AE 1.9 - Prosthetic Valve, Valve Repair, Hypertension

Major categories of prosthetic valves (4)

Mechanical

• bileaflet tilting disk

• single tilting disk

• ball cage

Bioprosthetic

• percutaneous (TAVR, mitraclip)

• human

• animal

  • stented porcine (typically no leaks or clots)

  • stentless porcine (AV only, large flow area, no real regurg)

  • bovine (regurg or stenosis common from leaflet thickening)

Homograft

• from cadaver

• usually only for aortic valve

• stentless

• low stenosis rate

• low thrombosis rate

• failure secondary (degeneration) to increasing regurgitation

Autograft (Ross Procedure)

• take own pulmonic valve & use it to replace the aortic valve

• replace the PV with a homograft

• coronary arteries reimplanted

• pediatrics w/congenital AS

• failure due to:

  • dilatation of autograft root leading to progression of aortic regurgitation

  • pulmonary homograft degeneration

Basic design characteristics of prosthetic valves

• all prosthetic valves have reduced orifice size and are inherently stenotic

• need to know type of valve & size

• inflow profile & regurgitation characteristics

Advantages & disadvantages of each prosthetic valve type

Mechanical

• high risk of clots / have to be on blood thinners

• clicking noise

• tissue overgrowth/pannus risk

• last very long / doesn’t degenerate

Bioprosthetic

• don’t last as long / degenerate over time

• endocarditis risk

• no need for blood thinners / low clot risk

• no clicking sound

• no inherent regurg

Mechanical valves

• More durable than tissue valves (some last decades)

• Made of carbon, polymeric silicone, or titanium

• May have overgrowth of a tissue around the valve perimeter called a pannus

• Typically more suitable for younger male patients or females who don’t intend to become pregnant

  • Will need blood thinners for life (Coumadin)

  • Problems with increased thrombogenicity

• Can hear the “clicking” sound outside of the body

• Physiological trivial regurgitation is normal

• ball & cage (rare)

• bileaflet tilting disk

• single tilting disk

Expected flow characteristics of mechanical valves

ball & cage

• non-central flow

• lateral flow around the ball occluder

• stenotic

• closing volume

bileaflet tilting disk

• 3 orifices/jets when open (1 small central, 2 larger lateral)

• high velocities in central one

• leakage volume / washing jets

  • built-in transprosthetic regurgitation aims to prevent thrombus formation at potential sites of stasis 

  • common in bileaflet valve 

single tilting disk

• 2 orifices/jets (1 major, 1 minor)

• leaking & closing volume regurgitation common around central strut & between disc & sewing ring

Expected flow characteristics of tissue valves

homograft

• similar flow characteristics as native valve

• central flow

• trivial/no regurgitation

• low stenosis rate

autograft

• native valve flow characteristics for both valves

• central flow

• trivial/no regurgitation

stentless valves

• large flow area

• trivial/no regurgitation

Expected normal regurgitation patterns of prosthetic valves

bioprosthetic valves

• trivial/no regurg

percutaneous valves (transcatheter)

• paravalvular leaks in AV

mechanical valves

• washing jets / built-in regurg

ball & cage and single tilting disk

• closing volume: blood displaced when the occluder shuts

• leaking common around central strut & between disk and ring

Which prosthetic valves require lifelong anticoagulation

• mechanical prosthetic valves

• high risk of thrombosis on valve

Indications for valve replacement vs repair

replacement

• valve itself is severely damaged

• can no longer function normally

• advanced stenosis, regurgitation, endocarditis

• usually the aortic valve is replaced

repair

• when cause is secondary to valve

  • annular dilation

  • chordal issue

• leaflets/cusps are not severely damaged or calcified

  • small perforation

• usually the mitral & tricuspid valves are repaired

Advantages of valve repair compared with valve replacement

• repair is always the best option when available

• lasts very long

  • much more durable / less chance of degeneration

• less complications with own native valve

  • less chance of infection

  • no need for blood thinners

Components of a comprehensive prosthetic valve evaluation

• on & off axis views

• Valve function

• Chamber measurements

• Systolic/diastolic function

• Color Doppler

• Spectral Doppler

  • CW peak/mean gradients

• Valve appearance

• Seating of valve within the native annulus

• Opening and closing motion of the leaflets

• Valve bed/appearance of sewing ring stability

  • “rocking motion” = dehiscence

• bioprosthetic leaflet thickness

Importance of knowing valve type & size

• so you know what to look for on echo

• normal hemodynamic values are based on this:

