1
Q
How does carotid USS differ from carotid CTA or MRA (or catheter angiography) in determining degree of carotid artery stenosis?
A
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
2
Q
What is the gold standard for diagnosing internal carotid artery stenosis?
A
Catheter cerebral аոgiοgrарhу BUT it is invasive, time consuming, assoc with stroke risk
3
Q
What is the preferred diagnostic strategy in symptomatic (eg stroke/TIA) carotid artery disease?
A
Usually CT or MR head and neck angiogram (given usually performed in ED at time of stroke presentation)
3
Q
What is the preferred diagnostic strategy for asymptomatic carotid artery disease?
A
Carotid duplex USS
3
Q
If a carotid stenosis less than 50% is identified on initial imaging, what further evaluation needs to be done?
A
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
4
Q
What further evaluation is indicated if a symptomatic carotid artery stenosis 50-99% is detected?
A
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
5
Q
What further evaluation is indicated if an asymptomatic carotid artery stenosis 50-99% is detected?
A
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
6
Q
If a patient is found to have complete carotid artery occlusion on CTA can you trust it?
A
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
7
Q
What are the advantages of CT (head and neck) angiogram for the detection of carotid artery disease?
A
Quick (an important advantage in patients who are uncooperative or claustrophobic)
Can be useful in situations of difficult anatomy e.g. severe kinking
8
Q
What are the disadvantages of CT (head and neck angiogram) for the detection of carotid artery disease?
A
Significant contrast bolus (same or higher dose than catheter angiogram) which poses risks to kidneys
+
Radiation risk
+
Pseudo-occlusion risk
9
Q
What are the advantages and disadvantages of carotid duplex USS for evaluation of carotid artery disease?
A
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)
10
Q
Is CDUS a good modality for detecting carotid artery dissection and why?
A
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
11
Q
After carotid artery intervention (ie endarterectomy or stenting) what is the best imaging modality to evaluate for restenosis?
A
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
12
Q
What is the definition of symptomatic extracranial carotid atherosclerotic disease?
A
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)
13
Q
Αthеrοѕϲlerоѕis of the internal carotid artery at the bifurcation accounts for what percentage of ischaemic strokes?
A
10-12%
14
Q
What is the mechanism by which carotid artery disease may cause an ischaemic stroke?
A
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)
15
Q
What is the treatment of symptomatic carotid artery disease?
A
Intensive medical management +/- carotid artery revascularisation
16
Q
What does intensive medical management of carotid artery disease entail?
A
1) Antithrombotic therapy
2) High-potency stаtiո therapy
+
3) Risk factor modification, including blood pressure control, glucose control, weight control, and lifestyle modification with smoking cessation, exercise, and recommended dietary modifications
17
Q
Which patients are most likely to benefit from carotid artery revascularisation?
A
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)
18
Q
What is the preferred modality of carotid artery revascularisation?
A
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
19
Q
Which patients are unlikely to benefit from carotid artery revascularisation?
A
- 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
20
Q
What are the benefits of carotid artery revascularisation?
A
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)
21
Q
In what circumstances may you consider carotid artery stenting over endarterectomy?
A
- 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
22
Q
Which factors influence the benefit and risk of Carotid endarterectomy?
A
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)
23
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
24
What is the annual stroke risk in patients with asymptomatic carotid artery disease?
0.5 to 1.0 percent annually
+
Also a marker for MI and vascular death
25
Does an isolated unilateral carotid stenosis cause vertigo, diplopia, lightheadedness or syncope?
No
26
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
27
What are the four key manifestations of acute pericarditis?
1) Chest pain
2) Pericardial friction rub
3) ECG changes
4) Pericardial effusion
28
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
29
Chest pain may be minimal or absent in patients with pericarditis due to which aetiologies?
Uraemia
Rheumatologic disorder eg SLE
30
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)
31
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
32
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
33
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
34
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
35
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
36
Does the absence of a pericardial effusion exclude pericarditis?
