UBC RCE Compiled Notes II Flashcards
What is rate of MI in EST? Death?
5/10 000, 1/10 000
What is normal increase in SBP per MET?
10% increase per MET
Criteria for Hypotensive Response?
-Decrease in SBP below resting BP
-SBP goes down by 10 or more points after initial increase
What is Heart rate reserve?
Age predicted max HR - Resting HR
**How to write an exercise prescription: 50-70%
-THR = ((Max HR - Resting HR) x 0.5) + RHR = Lower end
What is calculation for Chronotropic Index?
(Max HR - Baseline) / (Age predicted - Baseline)
< 80%
Definition of abnormal HR recovery?
Not going down 12 point in first minute of recovery
What is more predictive of CAD: CP or ST changes on EST?
CP
What are the absolute CI’s to EST? (9)
-Symptomatic Severe AS
-ACS in last 48h
-High risk unstable Angina
-Decompensated HF
-Myopericarditis
-PE
-Aortic Dissection
-Unable to walk
-Arrhyhtmia with HD compromise
Name all absolute indications to stop an EST?
-Moderate-Severe Chest Pain
-Pallor/Cyanosis
-CNS symptoms/Ataxia
-ST elevation in leads without Q waves
-Unstable Ventricular Arrhythmias
-Hypotensive response with signs of ischemia
-Patient request to stop
-Cannot safely monitor the patient
Describe the BRUCE protocol
Begins at a workload of 4 METS and increases the workload every 3 minutes by 3 MET increments
What is the prognostic significance of LBBB developing during Exercise? How about RBBB?
-LBBB: Predicts higher risk of death and major cardiac events
-RBBB: Associated with CAD, especially LAD disease
What happens to the following with EST?
-P wave
-PR segment
-QRS
-Q wave
-T wave
-U wave
-QT interval
-P wave: Magnitude increases
-PR segment: Shortens
-QRS: Increases in amplitude
-Q waves: Increase
-T wave: Decreases in amplitude
-U wave: No changes with exercise
-QT interval: Absolute QT decreases
What is equivocal STD?
> 1mm upsloping STD
Is it normal to have normalization of Early Repol with exercise?
Yes
Why is having Complete Heart Block a contraindication to EST?
Risk of precipitating VT
What is the most important prognostic variable on EST?
Exercise Duration: 1 MET greater exercise capacity is associated with a 12% reduction in risk of death
4 CI’s to using Persantine/Adenosine? Updated as per CP guidelines
-SBP < 90mmhg
-SBP > 200mmhg
-Mod-severe asthma with active wheezing
-Brady < 45bpm without a pacemaker
-2nd or 3rd degree AV block without a pacemaker
-Dypirimadole recent use
-Methylxanthine use in last 12 hours
-ACS in last 48 hours
When assessing Viability, what has the highest sensitivity for predicting Viability?
Improvement with Low dose Dobutamine
When assessing Viability, what has the highest specificity for predicting Viability?
Biphasic response (Wall motion better at low dose, worse at high dose)
What is viability determined by on DSE?
Improvement of at least one grade in 2 or more segments
5 high risk criteria on DSE?
2 on CCS statement, preferred for exam:
-2 or more inducible WMA’s
-WMA at low ischemic threshold (Dobutamine < 10mg/kg/min, or HR < 120 bpm)
Others in case they ask more:
-Peak LVEF < 45% AND Extensive ischemia
-Baseline LVEF < 35 % AND Extensive ischemia
-Transient Ischemic DIlatation
Describe the following Adenosine receptors (1, 2A, 2B, 3)
1- SA and AV nodal blockade
2A- Coronary Vasodilation
2B- Bronchoconstriction and Peripheral Vasodilation
3- Mast cell degranulation
What is unique about Regadenoson?
Selective 2A receptor agonist
6 High risk criteria on MPI?
-Large perfusion deficits (>10%)
-Increase lung or RV uptake
-Multiple Coronary territories
-TID
-LVEF < 45% at peak stress of LV decrease from baseline with ischemia
-Resting LVEF < 35% due to non coronary cause
What happens to Myocyte metabolism when there is low O2 supply?
Shift in metabolism from fatty acid metabolism to glycolysis (using glucose).
How is the change in metabolism in low flow states taken advantage of when assessing Viability with PET?
-Glucose transport and phosphorylation is easily tracked by the uptake and retention of 18-FDG, which can be detected by PET.
What is Hibernating Myocardium?
-Chronically dysfunctional, but has the ability to regain function through revascularization
What are 4 criteria that a hibernating myocyte needs to have?
-Adequate blood flow
-Intact cell membrane
-Intact mitochondrial membrane
-Preserved metabolic activity
What is the definition of Stunned myocardium?
