Increased riskol hemorrhage:1-2%/yr

<50 yr for aortic valves and <65 for mitral

valves

‘should only be performed In high volume centers with extensive experience in aortic root procedures and the Ross operation +

C55 Cardiology and Cardiac Surgery Toronto Notes 2023

Prosthetic Valve Management

Ross Operation

• En bloc removal of a patient's native

pulmonary root with valve (autograft)

and transposition of the autograft

into the aortic position to a replace

a diseased aortic valve that cannot

be spared

. The RVOT is then reconstructed with

a prosthetic valve,most commonly a

cryopreserved pulmonary homograft

(human donor)

• With proper technique,mitigation of

risk factors for early graft failure, and

strict postoperative blood pressure

control, the pulmonary autograft

adapts to the hemodynamics of the

LVOT and left heart with low rates of

reintervention

. Despite being more complex than

isolated aortic valve replacement,

morbidity and mortality arc

comparable to AVR with

bioprosthesis or mechanical valves

when done in experienced centres

Management and Follow-Up

• follow-up:dependent on valve type, residual heart disease, and clinical factors

TTE after prosthetic valve implantation to assess hemodynamics and ventricular function

if/when clinical symptoms orsigns of prosthetic valve dysfunction arise, repeat TTE;

additional investigations may be warranted if high clinical suspicion is present

TTE at 5 yr, 10 yr, and then annually thereafter is reasonable in otherwise asymptomatic

patients with a surgically implanted bioprosthetic valve (if transcatheter implantation was

used, annualTTE following the procedure isreasonable)

optimal dental care and endocarditis prophylaxis are required

• antithrombotic therapy: risk of bleeding must be considered and balanced whenever using/increasing

any antithrombotic therapy

• for patients with a mechanical valve, use anticoagulation with a vitamin K antagonist and INK

monitoring

• for patients with a bioprosthetic TAV1,bioprosthetic SAVR,or mitral valve replacement,short

term other antithrombotic oral anticoagulation or antiplatelet therapies may be indicated

Prosthetic Valve-Related Complications

• prosthetic valve dysfunction

no known medical therapies to prevent bioprosthetic or mechanical valve degeneration

« etiology:tissue degeneration, pannusformation, IE,thrombosis

presentation: prosthetic vascularstenosis or regurgitation

• investigations and treatment: depend on the type/severity of pathology,as well as patient

characteristics (see below)

• thromboembolic events Mechanical or Biological Prosthesesfor AorticValve and Mitral-Valve Replacencnt

NUM 2011:317:184? «

Purpose: lo elucidate inferencesin nechmlcal

n.biological prostheses in aortic-an)mitral-valve

replacements.

Methods:Patientswho underwent primary

aortic-valve or mitral- valve replacement in California

m Ihe period from IMS 2013 were analysed.

Outcomes included long-term mortality and rales of

re-operation,stroke, and bleeding.

Results: In aortic-valve replacement, biologic

prosthesis wasassocialed with higher IS- yr mortality

than mechanical prosthesis among patients aged

45-54 yr (30.6% vs.26.4%), but not among patients

aged 55-64 yr.lo mitral-valve replacement, biologic

prosthesis wasassocialed with higher mortality than

mechanical prosthesis among pa bents aged 40 49

yr (44% vs.21%).and among those aged 60-69 yr

(50.0% vs.45.3%).

Conclusion: The long term mortality benefit from

mechanical versus biologic prosthesis persisted until

20 yi among mitral-valve replacement patients, and

nntil 55 yr ameng aoibc-valve replacement patients.

ensure to assess anticoagulation adequacy, time spent in therapeutic range:rule out infective

endocarditis;screen for new-onset A!

'

;consider other sources of a potentially underlying

hypercoagulable state

patients with a mechanical aortic/mitral valve that were in therapeutic INR range on a vitamin K

antagonist at the time of event:consider increasing INR goal or adding low-dose daily aspirin

patients with a bioprosthetic aortic/mitral valve that were on antiplatelet therapy at time of event:

considerswitching to vitamin K antagonist anticoagulation

• valve thrombosis

mechanical valve thrombosis (generally a subacute-acute event):

often associated with inadequate anticoagulation; leads to rapid valve dysfunction

- recurrent thrombosis can be associated with pannusingrowth

symptoms/signs/presentation:rapid onset ofsymptoms, acute pulmonary edema,stenotic

murmur, muffled closing clicks

investigations: urgent multimodal imaging (TTE, TEE, fluoroscopy and/or multidetector CT

imaging)

treatment:if thrombosed valve is left-sided and symptoms of valve obstruction are present,

treat urgently with either fibrinolytic therapy or emergency surgery

• bioprosthetic valve thrombosis

most common in first 3 mo post-implantation; bioprosthetic valves are less thrombogenic

than mechanical valves

investigations:TTE or TEE or 4D CT imaging in suspected patients

treatment:if suspected or confirmed, treatment with a vitamin K antagonist is reasonable

(assuming hemodynamically stable and no contraindications)

• graft dysfunction after Ross operation

etiology:autograft dilatation and RVOT conduitstenosis and/or regurgitation

autograft within LVOT requires reintervention more often than pulmonary homograft within

RVOT

presentation:aortic regurgitation, pulmonary stenosis, pulmonary regurgitation,aortic root

aneurysm

investigations:echocardiography, MRI if aneurysmal root

treatment: when done in expert centers reintervention results in low mortality

» autograft dilatation:reoperation (autograft isspareable in majority of cases and survival

advantage isstill preserved)

RVOT'

graft dysfunction: transcatheter pulmonary valve replacement or surgical pulmonary

valve replacement (transcatheter is preferred)

r

L J

+

C-56Cardiology and Cardiac Surgery Toronto Notes 2023

Summary of Valvular Disease

General Principles for Evaluating Valvular Heart Disease

• initial evaluation

history and physical:symptom severity, valve disease, comorbidities, HF presence and severity

• TI E (standard initial investigation): chamber size/function, valve morphology,severity of

valvular heart disease, impacts to pulmonary/systemic circulations

-

ECU:rhythm, LVH, LV function

• further testing if indicated/needed

• CXR:particularly useful for symptomatic patient; assessesfor aortic and pericardial calcification,

intrinsic pulmonary disease, heart size and congestion of the pulmonary vessels

• TEE:assessment of mitral and prosthetic valve

• CMR:LV volume/function, aortic disease,severity of valvular disease

• PETCT:identification of infection/inflammation

• stress testing:exercise capacity

• catheterization: exercise- and drug-related hemodynamic responses,severity of valvular disease,

pressures within the heart and pulmonary'circulation

• future risk stratification

• biomarkers:surrogate measure for myocardial damage and filling pressures

• T EE strain:myocardial function

CMR:fibrosis

stress testing

• procedural risk:The Society of Thoracic Surgeons(STS) and TAVI scores

• frailty score

• preprocedural testing

dental exam:rule outsources of infection

• invasive coronary angiogram or CT coronary angiogram

• CT peripheral and cardiac (for transcatheter procedures)

Stages of Valvular Heart Disease

• stage A: at

-risk (asymptomatic)

• stage B: progressive (mild-moderate severity; asymptomatic)

• stage C:asymptomatic,severe

• Cl:compensated LV or RV

• C2:decompensated LV or RV

• stage D:symptomatic severe

r n

L J

+

C57 Cardiology and Cardiac Surgery Toronto Notes 2023

Table 18. Valvular Heart Disease

Aortic Stenosis Aortic Regurgitation r

8

s

1J

fcv/iVw :

*

s S: S , s, s: S 0

' ©

Etiology Definition

Congenital (bicuspid,unicuspid valve),calcification|wear and tear),rheumatic disease

Definition/Stages

Stage A:asymptomatic;congenital abnormality,bicuspid or sclerotic valve;aortic Vmax <2 mis

Leakage of blood across the aortic valve into the LV (i.e.aortic insufficiency). May be primary or

secondary AR

Etiology

Stage B;asymptomatic:can be mild AS (Vmax 2.0-2.9 m/s or mean pressure gradient «20 mm Hg) Supravalvular:aortic root disease (Marfan syndrome,atherosderosisand dissecting aneurysm,

or moderate AS (Vmax 3.0-3.9 mis or mean pressure gradient 20- 39 mm Hg)

Stage C:asymptomatic;can be severe AS (Vmax < 4 mis or mean pressure gradient - 40 mm Hg) or Valvular:congenital (bicuspidaortic valve,largeVSD).IE

very severe AS (Vmax >5 m/s or mean pressure gradient >60 mm Hg)iIV dysfunction

Stage D:symptomatic:can be severe AS or very severe AS;criteria also exist for low-flow,lowgradient AS with reduced LVEF and for low- gradient AS with either normal IVEF or paradoxical

low - flow severe AS

Pathophysiology

connective tissue disease)

Acute Onset:IE. aortic dissection,trauma, failedprosthetic valve

Pathophysiology

Volume overload

*

LV dilatation » increased SV.high sBPand low d8P

*

increased wall tension *

pressuie overload -*

LVH (low dBP•decreased coionary perfusion)

Symptoms

Outflow obstruction

*

increased EDP •» concentric LVH -*

LV failure CHF.subendocardial ischemia Usually only becomes symptomatic late in disease when HE symptoms.S0B0E,dyspnea.

