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Define Diastolic function

Limitation of the ventricle to fill to normal end-diastolic volume without an abnormal increase in end-diastolic pressure at rest or during exercise.

Loss of compliance/loss of relaxation with abnormal distensibility abnormal filling


What are echo signs of Diastolic dysfunction

1. Prolonged Transmitral E wave deceleration time (normally adults less than 220 ms)
2. Prolonged Isovolumetric relaxation time (interval in the cardiac cycle, from the aortic component of the second heart sound, that is, closure of the aortic valve, to onset of filling by opening of the mitral valve, greater then 80)
3. Reversal of transmitral E:A ratio (impaired relaxation (E:A reversal i.e. E is < A)
4. Delayed ratio of transmitral A wave duration to pulmonary atrial reversal wave duration ( > 30)
5.Blunting of systolic pulmonary vein flow to Diastolic ratio (systolic blunting, a decrease in the height of the S wave)


What are echo predictors of SAM post mitral valve repair

Septum > 15mm
Small LV cavity
Hyperdynamic LVEF 65%
Aorto mitral angle < 120 (some say 130)
Short coaptation-septal distance< 25 mm
Too small annuloplasty ring
Excessive height of posterior leaflet post repair (>15mm)


What are details of first generation LVAD

Pulsatile, volume displacement using a pusher plate system.
The pump senses when the chamber is full and activates the pusher plate. It has porcine xenograft valves.
35% device failure in 2 years;
Heartmate XVE


What are details of Second Generation LVAD

Continuous flow, rotary pump, smaller, eliminating the reservour chamber and valves that was needed for first generation.
Rotary blood pump is in axial blood flow path, with an internal rotor suspended on bearings.
Inflow at apex of LV and outflow in ascending aorta.
Risk of negative intraventricular pressure. INR 2.5- 2.5
Heart mate II


What are details of 3rd Generation LVAD

eliminated need for "bearings"
Using hydrodynamic or electromagnetic suspension of an impeller to reduce mechanical wear and trauma to blood cells

contact free rotation


List contraindications to LVAD

CVP < 16
Revised Columbia score > 5 (mortality 47% if score > 5)
likelihood of recovery low


What are features of Barlows mitral valve

young age, long history of symptoms
myxoid infiltration
Bulky, billowing and tall leaflets
multi-segment prolapse
Calcification of annulus
atrialization of leaflets
chordal thickening/elongation
late SEM with mid click


What are features of Fibroelastic defiencey

older, usually sudden onset
impaired connective tissue
thin leaflets
prolapse of single segment
ruptured chord
holosystolic murmur
thickened and excess chord only at prolapsing segment


What are criteria for Brain Death

Unresponsive to central pain stimulus
Absence of brain stem reflexes
a. no occular movements
b. no corneal reflex
a. measure po2 and pco2 after 8 minutes of apnea
b. if pco2 > 60 or 20 point increase
normothermia, no toxins, two physicians, clinical evidence of cns event keeping with brain death


List features of Ebstein Anomaly

Dysplasia of Triscuspid valve resulting in
1. fused perforated or absent leaflets and abnormal chordaie
2. apical displacement of the septal and posterior leaflets into the body of the right ventricle
3. thin atrialized right ventricle
4. right ventricle dysfunction
5. rhythm abnormalities (wpw)
6. often severe TR


What are echo features of TR

1. Vena contracta > 0.7cm
2. systolic flow reversal in hepatic vins
3. Effective Regurgitant volume > 45ml
4. Effective regurgitant orifice area > 0.40cm2


List features of Carcinoid Heart

How do you test for it

50% develop valve disease
Primary lesion is located in the small intestine
Mainly right sided lesions
Usually TR or TS
plaques are on the downstream of the valves leading to adherence of the leaflet on the underlying structures
Regurgitation and may constrict the annulus leading to stenosis
Pulmonary valve replacement
*test urine of 5-HIAA serotonin


Describe atrial senning operation

Atrial switch concept was first successful accomplished Senning in 1959
Relocating the walls of the right atrium and the atrial septum
Pulmonary and systemic venous return rerouted by incising and realigning the atrial septum over the pulmonary veins and using the the right atrial wall to create a pulmonary venous baffle.