Dysfunctional myocardium followed a brief ischemic insult that was followed by reperfusion
What % of myocardium is needed to have viability to have increase in LV function post revascularization?
for PET? 7%
What are the two results of PET and what do they mean with respect to viability?
-Mismatch = Absence of perfusion, preserved FDG -> viability
-Match = refers to absene of both perfusion and myocardial metabolism -> scar
Where is the pattern of scar on CMR with Fabry disease?
The LGE pattern is distinct with a basal-inferolateral wall predilection
What is CMR RV criteria for ARVC?
RVEDV > 110 ml/m2 in men and >100 ml/m2 in women
OR
RVEF < 40%
Describe the following in JVP?
a
x
c
x’
v
y
a = atrial contraction
x = atrial relaxation
c = bulge of TV/MV into RA/LA
x’= descent of the base of heart
v = passive filling of LA
y = rapid emptying of LA
What is Carabello’s sign?
> 10mmhg increase in arterial BP during pull back = critical AS
What happens to Aortic Stenosis Post PVC?
Large LV-aortic gradient, wider pulse pressure and persistently delayed upstroke of aortic pressure
What are three findings of severe AS on a hemodynamic tracing?
-Delayed arterial upstroke
-Late peak pressure
-Exaggerated anacrotic notch
What are 4 RA/JVP findings in CP?
-Prominent Y descent
-A and V waves equal in height
-Elevated
-+ Kussmaul’s sign
What is the classic finding in CP seen in the RV/LV filling?
-Square root sign/Dip and Plateau: Rapid early filling followed by abrupt cessation in early diastole (plateau)
What is the most specific hemodynamic criteria for Constriction?
Interventricular dependence leads to discordant LV/RV filling
What is different in the JVP waveforms in RCM compared to CP?
Prominent x and y descents in CP
5 hemodynamic differences between CP and RCM?
-Ventricular interdependence in CP not RCM
-Equalization of RV/LV end diastolic pressures in CP not RCM
-RVEDP/PASP > 1/3 in CP but not in RCM
-PASP elevated >55mmhg in RCM not in CP
-Rapid LV filling in CP (early filling wave > 7mmhg) in CP but not RCM
What is a large shunt by QP/QS?
> 2.0
Name three reasons for a ABI > 1.30
-Renal disease
-Long standing diabetes
-Heavily calcified arteries
What are 5 determinate of Plaque vulnerability?
-Location: Proximal and bifurcating lesions
-Inflammation in the atherosclerotic lesion
-Size of the necrotic lipid core
-Thickness of the fibrous cap
-Integrity of the fibrous cap
Describe the mechanism of Coronary Plaque Rupture?
Plaque rupture leads to intraplaque hemorrhage -> Exposure of highly thromboembolic material to circulating blood -> Platelet rich thrombus is formed at the site of rupture -> Following adhesion platelet activation ensues and release of procoagulant and vasoconstriction substances -> coronary artery constriction and platelet aggregation -> intrinsic and extrinsic -> coagulation cascade -> conversion of fibrinogen to fibrin
Name the three time courses for Stent Thrombosis?
Acute: 24 hours
Subacute: 1-30 days
Late: 30 days to 1 year
Very Late: > 1 year
What are three different UA presentations?
Rest angina
New onset angina of at least CCS III
Increasing Angina by 1 or more CCS class to at least CCS III
Name TIMI score (7)
Age > 65
Troponin elevation
ECG changes
3 CAD RFs
CAD established
Recurrent CP
ASA use in last 7 days
What is low, intermediate and high risk for TIMI and what risk does it correlate to ?
Low risk (0-1) : 5% 14 day MACE
Intermediate (2-4): 10-20% 14 day MACE
High: >4 : >20% 14 day MACE
Name 8 GRACE risk factors?
Age
Kilip class
SBP
HR
OHCA
ST changes
Troponin elevation
Creatinine
< 108 = 1% risk in hospital mortality
>140 = 3% risk in hospital mortality
Also estimated 6 month mortality
When should beta blockers be started in ACS?
< 24 hours (Class 1)
What is the pharmacology of Prasugrel?
-Prodrug, requires metabolism in a 1 step process, irreversible.
What are three contraindications to Prasugrel?
History of TIA/Stroke, Wt < 60kg, Age > 75
When does Prasugrel need to be discontinued before surgery?
7 days before OR
What is the pharmacology of Ticagrelor?
Reversibly binding P2Y12 inhibitor, binds to the allosteric site, and it is an active drug
What is dosing for UFH?
60 units/kg load and then 12 units/kg/hr infusion (ACT of 250-350)
If Fondaparinux is used for ACS treatment, what dose of UFH needs to be given prior to angiogram?
85 IU/kg
When should unstable patients get PCI? How about high risk but stable patients?
