View
216
Download
3
Category
Preview:
Citation preview
Valvular Heart Disease Overview: Prep for the Boards
Saturday, October 15, 2016
7:30 am - 4:00 pm
Sheraton Station Square
300 W Station Square Drive
Pittsburgh, PA
Valvular Heart Disease Overview: Prep for the Boards
Attention Attendees:
There will be no printed copies of these online meeting materials at the meeting this
year. In addition, the meeting will not have Wi-Fi accessible, so please make sure
you print or save these course materials.
This document will be updated as we receive changes or additions. A date will appear
at the bottom indicating when it has been updated. A * will mark revised sections.
To access this PDF offline you will need to save it to your computer. Click on the disk
icon in the top left or select Save from the File menu. If you are on a tablet, you will
need to open it in a PDF reader application (i.e.: iBooks, Amazon Kindle App).
These course materials can easily be navigated by turning on the bookmarks navigation
panel from under View.
Valvular Heart Disease Overview: Prep for the Boards Table of Contents
Agenda
Presentations
• Physical Exam Findings In Valvular Heart DiseaseFrederick W. Crock, MD, FACC
• Aortic Valve Overview – When Is It Appropriate To Intervene?Matthew E. Harinstein, MD, FACC
• Multi-Modality Imaging In Aortic Valve DiseaseJoao L. Cavalcante, MD, FACC
• TAVR OverviewDustin Kliner, MD, FACC
• A Surgeon’s Perspective – Will TAVR Prove to Be Appropriate for LowRisk Patients?Chris Cook, MD, FACS
• Paradoxical LF/LG Aortic StenosisRachel A. Hughes-Doichev, MD
• Case PresentationJohn T. Schindler, MD, FACC
• The Pathoanatomy Of Mitral RegurgitationWilliam E. Katz, MD, FACC
• Overview Of Mitraclip And Future DevicesJ. Conrad Smith, MD, FACC
• Surgical Strategies In Secondary MR?Walter E. McGregor, MD
• Double Valve DiseaseJohn T. Schindler, MD, FACC
• Tricuspid Regurgitation – Is This Disease Entity Overlooked?William E. Katz, MD, FACC
Valvular Heart Disease Overview: Prep for the Boards Table of Contents (continued)
• Surgical Approaches For Right Sided Valve Disease
Chris Cook, MD, FACS • Usefulness Of CMR In Valvular Heart Disease
Moneal B. Shah, MD • The Importance of Mitral Valve Anatomy When Considering Invasive
HCM Treatment Timothy C. Wong, MD, FACC
• Case Presentation Timothy C. Wong, MD, FACC
Exhibitor Thank You
Valvular Heart Disease Overview: Prep for the Boards
Saturday, October 15, 2016 7:30 am - 4:00 pm
Sheraton Station Square 300 W Station Square Drive
Pittsburgh, PA
7:30 am - 8:00 am
8:00 am – 8:05 am
8:05 am - 8:25 am
8:25 am - 8:45 am
8:45 am - 9:05 am
9:05 am - 9:25 am
9:25 am - 9:45 am
Registration and Breakfast Brighton Ballroom Welcoming Remarks – John T. Schindler, Course Director Fountain View Ballroom Physical Exam Findings In Valvular Heart Disease Frederick W. Crock, MD, FACC Aortic Valve Overview – When Is It Appropriate To Intervene? Matthew E. Harinstein, MD, FACC Multi-Modality Imaging In Aortic Valve Disease Joao L. Cavalcante, MD, FACC TAVR Overview Dustin Kliner, MD, FACC A Surgeon’s Perspective – Will TAVR Prove To Be Appropriate For Low Risk Patients? Chris Cook, MD, FACS
9:45 am -10:05 am Paradoxical LF/LG Aortic Stenosis Rachel A. Hughes-Doichev, MD
10:05 am - 10:35 am Morning Break – Visit Exhibitors Brighton Ballroom
10:35 am - 10:55 am Case Presentation John T. Schindler, MD, FACC
10:55 am - 11:15 am The Pathoanatomy Of Mitral Regurgitation William E. Katz, MD, FACC
11:15 am - 11:35 am Overview Of Mitraclip And Future Devices A. J. Conrad Smith, MD, FACC
11:35 am - 11:55 am Surgical Strategies In Secondary MR? Walter E. McGregor, MD
12:00 pm - 12:45 pm Lunch Brighton Ballroom
12:45 pm - 1:15 pm Double Valve Disease John T. Schindler, MD, FACC
1:15 pm - 1:35 pm Tricuspid Regurgitation – Is This Disease Entity Overlooked? William E. Katz, MD, FACC
1:35 pm – 1:55 pm Surgical Approaches For Right Sided Valve Disease Chris Cook, MD, FACS
Valvular Heart Disease Overview: Prep for the Boards
Saturday, October 15, 2016 7:30 am - 4:00 pm
Sheraton Station Square 300 W Station Square Drive
Pittsburgh, PA
1:55 pm - 2:20 pm Afternoon Break – Visit ExhibitorsBrighton Ballroom
2:20 pm - 2:40 pm Usefulness Of CMR In Valvular Heart Disease Moneal B. Shah, MD
2:40 pm – 3:00 pm The Importance of Mitral Valve Anatomy When Considering Invasive HCM Treatment Timothy C. Wong, MD, FACC
3:00 pm - 3:15 pm Case Presentation Timothy C. Wong, MD, FACC
3:15-3:30 pm Course Wrap-Up/Adjorn
10/7/2016
1
Sheraton Station Square
Pittsburgh, Pennsylvania
October 15, 2016
Frederick Crock MD, FACC
Assistant Professor of Medicine
University of Pittsburgh
DISCLOSURES
No Conflicts of interest to declare
UPMC Heart and Vascular Institute
10/7/2016
2
CXR
https://erikhultman.files.wordpress.com/2010/10/sixfingerhand.jpg
PREP
LABSCXREKG
PHYS
HX
ADAPTED FROM HARVEY
UPMC Heart and Vascular Institute
INSP
PALP
AUSCPULSE
JVP
GENAPP
https://erikhultman.files.wordpress.com/2010/10/sixfingerhand.jpg
ADAPTED FROM HARVEY
UPMC Heart and Vascular Institute
10/7/2016
3
Braunwald E, Zipes DP, Libby P, Bonow RO, eds. Heart Disease. 7th ed. WB Saunders Company 2005, Chap.19:457–489, page 475.UPMC Heart and Vascular Institute
Copyright © 2003 by Lippincott Williams and Wilkins
JVP
UPMC Heart and Vascular Institutecm H2O x 0.75 = mmHg
10/7/2016
4
JVP S1 S2
A
C
X
V
Y
HS1 S2
S1 S2
A
V
A
V
NORMAL JUGULAR VENOUS
PULMONARY HTN/TS
Examination of the Heart. Part II, Fowler et al. AHA 1972 UPMC Heart and Vascular Institute
CAROTID PULSES
Examination of the Heart. Part II, Fowler et al. AHA 1972 UPMC Heart and Vascular Institute
10/7/2016
5
PERIPHERAL PULSESPULSUS PARADOX PULSUS ALTERNANS
Examination of the Heart. Part II, Fowler et al. AHA 1972
UPMC Heart and Vascular Institute
, “ma‐ma”
S1
S2
OS
EJ
WS‐S2
S3
S4
MODIFIED FROM JULES CONSTANT, BEDSIDE CARDIOLOGY, LWW 1999 UPMC Heart and Vascular Institute
10/7/2016
6
FIRST HEART SOUND INTENSITY
Position of the AV valve at the onset of ventricular systole:
Structure of the valve : thickened or normal
Rate of pressure rise and tension development by the ventricle: contractility
SPLITTING
Normal in young
RBBB
UPMC Heart and Vascular Institute
FIRST HEART SOUND LOUD FIRST HEART SOUND
Short PR interval Mitral stenosis Left atrial myxoma Tachycardia Exercise, Anemia, Hyperthyroidism
SOFT FIRST HEART SOUND Long P‐R interval Severe hypertension Left bundle branch block Acute aortic regurgitation Severe LV dysfunction
UPMC Heart and Vascular Institute
10/7/2016
7
SECOND HEART SOUND
Normal Physiological Splitting Wide Splitting Paradoxical Splitting Narrow Splitting
Increased PVR (decreasedcapacitence)
Intensity High diastolic pressure =
Louder s2 (A2 & P2) sound
Shaver et al, Auscultation of the Heart, AHA, 1990UPMC Heart and Vascular Institute
WIDE SPLITTING OF S2DELAYED P2 CLOSURE
RBBB
LV PACING
PULMONIC STENOSIS
PULMONARY HTN WITH RV FAILURE
ACUTE SIGNIFICANT PULMONARY EMBOLISM
ATRIAL SEPTAL DEFECT (PERSISTENT)
EARLY CLOSURE A2
MR
VSD
UPMC Heart and Vascular Institute
10/7/2016
8
PARADOXICAL SPLITTING S2DELAYED A2 CLOSURE
LBBBRV PACING
PDASEVERE LV DYSFUNCTION
AORTIC STENOSISHOCMSEVERE HTN
UPMC Heart and Vascular Institute
FOURTH HEART SOUND Origin of S4
Physiologic vs. Pathologic
Organic Conditions
Aortic stenosis
Hypertension
Ischemia /CAD
Split S1 vs. S4
UPMC Heart and Vascular Institute
10/7/2016
9
THIRD HEART SOUND Origin of S3
Physiologic vs. Pathologic
Organic Conditions
Increased LVEDP
Severe MR
Large VSD, PDA
UPMC Heart and Vascular Institute
Shaver et al, Auscultation of the Heart, AHA, 1990UPMC Heart and Vascular Institute
10/7/2016
10
GRADING MURMURS GRADE I: Very faint, difficult to hear, intenseconcentration and patience needed, “attending only”
GRADE II: Faint, usually heard immediately
GRADE III: Intermediate intensity, not loud butlouder than Grade II
GRADE IV: Loud associated with a palpable thrill
GRADE V: Very loud, can be heard with one edge ofthe stethoscope head off the chest
GRADE VI: Very, very loud, can be heard the entirestethoscope head is off the chest ¼”.