No
37
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
38
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
39
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
40
What is the significance of finding elevated cardiac biomarkers in patient with acute pericarditis?
Indicates myopericarditis
41
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
42
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
43
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)
44
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
45
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
46
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
47
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
48
What is the classic triad of cardiac tamponade?
Soft heart sounds, elevated JVP, hypotension
49
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)
+
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
50
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
51
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
52
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
53
Which NSAIDs must be used in Dressler's syndrome?
Aspirin (+ Colchicine)
Avoid others since anti-inflammatory therapy may impair scar formation
54
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)
55
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
56
What is the role/benefit of colchicine in patients with pericarditis?
Reduces symptoms
Decreases the rate of recurrent pericarditis (HR 0.40)
57
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
58
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
59
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
60
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
61
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
62
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
63
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)
64
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)
65
What are the key tests to order in patients with myopericaditis?
Cardiac MRI with late gadolinium enhancement (within 2 weeks of symptom onset)
66
How do you treat myopericarditis?
Exclude ACS/myocarditis/perimyocarditis
Exercise restriction
+
NSAIDs + colchicine (as per pericarditis tx)
67
How do you treat Vaccinia-associated myopericarditis (ie myopericarditis assoc with smallpox vaccination)?
Same as pericarditis
Exercise restriction
+
NSAIDS/colchicine
68
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
69
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
70
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
71
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
72
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
73
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 (wtATTR) - previously called senile systemic amyloidosis caused by misfolding of wild-type/normal transthyretin
Hereditary amyloidosis (hATTR) - caused by gene mutations in the transthyretin gene
74
What is the typical mode of inheritance of hereditary amyloidosis?
Autosomal dominant inheritance with variable penetrance
75
In what population is wtATTR underdiagnosed?
Elderly patients with HFpEF
Patients with severe aortic stenosis
76
What are the clinical features of light chain cardiac amyloidosis?
Age >40
Multisystem involvement - liver, kidneys, spleen, autonomic and peripheral nervous system, lungs, heart
77
What is the main determinant of prognosis in AL amyloidosis?
Cardiac involvement/amyloidosis
78
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
79
Do patients with cardiac amyloidosis commonly present with ischaemic heart disease?
No - angina is uncommon but microvascular dysfunction is common
80
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
81
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
82
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)
83
Other than restrictive cardiomyopathy, what other cardiac condition is strongly associated with cardiac amyloidosis?
Severe aortic stenosis, particularly low-flow AS
84
What extra-cardiac manifestations may be seen in ATTR amyloidosis?
Autonomic neuropathy
Peripheral neuropathy - carpal tunnel syndrome
Spinal stenosis
Biceps tendon rupture
85
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
86
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
87
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
88
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%
89
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
90
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
91
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
92
Can cardiac MRI distinguish between AL amyloidosis and ATTR amyloidosis?
No
93
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%
94
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
95
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
96
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)
97
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
98
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
99
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)
100
What is the most definitive means for establishing the diagnosis of sustained monomorphic VT?
Electrophysiology studies
101
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
102
What are the pillars of chronic therapy for sustained monomorphic VT?
ICD insertion
Beta-blockers
Amiodarone
Sotalol
Catheter-based radiofrequency ablation
103
Along with symptoms and signs of structural or functional cardiac disease, what does the new definition of HF indicate you need?
Elevated BNP or objective evidence of pulmonary oedema
104
What are the 4 stages of HF?
A = asymptomatic but high risk
B = asymptomatic LV dysfunction
C = symptomatic HF
D = refractory HF eg marked symptoms at rest despite maximal therapy
105
What drugs are assoc with improved outcomes (mainly reduced hospitalisations) in HFpEF?
SGLT2i
Finerenone
106
What two signs are prognostic in HF?
3rd heart sound
JVP elevation
107
What are the two ways of slowing down progression in cardiac ATTR?
Tafamidis* - prevents misfolding of transthyretin which reduces new amyloid deposition
Vutrisiran* or Patisiran - RNA interference to reduce hepatic production
*both have mortality benefit
108
How does Levosimendan work in HF?