< 2 hours
< 24 hours
When should ECG be performed when STEMI is suspected?
Within 10 minutes
What should Clopidogrel dosing be for STEMI depending on if Lysed or Primary PCI?
-Lysis: 300mg then 75mg daily (No load if age > 75y)
-PCI: 600mg then 75mg daily
What is Prasugrel dosing?
60mg po daily and then 10mg daily
What are the indications for primary PCI in STEMI?
STEMI within 12h symptom onset (Class 1)
STEMI with failed Lysis (Class 1)
STEMI in CS regardless of timing (Class 1)
STEMI within 12-24h with ongoing symptoms/ECG evidence ischemia/HF (Class 2)
What is dosing of the following Lytics?
-Streptokinase
-TPA
-TNK
-Streptokinase: 1.5 million units over 30-60 minutes
-Alteplase/TPA: 15mg IV bolus then 0.75mg/kg IV infusion over 30 minutes
-TNK: weight based IV bolus x 1
What are the 9 CI’s for lytic?
Active bleeding
Bleeding diathesis
Uncontrolled Hypertension
Prior ICH
Stroke last 3 months
Spinal surgery last 2 months
Intracranial tumor
Aortic Dissection
Facial trauma
4 steps to reverse ACS anticoagulants in case of ICH?
-Cryoprecipitates
-Platelet transfusion for antiplatelets
-Protamine for UFH
-FFP
When should PCI be done after Lytic?
24 hours
What is the incidence of free wall rupture in the PCI era? Lytic Era? Account for total mortality?
-1%
-5%
-15%
What are the three types of Free wall rupture?
1) Occurs during the first 24 hours. Full thickness rupture.
2) Occurs 1-3 days post MI. Due to erosion of the myocardium at the site of infarction.
3) Occurs 5-7 days post MI. Aneurysm forms and ruptures at the border between infarcted and normal myocardium
Name 4 mechanisms of MR post MI?
-Pap muscle rupture
-LV dilation
-Ischemic papillary muscle dysfunction
-Severe RWMAs
When does pap muscle rupture occur post MI?
2-7 days
Which two populations should have NIV testing for CAD based on sex/age and chest pain characteristics?
-Adults > 30 with 2/3 features of classic chest pain
-Men > 40 or Woman > 60 with 1/3 symptoms
Name 4 high risk ECG criteria for EST?
-Sustained VT
-ST elevation
- 2 or more mm ST depression at low workload (5 METS) OR persisting into recovery
-Failure to increase to SBP > 120mmhg or sustained decreased > 10mmhg during exercise
Others:
-Unable to complete 5 METS
-Chest pain at low workload (<5 METS)
-More than 5 leads with ST Depression
-ST Elevation in Lead AVR
-Syncope on Treadmill
Name 6 MPI criteria
Increase pulmonary intake
TID
Multisegment Ischemia > 10% of the myocardium
Resting LV function < 35% not explained by ischemia
Resting perfusion abnormality > 10% of the myocardium
Severe stress induced LV dysfunction (Peak LV function < 45% or decrease in LVEF with stress.
Name 2 high risk Stress Echo criteria?
-Multiple segments of ischemia
-WMA abnormality developing at low dose of dobutamine (< 10mg/kg/min) or at a low heart rate (<120 bpm)
Others:
-Resting LVEF < 35% not explained by a non coronary cause
-Peak LVEF < 45% or decreased from baseline with extensive ischemia
-Transient ischemic dilation
-WMSI on effort > 1.7
Should echo be done in all patients with SIHD?
Yes (as per CCS 2014 guidelines)
Name 5 indications for revascularization in absence of symptoms as per ESC 2018 Revascularization guidelines?
-Left Main > 50%
-Proximal LAD > 50%
-Two or three vessel disease LVEF < 35%
-Large area of ischemia > 10%
-Singe remaining patent artery with stenosis > 50%
Name 4 indications for CABG > PCI
-3VD SYNTAX > 22
-LMCA SYNTAX > 32
-Proximal LAD disease
-Multivessel disease with Diabetes
What is the SYNTAX Score?
-Coronary Dominance
-Which artery is the lesion in
-CTO
-Trifurcation
-Bifurcation
-Severe Tortuosity
-Length > 20mm
-Heavy Calcification
-Thrombus
What is the definition of Heart failure?
A clinical syndrome with abnormal heart function resulting in, or increasing the risk of clinical symptoms and signs of reduced CO and pulmonary/systemic congestion at rest of with stress
Describe the AHA staging for heart failure?
A: At risk of structural heart disease (HTN, Cardiotoxic meds, DM, CAD etc)
B: Structural heart disease but without symptoms of HF
C: Structural heart disease with prior or current symptoms of HF
D: Refractory HF requiring specialized interventions
What does ischemia do to the contractile proteins/myocytes?