UPMC Heart and Vascular Institute
SYSTOLIC MURMURS
Shaver et al, Auscultation of the Heart, AHA, 1990UPMC Heart and Vascular Institute
10/7/2016
11
AORTIC STENOSIS 2nd RICS, 2 & 3rd LICS
Radiation to neck, shoulders
Radiation to apex‐Gallavardin Phenomenon Cycle Length: Variable intensity
Intensity, Duration
Time of Peak
A2 Intensity
Crescendo‐Decrescendo
Carotids: Parvus et Tardus
Paradoxical Splitting
UPMC Heart and Vascular Institute
Shaver et al, Auscultation of the Heart, AHA, 1990 UPMC Heart and Vascular Institute
10/7/2016
12
HYPERTROPHICCARDIOMYOPATHY
STEVE LOME, WWW.HEALIO.COM
UPMC Heart and Vascular Institute
POST PREMATURE BEATS Longer diastolicfilling period resultsin increased SV
Increased SV
Decreased afterload
Post‐systolicpotentiation –increasedcontractility
Brockenbrough–Braunwald–Morrow sign
Examination of the Heart. Part II, Fowler et al. AHA 1972 UPMC Heart and Vascular Institute
10/7/2016
13
PULMONIC STENOSIS
Shaver et al, Auscultation of the Heart, AHA, 1990 UPMC Heart and Vascular Institute
MITRAL REGURGITATION Holosystolic: Blowing, high frequency
Radiation
Apex to axilla
Apex to LSB
Acute vs. Chronic
MVP
Ischemic
Associated diastolic
rumble
Shaver et al, Auscultation of the Heart, AHA, 1990UPMC Heart and Vascular Institute
10/7/2016
14
CHRONIC MITRAL REGURGITATION
PALEY, H. AHA MONOGRAPH #46, 1975
UPMC Heart and Vascular Institute
ACUTE MITRAL REGURGITATION
COHEN, L AHA MONOGRAPH #46, 1975 UPMC Heart and Vascular Institute
10/7/2016
15
SEVERE CHRONIC MITRAL REGURGITATION
AORTA
LV
LA
S1 S2S3‐FLOW RUMBLE
PRESSURE
UPMC Heart and Vascular Institute
MITRAL VALVE PROLAPSE
Physiologic Principles of Heart Sounds and Murmurs. AHA Monograph 46 Leon & Shaver 1975UPMC Heart and Vascular Institute
10/7/2016
16
MITRAL VALVE PROLAPSE
O'Rourke RA, Crawford MH. The systolic click‐murmur syndrome: clinical recognition and management. Curr Probl Cardiol 1976;1:1–60.
UPMC Heart and Vascular Institute
TRICUSPID REGURGITATION Holosytolic
Location: lower left sternal border
Intensity: respiratory variation
JVP: V wave
RV lift
Associated diastolic rumble
UPMC Heart and Vascular Institute
10/7/2016
17
VENTRICULAR SEPTAL DEFECT Holosystolic
Location: Mid‐lower left sternal border
Crescendo‐decrescendo (mid systolic accentuation)
Intensity: small= louder (thrill)
Pulmonary HTN
Wide Splitting of S2
UPMC Heart and Vascular Institute
DIASTOLIC MURMURS Increased flow x MV
Severe MR Large left to right shunt
VSD PDA
Increased flow x TV Severe TR ASD (> 2: 1 shunt) Carey Coombs
Pathologic Obstruction MS, TS Myxoma
Relative Obstruction Austin Flint
UPMC Heart and Vascular Institute
10/7/2016
18
AORTIC INSUFFICIENCY Decrescendo: High Pitched
Location: 2nd RICS to LLSB
Positon: Sit up, lean forward, end expiration
Acute vs. Chronic
Bisferians Pulse
Shaver et al, Auscultation of the Heart, AHA, 1990 UPMC Heart and Vascular Institute
ACUTE VS. CHRONIC
REDDY, P.S. AHA MONOGRAPH #46, 1975
Examination of the Heart Part 4 Auscultation. AHA 1990 Shaver et al UPMC Heart and Vascular Institute
10/7/2016
19
Peripheral Signs of AorticInsufficiency carotids‐bisferiens (two upstrokes)
peripheral‐Corrigans (pistal shot) (waterhammer pulse)
peripheral‐Derozier (to/fro murmur bystethoscope pressure)
De Musset‐ head bobbing
Muellers‐bobbing uvula
BP wide pulse pressures
Quinckes pulses
UPMC Heart and Vascular Institute
MITRAL STENOSIS Opening Snap
Early diastolic with pre‐systolic accenuation
Location: apex
Low frequency rumble
Loud S1
Loud P2
A2‐OS intervel
Best: left lateral, Bell
Shaver et al, Auscultation of the Heart, AHA, 1990UPMC Heart and Vascular Institute
10/7/2016
20
A2‐OS INTERVAL
http://www.texasheart.org‐modified UPMC Heart and Vascular Institute
CONTINUOUS MURMUR
‐PDA‐SINUS OF VALSALVA ANEURYSM RUPTURE
‐AS/AI
Shaver et al, Auscultation of the Heart, AHA, 1990UPMC Heart and Vascular Institute
10/7/2016
21
PERICARDIAL FRICTION RUB Scratchy, leathery, high frequency
Location: LLSB, Xyphoid
3 Components
Ventricular systole
Early diastole
Late diastole (atrial systole)
UPMC Heart and Vascular Institute
BEDSIDE MANEUVERS Amyl Nitrate
Decrease preload and afterload
Deeper Inspiration Increase preload
All right sided events will increase except the ejectionsound of PS.
Leg raising Increase preload
Exercise Increased flow
UPMC Heart and Vascular Institute
10/7/2016
22
BEDSIDE MANEUVERS Standing
Decrease venous return
Reflex increase in HR
Squatting Increase Afterload
Increase Venous Return
Isometric Hand/Arm Increase SVR, BP, HR
40‐50”
Don’t Valsalva, breath normally
Contraindicated: recent MI, CVA, Ao Dissection
UPMC Heart and Vascular Institute
VALSALVA MANEUVER Forced expiraton against a closed glottis Phase I‐ increase intra‐pleural pressure & decrease invenous return
Phase II‐ decrease in heart size, SV, mean arterioal BP, &increase in HR
Phase III‐ further drop in BP at termination of strain, thenreflex baroreceptor response
Phase IV‐ increase venous return, increase SV, CO, arterialBP
10‐12” Assistance: push on abdomen, bear down against hand
blow out against thumb with forced expiration
UPMC Heart and Vascular Institute
10/7/2016
23
SYSTOLIC MURMURS INCREASED INTENSITY DECREASED INTENSITY
AORTIC STENOSIS PASSIVE LEG RAISEPOST PVC PAUSEAMYL NITRATESUDDEN SQUATTING
VALSALVA ISOMETRIC HAND GRIP
HOCM VALSALVASTANDINGAMYL NITRATE
SUDDEN SQUATTINGPASSIVE LEG RAISEISOMETRIC HAND GRIP
MVP VALSALVASTANDINGAMYL NITRATE
SUDDEN SQUATTINGPASSIVE LEG RAISEISOMETRIC HAND GRIP
PULMONARY STENOSIS AMYL NITRATEVALSALVA RELEASEPASSIVE LEG RAISEINSPIRATIONSUDDEN SQUATTING
STANDING
MITRAL REGURITATION SUDDEN SQUATTINGISOMETRIC HAND GRIP
AMYL NITRATE
TRICUSPIED REGURGITATION INSPIRATIONPASSIVE LEG RAISE AMYL NITRATESUDDEN SQUATTING
STANDING
VSD SMALLWO PULM HTN ISOMETRIC HAND GRIP AMYL NITRATE
VSD LARGE W PULM HTN AMYL NITRATE ISOMETRIC HAND GRIP
UPMC Heart and Vascular Institute
DIASTOLICMURMUR INCREASED INTENSITY DECREASED INTENSITY
AORTIC INSUFFICIENCY SUDDEN SQUATTINGISOMETRIC HAND GRIP
AMYL NITRATE
PULMONICINSUFFICIENCY
INSPIRATION AMYL NITRATESUDDEN SQUATTING
MITRAL STENOSIS EXERCISEISOMETRIC HAND GRIPAMYL NITRATE
TRICUSPID STENOSIS INSPIRATIONPASSIVE LEG RAISEISOMETRIC HAND GRIPAMYL NITRATESUDDEN SQAUTTING
EJECTION SOUND OF PULMONIC STENOSIS
INSPIRATION
S3 & S4 PASSIVE LEG RAISEISOMETRIC HAND GRIP(50% IN CAD/CHF)
STANDINGVALSALVA
UPMC Heart and Vascular Institute
10/7/2016
24
CONCLUSION I JUST TOOK THE HIGHLIGHTS FROM THE
LECTURE AS I ONLY HAD 20 MINUTES
FOR THE BOARDS
KNOW THE DIFFERENCE BETWEEN ACUTE VS.CHRONIC
WHAT MANEUVERS DO TO THE MURMUR
KNOW WHICH CLINCAL/AUSCULTATIVE FINDINGSPREDICT SEVERITY OF LESION
UPMC Heart and Vascular Institute
UPMC Heart and Vascular Institute
10/13/2016
1
MatthewHarinstein,MD,FACC,FASE,FASNCAssistantProfessorofMedicineUniversityofPittsburghSchoolofMedicineChief,Cardiology,UPMCMcKeesportCo‐Director,NoninvasiveImaging,UPMCShadysideUPMCHeartandVascularInstitute
Aortic Valve OverviewWhen is it Appropriate to Intervene?
• No conflicts of interest to declare
Disclosures
10/13/2016
2
• Epidemiology
• Pathophysiology
• Clinical presentation and physical exam
• Diagnostics and imaging
• When to intervene?
Aortic Stenosis: Overview
• Senile Calcific Aortic Stenosis- most common
• Rheumatic Valve Disease– Mitral involvement more common
• Congenital Heart Disease- more common inyounger patients
• Bicuspid Aortic Valve
• Most common form resemble accelerated SenileCalcific Aortic Stenosis (Present in 40’s, 50’s and60’s)
Aortic Stenosis: Epidemiology
10/13/2016
3
• 1-2% of generalpopulation
• Familial with autosomaldominance withincomplete penetrance– Incidence can be up to
10% in affected families
• Associated withaortopathy; Evaluateascending aortic size
Bicuspid aortic valve
• Mechanism of stenosis is similar to atherosclerosis1
– Mainly solid calcium deposits within the valve cusps
– Similar risk factors to Coronary Artery Disease (CAD)
– High coincidence of CAD and AS in same individual2
– Present in 60’s, 70’s, and 80’s
Aortic Stenosis: Senile degenerative
1Otto CM, Lind BK, et al. Circulation 1994; 90: 844-53.
2Otto CM, Lind BK, et al. New Eng J Med 1999; 341: 142-147.
