-associated myopericarditis (ie myopericarditis assoc with smallpox vaccination)?
Same as pericarditis
Exercise restriction
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NSAIDS/colchicine
How do you treat myocarditis/perimyocarditis?
General therapy (for all) + specific therapy (targeting specific causes)
General therapy
- standard HF therapy eg ACEI, evidence-based beta-blocker, MRA, diuretics as required
What are the treatment options for patients with myocarditis and haemodynamic instability or refractory HF despite Optimal Medical Therapy (OMT)?
Mechanical circulatory support e.g. ECMO / VAD
Cardiac transplantation
If arrhythmias develop in a patient with myocarditis, what therapy should be given?
None if asymptomatic APBs or VPBs or asymptomatic nonsustained arrhythmia (eg NSVT)
If indicated -
cardioversion
OR amiodarone (mainstay)
OR if no class IV HF cautious use of BB and CCB
Temporary pacing if CHB or symptomatic bradycardia - usually transient so doesn’t always require PPM
Avoid class I and II antiarrhythmic drugs due to proarrhythmic and negative inotropic effects
What should be avoided in the treatment of myocarditis/perimyocarditis?
NSAIDS - not effective and may increase mortality + exac HF
Heavy alcohol consumption - may enhance the severity of myocarditis
Exercise - 3-6 month abstinence from competitive sports
What are the two most common types of cardiac amyloidosis?
Transthyretin amyloidosis (ATTR Amyloidosis)
Light chain amyloidosis (AL amyloidosis)
These account for 95% of cases and are named after the precursor protein of the amyloid deposit eg transthyretin and immunoglobulin light chains respectively
What is the pathogenesis/pathophysiology and 2 main subtypes of ATTR amyloidosis?
ATTR amyloidosis results from the misfolding and deposition of tranthyretin in cardiac tissues
Transthyretin (formerly called pre-albumin) is a protein produced by the liver that normally functions to transport thyroid hormone and retinol (vitamin A)
There are 2 types:
Wild-type ATTR (wtARRT) - previously called senile systemic amyloidosis caused by misfolding of wild-type/normal transthyretin
Hereditary amyloidosis (hATTR) - caused by gene mutations in the transthyretin gene
What is the typical mode of inheritance of hereditary amyloidosis?
Autosomal dominant inheritance with variable penetrance
In what population is wtATTR underdiagnosed?
Elderly patients with HFpEF
Patients with severe aortic stenosis
What are the clinical features of light chain cardiac amyloidosis?
Age >40
Multisystem involvement - liver, kidneys, spleen, autonomic and peripheral nervous system, lungs, heart
What is the main determinant of prognosis in AL amyloidosis?
Cardiac involvement/amyloidosis
How does cardiac amyloidosis typically present?
SOB
Peripheral oedema
Elevated JVP
Hepatic congestion
Ascites
(ie symptoms consistent with restrictive cardiomyopathy and predominantly right ventricular failure
Do patients with cardiac amyloidosis commonly present with ischaemic heart disease?
No - angina is uncommon but microvascular dysfunction is common
Why do patients with cardiac amyloidosis commonly present with syncope or presyncope?
Due to bradyarrhythmias or advanced AV block OR postural/exertional hypotension secondary to excessive diuresis or autonomic neuropathy
Critical to recall that patients with ATTR amyloidosis often develop progressive conduction system disease and require PPM insertion
This is far less common in AL amyloidosis
Are patients with amyloid cardiomyopathy at increased risk for cardiac thromboembolism?
Yes - amyloid deposits in atrial and ventricular walls causes atrial dysfunction incl electromechanical dissociation during sinus rhythm associated with risk of atrial thrombus formation
What are the typical features of extracardiac involvement in AL amyloidosis?
Nonspecific symptoms eg fatigue, poor appetite, early satiety, weight loss
Kidney disease - asymptomatic proteinuria -> nephrotic syndrome
Peripheral nerve involvement - peripheral neuropathy incl carpal tunnel syndrome
GI involvement - incl hepatomegaly, GI bleeding
Tongue involvement - macroglossia (nearly pathognomonic)
Bleeding issues - incl periorbital purpura (nearly pathognomonic)
Other than restrictive cardiomyopathy, what other cardiac condition is strongly associated with cardiac amyloidosis?
Severe aortic stenosis, particularly low-flow AS
What extra-cardiac manifestations may be seen in ATTR amyloidosis?
Autonomic neuropathy
Peripheral neuropathy - carpal tunnel syndrome
Spinal stenosis
Biceps tendon rupture
What is the hallmark of cardiac amyloidosis on ECG?
Discordance between QRS voltage (often reduced) and LV wall thickness (e.g. on echocardiogram)
- low sensitivity
- more frequent in those with AL amyloidosis
What other ECG features may be seen in amyloidosis?
LV hypertrophy
LBBB
Pseudo-infarct patterns
AV block (in older patient with LVH should prompt consideration of cardiac amyloidosis)
AF
When should you suspect cardiac amyloidosis?