-Ischemia results in depletion of ATP and leads to failure of myosin (thick filament) to detach from actin (thin filament) -> this results in stiffening/diastolic dysfunction
Describe excitation-contraction coupling in the myocyte
-During the plateau phase of the action potential, extracellular calcium enters the myocyte and binds to ryanodine receptors, which leads to larger calcium release from the sarcoplasmic reticulum and initiates contraction
-In the setting of sympathetic stimulation ryanodine receptors can be phosphorylated which increases calcium flux and cardiac contractility
-Myocardial relaxation requires all calcium to be removed from the cytoplasm, which requires ATP
What changes the ESPVR and EDPVR?
Contractility (Slope increases with positive inotropes)
Not affected by pre load or after load
What leads to changes in the End Diastolic PV relationship?
Diastolic dysfunction/Impaired relaxation- Ischemia, fibrosis, hypertrophy, infiltrative disease
Leusotropy would improve it
What are the three determinants of MVO2?
Wall stress, Contractility and Heart Rate
What is LaPlace’s law?
Wall Stress = Intracavitary Pressure x (Radius/Wall Thickness)
So Wall thickness increases in an attempt to reduce wall stress
Name 5 Neurohormones involved in ventricular remodeling?
-Norepinephrine
-Angiotensin II
-Aldosterone
-Vasopressin
-Endothelin-1
What is screening interval for HCM if gene mutation is present?
Every 3 years until 30 years of age and then every 5 years there after
What is the screening interval for ARVC if gene positive?
Echo every year from 10-50 years of age
What is the screening interval for LVNC if gene positive?
Yearly in childhood every 1-3 years in adults
What is the screening interval for Restrictive CMO if gene positive?
Yearly in childhood, every 1-3 years in adults
What are three reasons for Large V waves on hemodynamic assessment?
MR
VSD
Diastolic dysfunction w/ impaired atrial compliance
What is something that will cause overestimation of CO using thermodilution versus underestimation?
-Overestimate: Severely reduced CO
-Underestimate: TR and Left to Right Shunt
What is limitation of Fick CO?
VO2 is approximated
What is the Jenni Criteria for LVNC?
-PSAX Echo > 2:1 ratio non compacted to compacted at end systole
-Communication with intertrabecular space demonstrated with color doppler
-Multiple prominent trabeculations
-Absence of coexisting cardiac abnormalities
What is CMR criteria for LVNC?
> 2.3:1 at end diastole
What are Diagnostic criteria for Takotsubo? (Mayo Clinic Criteria)
-Transient LV dysfunction beyond a single coronary distribution
-Absence of obstructive CAD or acute plaque rupture
-New ECG abnormalities or modest troponin elevation
-Absence of pheo or myocarditis
Additional as per INTER TAK:
-Emotional or physical or combined trigger may be present
-Can have concomitant CAD
-Can have Pheochromocytoma
What are two kinds of TTR Amyloid?
-Hereditary (Autosomal dominant)
-Wild type
What is only way to make Definite diagnosis for Cardiac Sarcoidosis?
Histological diagnosis from myocardial tissue showing non-caseating granuloma on histological examination of myocardial tissue with no alternative cause
How to make Probable diagnosis of Cardiac Sarcoid?
-Histological diagnosis of extra-cardiac sarcoidosis and one or more of:
-Steroid/immunosuppressant responsive CMO or heart block
-Unexplained LVEF < 40%
-Unexplained sustained VT
-Patchy uptake on PET
-LGE on CMR
-Heart block
-Other causes for cardiac manifestations have been included.
How should transient heart block be treated differently in Sarcoid?
PPM indicated
Immunosuppression indicated
What is Gaucher disease?
Deficiency of beta-glucosidase resulting in accumulation of cerebroside in spleen, liver, bone marrow, lymph nodes, brain, heart
Treat with enzyme replacement
What is inheritance of Hemochromatosis? What gene? What is this gene responsible for?
AR
HFE
Codes for protein which regulates iron uptake in the intestines and liver
What is inheritance of Fabry’s disease?
X-linked recessive deficiency of alpha-galactosidase A resulting in accumulation of glycosphingolipids within lysosomes
How to treat Fabry’s disease?
Recombinant alpha-galactosidase A administration
What is inheritance for ARVC?
Autosomal Dominant
What are the 6 Major ARVC criteria?
You need two Major criteria / One Major and 2 minor / 4 minor from different categories
-RV dilation (Echo PLAX > 32), FAC < 33%, CMR RVEDV > 110, RVEF < 40%, RV dyskinesia
-Residual myocytes < 60% with fibrous replacement of the RV free wall
-Repolarization abnormalities: TWI inverted in V1-V3
-Depolarization abnormalities: Epsilon wave
-Arrhythmias: VT with RVOT configuraition
-Confirmed in FDR
Can patients with ARVC participate in competitive sports?