10/13/2016
4
Aortic Stenosis
Outflow obstruction
Reduced coronary blood flow
Increased Afterload
LVH
Diastolic Heart Failure
O2 mismatch
↑ Demand
↓ Supply
Aortic Stenosis: Pathophysiology
Subendocardial ischemia
Pulmonary congestion
• Angina– Often complicated by concomitant coronary
artery disease
• Syncope– Exertional syncope
• Signs and symptoms of heart failure– Portends worst prognosis
Aortic Stenosis: Clinical Presentation
10/13/2016
5
Pellikka et al, Circulation 2005;111:3290‐3295
% ofPatients
Years of Follow-up
1 year: 82%2 years: 67%5 years: 33%
Survival Free of Symptoms
100
80
40
20
0
60
0 1 2 3 4 5 6 7 8 9 10
Markers of poor outcome:1. Advanced age2.Heavy Ca++
3.Velocities >4m/sec
Aortic Stenosis: Clinical Presentation
• Systolic ejection murmur– Crescendo-decrescendo
– Timing of the murmur correlates with severity ofstenosis (i.e. later the peak of the murmurworse the stenosis)
– Absent A2 is associated with more significantstenosis
• Tardus et parvus pulse
Aortic Stenosis: Physical examination
10/13/2016
6
• Assess LV size, dimensions and function
• 2D planimetry, if possible
• LVOT diameter, spectral Doppler of LVOT and AoV
• Location of the stenosis– Supravalvular
– Valvular
– Subvalvular
• Evaluate aortic regurgitation, coexistent mitral valvedisease and stroke volume
Aortic StenosisDiagnostics and Imaging: Echocardiography
Baumgartner et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice
Indicator: Mild Moderate Severe
Jet velocity (m/s) <3.0 3.0–4.0 >4.0Mean gradient (mmHg) <25 25–40 >40Valve area (cm2) >1.5 1.0–1.5 <1.0Valve area index <0.6
(cm2/m2)
Dimensionless Index < 0.25
Aortic Stenosis: Severity
Nishimura et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease. J Am Coll Cardiol 2014;63:e57-185.
10/13/2016
7
• 87 year old male
• PMHx: Coronary artery disease s/p PCI, hypertension anddyslipidemia
• Lives independently but chores have been more difficult andhe has noticed dyspnea on exertion with mild chestdiscomfort
• SPECT study revealed no ischemia with preserved ejectedfraction
• Echocardiogram was ordered
Aortic StenosisCase
Aortic StenosisEcho Evaluation
10/13/2016
8
Aortic StenosisEcho Evaluation
2 .
• 2 .
• 2 . . .
.0.6cm2
•
. /
. /0.22
• Therefore…SEVEREAorticStenosis
Aortic StenosisEcho Evaluation
10/13/2016
9
Ross J Jr, Braunwald E. Aortic stenosis. Circulation. 1968;38 (Suppl 1):61-7.Bonow RO, et al. Management strategies and future challenges for aortic
valve disease. Lancet 2016;387:1312-23.Kapadia SR, et al. 5-year outcomes of transcatheter aortic valve replacement
compared with standard treatment for patients with inoperable aortic stenosis (PARTNER 1): a randomised controlled trial. Lancet 2015;385:2485–91.
Aortic Stenosis: When to Intervene?
Aortic Stenosis: When to intervene
From: 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63(22):2438-2488. doi:10.1016/j.jacc.2014.02.537
10/13/2016
10
• Low dose dobutaminestress echo:
– Start at 2.5-5 mcg/kg/minwith incremental increaseup to 10-20 mcg/kg/min atapproximately 5 minuteintervals
Aortic Stenosis: Low Flow-Low GradientStress Echo Evaluation
Picano et al. The Emerging Role of Exercise Testing and Stress Echocardiography in Valvular Heart Disease. J Am Coll Cardiol. 2009;54(24):2251-2260.
• Etiology
• Pathophysiology
• Clinical presentation
• Physical exam
• Diagnostics and imaging
• When to intervene?
Aortic Regurgitation: Overview
10/13/2016
11
• Valvular– Degenerative/calcific
– Bicuspid
– Endocarditis
– Rheumatic
– Connective tissue disease
– Anorectic drugs
• Ascending Aortic– Degenerative
– Type A Dissection
– Marfan’s Syndrome
– Inflammatory
– Giant Cell Arteritis
• More common causes ofAcute AR:– endocarditis, aortic dissection,
blunt trauma and proceduralcomplications
• More common causes ofChronic AR:– idiopathic root dilatation,
congenital abnormalitiesincluding bicuspid valve,endocarditis, rheumatic anddegenerative valve disease
Aortic Regurgitation: Etiology
• Sudden large regurgitantvolume into the LV resulting in increased LVEDV, LVEDP, LAP and thus preload
• No acute LV enlargement, thusthere is an acute reduction in stroke volume
• Characterized by pulmonarycongestion, reduced CO, decreased BP and cardiogenic shock
• May be asymptomatic for aprolonged period of time as LV compensates and dilates
• Eventually there is increasedwall stress and the LVEDV continues to rise and the LVEF falls
• Commonly presents withdyspnea and reduced functional capacity
Aortic Regurgitation:Pathophysiology/Clinical Presentation
Acute Chronic
10/13/2016
12
• High-pitched decrescendodiastolic murmur
• May have ejection systolicflow murmur
• Possible S3 gallop
• Austin Flint murmur- low-pitched diastolic rumble dueto displacement on theanterior mitral valve leafletfrom the AR jet andturbulence from mixing of theAR jet and MV inflow
Aortic Regurgitation: Physical Exam
http://www.texasheart.org/Education/CME/explore/events/HSPS_aortic_regurg.cfm
• Few signs
• Quiet diastolic murmur
• Diastolic murmur
• Austin Flint murmur
• Bisferiens pulse- double peak pulse
• Wide pulse pressure
• Water hammer pulse
• Head nodding (de Musset’s sign)
• Capillary pulsation (Quincke’s)
• Rapid carotid upstroke and collapse(Corrigan’s pulse)
• “Pistol shot” femoral (systolic)(Traube’s)
• Diastolic murmur over femoral whencompressed with bell (Duroziez’s)
Aortic Regurgitation: Physical Exam
Acute Chronic
10/13/2016
13
• 2D examination for etiology: valvular versus aorticroot related
• Assess LV size and systolic function
• Severe aortic regurgitation– Vena contracta width > 0.6 cm
– AR color jet width/LVOT diameter (≥ 65%)
– Regurgitant volume ≥ 60 mL
– Regurgitant fraction ≥ 50%
– EROA ≥ 0.30 cm2
– Holodiastolic flow reversal in proximal descendingthoracic aorta
– Steep PHT < 200-250 ms
Aortic Regurgitation: Diagnostics and ImagingEcho assessment
Zoghbi et al. Recommendations for Evaluation of the Severity of Native Valvular Regurgitation with Two-dimensional and Doppler Echocardiography. J Am Soc Echocardiogr 2003;16:777-802.
Aortic Regurgitation
10/13/2016
14
Aortic regurgitation: When to Intervene
THANK YOU
10/11/2016
1
Dustin Kliner, MDClinical Assistant Professor of Medicine
Interventional Cardiology
UPMC Presbyterian/Shadyside
INTRODUCTION TO TAVR
DISCLOSURES
• Coinvestigator in trials involving Medtronic Evolut, Boston Scientific Lotusand St. Jude Portico
• No financial disclosures
10/11/2016
2
OBJECTIVES
• Examine the guidelines regarding use of TAVR in severe, symptomatic AS
• Illustrate the FDA approved devices
• Review the landmark trials leading to FDA approval for each device/use
• Discuss the delay between FDA approval and inclusion to availableguidelines
AORTIC STENOSIS IN THE ELDERLY
• Retrospective cohort study of 277 patients from a large university databasewith doppler derived AVA of ≤0.8cm2 and age >80
• Age 85 ±4 years, 53% male, AV area 0.68 �± 0.16 cm2, EF 52 �± 20%,CAD 47%, diabetes 17%
• Mean follow up of 2.5 years, during which 55 (20%) had AVR and 175deaths occurred
• In patients with AVR – 1-year, 2-year and 5-year survival rates were 87,78 and 68% respectively
• In patients without AVR - 52, 40 and 22%, respectively ( p < 0.0001)
Varadajan P et al. European Journal of Cardio-thoracic Surgery 30 (2006) 722—727
10/11/2016
3
AORTIC STENOSIS - SYMPTOMS
• Especially in TAVR patients, difficult to elicit, and can be nonexistent
• CHF – try to assess NYHA class
• Ask family members – Can they still keep up?
• If they don’t have CHF, why are they on Lasix?
• Syncope/Presyncope
• Angina – Late, ? CAD
• Fatigue?
TIMING OF INTERVENTION
Nishimura et al. 2014 AHA/ACC Valvular Heart Disease Guideline: Executive Summary
10/11/2016
4
Nishimura et al. 2014 AHA/ACC Valvular Heart Disease Guideline: Executive Summary
HISTORY OF TAVR
• Initially based on the observation that low pressure balloon inflation duringBAV opened the AV in a circular fashion, restenosis occurred soon after
• Started with stent placement in the AV in animals, and autopsy studiesshowing expansion
• A small startup in New Jersey began working on a transcatheter valve
• First human implant on April 16, 2002 in France, Dr. Alain Cribier
• 57 year old, EF 12%, inoperable, presenting with cardiogenic shock
• In 2004 the small startup was acquired by Edwards Lifesciences
10/11/2016
5
PARTNER
• First randomized trial of TAVR
• 358 patients in 17 centers with AVA <0.8cm2 and AV peak velocity >4 or MG>40mmHg with class II, III, or IV CHF were divided into two cohorts
• Cohort A - Operable despite high STS for mortality of 10% or greater
• Cohort B – Inoperable because of predicted 30 day mortality of 50%
• Exclusion criteria included bicuspid valves, AMI, CAD requiringrevascularization, EF < 20%, Severe MR or AI, TIA or CVA within 6 months,ESRD
• Those randomized to TAVR were treated with Edwards Sapien Valve
N Engl J Med 2010; 363:1597-1607
PARTNER
• Cohort B – Results
• AT 1 year, death rate was 30.7% with TAVI, 50.7% with standard medicaltherapy, 83.8% of which received BAV (hazard ratio with TAVI, 0.55; 95%confidence interval [CI], 0.40 to 0.74; P<0.001).