Symptoms

Exertional angina,syncope,dyspnea.PHD. orthopnea,peripheral edema,exertional dyspnea,

decreased exercise tolerance,HF symptoms,presyncope,syncope

Physical Exam

Harrow pulse pressure,brachial-radial delay,pulsus parvus et tardus,sustained PMI

Auscultation:crescendo-decrescendo SEM radiating to right davideand carotid,musical guality at pathology):best heard sitting,leaning forward,on full expiration; soft S1.absent S2,present S3

apex (Gallavardin phenomenon).S4.soft S2 with paradoxical splitting.S3 (late)

Investigations

ECG:LVH and strain.LB8B.LAE.AFib

orthopnea. PHD, syncope,and/or angina develop as a result of IV lailurc

Physical Exam

Waterhammer pulse,bisferiens pulse.femoral-brachial sBP >20 mmHg (Hill'stest:wide pulse

pressuie),hyperdynamic apex,displaced PMI.heaving apex

Auscultation:early decrescendo diastolic murmur at LLSB (cusp pathology) or RLSB (aortic root

(late)

Investigations

ECG:LVH.LAE

CXR:post stenotic aortic root dilatation,calcified valve,LVH. LAE.CHF

echo:etiology,valve area,valve morphology,hemodynamics.LV sice,systolic function,prognosis. echo/TIE:ctiologylscverity.quantify AR.leaflet or aortic root anomalies.IV sice,systolic function.

prognosis,timing of intervention

TEE. CMR. or cardiac catheterization if >moderate AR,suboptimal/inconsistent TIE:systolic

function,heart volumes,aortic site,AR severity

Cardiac catheterization lab|Cath lab):if >40 yr and surgical candidate -to assess for ischemic

heart disease

Exercise testing:hypotension with exercise

Treatment

Asymptomatic:serial echos,afterload reduction (e.g.ACEI.nifedipine,hydralazine)

Symptomatic:avoid exertion,treat CHF

Surgery il: symptomatic severe AR:chionic, severe AR with LVEF <55%;severe AR and otherwise

undergoing cardiac surgery;other specific situations

Surgical Options

Valve replacement

Valve repair

Bentall procedure:replacement of aortic root and valve

CXR:LVH, LAE.aortic root dilatation

timing of intervention

Other:low-dose dobutamine stress testing, CT imaging/aortic valve calcium score,andexercise

testing (contraindicatedil symptomatic)

Treatment

Calcific AS:statin based on standard risk score for atherosclerotic prevention

Stages A-C:treat HTH

Asymptomatic:serial echos (repealed based on seveiity).avoid exertion

Symptomatic:avoid nitrateslarterial dilatois andACEI in severe AS

Proceduial intervention considered in stage D. stage C.and other specific situations

Procedural Options

SAVR:if <65 yr old and >20 yr life expectancy,or if 1AVR contraindication

- Conduct prior to pregnancy (if AS significant)

TAVR: if >80 yr old.if <10 yr life expectancy, or if high/piohibitive surgical risk

If patient between 65- 80 yr old.decision between SAVR or 1AVR is catered to specific patient

Percutaneous aortic balloon dilation:bridge to AVR in critical patients

r m

L J

+

C58 Cardiology and Cardiac Surgery Toronto Notes 2023

Table 18. Valvular Heart Disease

Mitral Stenosis Mitral Regurgitation

5

-: : 5

s ea

T

ss ,i

o

s s,

:

s > Si

Etiology

rheumatic disease (most common),non-rheumatic calcilication. congenital

Definition

Severe MS:mitral valve area (MVA)

"

1.5cm2

.diastolic pressure half-time >150 ms

Pathophysiology

MS » fired CO and LAE -•increased LA pressure -•PVR and CHF; worse with AFib (no atrial kick),

tachycardia (decreased atrial emptying time) and pregnancy (increased preload)

Symptoms

S060E. orthopnea,fatigue,decreased exercise tolerance,palpitations,peripheral edema,raalai

Hush,pinched and blue lacies (severe MS)

Physical Exam

Af ib,left parasternal lift,palpable diastolic thrill at apex:if AFib.no “a* wave on JVP;if sinus,

piominenl“a” wave may be found on JVP

Auscultation:mid diastolic rumble atapex;best heard with bell in left lateral decubitus position

following exertion:loud S1,OS following loud P2 (heard best during expiration),long diastolic

murmur,and short A2 OS interval correlate with worse MS

Investigations

ECO:HSR , AFib, LAE (Pmitrale).RVH.RAD

CXR:LAE.CHF,mitral valve calcification

echo/ TTE: diagnosis/severity,hemodynamics,valvular lesions, valve analomy/morphology.LA

thrombus if percutaneous mitral balloon commissurotomy being considered

Exercise testing:rheumatic MS and resting echo inconsistent with symptoms

Cath lab:if concurrent CAD and patient >40 yr (male) or >50 yr (female)

Treatment

Avoid exertion,fever (increased LA pressure):treat AFib and CHF;increase diastolic filling time

O-blockers. digitalis)

Vitamin K antagonist anticoagulation:in rheumatic MS if AF.previous embolism, or LA thrombus

Heart rate control (for some patients)

Intervention if:symptomatic,severe MS

InvasiveOptions

Percutaneous mitral balloon commissurotomy (PMBC):symptomatic,severe rheumatic MSwith

acceptablemorphology.< moderate MR. and no LA thrombus (may be reasonablein other specific

situations)

Etiology

MVP.congenital dell leallets.IV dilatationiancurysm (CHF.DCM. myocarditis).IE abscess.Marfan's

syndrome,HOCM.acute Ml.myxoma,mitral valve annulus calcification,chordae/papillary muscle

traumafischemia/rupture (acute),rheumatic disease,leaflet perforation

Definition

Leakage of blood across the mitral valve from the LV into the LA; can be primary or secondary. Can

use Carpenlier's classification

Pathophysiology

Reduced CO *

increasedIV and LA pressure

*

LV and LA dilatation » and pulmonary HID

Symptoms

Dyspnea.PND,orthopnea,palpitations,peripheral edema,decreased exercise tolerance,SOBOE

Physical Exam

Displaced hyperdynamic apex,left parasternal lid. apical thrill

Auscultation:holosystolic murmur atapex radiating to axilla * mid diastolic rumble,loud S2 (if

pulmonary HTN).S3

Acute MR:sudden acute and hemodynamic instability (possibility duringfpost Ml)

Investigations

ECG: LAE,left atrial delay (bifid P waves),

* LVH

CXR:LVH.LAE,pulmonary venous HTN

echo/TTE: etiology and severity of MR. LV/RV function,leaflets,pulmonary artery pressure,

vegetations/abscesses,papillary musdc/choidal rupture. LA sice,mitral valve apparatus,extent

of remodelling

TEE:can be helpfulwith acute MR or if considering transcalheter interventions:also used when TTE

findings are insufficient/inconsistent;assess for MR severity/mechanism and IV function

Swan Gant Catheter:prominent LA "v" wave

Other:CMR,exercise testing,stress nudear/PET,stress echo,and serum biomarkers/novel

measurement of LV function

Treatment

Acute MR:vasodilator therapy (use limited by systemic hypotension):intra aortic balloon counter

pulsation or percutaneous circulatory assist device may be employed

Asymptomatic:serial echos

Guideline directed management and therapy lor patients with severe MR andIVsystolic

dysfunction or HFrEF (e.g.ACEt.ARBs,beta blockers,aldosterone antagonists.ARNIs, biventricular

Mitral valve surgery (repair,commissurotomy,or replacement):symptomatic,severe rheumatic MS pacing)

with contraindicalion/limited access for PMBC.previous failure of PMBC,or otherwise undergoing intervention if:acute MR with CHF,papillary muscle rupture;severe MR with symptoms or LV

cardiac suigery (note:lestenosis in 50% of patients In 8 yr after open mitral commissurotomy)