No, OK to enroll in recreational low intensity sports
9 things that differentiate HCM from Athletes heart
LGE on CMR
Diastolic dysfunction
Abnormal ECG
Abnormal VO2 max
Asymmetric thickening
SAM
Family history
LV cavity < 45mmhg
LA enlargement
When to consider Septal reduction in HoCM?
Severe symptoms due to LVOT-O despite medical management at a high volume center/experienced operator (Class 1)
NYHA II symptoms with:
-LVOT causing PHTN
-LVOT causing decreased functional capacity
-LVOT causing LAE and AF
-LVOT > 100mmhg in children
What is dose of PUFA for HF?
1 gram/day
When would you expect increased likelihood to experience significant improvement in LVEF after revascularization based on: SPECT, PET, Echo, CMR
- Large segment of Viable myocardium in SPECT (> 30% LV)
- > 7% hibernating myocardium on PET
- > 20% LV on Dobutamine stress Echo
- Less than 50% wall thickness scarring with LGE on CMR
What is the leading cause of mortality post transplant in first 30 days?
Graft failure
What is the leading cause of mortality post transplant in 1-3 years
Acute rejection
What is the leading cause of mortality post transplant after first 3 years?
Malignancy
What are 7 contraindications for transplant?
Pulmonary HTN (WU > 3, TPG > 15mmhg, no decrease in PVR to less than 2.5 in response to vasodilators
Severe systemic illness that limits life expectancy despite transplant
Severe systemic illness that has high probability of recurrence in the transplanted hear
Non cardiac organ failure that limits life expectancy (Liver, CVD, Lung)
Active infection
Active substance use
ABO incompatibility
Describe the Canadian Transplant Listing status:
Status 4: Mechanically vented, high dose single or dual inotropes on MCS (other than VAD), VAD malfunction or complications
Status 4s: 4 but highly sensitized (PRA > 80%)
Status 3.5: Hospitalized, high dose inotrope dependent, ineligible for VAD or not available OR acute/refractory ventricular arrhythmia
Status 3: Hospitalized on inotropes but not on above criteria
Status 2: Outpatient on inotropes
Status 1: All other patients
5 risk factors for rejection post transplant?
-Young
-Female
-CMV+
-HLA Incompatibility
-ABO Incompatibility
What are two strategies to lower PRA in sensitized patients?
-Plasmapheresis
-IVIG
How does Calcineurin inhibitors work? (Cyclosporin, Tacrolimus)
Blocks Calcineurin, which is reponsible for inhibiting transcription of IL-2
What are 5 adverse effects of CNI’s?
-Nephrotoxicity
-Hypertension
-Dyslipidemia
-Tremors
-Paresthesias
Name 9 meds that increase CNI concentration?
ABCDEF
A: Allopurinol, Amlodipine
B: Amphotericin B
C: Cimetidine
D: Diltiazem
E: Erythromycin + Vancomycin
F: Fluconazole + Ketoconazole
Name 3 meds that decrease CNI levels
Phenobarbitol
Dilantin
Ticlodipine
How do MMF and Azathioprine work?
-Blocks synthesis and proliferation of T and B lymphocytes
How do MTOR inhibitors work?
Block the target of rapamycin, which stimulates the growth and proliferation of T and B lymphocytes, smooth muscle cells and endothelial cells
What is hyperacute (minutes-hours) due to?
Preformed donor specific antibodies in the recipient
What is the histology of Antibody mediated rejection?
Scant cellular infiltrates with endothelial swelling and macrophage accumulation. Immunoglobulins and complement can be identified in capillaries with staining
What is the histopathology for CAV?
Thickening/Hyperplasia of the coronary intima, can be focal but usually diffuse
What are 7 RFs for CAV?
HLA mismatching
Rejection
CMV
Donor Age or CAD in the donor heart
Typical CAD RF’s: DM, HTM, DSL
What are three opportunistic infections the affect transplant patients in the first month?
Nosocomial
HSV
CMV
What are 6 causes of opportunistic infections in the intermediate course?
-CMV
-HSV
-PCP
-Aspergillosis
-Nocardia
-Toxoplasmosis
What two prophylactic meds do transplant patients need to be on?
-CMV: Ganciclovir 3-6 months if recipient seropositive or recipient seronegative and donor seropositive
-PCP: Bactrim for at least 1 year in all patients (Sulpha allergy: Dapsone or Pentamidine)
When does Malignancy take over as the leading cause of death post transplant?
3rd year post transplant
What is the most common cancer in post transplant?
SCC/Cutaneous (Followed by Lymphoma and then solid organ tumors)
How much does Tandem heart (LA to Aorta) device and LVAD increase CO by?