• The rate of the composite end point of death from any cause or repeathospitalization was 42.5% with TAVI as compared with 71.6% withstandard therapy (hazard ratio, 0.46; 95% CI, 0.35 to 0.59; P<0.001).
• At 30 days, TAVI, as compared with standard therapy, was associatedwith a higher incidence of major strokes (5.0% vs. 1.1%, P=0.06) andmajor vascular complications (16.2% vs. 1.1%, P<0.001).
N Engl J Med 2010; 363:1597-1607
10/11/2016
6
PARTNER – COHORT B
• TAVR better than nothing in inoperable patients
• Given the survival with “medical therapy”, this is not surprising
• What about TAVR vs SAVR?
PARTNER – COHORT A
• Multicenter, open-label, randomized controlled trial.
• 699 high-risk, symptomatic patients (median age=84.1) with severe aorticcalcific stenosis were randomized to either TAVI (n=348, 244 TF and 104 TA)or surgical AVR (n=351).
• TAVI vs surgical AVR:
• Mortality 30 days (3.4% vs. 6.5%, p=0.07) 1 year (24.2% vs. 26.8%,p=0.44)
• CVA 30 days (3.8% vs. 2.1%, p=0.2) 1 year (5.1% vs. 2.4%, p=0.07)
N Engl J Med 2011; 364:2187-98
10/11/2016
7
PARTNER – COHORT A
N Engl J Med 2011; 364:2187-98
COREVALVE PIVOTAL
• 795 patients underwent randomization at 45 centers in the United States.
• Severe AS was defined as AVA <0.8cm2 or indexed AVA < 0.5cm2, MG >40mmHg or AVA peak velocity >4m/s.
• High risk defined as 30 day mortality of 15% or greater as determined byestimated STS and “other factors” and agreed upon by 2 CT surgeons andone IC
• Death from any cause at 1 year was significantly lower in the TAVR groupthan in the surgical group (14.2% vs. 19.1%), P<0.001 for noninferiority; P =0.04 for superiority)
N Engl J Med 2014; 370:1790-1798
10/11/2016
8
CHOICE OF INTERVENTION
Nishimura et al. 2014 AHA/ACC Valvular Heart Disease Guideline: Executive Summary
AND VALVE IN VALVE…
• Edwards Sapien XT, Sapien 3, and Medronic Evolut are indicated for TAVRinside degenerated SAV
• Can be done for AS, AI, or a combination of
• Must be high risk for surgery (STS >8%)
• The type and size of the prior prosthesis must be known
• 19mm prosthesis are too small for TAV in SAV and not recommended (itsbeen done elsewhere, the mean gradients immediately post op are high20s)
• Cannot be done for mechanical valves
10/11/2016
9
GLOBAL VALVE-IN-VALVE REGISTRY
• 202 patients with degenerated bioprosthesis from 38 centers
• 42% (n=85) AS, 34% (n=68) AI, 24% (n=49) combined
• Successful implant 93.1% of cases, complications included malposition(15.3%) and coronary ostial obstruction (3.5%)
• Implanted devices – Corevalve (n=124) and Sapien (n=78)
• Mean gradient post implant 15.9 ±8.6mmHg
• 30-day follow up, all cause mortality 8.4%
• 1-year follow up, survival 85.8%
Dvir et al. Circulation. 2012;126:2335-2344
TAV IN SAV
10/11/2016
10
FDA APPROVAL• Edwards Sapien – November 2, 2011 – Inoperable – Partner B
• Edwards Sapien – October 19, 2012 – High risk (STS >8% mortality or >15%mortality at 30 days) – Partner A
• Medtronic CoreValve – January 2014 - High risk (STS >8% mortality or >15%mortality at 30 days) – CoreValve Pivotal
• Edwards Sapien XT – June 16, 2014
• Medtronic CoreValve – March 30, 2015 – Valve in valve
• Medtronic Evolut – June 2015
• Edwards Sapien 3 – June 17, 2015
• Edwards Sapien XT – October 15, 2015 – Valve in valve
• Edwards Sapien XT/Sapien 3 – September 2016 – Intermediate risk (STS >3%mortality)
FDA APPROVED DEVICES
A. Medtronic CoreValve. B. Medtronic Evolut. C. Edwards Sapien XT. D. Edwards Sapien 3
10/11/2016
11
IS MY PATIENT GOING TO BENEFIT FROM TAVR?
WHERE DO WE GO FROM HERE?
• Guidelines certainly do not keep up with available data
• New products or updated generation of products are common
• New patient populations have been shown to derive benefit
• TAV-in-SAV and intermediate risk approval are new since the mostrecent guidelines
• Low Risk patients are now being investigated
10/11/2016
12
INVESTIGATIONAL DEVICES
• Here
• Medtronic Evolut – Low Risk patients
• Medtronic Evolut - Intermediate risk patients
• St. Jude Portico – High risk patients
• Boston Scientific Lotus – High risk patients
INTERMEDIATE RISK
• PARTNER 2
• 2032 intermediate risk patients randomized to SAVR or TAVR
• Primary end point was death or disabling stroke
• Rate at 2 years 19.3% in the TAVR group, 21.1% in the SAVR group
• In transfemoral access cohort, TAVR rate of death or disabling CVA waslower (HR 0.79, 0.62-1.00, p=0.05)
• TAVR resulted in lower rates of bleeding, AKI, Afib
• Surgery had fever vascular complications and less PVL
Leon et al. N Engl J Med 2016;374:1609-20
10/11/2016
13
CONCLUSIONS
• TAVR is a viable alternative to SAVR in patients at prohibitive or high risk forconventional surgery
• TAVR is probably equivalent to SAVR in intermediate risk patients, especiallywhen iliofemoral access is available.
• Technology and use are evolving rapidly, and guidelines cannot keep up withdaily clinical practice
• Long term studies regarding valve durability are needed, and are underway
Paradoxical low flow, low gradient, severe AS
10/15/2016 RRachel Hughes-Doichev, M.D., FASE
Assistant Professor of Medicine Temple University School of Medicine Medical Director of Echocardiography
Allegheny General Hospital. AHN
Pittsburgh, PA
“ I have no disclosures.” O Rachel Hughes-Doichev, M.D., O 10/15/2016
Stages of Aortic Stenosis O A. At risk of AS (Bicuspid, sclerotic,
Vmax < 2m/s), No symptoms
O B. Progressive AS (Mild AS, Mod AS), No symptoms
O C. Asymptomatic Severe AS O C1. Normal LVEF O C2. Reduced LVEF (< 50%)
O D. Symptomatic Severe
Stage D Symptomatic Severe AS
O D1. High Gradient
O D2. Low Flow/Low Gradient, reduced LVEF
O DD3. Low Flow/Low Gradient with normal LVEF or paradoxical low flow severe AS
Stage, Definition, Sx
Valve Anatomy Valve Hemodyn Hemodyn Consequenc
Stage D: (SS)AS HF, angina, syncope, presyncope, exertional sx
AVA<=1.0 cm2 or AVAi <=0.6cm2/ms
Nishimura et al 2014 ACC/AHA Valvular HD Guidelines
D1, High Gradient
Severe leaflet Calcification.or congenital w/ Severely reduced leaflet opening
AVVmax >= 4m/s or mean grad >=40 mm Hg AVA may be larger if mixed AS/AR
-LV DD -LVH -poss PH
D2, LFLG reduced LVEF
Same as D1 but no congenital
AVVmax <4m/s or Mean grad < 40 mm Hg DSE shows AVA <1 cm2 with Vmax >=4 m/s at any flow rate
-LVDD -LVH -LVEF <50%
D3, LFLG Preserved LVEF (50%) “Paradoxical”
same as D2 SVI <35 mL/m2
Measured when SBP < 140 mm Hg
-Severe conc remodeling Small LV chamber -Low SV Restrictive DF LVEF >=50%
Definition of paradoxical LF LG SAS
O Severe AS– O AVA <=1.0 cm2 or AVAi<= 0.6 cm2/m2
O Low gradient- O Mean AVG < 40 mm Hg
O Low flow- O SVI < 35 mL/m2 3.14 * (LVOTrad)sq *LVOT vti / BSA
O Preserved LVEF- O LVEF>=50%
Incidence O Reported incidence 55-25% of severe AS
cases O Increased prevalence: O older age O Women O HTN O Metabolic syndrome O DM
Pibarot P ,Dumensil JG JACC.2012; 60:1845-53
Pathology(purists/splitters) O Pronounced concentric remodeling of the LV
with development of mmyocardial fibrosis(shown by MRI studies)
O Reduction in LV size, filling, and compliance
O Decreased Stroke Volume due to impaired filling and abnormal LV emptying
Doppler Echo Findings LV AV
O EF >=50% O Small LV size O RWT >0.5 O Diastolic dysfunction O Reduced GLS O Low SVI ( < 35 mL/m2
O Severely calc/thick leaflets with decreased opening
O AVA < 1.0 cm2, AVAi<0.6 cm2/m2, DVI< 0.25
O Mean Grad< 40 mm Hg O Valvulo-arterial
impedance > 4.5 mm Hg/mLm2
Zva=( SBP + mean AV grad) / SVI----(mmHg/mL/m2)
ASE’s Comprehensive Echocardiography. 2nd Edition
Contrasts with High Gradient and LFLG rEF SAS O HHigh Gradient: O LVH develops with normal LV chamber size
and normal stroke volume
O LF LG Reduced EF: O Dilated LV with reduced LVEF
Pathology of Paradoxical LFLG AS
Pibarot and Dumesnil JACC 2012;60:1845-53
Preserved LVEF does not mean normal LV systolic function
Patients with Paradoxical LFLG SAS have been shown to have decreased LV global longitudinal strain in several studies (<-15%)
Adda J et al. Circ Cardiovasc Imaging, 2012. 5:27-35
O 16 pts with paradoxical low flow low grad severe AS were identified from a group of 103 pts with severe AS and normal LVEF.
O Low flow defined as SVI < 35 mL/m2 by echo Doppler data.
O LF group found to have worse functional status, lower GLS, lower AVA, and higher valvuloarterial impedance than normal flow group.
Lee SP et al. JASE.2011;61:1799-1808
NNormal Flow Low Flow
Lee SP et al. JASE.2011;61:1799-1808
Natural History
O Paradoxical LF/LG AS (D3) portends a worse prognosis than High Gradient (D1)
O Study looked at prognostic implications of flow state with severe AS
O 1704 consecutive pts with severe AS (AVA < 1.0 cm2 and preserved EF(>=50%)
O Divided into 4 groups based on flow and gradient: O Low flow (SVI < 35 mL/m2) O Low grad (mean grad < 40 mm Hg)
Eleid et al. Circ 2013;128:1781-89
Results O NF/LG ( 352=21%) had best 2 year survival,
82% O NF/HG had 67% 2 year survival O LF/LG (53=3%) had 60% 2 year survival O LF/LG had lower LVEF in general, more atrial
fibrillation, heart failure, and reduced arterial compliance.