Nonrheumatic,calcific MS:if severe MS and severe symptoms,valve intervention can be

contemplated pending discussion with patient abouthigh procedural risk

systolic dysfunction;AFib;increasing LV siiefprcsence of IV dilatation:pulmonaiy hypertension;

decreasing exercise tolerance:can be reasonable in other situations if low mortality risk (<1%) and

high probability of successfut/durable repair (>95%) or if otherwise undergoing CABG

Procedural Options

Mitral valve surgery (preferably repair)is indicated and lifesaving in acute, severe,symptomatic,

primary MR

Valve repair (preferred over replacement if degenerative disease is the etiology):>75%of patients

with MR and myxomatous MVP - annuloplasty rings,leaflet repair,chordae translers/shorteningf

replacement

Valve replacement if:failure of repair,heavily calcified annulus

Advantage of repair:low rate of endocarditis,no anticoagulation,less chance of re-operation

Transcalheter cdgclo- edgc repair (TEER):reasonable in patients with severe, symptomatic

primary MR with high/prohibitive surgicalrisk or in severe,symptomatic secondary MR if

associated with LV dysfunction

r “i

L J

+

C59 Cardiology and Cardiac Surgery Toronto Notes 2023

Table 18. Valvular Heart Disease

Tricuspid Stenosis Tricuspid Regurgitation :

-

I

=:

ill s

i

-

cn S, s, S.2

'Vi

!

,

s s

Etiology

Rheumatic disease,congenital,carcinoid syndrome,fibroelastosis;usually accompaniedby MS

(in rheumatic heart disease),autoimmune disorders,atrial mysomas, blunt trauma,mctastascs,

congenital,drug-associated valvulopathy

Definition

Tricuspid orifice narrowing:blood flow from the RA into the RV is obstructed

Pathophysiology

Increased RA pressure •right HF » CO decreased and fined on exertion

Symptoms

Peripheral edema,fatigue,palpitations

Physical Exam

Prominent “a* waves in JVP.positive abdominojugular reflux. Kussmaul's sign,

diastolic rumble 4th left intercostal space

Investigations

ECG: RAF

Etiology

RV dilatation.IE (particularly due to IV

drug use),rheumatic disease,iatrogenic (deviceleads,endomyocardial biopsy),congenital

(Ebstein's anomaly),pulmonary HTN.RV overload,DCM.annular dilation,leaflet tethering. RA

dilatation,ischemic heart diseases,other (trauma,carcinoid,drugs,irradiation)

Definition

leakage of blood across the tricuspid valve(i.e.bicuspidinsufficiency):can be primary or

secondary

Pathophysiology

RV dilatation -» TR (and further RV dilatation)

-*

right HF

Symptoms

Peripheral edema,fatigue,palpitations.SOBOE. ascites

Physical Exam

elevated JVP.“cv" waves in JVP.positive abdominojugular reflux,holosystolic murmur at LLSB

accentuatedby inspiration,left parasternal lift.

Investigations

ECG:RAE, RVH.AFib

CXR: dilatation of RA without pulmonary artery enlargement

echo:diagnostic

Cardiac catheterization:large R A “a"wave (12-20 mm Hg); diastolic,mean pressure gradient of 4-8 CXR:RAE,RV enlargement

mm Hg (Increased RA pressure with a slow decrease in early diastole * diastolic pressure gradient echofllE:diagnostic - assess lor ctiology/severity of TR.IVC and right heart sice. RV systolic

is classic for 1$)

CMR:RV sice/function

function,left-sided disease and pulmonary artery systolic pressure

Invasive measurements (to address inconsistencies):cardiac index,right-sided diastolic pressure,

pulmonary artery pressures,pulmonary vascular resistance,ventriculography

Treatment

Treatment

Preload reduction (diuretics) for severe,symptomatic IS (caution:may exacerbate low oulpul)

Treatunderlying etiology

Slow HR

Preload reduction (diuretics):reasonable if right-sided HF related to severe TR

Therapies to treat HF etiology reasonable if right-sided HF related to severe secondary TR

Surgery:usually performed at time of other cardiac surgery (e.g.mitral valve surgery for rheumatic Surgery if:severe TR (stages C and D) and undergoing cardiac surgery for a left-sided valve:can be

reasonable inother specific situations.

Surgical Options

Annuloplasty (i.e.repair:rarely replacement)

MS)

Surgical Options

Valvotomyusing13balloons

Valve surgery:repair or replacement (open or transcatheter options for replacement)

Usually bicuspid surgery favoured over percutaneous balloon tricuspid commissurotomy or

valvuloplasty

Pulmonary Stenosis Pulmonary Regurgitation

S 5

S -§

-

•

'

i

.'

J

5 I

S S' Sr S Sion

' © '©

Etiology

Usually congenital,rheumatic disease (rare),carcinoid syndrome

Definition

Stiffening/narrowing of the pulmonic valve:blood llow into the pulmonary artery from the RV is

obstructed

Pathophysiology

Increased RV pressure *

RVH*

right HF

Symptoms

Chest pain,syncope,fatigue,peripheral edema

Physical Exam

Systolic murmur at 2nd left intercostal space accentuated by inspiration; pulmonary ejection click;

right-sided S4

Investigations

ECG:RVH

CXR:prominent pulmonary arteries,enlarged RV

echo:diagnostic

Treatment

Balloon valvuloplasty if severe symptoms

Surgical Options

Percutaneous or open balloon valvuloplasty

Etiology

Pulmonary HIH,IE. rheumatic disease, tetralogy of Fallot (post-repair),defective valvular

coaptation,annular dilatation,fibrinoid deposits

Definition

Insufficient closure of the pulmonicvalve during diastole:reversal of flow into the RV

Pathophysiology

Increased RV volume » Increased wall tension

-* RVH -•right HF

Symptoms

Chest pain,syncope,fatigue,peripheral edema

Physical Exam

Early diastolic murmur al USB:Graham Stecll (diastolic) murmur at 2nd and 3rd lell intercostal

space (increasing with inspiration)

Investigations

ECG:RVH

CXR:prominent pulmonary arteries if pulmonaiy HTH;enlarged RV

echo:diagnostic

Treatment

Rarely requires treatment:valve replacement (rarely done)

Surgical Options

Pulmonary valve replacement

rt

+

C60Cardiology and Cardiac Surgery Toronto Notes 2023

Table 18. Valvular Heart Disease

Mitral Valve Prolapse 04

04

click

c

ss : s i

63

Etiology

Myxomatous degeneration ol chordae:thick,bulky leaflets that crowd orifice:associated with

connective tissue disorders: pectus excavatum;straight back syndrome,other MSK abnormalities;

<3% of population

Definition

Valve lea(let|s) prolapse into the U;common cause of MR.(i.e.dick-murmur syndrome,Barlow's

syndrome,billowing mitral valve leaflets, or floppy valve syndrome)

Pathophysiology

Mitral valve displaced into LA during systole:no causal mechanisms found for symptoms.Generally

benign;however,presentation may he withsudden cardiac death,infective endocarditis,or

cerebrovascular accident

Symptoms

Can he asymptomatic. May have prolonged, stabbing chest pain or atypical chest discomfort;

dyspnea; anxietyi'panic attacks;palpitations: fatigue:presyncope.S060E.exercise intolerance;

low blood pressure:syncope; orthostasis;moodchanges:syncope

Physical Exam

Auscultation:mid-systolic dick (diagnostic - due to billowing of mitral leaflet into LA and tensing of

redundant valve tissue);followed by a mid to late systolic murmur at apex (murmur accentuated by

Valsalva and diminishedwhen patient squatting)

Investigations

ECG:non-specific ST-T wave changes,paroxysmal SVT,ventricular edopy

echo:diagnostic - systolic displacement of mitral valve leaflets above mitral annulus into LA:

assess mitral valve leaflet thickness

Cardiac calhcleritalionflefl ventriculography:if inconsistent clinical and echo findings; sometimes

picks up MVP incidentally

Treatment

Asymptomatic:often no treatment:reassurance.If MR associated,follow-up annually;if not.

follow-up q3- 5 yr

Sinus rhythm and high- risk MVP:aspirin may be considered

Systemic embolism,recurrent IIAs despite aspirin,ischemic stroke, or Afib: anticoagulation

Symptomatic: 8-blockers and avoidance of stimulants (e.g.caffeine) of significant palpitations;

anticoagulation ifAfib

Surgical Options

Mitral valve surgery (repair favoured over placement):if symptomatic and significant MR;may be

reasonable If asymptomatic with MR and systolic HF

Iranscatheter mitral valve repair considered if high/prohibitive surgical risk

EO

r.