Calcium sensitiser which increases sensitivity of the myocardial contractile apparatus to calcium, causing an increase in myofilament tension development and myocardial contractility
Also has PDE-3 inhibiting properties
109
How does milrinone work in HF?
PDE3i - decreases rate of cAMP degradation
Higher cAMP concentration leads to enhanced calcium influx into the cell, a rise in cell calcium concentration, and increased contractility.
110
What are the indications for biventricular pacing?
NYHA Class 2-4 despite optimal medical tx (note must be ambulatory IV)
LVEF <35%
SR with LBBB and QRS >150
Also recommended if:
- QRS >120
- EF 35-50% if another indication for pacing eg AV block, ICD
- AF who require pace-ablate
111
What are the indications for ICD implantation?
Survived cardiac arrest due to VF/VT (and not transient/reversible cause)
Spontaneous sustained VT in assoc with structural CHD
LVEF <30% >1 mth after MI or >3mths after CABG
Symptomatic HF with LVEF <35%
112
Above which age do you not see mortality benefit from ICD in non-ischaemic CM?
68
But often use frailty as marker
113
Which components of the 4 pillars of HF did not show significant benefit in MI?
ARNI & SGLT2i
114
What medication(s) can you substitute for those who can't take ACEI/ARB?
Hydralazine and nitrates
115
What did the HEART-FID study show?
No hospitalisation or mortality benefit for IV iron in HF
cf AFFIRM AF study which did show reduction in hospitalisation with IV iron
116
Is there a role for fish oil in HF?
Yes, mild reduction in mortality
117
What is the main side effect of ivabradine?
Selective inhibitor of the SA pacemaker modulating "F current" (funny channel)
Reduces HR
Main side effect = Sparkly vision
118
What is the indication for Ivabradine?
HFrEF LVEF <35% and persistent sinus HR>77 despite maximal BB therapy (or BB contraindicated)
119
When is Vericiguat used in px with HFrEF?
An oral soluble gyancyclase inhibitor
Enhances nitric oxide
Might have small role in reducing hospitalisations (not mortality) in px with optimally tx HF with recent decompensation event (eg hospitalisation for HF)
120
What are the indications for heart transplant?
Refractory cardiogenic shock OR continued dependence on IV inotropes
Refractory / Severe symptomatic ischaemia not amenable to revascularisation
Recurrent symptomatic ventricular arrythmias refractory to all therapies
121
What causes VT?
Ischaemia
Electrolyte disturbance
Drugs
Mechanical irritation
122
What are the causes of recurrent VT?
Old MI
Cardiomyopathy
Congenital heart disease
Valvular heart disease
Long QT
VT in normal heart
123
What is the most effective treatment of VT (if not compromised)?
Sotalol
124
What is the best intervention for secondary prevention of cardiac arrest?
ICD
125
How do ICD's commonly treat VT?
With overdrive pacing
If resistant - then cardioversion
If VF - then defibrillation
126
What do you give patients if they have ICD and are getting recurrent shocks?
Sotalol
127
What is the advantage of sotalol over amiodarone for reducing recurrent ICD shocks?
Reduces defibrillation threshold rather than increasing threshold (as amiodarone does)
128
What are the advantages, disadvantages and indications for leadless subcut ICDs?
Adv - less invasive, decreased risk of systemic infection, nil requirement to remove leads
Disadvt - larger, can defibrillate but can't pace for bradycardia or pace-terminate arrhythmias
Indication - for px with repeated infections (eg IE) or in young px who don't require bradycardia/overdrive pacing (eg Long QT or HCM)
129
What is the treatment hierarchy for VT in px with heart disease?
ICD + bb
if frequent episodes - add antiarrhythmic eg sotalol
if still - catheter ablation
130
How do you manage VT in absence of structural heart disease?
Anti-arrhythmics or catheter ablation
131
What are the indications for ICD insertion?