Describe ISHLT classification of rejection

Grade 0 No rejection
Grade 1A Focal, mild, no necrosis
Grade 1B Diffuse infiltrate, no necrosis
Grade 2 Focal, moderate, one focus of aggressive infiltration with myoctye damage
Grade 3A Multifocal aggressive infiltration
Grade 3B Diffuse--diffuse inflammatory, myocyte necrosis
Grade 4 Severe rejection,Hemorrhage, vasculitis, Diffuse aggressive, edema



Class 1: Critical cardiogenic shock
Class 2: progressive decline
Class 3: stable on inotropes
Class 4: recurrent Advanced Heart failure
Class 5: Exertion intolerant
Class 6: Exertion limited
Class 7: NYHA III


Describe HIT

What percentage of pts develop HITT type II and how many develops thrombosis

IgG antibody binds to complex of platelet factor 4 and heparin leading to the formation of an immune complex.

The immune complex binds to platelets via platelet Fc receptors producing intravascular platelet activation, thrombocytopenia, and thrombosis

1- 5% develop Type II HIT and 20% of those develop thrombosis


Contraindications to Ross

Pulmonary valve disease
Autoimmune disorders
Poor LV function/Anatomical issues
aberrant coronary anatomy
mismatch of PA and Aorta


Mechanism and dosing of Factor VIIa

Stimulates the coagulation cascade by activation of thrombin at the site of tissue injury by tissue factor dependent and independent mechanisms

Tissue dependent results in factor X activation and thrombin generation

Tissue factor independent mechanisms include activation, aggregation, recruitment and stabilization of platelets.

65 ug/kg to 100 ug/kg


What is Ticagrelor

Nonthienopyridine, oral pyrimidine derivative, direct-acting, and reversible antagonist of the ADP receptor P2Y12 with a plasma half-life of about 12 hours

More rapid, potent and consistent effect on platelet function compared with clopidogreal.

PLATO trial improved rates of MI/Death/Stent thrombosis


Who should get a PA band

Unbalanced AV canal
Multiple VSD "swiss cheese"
Contraindication to cardiopulmonary bypass "weight"
VSD with Coarctation
Late presentation TGA (3 weeks..then place for 1 week before doing switch)


List cancers associated with post transplant

Basal Cell
Squamous Cell
B cell lymphoma
Cervical *rare
Vulvar *
Kaposi sarcoma *


What are 5 signs of positive exercise stress test

Abnormal symptoms (chest pain, syncope)
Abnormal ECG (ST depression)
Abnormal Blood pressure (drop in BP)
Abnormal Heart rate
Inability to achieve 6 mets


List 7 factors that a rate responsive pacemaker will respond

Body vibration
Body temp
respiratory rate
shortened QT interval
Acceleration in motion
RV systolic pressure
RV systolic volume


What are 2012 indications for CRT

EF < 35%
Sinus rhythm
LBBB with QRS > 150 msec
on optimal medical therapy


List predictors for RVAD placement after LVAD

Cardiac index < 2.2
RV stroke work index < 0.25
Severe RV dysfunction
Pre-operative increase in serum creatinine
previous cardiac surgery
Systolic blood pressure < 90 mmg


List causes of restrictive cardiomyopathy

post radiation


What are features of Constrictive pericarditis

RAP and LAP are equal and > 10 mmhg
RVEDP = LVEDP (equalization within 5)
atrial size is normal
Ejection fraction is > 40%
Square root sign on right ventricle tracing
Pulmonary artery pressure is usually low


List health Edwards classification of Pulmonary artery hypertension

1. medial hypertrophy without intimal hyperplasia
2. media hypertrophy with intimal hyperplasia
3. medial hypertrophy with fibrosis
4. areas of vascular occlusion with fibrosis
5. angiomatoid lesions
6. necrotizing arteritis


What are causes of organic TR

Anorexectic drugs
Whipples disease


What are causes of functional TR

RV failure --ischemia
Pulmonary hypertension -mitral valve disease/left sided lesions
RVOT obstruction --Pulmonary embolism/chronic