& < E

- *

s s

s

w

_r a

o c

no - tto - e no -

iv :

LV e

AORTIC

PRtSSURE 90 90 -

*

iDROP 90 -

AORTA s

— |70 - J 70 - E 70 -

m 3 s 5

JS 50

-

<

2 50 - *2 50

az -

30 30 - '

30 -

to - 10 to -

TIME TIME TIME

HEART

SOUNOS:

HEART

SOUNOS:

HEART

SOUNOS If

'

l I.

S,S 1 s,s 1 ss 2

r T

Figure 47. Hemodynamics of aortic stenosis

Stenosis across the aortic valve results in the

generation of a significant pressure gradient

between the LV and the aorta, as well as a

crescendo-decrescendo murmur during systolic

contraction. The stenosis decreases the intensity

of aortic valve closure,hence diminishing S2

Figure 48. Hemodynamics of aortic

regurgitation

Regurgitation across the aortic valve during

diastole causes the aortic pressure to rapidly

decrease and a decrescendo murmur can be

heard at the onset of diastole (after S2). The

presence of regurgitant blood from the aorta

increases LV end diastolic volume

Figure 49. Hemodynamics of acute mitral

regurgitation

During systolic contraction, blood regurgitates

from the LV into the LA across the incompetent

mitral valve resulting in a short but audible

holosystolic murmur between S1 and S2.The

portion of left ventricular end diastolic volume

that regurgitates into the LA myocardium

increases left atrial pressures resulting in a tall

V-wave (in the JVP). Severe, acute MR usually

results in acute hemodynamic decompensation

c.J

+

C61 Cardiology and Cardiac Surgery Toronto Notes 2023

Transcatheter (TAVR ) or Surgical (SAYS) AorticValve Replacement in Intermediate disk Patients

{PARTNER IITrial)

NEJH 2016:374:1609-1620

Purpose: To determine il TAVR and SAVO result m

different survival rates amongintermediate-risk

patientswith AS.

Methods: Patients with AS were randomred to

either TAVR |IM011)or to SAVR |n-102lT The primary

endpoint was death Irom any cause or disabling

stroke at 2 yr.

Results: The death rate Irom any cause or drsablng

stroke was sim tar in the IAYR and SAVR groups

(P'0.001for noninferiority).In the translemoralaccess cohort TAVR resulted m a lower rate of death

or disadkng stroke than SAVR did (P'0.05). In the

transthoracic-access cohort,similar outcomes were

obserred in the TAVR and SAVR groups. TAVR resulted

in larger aortic valve are as and lower rates of AKI.

severe bleeding, and new onset AFib.Fewer major

vascular complications and less paravahrular AR were

observed in patients who underwent SAVR.

Conclusion: In intermediate-risk pabentswith AS.

TAVR an d SAVR resulted in similairates of all-cause

mortality and disabling stroke.

110 -

90 -

£

E

S 70 -

ui

3

(2 50 -

cc

30 -

10 -

HEART

SOUNDS:

lllllllijll

SS 2 OS s s

© Young M Kun 2010

Figure 50. Hemodynamics of mitral stenosis

First note that the left atrial pressure exceeds the left ventricular pressure during diastole due to MS and there is

a consequent generation of a pressure gradient across the LA and LV. In diastole, the stenotic mitral valve opens

(which corresponds to the OS) and the passage of blood across the MS results in an audible decrescendo murmur.

Left atrial contraction prior to S1 increases the pressure gradient resulting in accentuation of the murmur before S1

is audible

See landmark Cardiac Thais for more information on

PARTNER III which details Ihe outcomes of law -r.sk

patients who underwent TAVR or surgical aortic-valve

replacement.

Pericardial Disease

Anterior leaflet laceration to Prevent Ventricular

Outflow Tract Obstruction During Transcatheter

Mitral Valve Replacement (IAMP00N)

J Am Coll Cardiol.2019 Jut 30:?4|4|:59S

Background:Traiacathether mitral valve

replacement (1MYR) is routinely employed in patients

with valvular disease who are unsuitable foi open

surgical interventions.Ihe primary complication

of tins procedure is IV0Iobstruction as a result

of the anterior mitral leaflet impinging on the

interventricular septum.

Purpose lo study intent one iteration ol the

anterior mitral valve leaflet (IAHP00HI alongside

IMVR to prevent the tomplication ot LV01obstruction.

Methods: Between June 20IJand June 2018, 30

patients with severe MRIMS.hgh surgical risk, and

prohibitive risk ofIV0T obstruction,underwent

IMVR with LAMPOON.Ihe pr maryoutcomes were

technical success fur TMVR and LAMPOON (successful

laceration) procedures.IV0Igradient <30 mmHg.

freedom from emergentre-intervention,and

procedural mortality.

Nesults: Ihe IAMP00N laceration was deemed

successful in 1001of enrolled patients.100% of

patients survived immediately post-procedure, with

93% suinving 30 d after discharge. 90% of patients

had an LVOI gradient <30 mmHg (optimal range) after

IMVR.with100% of patients showing LV0T gradient

<60 mmHg (acceptable range). Ihe procedural

success rate was 73% from tie remaining 22 subjects.

Conclusions: In die studied population.LAMPOON

mitigates the risk of IV0Iobstruction with IMVR.

LAMPOON is technically leasibleand serves to enable

IMVR 1patients otherwise deemed ineligible due to

prohibitive risk olIVOI obstruction.

Acute Pericarditis

Definition

• syndrome involving the inflammation of the pericardium that may present with or without a

pericardial effusion

• pericarditis can be divided into:

• acute (<4-6 wk)

• incessant (>4-6 wk with no remission)

recurrent (symptom-free remission period of 4-6 wk followed by new onset of pericarditisassociated signs and symptoms)

chronic (>3 mo)

Etiology of Pericarditis/Pericardial Effusion

• idiopathic is most common (presumed to he viral)

searching for and identifying the etiology is not required in all patients; in nations with low TB

prevalence, the most common causes of pericarditis are generally benign

infectious only approximately 14%

viral: Coxsackie virus A, B (most common), echovirus. Parvovirus B19, Epstein-Barr virus

• bacterial; S. pneumoniae, S. aureus, B. burgdorferi, M. tuberculosis

HIV

• fungal: histoplasmosis, blastomycosis

• post-Ml: acute (direct extension of myocardial inflammation, 1 -7 d post-Ml), Dressler’

s syndrome

(autoimmune reaction, 2-8 wk post-Ml)

• post-cardiac surgery (e.g. CABCi), other cardiac procedures (e.g pacemaker insertion or TAVR), or

other trauma

• metabolic: uremia (common), hypothyroidism

• neoplasm: Hodgkin’

s, breast, lung, renal cell carcinoma, melanoma, lymphoma

• collagen vascular disease: SLE, polyarteritis, rheumatoid arthritis, scleroderma

• vascular: dissecting aneurysm

• other: drugs (e.g. hydralazine), radiation, infiltrative disease (e.g. sarcoidosis), vaccination (e.g.

smallpox)

• autoimmune diseases

• immune checkpoint-inhibitor-associated pericarditis (severe; requires immunosuppressive therapy)

• seel-

'

igure 51, C62 for a proposed approach to triaging pericarditis

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C62 Cardiology and Cardiac Surgery Toronto Notes 2023

Pericarditis?

( physical examination, ECG. chest x-ray,

echocardiogram, CRP, troponin) Phase 3 Trial ollnterleukin-1Trap Rilonacept in

Recurrent Pericarditis (RHAPSODY)

HEIM 2021:384:3141

Purpose: Evaluate the efficacy and safety of

rilonacept, an interifukir.-la and theytokine trap,at

a mediator ol recurrent pericarditis.

Methods: Patentswith acute symptoms of

recurrent pericarditis and systemic inflammation

(elevated CPP lenel|were enrolled in a 12-wtr rua-in

period, during winch lilonacept was in dialed and

background mediations discontinued.Patients

were randomized fid rat D) to receive continued

rilonacept monotherapy or placebo, administered SO

once weekly.Ihe primary endpoint wasrecurrence of

pericarditis symptoms.

Results: During the randomiied w thdrawa! period,

there weic too few recurrences in ihe rilonacept

group to calculate median recurrence lime.In the

placebo group,median recurrence1me was8.S wk

|95\Cl 4.0 toll.7; haia id ratio 0.04:95% Cl O.OIto

0.18:P- 0.001). Outing this period.2 of 30 patients

(7%) in the rilonacept group had a pericarditis

recurrence, as compared to 23 of 32 patients(74%) in

tteplacebogroop.