Secondary prevention - if prev VT/VF and no reversible cause
Primary prevention -
symptomatic HF with LVEF <35% despite 3mths optimal medical therapy and life expectancy >1yr
- ischaemic - usually wait >6 weeks after
- non-ischaemic - lower evidence (DANISH study negative but practice is still to do in most cases)
132
When is flecainide contraindicated?
Impaired LV function or severe ischaemic heart disease
133
What is the risk of Sotalol?
Prolonged QTc
134
What is now the method of choice for pulmonary vein isolation in AF?
Pulsed-field ablation
135
What is the new recommendations re AF management?
In px with recurrent symptomatic pAF catheter ablation is a reasonable initial rhythm-control strategy
136
What can you consider in px with CHADSVA score 2+ with contraindications to oral anticoagulant therapy?
Left atrial appendage occlusion device
137
Where does AF tend to originate?
Pulmonary veins
138
Where does Aflutter tend to originate?
Re-entrant circuit around tricuspid valve
139
How we divide causes of sudden cardiac death in the young?
Into structural and arrhythmogenic
Arrhythmogenic tend to have normal post-mortem exam
Structural:
- arrhythmogenic cardiomyopathy
- dilated CM
- hypertrophic CM
Arrhythmogenic:
Brugada
Long QT
Catecholaminergic Polymorphic VT (CPVT)
140
What is hypertrophic cardiomyopathy?
A primary myocardial disorder characterised by LVH in absence of loading conditions
Occurs in ~1 in 500
Autosomal dominant
Clinical heterogeneity
Genetic heterogeneity >1500 pathogenic variants identified to date
141
What are the most common genetic variants in hypertrophic cardiomyopathy?
Cardiac myosin binding protein C
AND
Cardiac beta-myosin heavy chain gene
142
How do you diagnose hypertrophic cardiomyopathy?
LVH >15mm in absence of loading conditions
OR
LVH >13mm in first degree relative of known case
143
Instead of HOCM, what is the preferred terminology now?
Obstructive HCM vs non-obstructive HCM
144
What are the main treatment principles for HCM?
Obstructive symptom control:
- BB + CCB
- disopyramide
- mavacamtem (myosin inhibitor)
- septal reduction therapy
Family screening:
All first-degree relatives need screening with ECG + TTE
Repeat screening is necessary and age dependent (ie every 1-2 years for kids, 3-5 yrs for adults)
Risk stratification for SCD
- use ESC or AHA/ACC calculators
145
What are the main risk factors of SCD in HCM that are used in risk calculators?
FHx of SCD
Massive LVH / LVOT gradient / LA diameter
Unexplained syncope
NSVT
Extensive scar
146
What is the magic number (risk) for primary ICD in HCM?
5yr >6% considered high risk
147
What is the definition of dilated CM?
LV dilatation and systolic dysfunction in absence of abnormal loading conditions or coronary artery disease
Defined as LVEDD >58mm (males) or >52mm in females
OR
LVEDVi >75ml/m2 (males) or >62ml (females)
148
What are the causes of dilated CM?
Prevalence ~1 in 500
Causes:
- idiopathic
- alcohol
- viruses
- drugs/toxins eg antracycline chemo
- familial (autosomal dominant)
- idiopathic
149
What are the most common genetic variants/causes in familial DCM?
DSP (desmoplakin)
TTN (titan)
LMNA (lamin)
PLN
BAG3
FLNC3
150
How do you manage dilated CM?
Optimise medical therapy
Family clinical screening
Avoid alcohol
Correct electrolytes and thyroid function
Consider ICD +/- CRT
151
What factors are now being included in determining which px with dilated CM should get primary ICDs?
MRI findings - certain high risk LGE/scar distribution
High risk genes (eg LMNA, FLNC, PLN, DSP) - even at EFs up to 45%
152
What is arrhythmogenic CM?