O LF/LG was the strongest predictor of mortality in multivariate analysis ( HR 3.26, 95% 1.71-6.22, P<0.001) vs. NF/LG
Eleid et al. Circ 2013;128:1781-89
Eleid et al. Circ 2013;128:1781-89
Eleid et al. Circ 2013;128:1781-89
Excluded patients O Prosthetic valves O HCM O Complex congenital O Supra or sub-aortic stenosis O MModerate or more severe valvular lesions----
may account for some of decreased prevalence of paradoxical LF LG pts in this study.
Eleid et al. Circ 2013;128:1781-89
Surgical Outcomes
O AVR afforded a 69% reduction in mortality for LF/LG and NF/HG
O ( HR 0.31, 95% 0.25-0.39, P<0.0001)
Eleid et al. Circ 2013;128:1781-89
Survival improved with AVR in Paradoxical LFLG SAS
AA. n=101 pts B. Propensity score matched-61 pts
Tarantini G et al Annals of Thor Surg.2011 91(6),1808-15
Myriad causes of LF pEF state ( Non-Purists—Lumpers)
Pibarot et al. Circ 2013.128:1729-32
Diagnosis O YYou must make sure the AS is truly severe.
O 1.Is the SV accurately measured by echo? O LVOT diameter measurement error is most
common: O LVOT diameter measured at base of AV
cusps
O LVOT PW sample volume in correct position O Verify measurements with another modality
Correct LVOT Measurement
MMeasure LVOT diameter in systole. Zoomed view. Measure at the level of the aortic leaflet insertion point at the septum and anterior leaflet
Clavel et al. JACC CV Imag;8(3):248-57
Diagnosis O 22.Are there other pathologies contributing to
low stroke volume?
O mitral regurgitation/stenosis, atrial fibrillation, tricuspid regurgitation, systemic arterial hypertension
Myriad causes of LF pEF state ( Non-Purists—Lumpers)
Pibarot et al. Circ 2013.128:1729-32
Diagnosis O 33. Is the patient hypertensive?
O HTN may contribute to symptoms and LF.
O Blood pressure should be optimized (SBP < 140 mm Hg) and the echo should be repeated to confirm AS severity
Diagnosis O IIs the AS truly severe?
O ?Role for DSE to assess AS at normalized stroke volume---Maybe.
O ?Role for MDCT to assess severity of AV leaflet calcification—Yes
ACC/AHA 2014 VHD Guidelines regarding paradoxical LF LG AS
O ““If the degree of valve calcification cannot be adequately assessed on TTE, TEE, CT imaging, or fluoroscopy may be considered.
O The patient should be evaluated for other potential causes of symptoms to ensure that symptoms are most likely due to valve obstruction.”
AVA by CT vs. Echo O AVA by CT is generally 0.1-0.2 cm2 larger than that
determined by echo due to LVOT area being more elliptical in shape.
O Severe AS by echo is AVA <=1.0 cm2 O Severe AS by CT is AVA <=1.2 cm2.
O Discrepancies in Echo guidelines definition. O AVA of 1.0 cm2 corresponds to mean pressure
gradient of 30-35 mmHg. O AVA 0.8 cm2 corresponds to mean grad of 40 mm
Hg.
Recommendations for Surgery
O If the AS is thought to be truly severe, and the patient is symptomatic --
O Class II A, level of evidence C recommendation for AVR or TAVR
ACC/AHA 2014 Valvular Heart Disease Guidelines
O Class IIa: O “AAVR is reasonable in symptomatic pts with low-flow/low-
gradient severe AS (stage D3) with an LVEF 50% or greater, a calcified aortic valve with significantly reduced leaflet motion, and a valve area 1.0 cm2 or less oonly if clinical, hemodynamic, and anatomic data support valve obstruction as the most likely cause of symptoms and data recorded when the patient is normotensive (SBP < 140 mm Hg) indicate ( Level of Evidence C):
O A. An AV V max < 4 m/s or mean grad < 40 mm Hg; and O B. SVI < 35 mL/m2; and O C. An indexed AVA 0.6 cm2/m2 or less
Case Study
Nishimura RA. ACC/AHA VHD Guidelines.JACC 2014
Nishimura RA et al. JACC 2014
Ongoing Study O Strain studies O Amyloid
Board Review Q1 O In which of the following patients is it
recommended to perform a DSE to assess AS severity?
O A. A O B. B O C. C O D. D
Copyright © The American College of Cardiology. All rights reserved.
From: Imaging of Low-Gradient Severe Aortic Stenosis
J Am Coll Cardiol Img. 2013;6(2):184-195. doi:10.1016/j.jcmg.2012.11.005
A. Normal LVEF, Normal Flow, High Gradient
B. Normal LVEF, Low Flow, Low Gradient
C. Normal LVEF, Normal Flow, Low Gradient
D. Decreased LVEF, Low Flow, Low Gradient
Copyright © The American College of Cardiology. All rights reserved.
From: Imaging of Low-Gradient Severe Aortic Stenosis
J Am Coll Cardiol Img. 2013;6(2):184-195. doi:10.1016/j.jcmg.2012.11.005
Copyright © The American College of Cardiology. All rights reserved.
J Am Coll Cardiol Img. 2013;6(2):184-195. doi:10.1016/j.jcmg.2012.11.005
CopCopCopCopCopCopCopopCopCopCopopCopCopCopopopCopCopCopCopCopCopCopCopCopCoppopCopCoppCoppCopCoppCopopppCopCopopCopCopCopCoppopopopopCoppopCopCopCopCopCopopppopopopCopopppCoppCoppCopCopCopppCoppopCoppCopCopppopppCoCoCoCoCoCoCoCooCooCoCoooCoCoooCoooooooCooCooooCoCooCoCoooooCoCooCoooCoCoooooooooCoCoooCoCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCC yriyriyriyriyriiyriyriyriyriyriyriyriyriyriyririyriiiriiriyriyriiririiiriyriyriiyriyriiiiyriiiriyriiyriyriiiririyryryryrrrryryrrryrrryrrrryrrrrryryryryryryryryrryryyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyy ghtghttghtghtghttttghtghththtghthtghthttthtthtthtghtghtghtghtghtghttthttghtghtghtghtghtghtghtghthttghthtghtgghtghthtghtghtghtghtghtghthtghttghtghttghthtghtghtghtghtghtghtghtghtghtghthtghttghtghtghtghththtghttghthghhhghhhghhhhghghghhhhghhhghghghhghghhhghghhhhhhhhhghghghhghghghhghhghghhhhghghhhhhhgggggggggggggggggggggggggggggggggggggggggggggggggg ©©© ©©©©©© ©©©©©©© ©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©© eeeeeeeeTheeTheTheeTheeheTheTheheTheehThThThThThhhhThhhThhThThThhhThThThThhThThThThhThThThThhThhhThhhhThhhhThhThThhThThThThThhThhTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTT American College of Cardiology. CopCopCoppopCoppCoppppppCopCoppppooooCCooooCoCoooooCCC yriyriyriyryyyyyyyyyyyyyyyyy ghtghttthg ©©©© eeeeeeeeeeTheTheThehTTTTTTTTT American College of CardiologyAllAllAllAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA iii hththt ddd
Copyright © The American College of Cardiology. All rights reserved.
From: Low-Flow, Low-Gradient Aortic Stenosis With Normal and Depressed Left Ventricular Ejection Fraction
J Am Coll Cardiol. 2012;60(19):1845-1853. doi:10.1016/j.jacc.2012.06.051
CT Calcium Score may be of benefit
Board Review Q2
O 75 year old woman with h/o DM, HTN, AS and diastolic heart failure comes in with worsening exertional SOB.
O HR 88 bpm, BP 160/90 mm Hg, BSA 2.2 m2 O Cardiac exam reveals. Normal JVP O 2/6 late peaking SM with radiation to the carotids, single S2,
no S3 O EEcho shows the following: O Normal LV size, LVH, LVEF 55%, calcified AV leaflets with
greatly decreased leaflet mobility O LVOT diam1.9 cm; LVOT VTI 16 cm O AV VTI 66 cm O Peak AV grad 55 mm Hg; mean AV grad 26 mm Hg O 1+ AI, 1+ MR, 1+ TR
What would be the most appropriate next step
O A. Refer for Surgical Consultation for AVR or TAVR
O B. Dobutamine Stress Echo to assess for severe AS
O C. Control blood pressure and repeat the echocardiogram
O D. Continue current medical therapy
O E. Add lasix to the patient’s regimen.
What would be the most appropriate next step
O A. Refer for Surgical Consultation for AVR or TAVR
O B. Dobutamine Stress Echo to assess for severe AS
O C. Controlling blood pressure and repeating the echocardiogram
O D. Continue current medical therapy
O E. Add lasix to the patient’s regimen.
ACC/AHA 2014 Valvular Heart Disease Guidelines
O Class IIa: O “AAVR is reasonable in symptomatic pts with low-flow/low-
gradient severe AS (stage D3) with an LVEF 50% or greater, a calcified aortic valve with significantly reduced leaflet motion, and a valve area 1.0 cm2 or less oonly if clinical, hemodynamic, and anatomic data support valve obstruction as the most likely cause of symptoms and data recorded when the patient is normotensive (SBP < 140 mm Hg) indicate ( Level of Evidence C):
O A. An AV V max < 4 m/s or mean grad < 40 mm Hg; and O B. SVI < 35 mL/m2; and O C. An indexed AVA 0.6 cm2/m2 or less
OTHANK YOU!!!
10/13/2016
1
1
William E. Katz, MD, FACC, FASE
Associate Professor of Medicine
Clinical Director of Echocardiography
The Pathoanatomy of Mitral Regurgitation
No Disclosures
The Mitral Valve Apparatus
Otto 2001;345:740-6
10/13/2016
2
Mitral Valve Scallops(Surgeon’s View / 3D TEE view)
WWW.VHLAB.UMN.EDU.
A1A2
A3
P1P2
P3C2
C1
Mitral Chordae
A1 A2 A3
P1
P2P3
AL PM
NORMAL BILLOWED/PROLAPSE FLAIL
RH
1
23
C
O’G
ara
JA
CC
Im
agin
g 2
008
Netter
WWW.VHLAB.UMN.EDU.