  • unique normal flow profiles

  • unique regurgitation patterns

  • unique normal hemodynamic values

Expected 2D appearance of prosthetic valves

post-op

• IVS paradoxical motion

mechanical

• very echogenic

• shadowing below valve

• microbubbles / degassing

bioprosthetic

• sometimes look like native valve

• 3 struts

Causes of acoustic shadowing & reverberation artifact

• Sewing rings & mechanical valves are strong echo reflectors – results in acoustic shadows & reverberations

  • Blocks imaging & Doppler abnormalities in shadow region

Purpose of baseline post-operative echocardiography

(4-6 weeks post-op)

• Full comprehensive echo

• Primary goal is to acquire hemodynamic data when valve is working normally

• Can serve as a “normal reference”

• Advantages:

  • recognizes PPM – prosthesis patient mismatch

  • detects prosthetic valve dysfunction

  • identifying infective endocarditis

Importance of comparing serial studies with baseline examinations

So many numbers to remember! (each valve has its own unique ones)

• This is why a high quality baseline echo is so important!!!

• Use the baseline as the fingerprint (new normal) and compare all serial echoes to this

• can see a change from “normal” values

• Comparison with post-operative studies is essential in cases of high gradients

Prosthesis-patient mismatch (PPM)

• Occurs when the effective orifice area (IEOA) of the prosthetic valve is too small in relation to a patient’s body size

• Resulting in high residual postoperative pressure gradients across the prosthesis

• More common in aortic valves

Prosthetic valve thrombosis

• Formation of blood clot around or over prosthetic valve

• Observed with bioprosthetic and mechanical valves

• More common in mechanical valves with inadequate antithrombotic therapy (INR ≤ 2.5)

• Can lead to obstruction &/or regurgitation

Pannus formation

growth of abnormal tissue around a prosthetic heart valve

Prosthetic valve obstruction

TAVR = HALT (hypo-attenuated leaflet thickening) 

Prosthetic valve endocarditis

• Infection of the valve leaflets or between the sewing ring and native annulus

• More likely in bioprosthetic valves

• Timing of the infection reflects different mechanisms

• May create regurgitation and/or stenosis

• May also cause other complications like leaflet perforation, abscesses, dehiscence, etc

• TEE often required

Paravalvular leak vs. transvalvular regurgitation

paravalvular

• a leak caused by a space left between natural heart tissue and the valve replacement from a previous transcatheter aortic or mitral valve replacement

• Color flow Doppler: arises outside the sewing ring, between the sewing ring and the native annulus

transvalvular

• Occurs within the sewing ring

• Most mechanical valves have physiologic regur

  • May be multiple jets - usually short, narrow and nonturbulent

• Most common cause of mechanical is thrombosis or pannus formation

• Most common cause of bioprosthetic is leaflet degeneration

Valve dehiscence

serious prosthetic valve complication characterized by “rocking” of valve at an angle far in excess of its normal excursion

Typical echocardiographic findings associated with each complication

PPM

• ↑ pressure gradients

• EOA & DVI normal

• ↓ IEOA

• No change ΔEOA/DVI (from baseline)

Thrombosis

• obstruction/regurg

• echodensity on the occluder or leaflets

• restricted motion

Pannus

• tissue on valve

Obstruction/Stenosis

• ↑ Pressure gradients

• ↓ EOA & DVI (AVR)

• ↓ EOA & ↑ DVI (MVR)

• ↑ PHT (MVR, TVR)

Endocarditis

• regurgitation / stenosis

• leaflet perforation, abscesses, dehiscence

Dehiscence

• rocking motion

• paravalvular leak

Mitral valve repair techniques

• Annuloplasty rings

  • used to reshape and strengthen the natural valve annulus

  • a ring is placed around a stretched-out valve

    • the ring shrinks the valve down so the leaflets can close better

• Gore-Tex

  • chordal replacement

• Leaflet resection

  • removing the damaged part of the leaflet and then sews the remaining edges together

Common post-repair complications

• Recurrent MV regurgitation

• Newly developed septal contact / SAM

  • systolic anterior motion of anterior MV leaflet

• Pericardial effusion/constriction

Tricuspid Annuloplasty

• implantation of an undersized ring (rigid, semirigid, flexible) or a flexible band