Previously known as ARVC
Results in fibrous or fibrofatty involvement of myocardium (traditionally thought RV, now recognised to affect both)
Cause = most of the gene mutations involve proteins that make up desmosomes (eg PKP2 [plakophilin], desmoplakin)
Often presents with VT
No diagnostic test
Rather constellation of hx, fhx, ECG, TTE, holter, MRI, genetic test etc
- need 2 major criteria on Padua criteria
153
What is the relationship between endurance exercise and arrhythmogenic CM?
Endurance exercise is assoc with:
- lower age at presentation
- higher risk of VT
- more rapid progression to HF
Even in genotype+/phenotype- px
Hence rationale for exercise restrictions
154
An LVEF below what number would be considered grossly abnormal in HCM?
<55%
Should trigger consideration of heart transplant
155
What is unique about Long QT Syndrome Type 3?
Caused by SCN5a gene gain of function mutation
Sodium channel issue (rather than potassium channel in Type 1 and 2)
Therefore, whilst can use BB also role for Mexiletine (sodium channel blocker)
156
What is catecholaminergic polymorphic VT?
Rare (1:10000) highly lethal inherited arrhythmia tends to cause syncope/SCD on exertion
Symptoms + Fhx key
Normal baseline ECG + TTE
Need to do exercise test or diagnosis can be missed
Causes: Adrenergically-induced bidirectional/polymorphic VT
157
What is the most common pathogenic variant in catecholaminergic PVT?
RYR2 gene (cardiac ryanodine receptor 2)
Less commonly CASQ2 Calsequestrin
158
What should you do in someone with suspected Brugada syndrome?
High lead ECG - may reveal spontaneous type 1 brugada
159
Is drug-induced Brugada ECG pattern diagnostic of Brugada in isolation?
No
160
What is the biggest risk factor for elevated calcium score?
Age
161
What is the relevance of coronary artery calcium score?
Marker of higher coronary artery disease burden and therefore cardiovascular risk
162
What is the 10yr risk of CV event in someone with CAC of 0?
<1%
163
What is the role of CAC?
Screening tool in asymptomatic population
Most value is in those with intermediate CV risk (based on calculator) to reclassify px into lower or high risk groups (ie to guide statin therapy)
Can also consider in lower risk px where you think traditional risk scores underestimate risk eg FHx of premature CVD, DM age 40-60yo
164
What is the CSANZ recommendation re who is appropriate to perform coronary artery calcium score in?
Asymptomatic
Aged 45-75
With intermediate CV risk
Consider in those with lower risk if:
- strong fhx
- diabetes 40-60yo
- indigenous >40
165
When is CTCA appropriate to perform?
Symptomatic patients (unlike CAC which is asymptomatic)
- particularly in those with low-intermediate (30-70%) likelihood of disease
Has greatest value in its negative predictive value - rule out test - excludes CAD
166
How long is the "warranty period' on a normal CTCA?
8 years
167
What does CSANZ suggest are the appropriate indications for CTCA?
Chest pain with low-to-intermediate pre-test probability of coronary artery disease
Chest pain with non-diagnostic stress test or imaging results
Normal stress test with continued/worsening symptoms
Suspected coronary or great vessel anomalies
Evaluation of symptoms in px with CABG grafts
New onset LBBB or HF to exclude ischaemic cause
168
When is CTCA inappropriate to perform?
As screening in asymptomatic px
For inpatients with typical angina who have high-probability of obstructive disease -> these px should proceed to Invasive CA
169
What is the importance of low grade coronary artery stenoses (<50%)?
Most myocardial infarctions are caused by low grade stenoses
170
What is the role of functional ischaemic testing?
Determines haemodynamic significance of lesion (ie does it cause angina)
Optimises need for coronary revascularisation
Prognostic
171
Where does cardiac stress testing fit in?
Most valuable in px with intermediate pretest probability
172
What are the contraindications to ECG stress testing?
Complete LBBB
Paced ventricular rhythm
Pre-excitation syndromes/WPW
>1mm STD
173
What are the adv/disadvantages of some of the main cardiac stress tests?