10/13/2016
3
• Pathoanatomic cause or mechanism of MRshould be described as primary or degenerative(annulus, leaflet, chordae tendiniae or papillarymuscle) or secondary (functional) due torestricted leaflet mobility and poor coaptationof otherwise normal leaflets
• Determining the mechanism guides theappropriate treatment, e.g mitral repair isrecommended for the asymptomatic primaryMR patient with high likelihood of success ifperfomed at a Heart Valve Center of excellence
Pathoanatomy of the Mitral Valve
5
Carpentier’s Classification of Pathology Causing Mitral Regurgitation
I: Annular dilatation Leaflet perforation
II: Excessive leaflet motion
III: Tethered leaflet motionA: RheumaticB: Ischemic
Filsoufi in Cohn Cardiac Surgery in the Adult 2003
10/13/2016
4
Primary
• Endocarditis / Perforation I
• Degenerative (Prolapse) II
• Rheumatic IIIA
• Congenital (clefts)
• Trauma
• Mitral annular calcification
• Tumors
• Radiation
Secondary (Functional)
• Nonischemic dilatedcardiomyopathy I
• Ischemic IIIB
• Hypertrophic cardiomyopathy
• Myocardial infiltrativediseases
Etiologies of Mitral Regurgitation
7
7.3. Chronic Primary MR
• 7.3.1.1. Diagnostic testing—initial diagnosis: Recommendations
Class I
• TTE is indicated for baseline evaluation of LV size and function, RVfunction and left atrial size, pulmonary artery pressure, and mechanism and severity of primary MR (stages A to D) in any patient suspected of having chronic primary MR. (Level of Evidence: B)
• TEE is indicated for evaluation of patients with chronic primaryMR(stages B to D) in whom noninvasive imaging provides nondiagnosticinformation about severity of MR, mechanism of MR, and/or status of LV function. (Level of Evidence: C)
Echo has a Central Role for Demonstrating the Mechanism of MR and Provides Other Measures that are Indications for Surgery
8
10/13/2016
5
Chronic vs Acute Mitral Regurgitation
Otto Textbook of Echocardioraphy
Natural History of MR
Carabello JACC 2008; 52:319
EF 66% EF 82%
EF 79% EF 58%
10/13/2016
6
• More common in undeveloped countries
• Younger patients pure MR
• Middle aged MS
• Older mixed
Rheumatic MR
11
• Abnormal systolic valve motion of the valve tip into the leftatrium (> 2mm beyond the mitral annulus).
• Most common cause of MR in the developed world
• Two distinctive types:– Barlow disease: Excessive myxomatous tissue which is an
abnormal accumulation of mucopolysaccharides resulting in thick,redundant billowed leaflets (body prolapses) and elongated chordae.Appears as bileaflet multisegmented prolapse. Diagnosed in youngadults and meet criteria for surgery in 4th or 5th decade
– Fibroelastic deficiency: due to abnormalities of connective tissueresulting in localized prolapse or elongated chordae or flail leafletdue to ruptured chordae. Present in the 6th decade with a shorthistory of MR
– Form Fruste: overlap of these 2 types: appear as fibroelasticdeficiency but subsequently have myxoid infiltration
Degenerative (MVP) Mitral Regurgitation
12
10/13/2016
7
3D TEE: MVP-Barlow’s Disease3D TEE-Multiple Leaflet Prolapse (Barlow’s)
Flail P2 Scallop Model: Fibroelastic Disease
10/13/2016
8
Post-op Systolic Anterior Motion
15
• Pathophysiologic outcome of ventricular remodeling arisingfrom ischemic heart disease– 20-25% of patient with acute MI
– Associated with worse outcomes due to worsened ventricularfunction, CHF and death
– Leaflet morphology is normal
– Outward and apical displacement of the posteromedial papillarymuscle occurs which tethers the mitral leaflets (posterior > anterior)into the LV restricting their ability to coapt at the annulus level.
– The annulus dilates and flattens and becomes essentially adynamicthroughout the cardiac cycle. Increases in anteroposterior dimension
– Leaflet growth occurs in an attempt to compensate for the decreasein leaflet coaptation.
Chronic Ischemic Mitral Regurgitation
16
10/13/2016
9
Mechanism of Ischemic MR
Levine NEJM 2004;1681
CHF
Evaluating Symptoms with < Severe MR: Exercise Echo Doppler
• Mitral regurgitation is dynamic with severitychanging with exercise / varying loadingconditions
• “exercise can…unmask the true severity ofwhat might otherwise be considered a mildlesion.” R. Levine NEJM 2004
10/13/2016
10
Class IIa
• Exercise hemodynamics with either Dopplerechocardiography or cardiac catheterization is reasonable insymptomatic patients with chronic primary MR where thereis a discrepancy between symptoms and the severity of MRat rest (stages B and C). (Level of Evidence: B)
• Exercise treadmill testing can be useful in patients withchronic primary MR to establish symptom status andexercise tolerance (stages B and C). (Level of Evidence: C)
Role of Exercise Testing
19
Requirements for Mitral Valve Repair
Alain Carpentier, pioneer ofmitral valve repair (1971):
1. “Understanding theanatomy and thepathology of the mitralvalve …
2. …excellent surgical exposure of the mitral valve by using large incisions in a patient’s chest wall to visualize the heart.”
10/13/2016
11
• Imaging is key for diagnosis of underlyingpathology
• Quantitation guides appropriate therapy
• Imaging is becoming integral tointerventions
• Follow up imaging can evaluate thesuccess of interventions
Pathoanatomy of Mitral Regurgitation Summary
21
10/13/2016
1
Mitraclip and Other Percutaneous Therapies for
Mitral RegurgitationAJ Conrad Smith, MD FACC FSCAI
University of Pittsburgh Medical Center
Indications for Surgery for Mitral Regurgitation
10/13/2016
2
Transcatheter Mitral Valve RepairMitraClip System
MitraClip® System
10/13/2016
3
Pre and Post Mitraclip
3D TEE with double orifice
10/13/2016
4
The MitraClip Clip Delivery System is indicated for the percutaneous reduction of significant symptomatic mitral regurgitation (MR ≥ 3+) due to primary abnormality of the mitral apparatus [degenerative MR] in patients who have been determined to be at prohibitive risk for mitral valve surgery by a heart team, which includes a cardiac surgeon experienced in mitral valve surgery and a cardiologist experienced in mitral valve disease, and in whom existing comorbidities would not preclude the expected benefit from reduction of the mitral regurgitation.
MitraClip® Indications
Transcatheter Mitral Repair
May be considered for prohibitive risk patients with primary MR and severe symptoms despite GDMT (class IIb)
ACC/AHA Guidelines – Primary MR
10/13/2016
5
MitraClip® Experience
EVEREST I Feasibility (n=55)
EVEREST II Pivotal Pre-Randomization (n=60)
HR Registry (n= 78)
Randomized (2:1 Clip to Surgery) (n= 279)
Worldwide Commercial Use: >15,000 patients
REALISM RegistryContinued Access (n=965)
Age: 82 ±9 years
Prior MI: 24%
Prior stroke: 10%
Diabetes: 30%
COPD: 32%
Renal disease: 28%
Mean STS Risk
13.2%
Lim et al. Improved functional status and quality of life in prohibitive surgical risk patients with degenerative mitral regurgitation after transcatheter mitral valve repair, JACC 2014;64:182‐192.
Prohibitive Surgical Risk DMR Cohort (n=127)
10/13/2016
6
95% implant success
No procedural deaths
LOS = 2.9 days
1.0
0.8
0.6
0.4
0.2
0.0
Eve
nt
Fre
e S
urv
ival
(N=127)
Days Post Index Procedure
0 100 200 300 400
Lim et al. Improved functional status and quality of life in prohibitive surgical risk patients with degenerative mitral regurgitation after transcatheter mitral valve repair, JACC 2014;64:182‐192.
Prohibitive Surgical Risk DMR Cohort (n=127)
Prohibitive Surgical Risk DMR Cohort (n=127)
Left Ventricular Volumes
Hospitalizations for Heart Failure
Left Ventricular End Diastolic Volume Left Ventricular End Systolic Volume
(N = 69)Paired
Data(N=69)
0.67
0.18
0.0
0.2
0.4
0.6
0.8
1.0
1 Year Prior… 1 Year Post…
HF Hospitalization Rate per Patient Year
73% Reduction
125
109
60
70
80
90
100
110
120
130
140
Baseline 1 Year
Vo
lum
em
L
‐16 mL
0
49
46
30
35
40
45
50
55
60
Baseline 1 Year
0
‐3 mL
Source: MitraClip Clip Delivery System Instructions for Use.See important safety information referenced within.
4+
4+
3+
3+
2+
2+
1+
1+
0%
20%
40%
60%
80%
100%
Baseline 12 Months
Patients (%)
Mitral Regurgitation Grade
0
1+
3+
4+
2+
IV
IV IV
III
III III
II
IIII
I
II
0%
20%
40%
60%
80%
100%
Baseline 30 Days 12 Months
Patients (%)
NYHA Functional Class
I
II
IV
III
10/13/2016
7
Global MitraClip® Experience
– Treating Centers: 587
– Implant Rate1: 96%
– Etiology2
• Functional MR3 65%
• Degenerative MR 21%
• Mixed 14%
Etiology2
FMR3
65%
DMR 21%
Mixed 14%
10/13/2016
8
Global MitraClip® Experience
Over 25,000 MitraClip Patients Worldwide
Current Global MitraClip Experience
Commercial Mitral Leaflet Patient RecordsSubmitted to the TVT Registry
50
1118
2500
0
500
1000
1500
2000
2500
3000
2013 2014 2015
Only commercial cases – does not include investigative cases (i.e. COAPT).
US catching up with >25K cases performed worldwide.
US use restricted to DMR in patients at prohibitive risk for surgery.
10/13/2016
9
Population1583 Patients
• Median age (% men)…………………..
• NYHA III/IV………………………………….
• HF hospitalization prior yr……………....
• Atrial fibrillation…………………………...
• Prior CVA……………………………………
• Diabetes…………………………………….
• Prior CABG…………………………………
• Prior MI……………………………………...
• Creatinine ≥2 g/dl………………………….
• O2-dependency……………………………
• Peripheral Arterial Disease……………...
82 yrs (56%)
85.0%
52.9%
64.4%
10.7%
24.5%
31.7%
26.5%
15.0%
14.4%
18.1%
• Frailty……………...........................................