Core Pulmonale-- congenital disease/left to right shunting


How does Milrinone work

What is loading dose and typical infusion rate

Inhibitor of Phosphodiesterase enzyme, which normally converts cAMP to its inactive form of 5 -AMP. So by being a phosphodiesterase inhibitor it increase the cAMP and subsequently creates a greater influx of calcium into myocardial cells

loading dose is 50ug/kg and 0.5ug/kg/min


How to adrenergic drugs effect cardiac contractility

stimulate adnylate cyclase which catayses the conversion of ATP to cAMP.
increases the amount of calcium introduced to into the cell for contraction


What does DDAVP stimulate

Increase VIII and vWF


What are ideal indications for fontan procedure

1. minimal age 4
2. sinus rhythm
3. normal caval drainage
4. right atrium normal
5. mean pulmonary pressure < 15 mmhg
6. pulmonary artery resistance < 4
7. no impairing effects of previous shunts
8. competent atroventricular vavle
9. normal ventricles
10. pulmonary-artery-to aorta-diameter ratio of > 0.75


What is natural history of AS

Median survival of 2-3 years after symptoms
Progression of decrease 0-15 mmHg/year
angina = 5 years, syncope = 3 years; dyspnea 1-2 years


What is natural history of AI

Latent period of 3-10 years
6%/year develop symptoms
3-5% develop LV dysfunction
25% will develop symptoms if LV is dysfunction
10%/year die when symptoms develop


Describe steps of Norwood stage I operation

Stage I reconstruction is performed shortly after birth via median sternotomy and deep hypothermic circulatory arrest (DHCA)”
1. atrial septectomy
2. Construction of a neoaorta from the pulmonary valve by division of the PA at the bifurcation and anastomosis of the aorta to the proximal PA
3. Placement of a systemic-to-pulmonary modified Blalock-Taussig shunt (mBTS) or RV to PA conduit


What is Natural History of VSD

80% close at birth
25% will close if not closed at 12 months
50% will develop pulmonary HTN at 20 years of age if left open


Surgical indications to close VSD

Failure to thrive beyond 6 months
Sub-arterial VSD at any age
History of endocarditis
plan for transvenous pacing


Define Left ventricular aneursym?
List 4 causes
What is natural history of symptomatic and asymptomatic LV aneurysms

Area of abnormal left ventricular diastolic contour with systolic or paradoxical bulging (dyskinetic movement)
1. 95% Coronary artery disease
2. Chagas Disease
3. Trauma
4. Sarcoidosis
5. Congenital
Excellent 10 year survival about 80-90% if no symptoms
50% 10 year year survival if symptomatic


What are contraindications for LV aneursym surgery

Excessive anesthetic risk
Impaired function of residual myocardium outside the aneurysm
Resting CI less then 2.0
Significant MR
Evidence of nontransmural infarction (hibernating myocardium)
lack of discrete and thin walled aneurysm with distinct margins


List clinical ways to distinguish between post MI VSD and papillary muscle rupture

1. murmur of septal rupture is more prominent @ the left sternal border and is louder and associated with a thrill.
2. murmur of pap muscle rupture is best heard at apex and is softer with no thrill.
3. VSD rupture is most likely associated with anterior infarctoin and conduction abnormality while a pap muscle is likely posterior with no conduction

***bonus criteria**
septal rupture show > 9% step up in oxygen saturation between RA and PA
papillary muscle shows classic V waves in the pulmonary artery wedge tracing


List 4 major differences between true aneurysm and false aneurysm

The wall of false aneurysm contains no viable myocardial cells
False aneurysm are more likely to form posteriorly
False aneurysm have a narrow neck
False aneurysm have an increased risk of rupture


List risk factors associated with needed redo CABG

Young age, Normal LV function, single and double vessel disease at time of initial operation
Not using ITA, incomplete revascularization
NYHA status III or IV at time of initial operation


What are survival indications to perform redo CABG

Atherosclerotic (late > 5 years) stenosis with vein grafts to LAD
multiple stenotic vein grafts that supply large areas of myocardium
multi-vessel disease with proximal LAD lesion/and or abnormal LV function based on native vessel or stenotic vein grafts or a combination of the two.