Unexplained LV hypertrophy
# HF and unexplained LV hypertrophy
# Patients with cardiac symptoms and unexplained LVH
# Patients with Aortic stenosis + low-flow, low-gradient or impaired longitudinal strain
# Patients with HF and other typical features eg history of bilateral carpal tunnel syndrome
# Patients with condition highly assoc with cardiac amyloidosis eg systemic AL amyloidosis
What finding on echocardiogram is more suggestive for cardiac amyloidosis?
Reduction in global longitudinal stain with relative apical sparing of longitudinal strain
One of the earliest markers is reduced GLS; pattern of relative apical sparing can help differentiate cardiac amyloidosis from other hypertrophic phenocopies
Sens 93%, spec 82%
What is the typical approach to evaluation in patient with suspected cardiac amyloidosis?
1) Echocardiogram - often non-specific but may be suggestive
2) Cardiac MRI
If cardiac MRI suggestive:
3) Test for evidence of monoclonal protein (serum free light chain assay + SPEP + UPEP)
If monoclonal protein detected -> often go on to have bone marrow biopsy
If monoclonal protein not detected -> cardiac scintigraphy with 99mtechnetium to identify presence/extent of cardiac uptake
Is the presence of a monoclonal protein specific for AL amyloidosis in patient with suspected cardiac amyloidosis?
No - whilst suggestive, can also be seen in ATTR with MGUS
Is bone scintigraphy helpful in patients with systemic AL amyloidosis and CMR suggestive of cardiac amyloidosis?
No it is not and cardiac MRI usually sufficient
Can cardiac MRI distinguish between AL amyloidosis and ATTR amyloidosis?
No
What is the characteristic appearance of cardiac amyloidosis on CMR with late gadolinium enhancement?
Initially diffuse subendocardial LGE
Later transmural myocardial LGE pattern
Sens 85%, spec 92%
What is a key limitation for cardiac MRI in the evaluation of cardiac amyloidosis?
Gadolinium-based contrast agents relatively contraindicated in patients with severe renal dysfunction which is fairly common in AL amyloidosis
If you are uncertain whether a wide complex tachycardia is SVT with aberrancy or VT - what are you best to treat it as?
VT
Inadvertently treating VΤ as though it were SVΤ could precipitate hemodynamic collapse and/or cardiac arrest, while “mistreating” SVΤ as though it were VΤ will rarely cause a clinically significant adverse effect
What ECG features suggest VT as the cause of wide complex tachycardia?
Regular rhythm (although polymorphic VT can be irregular)
Extreme right axis deviation or any axis shift >40deg from baseline (OR QRS to left of -30deg in px with RBBB-like WCT or to right +90deg in LBBB-like WCT)
AV dissociation (atrial activity independent of ventricular activity)
Fusion beats (QRS complex has a morphology intermediate between that of a sinus beat and a purely ventricular complex)
Capture beats (QRS complexes during a WCT that are identical to the sinus QRS complex)
‘Warm up phenomenon’ - a period of some irregularity and acceleration
Wide QRS >160msec
Concordance (QRS complexes in all precordial leads are monomorphic and of same polarity ie lack biphasic QRS)
What is the Brugada criteria for VT?
1 - inspect V1-V6 for RS complex (biphasic QRS) - if nil RS = concordance present = VT
2) If RS complex present measure interval between onset of R wave and nadir of S wave - if longest RS interval is >100ms and R wave is wider than S wave = VT
3 - if longest RS interval is <100ms, assess for AV dissociation - if present = VT
4 - if nil AV dissociation, assess QRS morphology in V1 or V2 and V6 - if
What are the causes of VT?
Coronary heart disease
Dilated cardiomyopathy
Infiltrative cardiomyopathy
Chagas heart disease
Complex congenital heart disease
Cardiac sarcoidosis
Arrhythmogenic right ventricular cardiomyopathy
Left ventricular noncompaction
Drugs - flecainide
Idiopathic eg RVOT VT or LVOT VT
Congenital long QTc
Inherited long QTc eg drugs
What is the role of cardiac MRI in the evaluation of patients with sustained monomorphic VT?
Can identify certain diagnoses eg arrythmogenic RV cardiomyopathy, cardiac sacroidosis, other infiltrative cardiomyopathies
Can guide ablation (ie finding areas of delayed gadolinium enhancement)
What is the most definitive means for establishing the diagnosis of sustained monomorphic VT?
Electrophysiology studies
How do you treat patients with sustained monomorphic VT?
Unstable and pulseless - advanced life support eg prompt defibrillation
Unstable but responsive/has a pulse - urgent cardioversion
Stable - pharmacological or electrical cardioversion
- pharm = IV amidarone, IV lidocaine or IV procainamide, IV sotalol
Ongoing/other measures:
- beta-blockers to reduce sympathetic facilitation esp in px with frequent recurrences of VT within short time period
- correct hypokalaemia and hypomagnesaemia (although electrolyte abnormalities alone should not be accepted as cause of VT)
- cease pro-arrhythmic drugs
- interrogate ICD (if present)
- urgent coronary revascularisation if active myocardial ischaemic felt to be contributing factor
What are the pillars of chronic therapy for sustained monomorphic VT?
ICD insertion
Beta-blockers
Amiodarone
Sotalol
Catheter-based radiofrequency ablation