• has importance among patients with functional TR

• annuloplasty rings or bands do not cover the whole tricuspid annulus, but remain open at the septal annulus to avoid injury to the conduction system

Valve-sparing aortic root repair

• Feasible in some instances:

  • leaflets are not deformed, scarred, or calcified

• Indications for AV repair include

  • 1. bicuspid valve with prolapsed of a single leaflet

  • 2. tricuspid valve with prolapsed of one leaflet

  • 3. normal aortic leaflets with dilated sinotubular junction

  • 4. Limited cusp destruction caused by infective endocarditis may also be amenable to repair in select instances. However, such repair should preferably be done at centers with specialized expertise

Definition & classification of systemic hypertension

• Begins at 130/80

• Should be based on the mean of 2+ readings on two separate visits

• 1. Essential

  • Known as primary or idiopathic

  • No identifiable cause

  • Approx 90-95% of patients will have essential systemic HTN

• 2. Secondary

  • Has identifiable mechanism

    • Arterial renal disease, aortic coarctation, endocrine diseases, drugs, food ingestion

Modifiable & non-modifiable risk factors (systemic hypertension)

Modifiable risk factors

• Smoking 

• Type 2 Diabetes

• Obesity (esp abdominal) 

• Hypercholesteremia

• Inactivity 

• Unhealthy diet

• Sodium intake 

• Alcohol consumption

• Emotional stress

Non-Modifiable risk factors

• Chronic Kidney Disease 

• Family History

• Increased age

• Male

• Race (higher in African Americans)

• Low socioeconomic status

• Obstructive Sleep Apnea

Common complications (systemic hypertension)

• Atherosclerotic complications

• Left ventricular hypertrophy

• Heart failure associated symptoms

• TIA/stroke

• Hypertensive encephalopathy, intracerebral hemorrhage, dementia

• Renal disease (nephrosclerosis, renal failure, glomerulosclerosis)

• Hypertensive retinopathy, optic neuropathy

• Aortic aneurysm (ascending aorta, abdominal aorta)

• Aortic dissection

Basic treatment approaches (systemic hypertension)

• Behavior modification

  • Weight loss, healthy diet, reduce alcohol consumption, exercise, tobacco cessation, stress reduction

• Pharmacologic

  • Diuretics, Beta blockers, ACE inhibitor, Calcium channel blocker, vasodilator

Role of echocardiography in patients with systemic hypertension

• Evaluate secondary complications

  • LVH/increased mass

  • LV systolic & diastolic function

  • LAE

• Exclude any causes

Left ventricular mass

• LV mass is the weight of the LV

• Typically measured using wall and LV dimensions

Relative wall thickness (RWT)

• A ratio that indicates the relationship between the wall thickness and cavity size of the left ventricle

• RWT = 2 x PW / LVID_d 

LV Geometric Patterns (Left Ventricular Remodeling)

Concentric hypertrophy

• thicker walls

• normal cavity

• increased mass

• higher ratio between wall and cavity

Eccentric hypertrophy

• normal thickness walls

• increased cavity size

• increased mass

• lower ratio between wall and cavity

Concentric remodeling

• thicker walls

• normal or smaller sized cavity

• normal mass

• higher ratio between wall and cavity

Echocardiographic findings associated with chronic systemic hypertension

EKG

• thickened LV wall leads to prolonged depolarization (increased R wave peak time)

• delayed repolarization (ST and T-wave abnormalities) in the lateral leads

Echo

• LVH

• LAE

• Ao root dilation

• diastolic dysfunction

Increased Wall Thickness vs LVH

• Increased Wall Thickness

  • Thick walls can happen for several reasons, some of which are not due to true muscle hypertrophy (cell growth)

  • Processes can cause an increase in wall thickness which is not due to hypertrophy of the myocardium

    • Infiltrative disease, tumors, transplant rejection

  • Typically result in an increased mass

• LVH

  • From pressure overload 

  • From increased afterload 

Definition & classification of pulmonary hypertension

• A clinical condition characterized by elevated pulmonary vascular pressure

  • Plaque, fibrosis, and narrowing

  • Increased pulmonary vascular resistance (afterload) 

• Over time sustained increased pressure in the arterial bed leads to increased right ventricular RV) afterload and eventually RV failure

• Can occur at any age

• Cause: idiopathic (no real reason) or secondary (has a reason) 

5 groups & their underlying causes (pulm htn)

1) Pulmonary Arterial Hypertension (PAH)