Define peak oxygen consumption and list cut offs for long term outcomes

peak oxygen consumption during exercise provides an index of overall cardiovascular reserve

value of 10 to 14 ml/kg/min or lower indicates a very poor prognosis and is generally the cuff off for transplantation


Define Hibernating and Stunned myocardium

Hibernating: contractility depressed myocardial function secondary to chronic ischemia that improves clinically immediately after revascularization

Stunned myocardium: left ventricular dysfunction without cell death that occurs after restoration of blood glow after an ischemic/reperfusion episode


4 ways to repair free wall rupture

Horizontal mattress sutors with felt
Infarct excision and closure with a patch
Horizontal mattress with felt and teflon patch
Simply Glue a patch to the epicardial surface


List 2007 AHA recommendations for antibiotic prophalaxis

Prosthetic heart valves
Previous infective endocarditis
Cardiac transplantation recipients who develop cardiac vavlulopathy
Serious Congenital conditions including unrepaired or incompletely repaired cyanotic congenital heart disease
a. palliative shunt/conduits/ TOF/TGA/Ebsteins/Tricuspid/interrupted arch/coarctation of aorta
Completely repaired CHD with prosthetic or device during first 6 months after procedure


What is mechanism of LVAD reverse remodelling

Improvement in myocardial contractility and calcium handling
altering the extracellular matrix
decreasing myocardial fibrosis
up-regulation of Beta receptors


What is evidence for IABP in a pt with cardiogenic SHOCK

what is mortality in pt with SHOCK post MI

80 % mortality for pt presenting in SHOCK

evidence for IABP is minimal. No improvement in survival with SHOCK II trial. mortality at 300 days was same


What are surgical options for anomalous coronary artery

Unroofing procedure: Open the slit-like ostium longitudinally start at the anomalous coronary os continuing into the correct sinus. A segment of the common wall between the aorta and the coronary is excised and the intimal surfaces are approximated.

creation of neo-ostium: probe passed through the intramural segment of the ACA into the correct sinu. The coronary artery is opened where it exits the aortic wall and then neo-ostium is created there.

Coronary artery translocation with reimplntation: coronary artery is excised with a button

Coronary bypass with either vein or artery can be performed.


What are contraindications for TAVI

Absolute contraindications
Absence of a heart team and no cardiac surgery on the site
Appropriateness of TAVI as an alternative to AVR, not confirmed by a heart team
Estimated life expectancy of < 1 year
Improvement of quality of life by TAVI unlikely because of comorbidities
Severe primary associated disease of other valves with major contribution to the patients symptoms that can treated only by surgery
Inadequate annulus size ( < 18 mm or > 29 mm)
Thrombus in the left ventricle
Active endocarditis
Elevated risk of coroanry ostium obstruction (asymmetric valve calcification, short distance between annulus and coronary osium, small aortic sinuses)
Plaques with mobile thrombi in the ascending aorta or arch
For transfemoral/subclavian approach: inadequate vascular acess (vessel size, calcification, tortuosity)
Relative indications
Bicuspid or non calcified valves
Untreated CAD
LVEF < 20%


What are factors in Child classification of Liver failure and risk of cardiac mortality

Bilirubin, Albumin , INR , encepalopathy , ascities
<7 cardiac surgery mortality is not affected
7-9 cardiac mortality is 41 to 80%
> 9 (1-3 month survival, cardiac surgery mortality is 100%)


List 4 types of Experimental Validity

Internal Validity
External Validity
Construct Validity
Statistical conclusion validity


List Bias associated with meta anlalysis studies

What techniques can be done to reduce bias?

What technique to test for Heteogenity

List 2 strengths of Meta-analysis

1. Publication bias/Search Bias/Selection bias
2. "Funnell plot"
3. Forest Plot--and a subsequent cochran Q- test
4. Strengths:
a. Increased Effective sample size which greatly increases more outcomes and variable that can be examined
b. Allows examining of rare events


What is major strength of RCT compared to Observational study?