Conclusion: Among patients with lec orient

perxarditis,rilonacept ltd to faster resolution of the

current episode and lower recurrence.

No 1 Yes

T V

Diagnostic criteria not satisfied Specific etiology highly suspected

Search for alternative diagnoses or any predictor of poor prognosis

Yes 1 Empiric trial with NSAID No

Predictors of Poor Prognosis

Major

• Fever >39C

•Subacute onset

• Large pericardial effusion

•Cardiac tamponade

• Lack of response to ASA or

NSAIDs after at least a week

ol therapy

V T

High Risk Cases

Admission and etiology

search (major or minor

prognostic predictor)

Non-High Risk Cases

No admission and etiology search

Response to NSAIO?

No Yes

£ I

Moderate Cases

Admission and etiology search

Low Risk Cases

Outpatient follow-up Minor

* Myopericarditis

• Immunosuppression

•Trauma

* Oral anticoagulant therapy CRP = C-reactrve protein

Proposed triage of acute pcricaditis accordint to epidemiological background and predictors of poor prognosis at presentation. At least

one predictor of poor prognosis is sufficient to identify a high risk case. Maior criteria have been validated by multivariate analysis,

minor criteria are based on expert opinion and literature review.Cases with moderate risk are defined as cases without negative

prognostic predictors but incomplete or lacking response to non-steroidal anti-mflammatory drug (NSAID) therapy. Low risk cases

include those without negative prognostic predictors snd good response to anti-inflammatory therapy Specific etiology is intended as

non-idcopathic etiology

Figure 51.Proposed triage of pericarditis

Clinical Presentation, Investigations, and Diagnosis

• 2 of the following 4 needed for diagnosis

1. chest pain

sharp, rapid onset ( may be dull or throbbing)

pain commonly radiates to the trapezius ridge

pleuritic; pain related to inspiration, coughing, and potentially hiccoughs

improves with sitting up/leaning forward

2. pericardial friction rub

with patient leaning forward or on elbows and knees, friction rub heard on left sternal border

classically triphasic; may be mono- or biphasic

varies in intensity over time; repeated examinations necessary

highly specific finding

3. ECG changes(only about 60% of patients have sequential changes)

stage 1: PR depression and generalized ST elevation (a generally specific finding but up to 40%

have nondiagnostic and atypical changes)

stage 2:stage I findings reversed;|points on baseline prior to flattening of T waves

stage 3:inversion of T-waves

stage 4: all changes normalized

changes noted on ECG can be localized or diffuse; PR depression may he the only sign

4. pericardial effusion (new or worsening)

• other physical exam findings:+ malaise, ± sinus tachycardia, ± low-grade fever, ± non-cardiac

findings if the acute pericarditis is related with a systemic condition (e.g. rash, arthritis, weight loss,

night sweats)

• other investigations may aid in diagnosis/monitoring

• biomarkers/inflammatory markers

cardiac-specific troponin 1 or T elevation (£30% of patients)

-evidence of myocardial

involvement (could be myopericarditis or perimyocarditis).Imaging modalities such as echo

or CMK may also provide evidence of myocardial involvement

elevated CRP, ESR, and/or WBC count found in majority of patients, but not sensitive or

specific (elevated high-sensitivity CRP can predict recurrence risk)

• imaging

• CXR

- usually normal heart size (effusion >300 mL needed to increase cardiothoracic index)

- patients with a new/unexplained increase in heart size should he worked up for acute

pericarditis (especially when lung fields are clear)

- may demonstrate evidence of pleuropericardial involvement in the setting of

pleuropulmonary disease

- cause of pericarditis can sometimes be identified

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C63 Cardiology and Cardiac Surgery Toronto Notes 2023

echo:often the only necessary modality for imaging (THE > T I E) -» normal in 40%

- applications include:

- identifying pericarditis-associated complications (e.g. cardiac tamponade,

constrictive pericarditis) or components of myocarditis (e.g. ventricular

dysfunction)

- monitoring pericardial effusion and efficacy of therapy

- providing real-time evaluation during pericardial drainage

( MR,CT may also have applications in the setting of pericarditis; assess for inflammation of

pericardium

•differential diagnosis includes:Takotsubo syndrome, Ml, myocarditis

Prognosis

•based on etiology (e.g. overall good prognosis = idiopathic/viral pericarditis (although significant

recurrence risk), pericarditis with myocardial involvement; purulent and neoplastic pericarditis have

a reported mortality rate between 20-30%)

negative prognostic factors:subacute onset, fever >38°C, >20mm pericardial effusion on echo,

tamponade, lack of response following 1 wk of anti-inflammatory treatment -» hospitalize

patients with these factors and those with an elevated tamponade and/or constriction risk

minor negative prognostic factors:oral anticoagulation, trauma,immunosuppression

Treatment

•treat the underlying disease

•anti

-inflammatory agents remain the mainstay for treatment (e.g. NSAIDs/ASA)

ketorolac may be employed in patients with severe pain or patients unable to take oral

medication; use should be limited to 5 d

•colchicine may reduce symptom persistence and recurrent rates

•corticosteroid use is controversial but may be indicated in patients with incomplete response,failure

of other anti-inflammatory medications, and/or other indicated situations (e.g. autoimmune diseaseassociated or immune checkpoint inhibitor-associated pericarditis)

•purulent pericarditis (rare but life-threatening): pericardial drainage and antimicrobial therapy

catered to the culprit etiologic agent and/or local fibrinolytic therapy

•tuberculous pericarditis:multidrug regimen for several months (corticosteroids and pericardiectomy

sometimes considered)

•pericarditis in the setting of viremia ( particularly in immunocompromised patients):antiviral

treatment

physical activity restriction until symptom resolution

Complications

•recurrent episodes of pericarditis, atrial arrhythmia, pericardial effusion,tamponade, constrictive

pericarditis

Pericardial Effusion

Definition

• fluid accumulation in the pericardialsac (note:the pericardialsac normally hosts 10-50 mL of

lubricating pericardial fluid). The composition of the fluid can include exudate, transudate, blood, and

rarely air/gas

Etiology and Classification

• effusion isfound incidentally on x-ray or echo for a significant proportion of patients

for these patients in developed countries, etiologies include:

idiopathic (up to 50%)

cancer (10-25%)

infections (15-30%)

iatrogenic causes(15-20%)

connective tissue diseases (5-15%)

• in developing countries, I B is the predominant cause (>60%)

• for pericardial effusion with pericarditis, the prevalence of malignant/infectious etiologiesis 15-50%

• transudative causes

• increased systemic venous pressure or hydrostatic pressure:CHE, pulmonary HTN

decreased plasma oncotic pressure: cirrhosis, nephrotic syndrome, hypoalbuminemia/

hypoproteinemia

• exudative causes (serosanguinous or bloody)

• pathologic process -> inflammation -> possible increased production of pericardial fluid

causessimilar to the causes of acute pericarditis

may develop acute effusion secondary to hemopericardium (trauma, post-Ml myocardial rupture,

aortic dissection)

• can be classified according to onset,distribution, hemodynamic impact,composition,and size

• physiologic consequences depend on type and volume of effusion,rate of effusion development, and

underlying cardiac disease

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C61Cardiology and Cardiac Surgery Toronto Notes 2023

Signs and Symptoms

• rate of development of pericardial effusion determines clinical presentation

• may be asymptomatic orsimilar to acute pericarditis

• classic symptoms: dyspnea on exertion (progressing to orthopnea), chest pain and/or fullness

• symptoms related to local compression of extracardiac structures may include: nausea, dysphagia,

hoarseness, hiccoughs; may cause esophageal/recurrent laryngeal nerve/trachea-bronchial/phrenic

nerve irritation

• non-specific symptoms related to compression of related structures or reduced blood pressure

and secondary sinus tachycardia: cough, weakness, fatigue, anorexia, palpitations, fever (may be

associated with pericarditis)

• physical exam findings:

J VP increased with dominant “x"

descent

arterial pulse normal

-to-decreased volume;decreased pulse pressure

auscultation:distant heartsounds ± rub

• Ewart'

ssign

« often normal in patients without compromise to hemodynamic status;if tamponade present,

findings can include fatigue, dyspnea, elevated|VP, neck vein distension, edema, pulsus

paradoxus, muffled heart sounds(in moderate-large effusions).Rarely friction rubs heard

(usually appreciated with concomitant pericarditis)