3.5-4 L/min
What are 4 contraindications for LVADs?
Mechanical Aortic Valve, LV thrombus, Coagulopathies, Severe PAD
6 complications with LVAD?
Bleeding
Arrhythmias
Strokes
Pump Thrombosis
Aortic insufficiency
LV suction events
What RA/PCWP ratio is associated with increased risk of RHF post LVAD?
-RA/PCWP > 0.63
Name 9 viruses that cause myocarditis
-Parvo 19
-CMV
-HCV
-HIV
-Adenovirus
-Cocksackie
-HHV-6
-EBV
-Enterovirus
What is the hallmark of the acute phase of Chagas CMO?
-Acute phase: Pericardial Effusion
What is the hallmark of the chronic phase of chagas?
-BiV enlargement, WMA, mural thrombi, heart blocks
What is the treatment for Chagas CMO?
Benznizadole
What is EMB sensitivity for GCA?
85%
What is the Lake Louise criteria?
CMR criteria for diagnosing Myocarditis:
-Regional or global myocardial signal intensity in T2 weighted edema images
-Increased global myocardial early gad enhancement ratio between myocardium and skeletal muscle in T1 weighted images
-There is at least one focal lesion with non ischemic regional distribution in inversion recovery-prepared gadolinium-enhanced t1 weighted images
Name three patient related Rfs for cardiotoxicity with Chemo?
-Pre existing CVD
-Advanced Age
-Multiple or poorly controlled CVD Rfs
Also Female
What is GLS cut off for picking up abnormalities?
> 15% relative change
Echo frequency when on Trastuzumab?
q3 months
When to start LV enhancement in chemo induced CMO? When to consider it ?
-LVEF < 40%
- > 10% decrease in LVEF from baseline or LVEF < 53%
What is life time dose limit for anthracyclines?
-400-450 mg/m2 for Doxorubicin
-800-900 for Epirubicin
-600 for Daunorubicin
-100 Idarubicin
What do Antimetabolites (5-FU/Capecitabine) cause?
Coronary spasm
What do small molecule tyosine kinase inhibitors cause?
Hypertension
What is most common BAV morphology? 2nd most?
-RCC-LCC
-RCC-NCC
What level of Contractile reserve correlates with poor prognosis?
20% (Makes no difference after TAVR, poor outcomes with SAVR)
What is the Hakki formula?
AVA = CO / (Square root MG)
What is the Gorlin formula?
AVA = CO / ((SEP x HR x 44.3(SqRt MG))
What is low risk STS?
< 4%
What is Intermediate risk on STS?
4-8%
What is high risk on STS?
> 8%
What is definition of Prohibitive surgical risk for SAVR?
predicted Major morbidity > 50%
Also
-Procedure specific impediment
-More than one organ dysfunction not expected to improve post procedure
-More than one frailty index not expected to recover post procedure
What % of patients with severe AI progress to having symptoms or LV dysfunction?
4% / year
When would you consider a Ross procedure?
-Young patient and VKA is contraindicated
What is PPM for AVR? Severe?
0.85
0.65
What is PPM for MVR? Severe?
< 1.2
< 0.9
What are indications for lytic/surgery in left sided PV thrombus?
Left sided HF if mechanical
If bioproshetic -> can be treated with intitiation of VKA
What to do if mechanical valve, thrombotic event despite therapeutic inr?
Increase INR by 0.5
What is contour of the jet velocity in PV stenosis?
-Rounded symmetrical contour (as opposed to early peaking)
What is EOA or severe PV stenosis?
< 0.8
What is DVI of severe AV PV stenosis?
< 0.25
What is MG of severe AV PV stenosis?
35mmhg
What is peak velocity of significant PV stenosis?
4m/s
What is Colchicine dosing for Pericarditis based on weight?
0.5mg BID if Wt > 70kg (daily is Wt < 70kg)
What is Colchicine duration if recurrent Pericarditis?
> 6 months
What is prednisone dosing in Pericarditis?
0.25-0.50 mg/kg/day
When tapering: 10mg/day every 1-2 weeks decrease
What are 6 predictors of poor survival with Pericardectomy?
Prior radiation
Renal dysfunction
Increased PASP
LV systolic dysfunction
Increased Age
Hyponatremia
What are 4 echo findings of Constriction?
-Septal bounce
-Tissue doppler e’ > 8 cm/s
-Respiratory inflow variation
-Pericardial thickening and calcifications
-What is ferritin and tsat cut off for Hemochromatosis?
-Ferritin > 200 in women and > 300 in men
-TSat > 45% in women and >50% in men
-How to treat Iron overload CMO or Hemochromatosis?
Iron removal usually by phlebotomy of iron chelation therapy
Describe the two phases of Chagas Cardiomyopathy?