List 2 ways that Observational studies attempt to account for weakness

List 3 potential limitations of RCT

RCT eliminates selection bias

Propensity analysis and Risk adjustment techniques (such as regression or analysis of variance)

weakness of RCT
a. decreased generalizability--specific inclusion/exclusions
b. Inadequate statistical power --expensive to enroll pts
c. Follow-up and approach to treatment may not be representative of real life


What is Everst II study

N = 279 pts (2:1 radndomization)
184 to mitra clip and 95 mitral repair
Primary composite endpoint---freedom from death, surgery for mitral dysfunction, and freedom from MR > 3+ at 12 months
Primary safety endpoint---included transfusion of >2U of Blood


What is results of Everest II study

mitral clip 55%
Surgery 73%

safety event was 15% with mitral clip and 48% with surgery. This was because of the blood transfusion data.


What is current for off pump CABG

What was difference between CORONARY and ROOBY

rate of Death, myocardial infarction, stroke, or new renal failure as a composite outcome showed no difference at 30 days or 1 year (12.1% vs 13.3%)--CORONARY

Repeat revascularisation has trend toward increase in off pump

rate of bleeding requiring, respiratory complications, and rise in serum creatinen were trending to wards benefit in off pump.

CORONARY had more pts (over 4000, expert based surgeons, more women and more left main)


What are microscopic features of HOCM

1. Disorganized myocytes and contractile elements withing cells (myofiber dissarray)
2. Extreme myocyte hypertrophy
3. Interstitial fibrosis


What is physiology of allograft Coronary artery disease

1. Diffuse, distal disease
2. Few collaterals
3. Concentric and neointimal proliferation
4. Months to develop
5. Not amenable to revascularization
6. always multivessel


What are allograft risk factors

1. Total ischemic time
2. CMV
3. Hyperlipidemia
4. Number of acute refection episdoes
5. Catecholamine-indiced ischemic injury in the donor


5 complications of the senning/mustard procedure

Sudden death (7-15%)
RV failure
L-sided pulmonary vein stenosis
SVC/IVC thrombosis
Baffle leak
Brady/tachy rhythms
Pulmonary HTN


What factors to consider when planning a Biventricular repair in pulmonary atresis with intact ventricular septum

1. echo criteria for RV size which is based on the tricuspid Z score of RV hypoplasisa
2. RV morphology
3. Presence of RV dependent coronary circulation
4. Presence of Ebsteinoid TV with severe TR


5 effects of NO on vascular endothelium

inhibits platelet aggregations and adhesion
inhibits vascular smooth muscle growth
Inhibits neutrophil adhesion
inhibits adhesion molecule expression


What are types of Pulmonary atresia with intact VSD

Type A: Confluent central PA and no MAPCAS
Type B Confluent central PAs with MAPCS
Type C: Non-confluent central PA with MAPCS (2 to 6)


What are the types of MAPCAS

Bronchial arteries
Indirect arteries arising from the aortic arch
Primitive intersegmental arteries that failed to involute


What is natural history and pathology of Pulmonary atresisa with intact ventricular septum

Complete obliteration of the RVOT at the level of valve and the pulmonary arteries are usually normally developed.
Severe cyanosis on the first day of life
Source of pulmonary blood flow is exclusively from PDA- MAPCAS are rare
Coronary flow is from coronary sinusoids or RV-coronary fistula


What are features of Congenital corrected TGA

L-Looping TAG--aorta anterior and to the left of the PA
AV and VA discordance
Blood flow--RA-LV-PA: and LA-RV-Aorta
95% have a VSD
90% have Tricuspid anomalies
15% have complete heart block


What are components of the Norwood operation

Atrial septectomy
Division of the PA and enlarging it with the PA patch
A modified BT shunt or RV-PA conduit
Arch augmentation with a patch


What are acceptable Epicardial pacing thresholds

ventricular pacing threshold < 0.7mV
R wave(sensing) amplitude > 5mV
P wave(sensing) amplitude > 1.5mV
Lead impedence 400 to 1000 ohms
absence of diaphragmatic pacing at 10mV


What type of Pacemaker in who

Bradycardia with intact AV node---DDI
Bradycardia with unreliable AV node--DDD
Bradycardia with episodes of atrial tachy--VDD or DDD
Bradycardia with chronic atrial tachy---VVI
SA incompetence with intact AV node---AAI
SA incompetence with unreliable AV node--DDD