Ewart's Sign

Egophony. bronchial breathing,and

dullness to percussion at the lower angle

o( the left scapula in pericardial effusion

due to effusion compressing left lower

lobe of lung

Investigations

• KCG:sinus tachycardia,low voltage (should raise concern for effusion with tamponade when present

with sinus tachycardia; however, not specific for pericardial effusion), flat T waves, electrical alternans

(highly specific for pericardial effusion (generally with tamponade), but not a sensitive sign to exclude

effusion/tamponade)

• be cautious in diagnosing STEM1in a patient with pericarditis and an effusion as antiplatelets

may precipitate hemorrhagic effusion

• CXR:± cardiomegaly with dearlung fields, ±

• emergency room: bedside U/S with subxiphoid view showing fluid in pericardial sac

• echo/TTE (procedure of choice):fluid in pericardial sac;assess effusion size and hemodynamic effects,

and assist in needle placement in pericardiocentesis

• pericardiocentesis: definitive method of determining transudate vs. exudate, identify infectious

agents, and investigating neoplastic involvement

• CT/CMR: compared with echo, provide greater field of view -> enable loculated effusion detection,

identification of masses or thickening associated with the pericardium, assessment for chest

abnormalities (however, echo still preferred due to availability/portability/low cost)

• biomarkers: assessment of inflammation markers (e.g.CRP) recommended

Treatment (see Figure 52,C65)

• triage: based on size, hemodynamic effects (particularly assess for tamponade), inflammatory

markers, concomitant pathologies -> high risk patientsshould be admitted

• treat underlying etiology (60% of effusions associated with known disease)

• if inflammatory signs are present, or if associated with pericarditis, treat as if pericarditis; if elevated

markers of inflammation, can try NSA IDs/colchicine/low-dose corticosteroids; if associated with

systemic inflammation, Aspirin"

/NSAlDs/colchicine recommended

• pericardiocentesis or cardiac surgery if: cardiac tamponade,symptomatic moderate-large effusion and

unresponsive to medical therapy,or unknown bacterial/neoplastic etiology suspected

• prolonged drainage using pericardiocentesis should also be considered if symptomatic effusion

without evidence of inflammation or unresponsive to anti-inflammatory agents

if no inflammation and large, isolated effusion, pericardiocentesis alone may be required (no

evidence for medical therapy), but recurrences are common

consider pericardiectomy or pericardial window (subxiphoid or video assisted thoracoscopic) if:

re-accumulation of fluid, loculated effusion, biopsy required

• follow-up/frequent observation if no evidence/suspicion of:

tamponade

bacterial/neoplastic etiology

elevated inflammatory markers

associated pathology

large effusion (>20 mm)

Note:follow-up based on symptoms, effusion size and evolution,inflammatory markers, etc.

rounded cardiac contour

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C65Cardiology and Cardiac Surgery Toronto Notes 2023

Empiric anti-inflammatory therapiesshould be considered

if a missed diagnosis ol pericaditis is presumed

Cardiac tamponade or suspected

bacterial or neoplastic etiology?

*

Yes No

i

Periacardiocentesis

and etiology search

Elevated inflammatory

markers?

Yes I No

T T

Empiric anti-inflammatory

therapy (treat as pericaditis)

Known associated

disease?

Yes No No Follow-up V y

Pericardial effusion

probably realted

Treat the disease

Large < >20 mm)

pericardial effusion?

Consider

periacardiocentesis

and drainage if

chronic (>3 mo)

Figure 52. Triage/management algorithm for pericardial effusion

Cardiac Tamponade

Definition

• accumulation of fluid, pus, blood, clots or gas in the pericardium leading to life-threatening,slow or

rapid compression of the heart

Classic Ouartet of Tamponade

• Hypotension

- Increased JVP

• Tachycardia

• Pulsus paradoxus

Etiology

• can he caused by inflammation, trauma, rupture of the heart or aortic dissection

• major complication of rapidly accumulating peric

• cardiac tamponade is a clinical diagnosis

• common causes: pericarditis,TB, iatrogenic, trauma, neoplasm/malignancy

• uncommon causes: collagen vascular diseases (e.g.SLE, rheumatoid arthritis,scleroderma), radiation,

post-MI, uremia,aortic dissection, bacterial infection, pneumopericardium

Pathophysiology

• high intra-pericardial pressure -> decreased venous return -> decreased diastolic ventricular filling »

decreased CO -> hypotension and venous congestion

Signs and Symptoms

• tachycardia, hypotension, increased ) VP

• tachypnea, dyspnea,shock, muffled heart sounds

• pulsus paradoxus (inspiratory fall in sBP >10 mmHg during quiet breathing)

•|VP “x” descent only, blunted “y” descent

• hepatic congestion/peripheral edema

• severity ofsigns/symptoms depend on rate of accumulation, volume of pericardial contents,

pericardial distensibility,cardiac filling pressures, and chamber compliance

ardial effusion

Beck'

s Triad

• Hypotension

. Increased JVP

• Muffled heart sounds

Investigations

• ECCi: electrical alternans (pathognomonic variation in R wave amplitude), low voltage

• CXR:enlarged cardiac silhouette;slow-accumulating effusions

• GT/GMR: less available; usually only necessary if Doppler echo is infeasible

• echo (diagnostic modality of choice):pericardial effusion (size,location, hemodynamic impact),

swinging of the heart, compression of cardiac chambers(RA and RV) in diastole, etc. -> echo also used

for the purpose of guiding pericardiocentesis

• cardiac catheterization (rare)

Treatment

• urgent drainage: needle pericardiocentesis recommended (with echo or fluoroscopic guidance);

surgery (i.e. pericardiotomy) is an alternative drainage approach (e.g. with purulent pericarditis or in

an urgent situation involving bleeding into the pericardium)

• avoid diuretics and vasodilators (these decrease venous return to already under-filled RV -> decrease

LV preload -> decrease CO) as well as mechanical ventilation

• IV fluid may increaseCO

• treat underlying cause

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C66Cardiology and Cardiac Surgery Toronto Notes 2023

A. No pathology B. Cardiac tamponade {inspirationI

Ventricular wall

collapse on

inspiration

Pericardial effusion

F— Pericardial fluid

pressure

on cardiac

chambers

Interventricular

septum

Pericardium

(pericardial sac

i

pericardial fluid)

C.Cardiac tamponade (expiration) 0.Pericardiocentesis

-Improvement in

cardiac

output on

expiration

Resolution of

ventricular

wall collapse

•

Pericardial effusion

-Pericardial fluid

pressure

on cardiac

chambers

Removal of excess

pericardial fluid

©Jennifer Lee 2021

Figure 53.Cardiac tamponade pathophysiology

Constrictive Pericarditis

Definition

• loss of pericardial elasticity caused by granulation tissue formation; leadsto restricted ventricular

filling

Etiology

• chronic pericarditis resulting in fibrosed, thickened, adherent,and/or calcified pericardium

• any cause of acute pericarditis may result in chronic pericarditis

• major causes are idiopathic, post-infectious (viral, bacterial pericarditis/purulent pericarditis,TB),

radiation, post-cardiac surgery, uremia,Ml,collagen vascular disease

• any pericardial disease process can cause constrictive pericarditis; risk of progression to constrictive

pericarditisis based on the etiology of the pericardial disease

Pathophysiology

• rigid,fibrous pericardium impairs ventricular filling during diastole -» decreased venous return to

the heart -» rise in systemic venous pressure -> signs and symptoms of right-sided HF (classically with

preserved ventricular function and otherwise no myocardial disease)

in advanced cases,there can be systolic dysfunction if myocardial fibrosis or atrophy present

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C67 Cardiology and Cardiac Surgery Toronto Notes 2023

Signs and Symptoms

• dyspnea,fatigue, palpitations

• abdominal pain

• may mimic CHF (especially right-sided HI-

'

)

• venous congestion, ascites, hepatosplenomegaly, edema, pleural effusions

• increased|VP, Kussmaul'

s sign (paradoxical increase in )VP with inspiration), Friedreich’

ssign

(prominent “y” descent)

• BP usually normal (and usually no pulsus paradoxus)

• precordial examination: ± pericardial knock (early diastolic sound)

• see Table 19 for differentiation from cardiac tamponade

Investigations

• HCG: non-specific findingslow voltage, flat T wave, ± AFib

• CXR:pericardial calcification, effusions

• echo/CF/CMR: pericardial thickening, calcification ± characteristic echo-Doppler findings(Note:

CMR is discouraged if patient is hemodynamically impaired)

• cardiac catheterization:indicated if other, non-invasive imaging modalities are insufficient to make

diagnosis; assessfor equalization of end-diastolic chamber pressures

• diagnosis:right HF symptoms + diastolic filling impairment caused by constriction (documented on