• Hostile chest…………………….....................
• Porcelain aorta………………….……………..
• RV dysfunction with severe TR….…....…..…
• Immobility………………………………....……
• Severe liver disease (MELD >12)……..........
• IMA at high risk of injury…………………..….
• Unusual extenuating circumstance……….…
• Chemotherapy ………………………………..
Descriptors of Prohibitive Risk
50.0%
7.4%
2.2%
7.8%
8.7%
1.4%
4.6%
28.7%
4.6%
10/13/2016
10
1 Clip= 54%, 2 Clips= 40%, ≥ 3 Clips= 5%Clip implanted = 97.7%
Site Reported MR Reduction
0%
20%
40%
60%
80%
100%
Baseline Post
Grade 4
Grade 3
Grade 2
Grade 1
Mitral Regurgitation
92.9% MR ≤2
62.0% MR ≤1
54% 46%
Evolution of Mitraclip Use
73%
27%
EVEREST II(Randomized Controlled Trial)
• 178 patients• Implant rate – 89%
= DMR = FMR
53% 47%
REALISM(Continued Access Registry)
34%
66%
Commercial(Europe, Canada, Asia, Australia)
• 571 patients• Implant rate – 94%
• > 10,000 patients• Implant rate – 95%
90%
10%
= Standard Risk = High Risk
75%
25%
10/13/2016
11
Outcomes of Mitraclip Everest II vs Registries
Percutaneous TMVR LandscapeEdge-to-edge
• MitraClip
Direct annuloplasty MitralignBident
• GDS Accucinch• Valtech Cardioband• Quantum Cor (RF)
• Micardia enCor
Otherapproaches
• Cardiosolutions• Mitra-Spacer
• St. Jude leaflet plication• TransCardiac Mitraflex
• NeoChord• Valtech Vchordal
• Mardil BACE• Mitralis
• Millipede
Coronary sinusannuloplasty
• Cardiac Dimensions Carillon
MV replacement• Tendyne• Neovasc• CardiAQ• Twelve
• EndoValve• Valtech Cardiovalve
• ValveXchange• Medtronic• Edwards
10/13/2016
12
Direct Mitral “Annuloplasty”
MitralignValtech
Cardioband
‐ Trans‐aortic
‐ 1‐3 annular pairs of pledgets via LV
‐ FIH done
‐ Trans‐septal
‐ Posterior annulus band in LA
(screw fixation)
‐ FIH done
10/13/2016
13
NeoChord DS1000 Device
Current activity: 420+ cases
• ITALY 170 (Torino, Milano, Brescia, Padova, Reggio Emilia, Bologna, Rapallo, Roma, Palermo, Bari, )
• LITHUANIA 75 (Vilnius)
• GERMANY 55 (Frankfurt, Leipzig, Trier, Goettingen, Duisburg, Munich, Hamburg, Dresden, Cologne, Aachen)
• TURKEY 29 (Ankara, Antalya, Istanbul area)
• FRANCE 20 (Bordeaux, Lyon, Nantes)
• FINLAND 9 (Helsinki, Turku, Tampere)
• OTHER COUNTRIES: LATVIA, POLAND, BELGIUM, SWITZERLAND, CANADA, NETHERLANDS, AUSTRIA (1‐8 cases each)
10/13/2016
14
Preoperative Screening (TEE)
Patient Stratification (Anatomical)Type A “Ideal” Patient:
• Central P2 prolapse • >5 mm predicted coaptation length with repair• OR Anterior Leaflet covering >70% AP diameter
Type B “Adequate” Patient: • 2 - 5 mm coaptation length• Prolapse extending to portions of P1 or P3
Type C “Challenging” Patient:• Prolapse involving commissures• LV dilatation with partial tethering of leaflets• Central regurgitant jet component
10/13/2016
15
10/13/2016
16
Ideal Patient
10/13/2016
17
Courtesy Dr. Andrea Colli, Univ. of Padova
10/13/2016
18
10/13/2016
19
a
10/13/2016
20
10/13/2016
21
Fortis TMVR
10/13/2016
22
Tiara and Fortis TMVR
Fortis
Tiara
Twelve and Tendyne TMVR
10/13/2016
23
TMVR and LVOT
Percutaneous MV Replacement• CardiAQ• Tendyne
• Valtech Cardiovalve• ValveXchange• Neovasc Tiara
• Medtronic Twelve
Challenges
10/13/2016
24
Conclusions
• Mitraclip device has a large worldwide experience with steep learning curve and improved success compared to early clinical trials.
• It provides a durable repair and can be used in a wider range of valve pathologies than at first recognized
• It does have some limitations: MS, calcified valve leaflets, still 20% with significant MR
• Alternative mechanism for percutaneous MV repair are still being studied and show some promise
• TMVR is the holy grail, but its implementation will be more challenging than its aortic cousin
Fortis
10/13/2016
25
Echo Quantification of Primary Mitral Regurgitation
Echo Quantification of Secondary Mitral Regurgitation
10/13/2016
26
Status of TMVReplacement as of March 1st 2016
Badhwar, Mack JTCVS 2016
10/13/2016
27
Mitral Regurgitation: Carpentier Classification
10/7/2016
1
John Schindler, MD, FACC, FSCAICo-Director, Center for Aortic Valve DiseaseUniversity of Pittsburgh Medical Center
Multi-Valve Disease
• I have no financial disclosures relevant to this topic
Double Valve Disease
10/7/2016
2
• 20.2% of patients seen with native valve dz– Euro Heart Survey
• 10.9% of patients undergoing valve surgery– STS Database
• 58% aortic/mitral
• 31% mitral/tricuspid
• 3% aortic/tricuspid
• 8% triple valve surgery
• Demographics– Mean age 64
– Predominantly male
What is the scope of the problem?
Eur Heart J 2003;23:1231-1243
Ann Thorac Surg 2011;91:677-684
• Acquired– Rheumatic heart disease
• Decreased significantly in developed countries in recent decades
• Most common is mitral and aortic pathology
– Endocarditis
– Mediastinal chest radiation
– Adverse drug effects
– Ehlers Danlos
• Mitral valve prolapse/aortic annular dilation (AI)
– Calcific disease
• AS/MS from severe MAC
– Carcinoid
• Combined tricuspid and pulmonic disease
Multiple Valve Disease
10/7/2016
3
• Recommend referral to a Heart Valve Center of Excellence– Multi-disciplinary
– Offer all available therapies
• Complex repair – trans-catheter therapies
– Participate in national registry
• TVT registry
– Demonstrate adherence to national guidelines
– Participate in continued QI and self-evaluation to enhance patient outcomes
– Publicly report outcomes
2014 Valvular Heart Disease Guidelines
• Significant stenosis and regurgitation can be found on the same valve. Disease of multiple valves may be encountered in several conditions, but particularly in rheumatic heart disease and, less frequently, in degenerative valve disease. There is a lack of data on mixed and multiple valve diseases.
• The lack of data does not allow for evidence-based recommendations.
European Guidelines - 2012
10/7/2016
4
• What to do when confronted with a complex multi-valve disease patient…
• Attempt to figure out the predominant lesion.
#1
10/7/2016
5
• Besides the separate assessment of each valve lesion, it is necessary to take into account the interaction between the different valve lesions.– Hemodynamic interaction between valve lesions can promote,
exacerbate or by contrast blunt the clinical expression of each singular lesion
#2
• Indications for intervention are based on global assessment of the consequences of the different valve lesions, i.e. symptoms or presence of LV dilatation or dysfunction.
#3
10/7/2016
6
• The decision to intervene on multiple valves should take into account the extra surgical risk of combined procedures.
#4
• The introduction of transcatheter valve therapies is changing the therapeutic paradigm. – AS/MR - TAVR prior to MV therapy
#5
10/7/2016
7
– AS/MR
– AS/MS
– AR/MR
– AR/MS
– TR and left sided disease
• Mod-Severe MR present in 20% of patients in PARTNER trials
• Effect of AS on MR– Increased systolic transmitral
gradient results in an increased regurgitant flow rate/volume for any given mitral regurgitantorifice area
• Effect of MR on AS – Low flow state resulting in a low
trans-lesional pressure gradient despite a small aortic valve area
Aortic Stenosis Combined with Mitral Regurgitation
N Eng J Med 2010;363:1597-1607
10/7/2016
8
• Infrequent in developed countries
• Poorly tolerated hemodynamically because both lesions inhibit forward cardiac output
• Underestimation of the severity of both disease states
• More common condition is degenerative/calcific mitral stenosis from severe MAC combined with senile calcific AS– MS is less severe when compared to RHD
Aortic Stenosis and Mitral Stenosis
TTE
10/7/2016
9
• Characterized by severe volume overload leading to severe LV dilation as well as mild increase in afterload
• Pattern of hypertrophy is eccentric (low ratio of wall thickness to cavity diameter)
• Pattern of premature closure of the mitral valve is absent leading to worsening LA pressure and pulmonary edema
Aortic Regurgitation and Mitral Regurgitation
TTE
10/7/2016
10
• Opposite loading conditions on the LV
• The increase in SV typically seen with AR may be blunted
• Patients tend to tolerate AR longer in this situation as compared to a patient with AR/MR
Aortic Regurgitation and Mitral Stenosis
• Common in mitral and aortic disease
• Associated with worsened postoperative survival
• Complex interplay of annular dilation, RV enlargement and dysfunction and pulmonary HTN
• Severity is highly sensitive to changes in loading conditions
• “Old” teaching that TR disappears after treatment of left sided disease is false
Tricuspid Regurgitation and Left Sided Valve Disease
Ann Thorac Surg 2005;79:127-132
10/7/2016
11
Prevalence of Significant TR with Left Sided Disease at UPMC
Schindler 2016 TCT abstract 3831 Washington DC
66/505 (13%) patients with >mod TR
Post TAVR 55%continued to have >mod TR
ECHO Considerations with Multi-Valve Disease
Heart 2011:97 (4);272-277
10/7/2016
12
Open Surgery
• The prevalence of multi-valve disease is increasing despite the reduction in rheumatic heart disease which is mainly due to aging of the general population.
• Despite the challenges, determination of the global consequences of all lesions is of the utmost importance and requires the use of multi-modality imaging.
• Patient centered therapeutic decisions should be made by a multi-disciplinary heart valve team to optimize patient outcomes.
Conclusions
10/7/2016
13
• Much needed randomized trials are underway which will hopefully allow for more evidenced based decision making in these complex patients.