*can add rate modulation to any of the above for you and active patients


List 4 meds that most patients should be on post CABG and why

ASA--improved vein graft patency and survival benefit
beta blocker-reduce post op arhythmias, and survival benefit in post MI pts
Statin: improved graft patency with reduction in inflammation prevent disease progression
ACE- reduced afterload and enhance LV remodeling in pts with low EF/DM


What are indications for LVAD

1. Class 4 Heart failure and failed OMT for at least 60 to 90 days
2. Left ventricular ejection fraction of < 25%
3. Functional limitation with a peak oxygen consumption of < 12 ml/kg/min or
4. Continued need for intravenous inotropic therapy owing to symptomatic hypotension, decreasing renal funtion, or worsening pulmonary congestion
5. Appropriate body sise (BSA > 1.5)

1/3 of BTT pts are lose transplant candiancy
17% of DT receive transplant


Clinical differences between VSD and pap muscle rupture

1. murmur of septal rupture is more prominent @ the left sternal border and is louder and associated with a thrill.
2. murmur of pap muscle rupture is best heard at apex and is softer with no thrill.
3. VSD rupture is most likely associated with anterior infarction and conduction abnormality while a pap muscle is likely posterior with no conduction

***bonus criteria**
septal rupture show > 9% step up in oxygen saturation between RA and PA
papillary muscle shows classic V waves in the pulmonary artery wedge tracing


List 2 ways to assess patency of intra operative bypass grafts

1. Transit time Doppler
>50 percent diastolic flow and PI < 5
2. Immuno fluorescence imaging


What has CRT been shown to benefit

Quality of Life
Functional Class
Exercise Capacity
degree of MR


What are primary prevention indications for AICD

Dilated Cardiomyopathy or IHD > 40 days post MI
LVEF < 35%
NHYA function II, or III despite OMT
Reasonable expectation of survival with a good functional status for more then 1 year


What are secondary prevention indications for AICD

Current or prior heart failure symptoms
Reduced LVEF < 35%
A history of Cardiac arrest, ventricular fibrillation, or hemodynamic destabilizaing ventricular tachycardia


What are Class I indications for CRT

LVEF < 35%
Sinus rhythm NHYA II, III, or IV on OMT
QRS > 150 w LBBB (CCS guidelines)
QRS > 120 (AHA)
*whatever you say add that it's cardiac dyssynchrony


What is most common test and results for Hemolysis

The blood smear--confirms it

Demonstrates microangiopathic red cell changes

other histological RBC changes are 1) schistocytes 2) burr cells 3) Fragmented red cells 3) elevated indirect bilirubin


What other tests for Hemolysis and expected results

Serum LDH--elevated
Serum Haptoglobin--depressed
Reticulocytosis--fragmented and in RBC peripheral smear
Increase Serum hemoglobin


List 5 items which may be tracked and used to modulate the rate in a rate responsive pacemaker

Carbon dioxide
Lactic acid
Intra-cardiac pressure
QT interval


How does a rate responsive pacemaker work

The particular item is a product of increased metabolism and will be sensed by a transducer.
This results in an electrical signal being sensed by the pacemaker electronic circuit and changes the pacemaker automatic interval and therefore the escape rate.

As the detection of the item increases, the pacemaker output rate will increase; as the sensed parameter decreases, the pacemaker response will also decrease


Quickly list locations for all VSD

1. Membranous VSD--under the commissure of the anterior and septal leaflet of TV. Bordered superiorly by ventricular infundibular fold, anteriorly and inferiorly by the septum and posteriorly by tricuspid
2. Inlet: under the commissure of the septal and posterior leaflet.
3. Muscular: surrounded by rim of muscle. located anywhere in interventricular septum
4. Doubly committed sub arterial VSD: fibrous continuity between the leaflets of the pulmonary and aortic valve.


4 week old with Tricuspid Atresia. List the 3 operations that would be used for a staged repair and the age at which each should occur

BT shunt--control cyanosis in newborn period.

