Valvular Heart Disease Overview: Prep for the · PDF fileValvular Heart Disease Overview: Prep...

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


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


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


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


INSP

PALP

AUSCPULSE

JVP

GENAPP

https://erikhultman.files.wordpress.com/2010/10/sixfingerhand.jpg

ADAPTED FROM HARVEY


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


10/7/2016

5

PERIPHERAL PULSESPULSUS PARADOX PULSUS ALTERNANS

Examination of the Heart. Part II, Fowler et al. AHA 1972


, “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


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


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


10/7/2016

8

PARADOXICAL SPLITTING S2DELAYED A2 CLOSURE

LBBBRV PACING

PDASEVERE LV DYSFUNCTION

AORTIC STENOSISHOCMSEVERE HTN


FOURTH HEART SOUND Origin of S4

Physiologic vs. Pathologic

Organic Conditions

Aortic stenosis

Hypertension

Ischemia /CAD

Split S1 vs. S4


10/7/2016

9

THIRD HEART SOUND Origin of S3

Physiologic vs. Pathologic

Organic Conditions

Increased LVEDP

Severe MR

Large VSD, PDA



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”.


SYSTOLIC MURMURS


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


Shaver et al, Auscultation of the Heart, AHA, 1990 UPMC Heart and Vascular Institute

10/7/2016

12

HYPERTROPHICCARDIOMYOPATHY

STEVE LOME, WWW.HEALIO.COM


POST PREMATURE BEATS Longer diastolicfilling period resultsin increased SV

Increased SV

Decreased afterload

Post‐systolicpotentiation –increasedcontractility

Brockenbrough–Braunwald–Morrow sign


10/7/2016

13

PULMONIC STENOSIS


MITRAL REGURGITATION Holosystolic: Blowing, high frequency

Radiation

Apex to axilla

Apex to LSB

Acute vs. Chronic

MVP

Ischemic

Associated diastolic

rumble


10/7/2016

14

CHRONIC MITRAL REGURGITATION

PALEY, H. AHA MONOGRAPH #46, 1975


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


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.


TRICUSPID REGURGITATION Holosytolic

Location: lower left sternal border

Intensity: respiratory variation

JVP: V wave

RV lift

Associated diastolic rumble


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


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


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


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


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


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


10/7/2016

21

PERICARDIAL FRICTION RUB Scratchy, leathery, high frequency

Location: LLSB, Xyphoid

3 Components

Ventricular systole

Early diastole

Late diastole (atrial systole)


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


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


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


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


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


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



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


2 .

• 2 .

• 2 . . .

.0.6cm2

•

. /

. /0.22

• Therefore…SEVEREAorticStenosis


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


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


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


From: Imaging of Low-Gradient Severe Aortic Stenosis




CopCopCopCopCopCopCopopCopCopCopopCopCopCopopopCopCopCopCopCopCopCopCopCopCoppopCopCoppCoppCopCoppCopopppCopCopopCopCopCopCoppopopopopCoppopCopCopCopCopCopopppopopopCopopppCoppCoppCopCopCopppCoppopCoppCopCopppopppCoCoCoCoCoCoCoCooCooCoCoooCoCoooCoooooooCooCooooCoCooCoCoooooCoCooCoooCoCoooooooooCoCoooCoCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCCC yriyriyriyriyriiyriyriyriyriyriyriyriyriyriyririyriiiriiriyriyriiririiiriyriyriiyriyriiiiyriiiriyriiyriyriiiririyryryryrrrryryrrryrrryrrrryrrrrryryryryryryryryrryryyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyy ghtghttghtghtghttttghtghththtghthtghthttthtthtthtghtghtghtghtghtghttthttghtghtghtghtghtghtghtghthttghthtghtgghtghthtghtghtghtghtghtghthtghttghtghttghthtghtghtghtghtghtghtghtghtghtghthtghttghtghtghtghththtghttghthghhhghhhghhhhghghghhhhghhhghghghhghghhhghghhhhhhhhhghghghhghghghhghhghghhhhghghhhhhhgggggggggggggggggggggggggggggggggggggggggggggggggg ©©© ©©©©©© ©©©©©©© ©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©©© eeeeeeeeTheeTheTheeTheeheTheTheheTheehThThThThThhhhThhhThhThThThhhThThThThhThThThThhThThThThhThhhThhhhThhhhThhThThhThThThThThhThhTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTT American College of Cardiology. CopCopCoppopCoppCoppppppCopCoppppooooCCooooCoCoooooCCC yriyriyriyryyyyyyyyyyyyyyyyy ghtghttthg ©©©© eeeeeeeeeeTheTheThehTTTTTTTTT American College of CardiologyAllAllAllAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA iii hththt ddd


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.



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

Date post:	24-Mar-2018
Category:	Documents
Upload:	vuongnhu
View:	215 times
Download:	3 times

Valvular Heart Disease Overview: Prep for the · PDF fileValvular Heart Disease Overview: Prep...

Documents