SI imaging modality including echo,CT,CMR, and/or catheterization)

• note:in up to 20% of patients, constriction can occur even with normal thickness of the pericardium

(pericardiectomy equally efficacious in these patients)

DDx Pulsus Paradoxus

• Most etiologies of RV failure except

restrictive cardiomyopathy (e.g.

acute RV Ml)

• Constrictive pericarditis(rarely)

• Severe obstructive pulmonary

disease (e.g.asthma)

. Pneumothorax

. PE

• Cardiogenic shock

• Cardiac tamponade

• Effusive-Constrictive pericarditis

Treatment

• surgery (pericardiectomy):mainstay treatment for chronic, permanent constrictive pericarditis

• medical therapy:can be used in 3 situations

1. for specific pathologies/etiologies (e.g.TB)

2. for transient constriction that is temporarily caused by pericarditis,or new constriction

diagnosis with evidence of inflammation of the pericardium (use anti-inflammatories)

3. supportive when high/prohibitive surgical risk (goal isto relieve congestive symptoms with

diuretics,salt restriction)

• prognosis best with idiopathic or infectious cause and worst in post-radiation

• death may result from HF

Table 19. Differentiation of Constrictive Pericarditis vs. Cardiac Tamponade

Characteristic Constrictive Pericarditis Cardiac Tamponade

JVP V»V -x- »

V

Kussmaul Absent 's sign

Pulsus paradoxus

Pericardial knock

Hypotension

Present

Uncommon Always

Present Absent

Variable Severe

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C68Cardiology and Cardiac Surgery Toronto Notes 2023

Extracorporeal Circulation

lOrtic cross-clamp

Systemic flow line

Pressure (Temperature 3 Cardioplegia delivery line iLiS

nj

'

i

Aortic root suction

Cardioplegic

Cardiotomy solution suction

vj 1 Left ventricular vent

One-way

valve

HKHk t 1 1 t 1 1 i t

Venous

clamp

Cardiotomy

reservoir

Filter

Lrf 0

Vent Suction Suction

^

/ cardioplegia

Arterial filter pump

and bubble Venous

reservoir 1

Level sensor

trap

Gas fitter |—| y~~ a

I

Oxygenator i

'

X /

Flowmeter

1 Systemic

blood pump

l vs\SCooler heater

water source

Air

02

Anaesthetic Blender

vaporiser meter ®Hoorn*

Znan2021 J

Figure 54.Cardiopulmonary bypass schematic

Modified from Cardiac Surgery in the Adu:t

_ second edition.Robert A.E Dion.p.729.Copyright(2020).withpermission from Elsevier

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C69 Cardiology and Cardiac Surgery Toronto Notes 2023

Cardiopulmonary Bypass

Overview

•CPB is commonly used in cardiac and thoracic aortic surgeries to obtain a still, bloodlesssurgical field

by circumventing the heart and lungs while supplying blood to the systemic circulation

•essential functions of CPB:oxygenation, ventilation, circulation, temperature control

Components

•the standard components of a CPB circuit:

arterial cannula (aortic,femoral, or axillary) and line (3/8” heparin-coated tubing)

oxygenator (membrane oxygenator,defoamer, and heat exchanger)

pump (peristaltic/roller or centrifugal)

venous cannula (RA,SVC and IVC,or femoral) and line (1/2” heparin-coated tubing)

venous reservoir (rigid high capacitance reservoir or closed soft reservoir)

Mechanics

•venous blood is drained into venous reservoir. The blood is oxygenated, and CO i is eliminated, heated,

or cooled (if applicable) and returned to the systemic circulation via the arterial cannula

heparin is first administered so that pump suckers can be turned on when the patient'

s ACT is

>400 s and CPB initiated when ACT is >480 s

•

ACT is measured every 30 min while on CPB and additional heparin boluses are administered

to maintain ACT >480 s

anticoagulation is reversed following separation of CPB by administering protamine which

neutralizes heparin

the rate of blood draining into the venous reservoir is determined by the:CVP, height differential

between venous cannula and venous reservoir,luminal radius of venous cannula and tubing,

presence of air within the tubing

arterial cannulation is typically performed at the distal ascending aorta, distal to the aortic

cross clamp, with alternative sites for cannulation including the aortic arch, innominate artery,

subclavian artery, axillary artery, femoral artery, and LV apex

optimal flow rate is calculated to achieve a cardiac index of 2.4 L/min/mpatient parameters measured during CPB:ECG, BP,CVP,SaO 2,ETC02, peripheral and core

temperature, urine output, ABG

CPB pump parameters measured duringCPB:blood flow rate, roller pump/centrifugal speed, gas

flow, pump blood temperature, heat exchanger water temperature, arterial line pressure, arterial

and venous line 02 saturations, delivered O 2 concentration

Complications

•reaction to non-endothelialized foreign surfaces:systemic inflammatory response, hemolysis,

coagulopathy

•vessel injury from cannulation:aortic dissection and embolization of aortic debris (e.g. porcelain

aorta)

•heparin-related:heparin-associated thrombocytopenia, heparin-induced thrombocytopenia (HIT)

•systemic embolization:cerebrovascular accident, renal and splanchnic hypoperfusion

includes biologic and nonbiologic microemboli as well as air/gas/bubble emboli

cardiotomy reservoir must be filtered to reduce risk of microemboli

Cardiac and Neurological Protection during Cardiopulmonary

Bypass

Myocardial Protection Techniques

• myocardial protection reduces myocardial ischemia during CPB by reducing myocardial oxygen

consumption and maintaining oxygenated myocardial perfusion

• methods of myocardial protection to reduce oxygen demands include: unloading the heart (CPB),

stopping the heart (cardioplegic diastolic arrest), cooling the heart (core hypothermia, cold saline

external washing, hypothermic cardioplegia solutions)

• cardioplegia (given continuously or intermittently) induces diastolic arrest by altering myocytes'

resting potential and ionic gradients via concentrated K+ solutions

• crystalloid cardioplegia

extracellular solutions(high sodium) (e.g.St. Thomas'

solution,del Nido solution) increase

extracellular K+ concentration to prevent cardiomyocyte repolarization

intracellularsolutions(low sodium) lower extracellular Na+ concentration thereby blocking

depolarization

blood cardioplegia: autologous cold blood combined with tailored crystalloid solutions in various

ratios

» blood typically comprises majority of overall solution (e.g.8:1, 4:1, 2:1)

Special Consideration of Blood

Conservation forJehovah's Witness

(Clients

• Preoperatively:

• Administer erythropoietin

• Stop all anticoagulant and

antiplatelet medicationsfor 7 d, if

possible

• Intraoperativety:

• Continuous cell salvage circuit

• Meticulous hemostasis

. OPCAB

• Pharmacological adjuncts

(tranexamic acid or aprotinin)

• Postoperatively:

• Low threshold for rcsternotomy due

to bleeding

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C70 Cardiology and Cardiac Surgery Toronto Notes 2023

Cerebral Protection

• cerebral protection techniques are required when CPB cannot supply the head vessels,such as during

surgery on the aortic arch

• methods of cerebral protection to reduce oxygen demands include: hypothermia (most important)

and anterograde/retrograde cerebral perfusion

Deep Hypothermic Circulatory Arrest

• deep hypothermic circulatory arrest reduces cerebral metabolism and oxygen consumption to the

point that CPU can be discontinued

• (3(M0 min safe circulatory arrest at 20°C;

-15-60 min safe circulatory arrest at 16“C)

concurrent ACP enables circulatory arrest at higher temperatures than DHCA alone

• liECi monitoring occurs throughout to confirm adequate cerebral protection

• mannitol (reduces cerebral edema ) and steroids (decrease cerebral inflammation) are used

adjunctively

complications related to deep hypothermic circulatory arrest include: coagulopathy and platelet

dysfunction,systemic inflammatory response, neurological injury secondary to ischemia in

watershed areas (neurologic dysfunction may be persistent or transient depending on etiology)

Common Medications

Table 20. Commonly Used Cardiac Therapeutics

Drug Class Examples Mechanism of Action Indications Contraindications Side Effects

ANGIOTENSIN CONVERTING ENZYME INHIBITORS ( ACEI)

enalapril (Vasotec'

),

perindopril (Coversyl '

),

ramipril (Allaccs).

lisinopril (Zestril '

)