ECG stress test - cost effective but least sensitive, risk of false neg and lower diagnostic accuracy in women
Echo - high specificity and nil radiation; false neg risk in single vessel/circ territory
Nuclear perfusion study- high sens but radiation, false positives
CTCA - high NPV, cannot assess functional significance
174
When is Cardiac MRI useful/indicated?
MINOCA
Myocardial viability assessment/surgical planning
Congenital heart disease
Aortopathies
Cardiac masses/tumours
Cardiomyopathy
175
What is the gold standard of LVEF measurement?
cardiac MRI
Also gold standard for RV chamber quantification and function
176
When is cardiac MRI with gadolinium contraindicated?
IN px with eGFR <30 due to risk of nephrogenic systemic fibrosis (NSF)
177
How does ischaemia appear on cardiac MRI?
Subendocardial or transmural scar
Cf
patchy or midwall fibrosis/scar in non-ischaemic
178
What is the general rule re cardiac myocardial viability on cMRI?
More transmural = less viable
179
What is the disadvantage in assessing myocardial viability on PET cf cMRI?
Less spatial resolution
180
What LV wall thickness suggests need for ICD in px with hypertrophic CM?
>30mm
181
Why might you have two murmurs in HCM?
1 = LVOT murmur
2 = SAM causing functional MR
182
What is cardiac amyloidosis?
A rare form of restrictive CM
Histopath = congo red histology demonstrating green birefringence (pathognomonic)
Vast majority the causative amyloid fibril deposits are of monoclonal light chain (AL) or ATTR amyloidosis
Presents with CCF but suspicion for amyloidosis should also be raised if syncope, arrhythmia or unexplained LV wall thickening on TTE
183
What is the best test to diagnose AL amyloidosis?
Fat pad biopsy
Or biopsy of salivary gland or rectum
184
Which is harder to get a confirmatory histopathological diagnosis for - AL or ATTR amyloidosis?
ATTR - often requires endomyocardial biopsy which is risky
185
What is the classical finding on TTE of amyloidosis?
LV wall thickening
Restrictive filling
Abnormal strain ("apical sparing" pattern)
Atrial septal thickening
However TTE neither sens nor specific for amyloidosis
186
What test should you perform in suspected ATTR amyloidosis?
Nuclear bone scan
187
What is the standard for biopsy-free diagnosis of acute myocarditis?
Cardiac MRI
- Lake Louise criteria - oedema, hyperaemia, patchy delayed LGE
188
What is the Gold standard for myocarditis diagnosis?
Endomyocardial biopsy
- Dallas criteria = lymphocytic infiltrates in assoc with myocyte necrosis
189
How do you diagnose pericarditis?
Clinical diagnosis
Supportive ECG/inflammatory markers + pericardial effusion on echo
190
What is the difference between pericarditis and myopericarditis?
Pericardial inflammation without troponin elevation = pericarditis
Pericardial inflammation with troponin elevation = myopericarditis
191
What qualifies at high CV risk?
Established ASCVD
Diabetes >60yo
Diabetes + albuminuria
Mod-severe CKD
Familial hypercholesterolaemia
TC >7.5
Severe HTN >180/110
192
What is the LDL target in high risk px?
<1.8
(Europeans say <1.4)
193
What are some of the key differences in P2Y12 receptor inhibitor characteristics?
Clopidogrel and Prasugrel are both prodrugs and provide irreversible competitive blockade and have once daily dose cf ticagrelor which is not a prodrug and is reversible, non-competitive binding and has two daily dosing
Ticagrelor and prasugrel work within 30mins-4hrs; ticag wears off in 3-5 days cf clopidogrel which takes 2-8hrs to work and wears off in 5-7 days
194
Which STEMI patients do not benefit from thrombolysis (where PCI cannot immediately be performed)?
Cardiogenic shock px
- evidence for these is culprit-only PCI
195
What should you do in STEMI px who have not reperfused with fibrinolysis?