-Acute phase: myocarditis and pericarditis
-Chronic phase: Cardiomyopathy
Describe the pathophysiology of Chagas CMO?
-Direct tissue damage from large number of parasites
-Immune mediated inflammatory damage of myocytes
-Leads to degeneration of muscle fibers and necrosis
-Neuronal damage with decreased parasympathetic nervous system input to SA node
-Occlusive thrombi in epicardiac and coronary vessels
What is ESC 2016 criteria for Takotsubo?
Transient RWMAs of LV frequently preceded by a stressful trigger
Beyond single epicardial territory
Absence of culprit ASCVD
New and reversible ECG changes
Elevated BNP
Positive but relatively small troponin elevation
Recovery of ventricular systolic function on cardiac imaging at follow up
Diagnostic criteria for Microvascular Angina?
-Typical angina
-Findings compatible with myocardial ischemia (EST, MPI, PET. CMR)
-Normal or near normal < 20% coronary arteries on angiography. Ancillary findings include CFR < 2, IMR > 25, Increased Myocardial Blush grade
-Absence of any other specific cardiac disease
What are the 3 pathophysiology of Microvascular angina?
-Abnormal Vasodilation
-Pro-thrombotic state
-Arterial remodeling
7 RF’s for Microvascular angina?
-Dyslipidemia
-Smoking
-Hypertension
-Elderly
-Diabetes
-Obesity
-Family history of early CAD
What are three invasive angiographic findings for Microvascular angina?
-Normal Epicardial coronary arteries
-Coronary Flow Reserve < 2.5
-Increased Myocardial blush grade, the number of heart cycles required for contrast to fade out of the coronary artery
3 mechanisms of Neprilysin inhibitors?
-Increase levels of endogenous vasoactive peptides
-Degrading counter-regulatory vasoactive peptides
-Degrades deleterious neuro0hormone angiotensin II
-Decreases renin production via increase in NP
When to Cath in new HF?
-Reasonable in all HFrEF if revascularization candidate
-Angina or equivalent if revascularization candidate
-NIV testing positive if revascularization candidate
When to Cath prior to AVR?
-Anginal symptoms
-Ischemia on NIV
-LV dysfunction
-History of CAD (even if stable)
-Men > 40 and Post menopausal Women
-If chronic severe secondary MR
Review Clinical factors increasing risk of TDP when Long QT seen on ECG
What are 2 associated abnormalities of Dextrocardia?
TGA
Right sided Aortic arch
What are 5 RFs for Patient Prosthetic Mismatch?
-Smaller aortic root and annulus
-Female gender due to smaller aortic roots
-Advanced age
-Smaller LV diameters
-Bioprosthetic valves
What are the 4 pathologic mechanisms that OSA causes LV dysfunction?
-Transient Hypoxic insults
-SNS Stimulation
-Increased afterload with marked fluctuations in intrathoracic pressures
-hypertension
What are predictors of adverse events in Takotsubo?
- Age > 75
- Physical trigger
- Neuro trigger
- LVEF < 45%
-Men > Women
-HD instability
Three mechanisms by which cocaine leads to MI?
1) Increased Demand
2) Vasoconstriction
3) Platelet activation/aggregation
Name parts of STS Score and what is it used for?
STS Score: Allows one to evaluate a patients risk of mortality and morbidity for a given procedure
-Type of OR
-Age
-Gender
-Race
-WBC
-Hct
-Plt count
-Creatinine level/Dialysis
-Hypertension
-Immunocompromise
-PAD
-CVD
-DM
-Cancer within 5 years
-Mediastinal radiation
-LVEF
-Arrest
-ECMO/VAD/IABP
-Degree of Coronary Stenosis
-Other valvular disease
-
Define Restrictive Cardiomyopathy (4)
A disease of the myocardium that is characterized by:
-Marked ventricular stiffness
-Restrictive filling pattern
-Reduced diastolic filling volumes
-Normal or near normal systolic function
Review causes of Restrictive CMO
5 high risk Echo findings of PE?
RV dilatation
RV dysfunction (decreased TAPSE)
Mcconell’s sign (decrease movement of RV free wall)
Increased RV-LV ratio
Increase TR Velocity
5 findings that portend a good prognosis in PPCM?
-Non black
-LVEF > 30%
-LVEDD < 60mm
-Post partum diagnosis
-Low BNP/Troponin
5 findings that portend a poor prognosis in Aortic Dissection?
-Age > 70
-Hypotension/Tamponade
-Stroke
-Visceral Ischemia
-Renal dysfunction
What is Jones criteria for Rheumatic Carditis?
Major:
-Sydenham’s chorea
-Carditis
-Migratory arthralgias
-Subcutaneous nodules
-Erythema Migrans
Minor:
-Fever
-Polyarthralgias
-ESR > 30
-Prolonged PR interval
2 Major, 1 Major and 2 Minor
What are three CCS scenarios where Myocarditis should be suspected?