Inhibit ACE-mediated

conversion of angiotensinI

to angiotensin II(AT II),

causing peripheral

vasodilation and decreased

aldosterone synthesis

HTN.CAD,CHE,post Ml, DM Bilateral renal artery stenosis. Dry cough (10%).hypotension,

pregnancy,caution in

decreasedGER

fatigue,hyperkalemia,renal

insufficiency,angioedema

ANGIOTENSIN IIRECEPTOR 8L0CKERS (ARBs)

candesartan.irbesartan,

losartan. olmesarlan.

lelmisarlan. valsartan

Same as ACEI Similar lo ACEI. but do not

cause dry cough

Bloch AT IIreceptors,causing Same as ACEI,although

similar effects as ACEI evidence is generally less lor

ARBs:often used when ACEI arc

not tolerated

ANGIOTENSIN RECEPTOR - NEPRILYSIN INHIBITOR (ARNI)

sacubilril/valsarlan (Entreslo ') Sacubilril inhibits neprilysin HFrEF

which leads to vasodilation

and natriuresis

Valsartan (ARB)

- see above

Angioedema.hyperkalemia,

hypotension,renal

insufficiency

Angioedema. pregnancy

DIRECT RENIN INHIBITORS (ORIs)

HTN (exact role of this drug

remains unclear)

Not recommended as initial

aliskiren Directly blocks renin thus

inhibiting the conversion

of angiotensinogen to

angiotensin I;this also causes therapy

a decrease in AT II

Pregnancy.severe renal

impairment

Diarrhea, hyperkalemia (higher

risk if used with an ACEI).rash,

cough,angioedema,reflux,

hypotension,rhabdomyolysis,

seizure

P-BLOCKERS

P1antagonists HTN.CAD, acute Ml,post- MI,

receptors,decreasing HR, BP. CHF (start low and go slow),

contractility,and myocardial AFib,SVT

oxygen demand;also slow

conduction through the AV

node

Block p-adrenergic Sinus bradycardia,2nd or

3rd degree heart block,

hypotension

Caution in asthma,

claudication.Raynaud's

phenomenon,and

decompensated CHF

Hypotension,fatigue,

light-headedness.

depression,bradycardia,

hyperkalemia, bronchospasm.

impotence,depression of

counterregulatory response to

hypoglycemia, exacerbation of

Raynaud's phenomenon, and

claudication

atenolol,metoprolol,

bisoprolol,

propranolol,

labetalol,carvedilol,

accbutolol

pifp2 antagonists

a1.'B1fp2 antagonists

P1antagonists with

intrinsic sympathomimetic

activity

CALCIUM CHANNEL BLOCKERS

Bcnzothiazcpines

Phenylalkylamincs

(non- dihydropyridines)

Block smooth muscle and HIN.CAD, SVT.AFib,diastolic

myocardial calcium channels dysfunction

causing effects similar to

0-blockers

Also vasodilate

Block smooth muscle calcium HIN.CAO

channels causing peripheral

vasodilation

Sinus bradycardia,2nd or

3rd degree heart block,

hypotension.CHF

dllliacem

verapamil

Hypotension,bradycardia,

edema

amlodipine (Notvasc ').

nifedipine (Adalaf ),

felodipine (Plendil )

Severe AS and liver failure Hypotension,edema.Hushing,

headache,light-headedness

Dihydropyrldines

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C71 Cardiology and Cardiac Surgery Toronto Notes 2023

Table 20. Commonly Used Cardiac Therapeutics

Drug Class Examples Mechanism of Action Indications Contraindications Side Effects

SODIUM-GLUCOSE COTRANSPORTER - 2 (SGLT2) INHIBITORS

Severe CKO (dapagliflozin

contiaindKated in patients

with cGER <30ml/

multiple other SGLI2 inhibitors mm/U3m;

).11DM.history of ketoacidosis,decreased bone

OKA. advise holding during mineral density

dapaglilloiin has received sick days

guideline recommendations

in Canada,US and EU lor use

in HFrEF,no SGLT2 inhibitors

have formal approval for HFrEF

without DM by HealthCanada

HFpEF (see EMPEROR-Preserved

Veasl inlections.Urinary trad

Infections,hypoglycemic

episodes, diabetic

canaglillocm

dapaglillonn

empaglillocln

erluglillocin

Dapaglilloiin trial(DAPAHF)

include: osmotic diuresis and Indicates potential use in

natriurcsis reducing preload: HFrEF with DM/non- OM,with

vasodilation leading to

reduced afterload: myocardial trials underway.Although

metabolic stabilnatron

Pioposed mechanisms

trial)

DIURETICS

Reduce (In'reabsorption in HTN (drugs ol choice for

the distal convoluted tubule uncomplicated HTN)

(OCT)

Blocks HafK'

-ATPase in thick CHE. pulmonary or peripheral

ascending limb of the loop edema

of Henle

Antagonize aldosterone HTN. CHE,hypokalemia

receptors

Thiazides hydrochlorothiazide, Sulfa allergy,pregnancy

chlorthalidone,metolazone

Hypotension,hypokalemia,

polyuria

Loop diuretics furosemide (Lasix -) Hypovolemia,hypokalemia Hypovolemia,hypokalemic

metabolic alkalosis

Aldosterone receptor

antagonists

spironolactone

eplenerone

Renal insufficiency,

hyperkalemia,pregnancy

Edema,hyperkalemia,

gynecomastia

INOTROPES

Inhrbit Nd/K'

-AIPasc, leading CHE,AEib

to increased intracellular

Na-andCa ^concentration,

and increased myocardial

contractility

Also slows conduction through

the AV node

2nd or 3rd degree AV block,

hypokalemia

digoxin (Lanoxin '

) AV block,junctional

tachycardia,bidirectional VT.

bradyarrhythinlas,blurred

or yellow vision (van Gogh

syndrome), anorexia. N/V

ANTICOAGULANTS

Coumarins warlarin (Coumadin '

) AFrb.LV dysfunction, prosthetic

valves, venous thrombosis

Recent surgery or bleeding. Bleeding (by tar the most

bleeding diathesis,pregnancy important side elfect),

paradoxical thrombosis, skin

necrosis

Recent surgery or bleeding. Bleeding,osteoporosis,

bleeding diathesis. heparin-induced

thrombocytopenia,renal thrombocytopenia (less in

insufficiency (for LMWHs) LMWKs)

Severe renal impairment. Bleeding,Gl upset

recent surgery,active bleeding

Idarucizumab:FDA approved

agent for reversal of

dabigatran for bleeding

Hepatic disease,active Bleeding,elevated liver

bleeding,bleeding diathesis, enzymes

pregnancy,lactation

Andeianet alfa FDA approved

agent for reversal of apixaban

and rivaroxaban for bleeding

Antagonizes vitamin K,

leading to decreased

synthesis of dolling factors II,

VII.IX.and X

Unfractionated heparin

LMWHs:dalteparin.enoxapaun,

linzaparin

Antithrombin III agonist, Acute MI/ACS:(when immediate

leading to decreased clotting anticoagulant effect needed).

PE,venous thrombosis

Heparins

factor activity

Competitive,direct thrombin AEib,venous thrombosis,PE

inhibitor,thrombin enables

fibrinogen conversion to

fibrin during thecoagulation

cascade

Direct,selective and

reversible inhibition of

factor Xa in both the intrinsic

and extrinsic coagulation

pathways

Direct thrombin inhibitors dabigatran

Direct factor Xa inhibitors rivaroxaban

apixaban

edoxaban

AEib, venous thrombosis.PE

ANTIPLATELETS

Salicylates ASA (Aspirin 1

) CAD. acute Ml, post- MI, post- Active bleeding or PUD

PCI.CABG

Bleeding,Gl upset,Gl

ulceration,impaired renal

perfusion

Irreversibly acetylales

platelet COX-1,preventing

thromboxane A 2-medialed

platelet aggregation

P2Y12 antagonist (block

platelet ADP receptors

Ihienopyridines clopidogrcl (Plavu'

).

liclopidine (liclid )

Acute Ml. post Ml. post PCI, Active bleeding or PUD Bleeding,thrombolic

thrombocytopenic purpura,

neutropenia (liclopidine)

CABG

P2Y12 antagonist (but

diflerenl binding site than

Ihienopyridines)

Block binding of fibrinogen to Acute Ml,particularly if PCI is

planned

Nucleoside analogues licagrelor (Brillinta )

Glycoprotein llb/llla inhibitors eptifibatide,tirohban.

abeiximab

Recent surgery or bleeding,

bleeding diathesis

Bleeding

Gp lib,Ilia

THROMBOLVTICS r i

i L J I

Convert circulating

plasminogen toplasmin.

which lyses cross-linked fibrin

alteplase,reteplase. Acute STEMI See fable 10.C34

tenecteplase.streptokinase

Bleeding

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