Rescue PCI within 12 hours
- rather than nothing or another attempt at fibrinolysis
196
What is the preferred P2Y12 receptor inhibitor in ACS?
Ticagrelor or prasugrel rather than clopidogrel
- reduces CV death / endpoints albeit at increased risk of non-CV bleeding
197
What does the evidence favour in non-shock STEMI px or NSTEMI px?
Complete revascularisation over culprit-only PCI
- however nil timeline, can bring them back for non-culprit lesions
198
Following Fontan procedure, what atrium has higher pressure?
RA - as it drives blood through altered circulatory system
(cf normal = LA > RA)
199
What is the most common consequence of chronic cyanosis?
Polycythaemia - because bone marrow
200
What are some other consequences of chronic cyanosis?
Acne
Gallstones
Gout - uric acid - turnover
201
What is the most common ASD?
Ostium secundum
202
What is sinus venosus ASD associated with?
Anomalous pulmonary venous drainage (ie right pulmonary veins go to RA or SVC rather than LA)
203
What type of ASDs can be closed percutaneously?
Ostium secundums
204
What are the indications for closing PDA?
Left heart volume overload OR right heart pressure overload
205
What is aortic coarctation commonly associated with?
Bicuspid aortic valves 80%
HTN post-repair 40%
Aneurysm or re-co-arctation at repair site
206
What are the 4 components of Tetralogy of Fallot?
RVOT
RVH
Aortic override (over RV)
VSD
207
What are the common associations with TGA?
VSD
Pulmonary stenosis
208
What are the two definitive operations for TGA?
Atrial switch
Arterial switch
209
When does atrial function MR occur?
In HFpEF, due to LA dilatation
210
What is the rule of 60 in MR?
We should intervene if LVEF <60% or LVEDD >60mm
(as those are thresholds for compensated MR)
211
Which is better - mitral valve repair or replacement?
Repair
- only in rheumatic heart disease, can be difficult to repair
212
What is aortic sclerosis?
Irregular thickening or calcification of aortic valve leaflets without stenosis
Progresses to AS at 2% per year
213
What are the consequences of AS?
Valve obstruction -> LV obstruction -> increased LV pressure load
In response, LV hypertrophies - microcirculation can't keep up so myocardium fibroses
This results in diastolic dysfunction (impaired relaxation) and increased LVEDP
Then LA pressure goes up -> LA dilates
LA squeeze/kick increases to contribute 50% of LV filling (as opposed to normal 20%) hence why ppl with AS do poorly if they develop AF (lose squeeze + diastole shortens)
214
How do you manage AS?
Mild-mod - clinical and echo surveillance
Severe
- and symptomatic = intervene
- and asymptomatic but LVEF <50% = intervene (if low LVEF due to AS)
- and asymptomatic and rapidly progressive disease
- asymptomatic with EF >50% = watchful waiting
215
When is surgery indicated in AR?
Rule of 55
Aortic root dilatation >55mm
Operate before LVEF <55%
216
What are the causes of tricuspid stenosis?
Rheumatic heart disease
Carcinoid syndrome
Tumour
Rare congenital malformations
217
Which is the only cardiac valve lesion that can be fixed percutaneously?
Aortic regurgitation
218
What is the definition of pulmonary HTN?
mean PAP >20mmHg
219
What is Pulmonary Arterial Hypertension?
Pulmonary HTN with PCWP <15mmHg
220
What gene is most commonly found in idiopathic Pulmonary Arterial Hypertension?
BMPR2
221
What condition has worse prognosis - IPAH or PAH-SSc?
PAH-SSc
222
What is the only treatment shown to improve survival in idiopathic PAH?
Epoprostenol (IV prostacyclin)
223
What is the preferred approach to PAH treatment?
Dual upfront therapy rather than monotherapy
- has survival benefit
224
How do you detect the 5% of px with IPAH who are vasoreactive and therefore sensitive to calcium channel blockers?
Give nitric oxide at pulmonary artery catheterisation - if pulmonary artery pressure drops = vasoreactive
BPT
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