• Further advances in transcatheter technology will continue to transform the delivery of care to those with mitral and tricuspid pathology and those with aortic conditions beyond pure aortic stenosis.
10/11/2016
1
1
William E. Katz, MD, FACC, FASE
Associate Professor of Medicine
Clinical Director of Echocardiography
No Disclosures
Tricuspid Regurgitation-Is this Disease Entity Overlooked?
• Tricuspid Valve Anatomy
• Prevalence of tricuspid regurgitation (TR)
• Utility for estimation of pulmonary arterysystolic pressure
• TR etiologies
• Grading severity of TR
• Clinical impact of TR
Outline
2
10/11/2016
2
Tricuspid Valve Anatomy
3
Tricuspid Valve Complex
• Continuous structure with 3 leaflets: septal, anterior and posterior
• Well visualized by TTE as it lies anterior in the chest in the near fieldof the transducer:
– RV inflow view: septal and anterior leaflets
– Parasternal short axis: anterior or septal / posterior leaflets
– Apical 4 chamber:
• anterior / septal leaflets
• More apically situated than the mitral valve
• Leaflets are attached via chordae to separate papillary muscles
• Annulus is D shaped
– Susceptible to dilatation
– Tricuspid annulus measured at end diastole in Ap 4C
• Normal < 4 cm
• Right Ventricle / Right atrium Dreyfus Ann Thor Surg 2005;79:127
10/11/2016
3
• Frequently asymptomatic and not detected onphysical exam
• Signs and symptoms of right heart failure
• Small degree of TR is present in 70% of adults ontransthoracic echocardiography and is called“normal” or physiologic.
• 90% of those with established heart disease haveTR.
Detection of Tricuspid Regurgitation
5
Prevalence of TR on Echo
6
Nath JACC 2004; 43: 405-9
• 88% of patients undergoing echoes at 3 VAs had TR
10/11/2016
4
Utility of Tricuspid Regurgitation Velocity to Estimate Pulmonary Artery Systolic Pressure
• The TR velocity measured by spectral Doppler can be used to estimate the RV systolic pressure = PA systolic pressure (assumes no pulmonic stenosis)
• Even trace TR may have a Doppler velocity signal to allow for this measurement
• Doppler interrogation – Attempted from multiple windows to obtain the most accurate TR velocity.
– Injection of agitated saline / microbubble contrast can be used to augment the spectral signal strength of the TR velocity
• Limitations:
– With severe TR due to leaflet pathology, the RA and RV may operate as a common chamber and the TR flow is laminar, thus the Bernoulli equation may not be applicable
– Respiratory variation in the TR velocity
Doppler Estimation of PA Systolic Pressure
Yock Circ 1984;657-62
ΔP = 4 TR Velocity2
PAS = Δ P + RA Est RA pressure
Normal 3 mmHg
Intermediate 8 mmHg
High 15 mmHg
IVC Diameter < 2.1 cm < 2.1 cm > 2.1 cm
> 2.1 cm
Collapse with sniff
> 50% < 50% > 50% < 50%
PAS
TR velocity
10/11/2016
5
• Myxomatous TVP
• Rheumatic
• Flail leaflet from biopsy OHTX
• Endocarditis
• Chest trauma
• Ebstein’s anomaly
• Carcinoid syndrome
• Pacer/defibrillator lead
• Radiation
• Anorectic Drugs__________
=>RV Volume overload
PAS < 50 mmHg
• Severe pulmonary HTN– Primary PH
– Secondary PH
• Acute pulmonary embolism
• L heart disease
• RV myocardial disease– Dysplasia, infarct, post TX
• TV Annular dilatation– RV dilatation e.g. ASD, VSD
– RA dilatation from chronic atrialfibrillation
Etiology of Tricuspid Regurgitation
9
Primary Functional (80%)
• EKG limited: RV infarct; P-pulmonale withsevere PH
• CXR: RA enlargement; pleural effusions
• Echocardiography main diagnostic tool foridentification and evaluation of TR (Class IIndication, Level of Evidence C):– Severity of TR
– Etiology of TR
– Estimate PA systolic pressure
– Measure sizes of right-sided chambers and IVC
– Assess RV systolic function
– Characterize any associated left-sided heart disease
Tricuspid Regurgitation Evaluation
10
10/11/2016
6
• Many patients with pulmonary hypertension(PH) have only mild TR (65% of patients withPASP 50-69 mmHg and 46% of those with PASP> 70 mmHg
• Abnormal degrees of TR are mainly functionalwith normal leaflets and chords and are relatedto tricuspid annular dilatation or leaflettethering in the setting of RV pressure orvolume overload
• VA study of 5223 adults showed moderate tosevere TR was present in 15.7% and 92% weredue to a functional cause
Tricuspid Regurgitation Evaluation
11
Grading Tricuspid Regurgitation Severity
12
JASE 2003;16:795
(Nyquist limit 28 cm/sec)
10/11/2016
7
13
JASE 2003;16:796
Grading Tricuspid Regurgitation Severity TR
Lead Associated TR
14
Al-Bawardy Clin Card 2013; 36:249
• The prevalence of TR is between 25% to 29% of patients with PPM• Worsening of preexisting TR by 1 or 2 grades in 11% to 25% of
patients, over a period of 1 to 827 days after PPM or ICD placement
10/11/2016
8
TR Severity Predicts Survival
15
Nath JACC 2004; 43: 405-9
16
10/11/2016
9
Predictors of Survival with TR
17
Nath JACC 2004; 43: 405-9
TR after Mitral Valve Repair Surgery
18
Dreyfus Ann Thor Surg 2005; 79:127
10/11/2016
10
Late TR after MVR Predicts Survival and CHF
19
Stages of Functional Tricuspid Regurgitation
20
10/11/2016
11
21
Dreyfus JACC 2015; 65:2331-6
Summary
• Physiologic TR is very common
• Abnormal TR is most commonly functionalcaused by dilatation of the RA, RV, TVannulus and tethering of the TV leaflets
• The are multiple causes of primary TR
• Signs and symptoms of severe TR are rightheart failure
• Echo is the main diagnostic modality forevaluation of TR and its etiology
• TR is associated with increased mortality
• Repair for TR for mild TR with annulardilatation improves survival
22
10/14/2016
1
USEFULNESS OF CMR IN VALVULAR HEART DISEASE
Moneal Shah10/15/2016
We can do it too
• Visual assessment
• Quantification
10/14/2016
2
10/14/2016
3
Mitral regurgitation
Quantification
• Regurgitant volume
• Regurgitant fraction
• Phase velocity mapping and 3D volumetrics
10/14/2016
4
Short axis stack
LVEDV-LVESV=
Stroke volume
Phase contrast mapping
10/14/2016
5
Uretsky et al. JACC 2015
10/14/2016
6
Uretsky et al. JACC 2015
Aortic Regurgitation
10/14/2016
7
10/14/2016
8
Ribeiro et al. JACC 2016
Mitral stenosis
10/14/2016
9
Aortic stenosis
Phase contrast
10/14/2016
10
• Phase contrast for peak velocity assessment
• continuity equation
Pulmonic regurgitation
10/14/2016
11
• Phase contrast forvelocity andregurgitationassessment
Tricuspid regurgitation
10/14/2016
12
ACC Guidelines
• Class I: CMR in indicated in patients with moderate or severeAR and suboptimal echocardiographic images for theassessment of LV systolic function, systolic and diastolicvolumes and measurement of AR severity.
• Class I: Serial evaluation of size and morphology of the aorticsinuses and ascending aorta by echocardiography, CMR orCT angiography is recommended in patients with a bicuspidaortic valve and an aortic diameter greater then 4.0 cm, withthe examination interval determined by the degree and rateof progression of aortic dilatation and by family history. Inpatients with an aortic diameter greater then 4.5cm, thisevaluation should be performed annually.
• Class I: CMR is indicated in patients with chronicprimary MR to assess LV and RV volumes,function or MR severity and when these issues arenot satisfactorily addressed by TTE.
• Class I: Noninvasive imaging (including CMR) isuseful to establish etiology of chronic secondaryMR and/or to assess myocardial viability, which inturn may influence management of functional MR.
• Class IIb: CMR or real-time 3D echo may beconsidered for assessment of RV systolic functionand systolic and diastolic volumes in patients withsevere TR and suboptimal 2-D echocardiograms.
10/13/2016
1
The significance of mitral valve anatomy and invasive therapy for LVOT obstruction in hypertrophic
cardiomyopathy
Timothy Wong, MD MS
Director, UPMC HCM Center
October 15, 2016
Disclosures
• Site principal investigator, LIBERTY‐HCM trial(Gilead Sciences)
10/13/2016
2
Overview
• Left ventricular outflow tract (LVOT)obstruction in HCM
–Mechanism / Prevalence
–Management
• medical versus septal reduction therapy
• mitral valve consideration
• Case studies
LVOT obstruction
Ommen et al Heart 2008
10/13/2016
3
LVOT obstruction
LVOT obstruction
• Quantified by the peak instantaneous gradient by Doppler echocardiography(or peak to peak by cath)
• Basal obstruction: 25%
• For those w/o basal obstruction, 60‐70% have exercise induced LVOTO.
Gersh et al Circulation 2011Shah et al Heart 2008Maron et al Circulation 2006
10/13/2016
4
LVOTO medical therapy
• Beta‐blockade
– metoprolol succinate (often BID)
• Non‐dihydropyridine calcium channel blockade
– verapamil, diltiazem
• Disopyramide (anti‐arrhythmic with anti‐inotropic effects)
• Other: hydrationGersh et al Circulation 2011Sherrid JACC 2005
LVOTO therapy
ACC/AHA Guideline Class I Recommendation
“Septal reduction therapy should be performed … only for the treatment of eligible patients* with severe drug refractory symptoms and LVOT obstruction.”
*Eligible patients = severe symptoms despite medical therapy, rest or provoked LVOT gradient > 50 mm Hg and associated with SAM, septal anatomy is suitable
Gersh et al Circulation 2011
10/13/2016
5
Mitral valve considerations• Mitral regurgitation
– Is it “just” due to systolic anterior motion?
– Are there intrinsic mitral valve abnormalities• If yes, should mitral valve repair be considered?
Desai et al Circ CV Imag 2011
Mitral valve
Maron et al Circ CV Imag 2011
10/13/2016
6
Mitral valve
Mitral valve
10/13/2016
7
Case 1
Case 2
10/13/2016
8
Case 3
We would like to send a special Thank You to the following companies for their Exhibitor support of the
2016 FIT Educational Conference
Edwards Life Sciences Medtronic
Philips
Recommended