• Arteries in the lungs become narrowed, thickened or stiff

• Right heart must work harder to push blood through these narrowed arteries

• Extra stress can cause the heart to lose its ability to pump enough blood through the lungs to meet the needs of the rest of the body

2) PHTN due to left heart disease

• Arteries and lungs are not as thick or stiff as Group 1

• Caused by:

  • Systolic or diastolic dysfunction

  • Left sided valve disease (MR backs up into pulm vns → lungs → right side) 

• “backup” of blood raises pressure in the lungs

3) PHTN due to lung disease

• Arteries in the lungs tighten so that blood can only go to areas of the lungs that are receiving the most air and oxygen

  • This tightening leads to high blood pressure throughout the lungs

• Restrictive lung disease in which the lungs have a tough time expanding when one inhales (ILD, pulm fibrosis)

• Lung airways narrow and make it harder to exhale (COPD/Emphysema)

• Sleep apnea

4) PHTN due to chronic blood clots in the lungs

• CTEPH – Chronic Thromboembolic Pulmonary Hypertension

  • Body is unable to dissolve blood clots in the lungs

  • Leads to scar tissue in the blood vessels of the lungs

  • Makes right side work harder

5) PHTN due to unknown causes

• Not really understood

• Associated conditions include sarcoidosis, sickle cell anemia, certain metabolic disorders

PAH

• Pulmonary Arterial Hypertension

• Idiopathic PAH occurs without a clear cause

• Heritable PAH is linked to genes that are inherited from family members

• PAH developed in association with:

  • congenital heart disease, liver disease, HIV and connective tissue diseases such as scleroderma and lupus

  • past or present drug use, such as methamphetamine or certain diet pills

• While there are treatment options for PAH, there is no known cure

Gold standard for diagnosis (pulm htn)

right heart catherization

Dicrotic notch = SL valve opens

Mean PA pressure > 20 mmHg

Role of echocardiography in evaluation (pulm htn)

• Identify potential cause of PHTN

• Estimate PA pressures

• Estimate RAP

• Assess RV structure, thickness, and function

• Observe for shunts or other hemodynamic flow abnormalities

• Assess PA

• RV

  • On-axis: measurements & size

  • Off-axis: function & doppler 

m-mode

• Mid-systolic notching (flying W) of pulmonary valve cusps

  • Flying “W” 

• Reduced RV TAPSE

Right ventricular adaptation to chronic pulmonary hypertension

hypertrophy

dilation

echo findings

• RV dysfunction

• TV annulus dilation

• PA dilation

• RA dilation (RAE)

• D-shaped LV

• Dilated IVC

Septal flattening in pressure overload versus volume overload

pressure

• during systole

volume

• during diastole

Assessment of RV systolic function

• 2D RV fractional area change

  • >35%

• TAPSE

  • >1.7 cm

• Tissue Doppler s’

  • >9.5 cm/s

• RV longitudinal strain

  • > -20%

• RVEF%

  • >45%

• 3D RV volumes

  • <90 mL/m²

• RV free wall

  • < 5mm

Qualitative assessment of RV size

• “Eyeball” for initial judgement

• From a non-foreshortened A4C view (location of probe not too medial)

  • Normal: RV area or mid-cavity diameter should be less than 2/3 of LV

  • Moderate dilatation: RV same as LV, share the apex

  • Severe dilatation: RV exceeds LV, RV forms apex

Estimation of right ventricular systolic pressure (RVSP)

• TR velocity

  • RVSP = PASP (as long as no PS)

• Evaluate RAP with IVC

• Hepatic vein flow

Relationship between RVSP & pulmonary artery systolic pressure

RVSP = PASP (as long as no PS)

Use of tricuspid regurgitation velocity & estimated right atrial pressure

RVSP = Tricuspid Regurgitation Pressure Gradient + RA pressure

TR = 4V²

RAP = IVC size + collapsibility

Evaluation of the inferior vena cava (IVC)

• sniff test

• size of IVC (is it dilated)

• does diameter decreases > 50%

Hepatic vein Doppler

• PW Doppler of hepatic veins

• Looking for s & d  (forward flow) 

• Sample Volume size of 3-4 mm

• Placed at 1-2 cm into the hep veins using color guidance

Pulmonary acceleration time (PAT)

• Time to get from baseline to peak of RVOT 

• Short = increased pressure (Pulm Art Pres)