-Shock with LV dysfunction with no other apparent cause
-LV systolic dysfunction with no other apparent cause
-Myocardial damage (biomarker elevation) with no CAD cause
What are the 4 major elements of Myocarditis diagnosis?
-Symptoms and clinical findings consistent with myocardial damage
-Evidence of myocardial injury with no epicardial coronary cause
-Evidence of hyperemia, edema or irreversible injury on CMR imaging
-Presence of inflammatory cell infiltrate or positive viral genome on EMB
Name 4 indicators of poor prognosis in Myocarditis
1) LVEF < 50%
2) sustained ventricular arrhythmia
3) heart failure/cardiogenic shock
4) etiology (eg GCA)
What is pathogenesis of myocarditis?
Direct viral myocyte injury -> activation of cytotoxic T cells -> Activation of aquired immune system -> 2 choices from here:
-Viral clearance and down regulation of immune system -> recovery
-Ongoing viral insult and ongoing immune system -> chronic LV dysfunction
Name 4 biomarkers that relate to plaque Instability (2014 exam, 6 answers)
-HS CRP
-Lp(a)
-Interleukin 6
-Myeloperoxidase
-Fibrinogen
-Homocystein
5 alterations in biology for the failing Myocyte ? (2014 exam)
-Cardiac Myocyte Hypertrophy
-Alterations in Excitation-Contraction coupling
-Beta-adrenergic desensitization
-Reduced SR calcium release
-Abnormalities in contractile and regulatory proteins
8 clinical factors that increase risk of limb loss with critical limb ischemia? (2014 exam)
-Older age
-Smoking
-Diabetes
-Hypertension
-Distal Disease
-Limited life expectancy due to comorbid disease
-Sepsis
-Ischemic Rest Pain
-Paresis of the extremity
-Uncorrectable flexion contracture
-Significant necrosis of weight bearing parts of the foot in ambulatory patients
What is lytic dosing for Prosthetic Valve thrombosis? What to determine if further lytic needed?
-Alteplase 25mg IV over 25 hours followed by UFH 70 units/kg and then 16 units/kg/hr to maintain aPTT 1.5-2x normal for 6 hours
Then do an echo if shows reduced gradient -> do TEE if shows > 75% reduction -> UFH and warfarin
If < 75% reduction or no reduction in gradient -> another 25mg IV infusion
5 reasons to choose surgery over lytic for PV thrombus?
-Patient preference
-Access to surgical expertise
-CI to lytic
-Large clot > 0.8 cm
-Low surgical risk
-NYHA IV
-Recurrent Thrombosis
-Concomitant CAD in need of revascularization
What are two manoeuvres to distinguish PR and AR?
Inspiration will increase PR but leave AR the same
Valsalva release will lead to immediate increase in PR murmur as RV preload will increase and then in 4-5 beats AR murmur will increase
It is also different as AR starts at A2
What are 4 muscular dystrophies that have conduction system involvement?
KEMP
Kearn’s Sayre
Erb’s
Myotonic
Peroneal muscular atrophy
What are 5 muscular dystrophies with cardiac involvement?
-Myotonic Dystrophy (AD)
-Duchenne’s (X Linked)
-Beckers (X Linked)
-Limb-girdle (AR)
-Fascioscapulohumeral muscular dystrophy (AD)
What is MRI seen on Hemochromatosis?
-Iron deposition that can be quantitatively assessed with T2 sequences
When can Hakki/Gorlin inaccurate? (3)
-Inaccurate CO measurement
-Inaccurate extremes of CO and HR
-SEP and DFP are inaccurate with PVC’s or Afib
Why does Flamm flow incorporate more SVC than IVC?
-Renal blood flow is high but extraction is low (shunting, higher O2), SVC includes blood flow from brain which has much higher extraction
What is definition of reinfarction vs. recurremt MI
Within 28 days or after
What is definition of Type 4a MI?
Trop > 5x/99%-tile when pre procedure was below OR >20% from pre trop
What is Type 4b and what are the timelines?
Type 4b: Stent Thrombosis on angio/autopsy
Acute: < 24h
Subacute: 1-30 days
Late: 30d-1y
Very late: > 1y
What population did Enoxaparin vs. UFH show benefit?
-Medically managed: ESSENCE
-More bleeding with no less MACE in PCI: SYNERGY
What benefit does Bivalirudin have vs. Enoxaparin/UFH?
Reduction in bleeding, no reduction in MACE (ACUITY)
What are two benefits of Fonda vs. Enoxaparin?
OASIS-5: No ischemic benefit but lower mortality and less bleeding, increased catheter thrombosis