Bidirectional Glenn anastomosis--6 to 12 months of age

Fontan operation after 3 year


List 4 anatomical vascular rings

1. Double aortic arch
2. Right aortic arch with left ligamentum arteriosum and left subclavian
3. Pulmonary Sling
4. Anomalous innominate artery compression syndrome
5. Anomalous right subclavian artery (dysphagia lusoria)

* Pulmonary artery sling--the left pulmonary artery passes anterior to the esophagus while all other vascular rings run posteriorly.


List 3 components of the Rastelli repair for TGA with LVOT obstruction

Tunneling of VSD to aortic root
RV-PA conduit
closure of main PA
closure of ASD *not really part of it*


What percentage of pts Do NOT have a intact circle of Willis and what do you do?

about 10 to 15%

Place a balloon tipped cath selectively into the Left common carotid.

Check with NIRS and you should see return from the left even before you place balloon tipped. Look for this


List Carpentiers classification of Ebsteins's Anomaly

Type A: small atrialized, normal RV
Type B: large atrialized--mobile anterior leaflet, normal to wall RV
Type C: restricted leaflet motion, small RV
Type D: triscuspid sac "Uhl's syndrome"


List 3 subsets of single ventricle anomalies

Tricuspid atresia
Double inlet left ventricle
mitral atresia


List the classification of tricuspid atresia

Type I: 70%--Normally related great vessels
Type II: 30 %--D-TGA
Type III --L-TGA (super rare)

Subsets--A pulmonary atresia
B pulmonary stenosis
c- normal pulmonary valve


what other lesions are associated with Vascular rings?



List anatomy of Hypoplastic left ventricle

Hypoplastic LV and ascending aorta
Aortic atresia/stenosis
mitral atresia/stenosis

restrictive inter-atrial communication
Coarctation in 80% of cases


Describe 2 posterior and 1 anterior root enlargement techniques

Nicks: incision through non coronary sinus and annulus, up to attachment of anterior mitral leaflet

Manougian: incision between the left coroanary and non coronary sinus, through the intravlvular trigone and the central fibrous origin of the anterior mitral leaflet

Konno: longitudinal incision in the anterior wall extended to the left of the RCA across the annulus and into both the IV septum and the RV anterior wall
dacron patch sewn to the LV side of the IV septum to close the VSD, prosthetic valve inserted, rest of dacron used to close aortotomy.
pericardial patch to close the RVOT


What are factors to consider when planning a repair for pulmonary atresia with intact ventricular septum

right ventricular dependent coronary artery ciculation
size of triscuspid valve
size of right ventricle
Morphology of right ventricle


What are clinical manifestations of rheumatic fever

Polyarthritis: temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
Carditis: Inflammation of the heart muscle which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
Subcutaneous nodules: Painless, firm collections of collagen fibers over bones or tendons.
Erythema marginatum: A long-lasting reddish rash that begins on the trunk or arms as macules, which spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake-like appearance.
Sydenham's chorea (St. Vitus' dance): A characteristic series of rapid movements without purpose of the face and arms.


What are factors of Severe AI

Regurgitant fraction ≥ 50%,
vena contracta width (narrowest diameter of the flow stream) > 6 mm,
regurgitant volume ≥ 60 mL,
jet width/LVOT ≥ 65%,
effective regurgitant orifice (ERO) area ≥ 0.3 cm2.”


What are measurements of severe MR

“Severe MR is characterized by a vena contracta width ≥ 0.7 cm,
ERO ≥ 0.4 cm2,
regurgitant volume ≥ 60 mL,
regurgitant fraction ≥ 50%,
jet area > 40% of LA area.”


What is mechanism of action of Dabigitran?

Name two other meds in this class with similar action?

What was study and outcome that was assessed with this drug?

Oral, direct competitive thrombin, inhibitor

Rivaroxaban and Apixaban

Re-Ly study showed in AF that 110 vs warfarin was equal and 150 vs warfarin resulted in less stroke 1.69 vs 1.11% with similar bleeding

Limitation was the time spent in therapeurtic range on warfarin was limited for pt. when pts were in therapeutic range greater >70%) of time there was no difference.

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