curs de chirurgie cardiaca pt studenti

8/3/2019 Curs de Chirurgie Cardiaca Pt Studenti

1/86

Surgery for

Acquired Heart Disease

Sef de lucrari dr. Adrian MolnarCardiovascular Surgery Clinic

HEART INSTITUTE


2/86

Cardiac Surgery the bad

Medical School

5 years General Surgery

2 years clinical/basic scienceresearch

2 years CT Fellowship

1 year advanced Fellowship Job opportunities

Stress/Work hours


3/86

Cardiac Surgery the good

You operate on the heart

Huge impact on patients lives!

Potential to fix the sickest patients in thehospital.

Technically and intellectually challanging.

Worse ways to make a living


4/86

Introduction

Cardiopulmonary Bypass

Coronary Artery Disease

Valvular Heart Disease

Transplant

Mechanical Assist Devices


5/86

The Father of Bypass

(John H. Gibbon (1903-1973)


6/86

CPB: Basic Principles

Full anticoagulation Heparin

Venous drainage

Right atrium SVC/IVC

Oxygenator

Pump

Arterial Inflow Aorta

Femoral artery

Axillary artery


7/86

CPB: Cardiac Arrest

Cardiopledgia

K+ (hyperkalemic arrest)

Energy substrates

Free radical scavangers

Antegrade aortic root

Retrograde coronarysinus

Deep HypothermicCirculatory Arrest


8/86

CPB: Myocardial Oxyge

nDema

ndUnloading the heart

Allen BS, Rosenkranz ER, Buckberg GD, et al: Studies of controlled reperfusion afterischemia, VII: high oxygen requirements of dyskinetic cardiac muscle. J Thorac

Cardiovasc Surg 1986; 92:543.)


9/86

CPB: Myocardial Oxyge

nC

onsumptio

n

Influence of temperature


10/86

CPB: Factor Activation

Bleeding

CoagulopathyFactor activation

doesnt help that we

have to heparinize!


11/86

CPB: Inflammatory Activation

Reactive Oxygen Species Ischemia/Reperfusion


12/86

CPB - Pros andCons

Hemolysis

Consumption

platelets

clottingfactors

Cytokineactivation

Embolism

Rest myocardium

Operate on still

heart Bloodless field

Allows opening ofchambers

Keeps patientstable


13/86

nevertheless a cornerstone


14/86

Coronary Artery Disease


15/86

Anatomy: RightCoronary Artery

RCA

anterior on aorta

R A-V groove

nodal arteries

acute marginal

postero lateral posterior

descending


16/86

Anatomy: Left Anterior Descending

LAD

branch of Left

main septal

diagonal

apex


17/86

Anatomy: LeftCircumflex Artery

Left A-V groove

obtuse marginals

posteriordescending

postero lateral


18/86

CAD: What is it?


19/86

CAD: Why is it a problem?


20/86

0 No angina

1 Angina only with strenuous or prolonged exertion

2 Angina with walking at a rapid pace on the level, on a grade,or up stairs (slight limitation ofnormal activities)

3 Angi

na with walki

ng at a

normal pace less tha

n2

blocks orone flight of stairs (marked limitation)

4 Angina with even mild activity

Can

adian

C

ardiovascular SocietyAngina Classification


21/86

CAD: Goals ofTherapy

IMPROVE BLOOD FLOW

Relief of symptoms

Prevention of complicationsMortality

MI

CHFArrhythmias

Prolong quality and quality of life


22/86

CAD: Outcomes /Prognosis


23/86

Coronary Artery Disease - Treatment

Medical Beta blockers, ASA, Nitrates

Risk factor modification Smoking, Lipid control, diet, activity

Interventional PTCA

Stents

Surgery CABG Coronary Artery Bypass Grafting

TMR Transmyocardial Revasc.

Transplant


24/86

AHA/ACCGuidelines forCABG:

Asymptomatic/mild/stable Angina

Asymptomatic/mild Angina Class I

left main stenosis

left main equivalent (proximal LAD and proximal circumflex)

triple-vessel disease

Class IIa

proximal LAD stenosis and one or two vessel disease

Class IIb

one or two vessel disease not involving proximal LAD

Stable angina Class I

left main stenosis

left main equivalent (proximal LAD and proximal circumflex) triple vessel disease

two vessel disease with proximal LAD stenosis and EF


25/86

AHA/ACCGuidelines forCABG:

Unstable Angina / Acute MI

Unstable Angina Class I

proximal LAD stenosis with one vessel disease

one or two vessel disease without proximal LAD stenosis, but with a moderateterritory at risk and demonstrable ischemia

ongoing ischemia despite medical therapy

Class IIa

proximal LAD stenosis and one or two vessel disease

Class IIb

one or two vessel disease not involving the LAD

ST segment elevation (Q-wave) MI Class I None

Class IIa Ongoing ischemia despite medical therapy

Class IIb

progressive heart failure with remote territory at risk

primary reperfusion within 612 hours


26/86

CAD Treatment MovingTarget

Safer surgery

Myocardialprotection

Anesthesia

Better peri-operative care

Better

medications Statins

Beta-blockers

Sicker patients

Higherexpectations

Lifestylemodification


27/86

Surgery CABG

CPB arrested heart

Off-pump (20%)

Conduits

IMA (L/R)

Aorto-Coronary

Vein (Saphenous)

Radial Artery

Other / Exotic NOT:

Prostetic

Non-autologous


28/86

CABG: OnPump

Benefits Comfortable for the surgeon Bloodless field

Motionless field Myocardial protection Exposure to all vessels for total

revascularization

Risks

Aortic cannulation Cerebral Emboli Dissection

Negative effects of cardiopulmonary bypass


29/86

CABG OffPump

OPCAB

Beating heart

No CPB

Lower heparin

Lower risk

Technically difficult

?outcome?


30/86

CABG Durability: ConduitPatency

1967 1989(even better with modern meds!)

P

ercentPate

nt

P

ercentPate

nt

100100

8080

606011 22 33 44 55 66 77 88 99 1010 1111 1212

YearsYears

N= 5657N= 5657

N=24145N=24145

ITAITA

SVGSVG

1389138910541054

456456 402402 415415

343343338338 291291 222222

175175 167167405405

5796579647804780

17561756

13661366

15351535

15891589

1553155313451345

1183118310291029

738738 14751475


31/86

CAD: CASS Registry Survival

Caracciolo, E., et Al., Circulation 1995; 91: 2325-2334.

100100

8080

6060

4040

2020

00

00 55 1010 1515

MedicalMedical

SurgicalSurgical

27%27%

37%37%

%%

YearsYears


32/86

CAD Treatment

What about people who you cant doa CABG on?

Previous CABG Growing number of redo-CABGs

Poor targets

No conduitToo sick


33/86

Transmyocardial Laser Revascularization

Create Reptilian Circulation

Patients deemed non

revascularizable Documented ischemia

Carbon dioxide / HolmiumYAG laser

30-40 holes drilled

Thoracotomy


34/86

Transmyocardial Laser Revascularization

Outcomes

improved angina

increased exercise tolerance

increased quality of life scores

decreased medical regimen

higher rate of survival free of cardiacevents

NEJM vol. Sept 1999341:14


35/86

Valve Disease

Tricuspid

Pulmonic

Mitral

Aortic


36/86

Valve Surgery: Repair vs Replacement

No CoumadinLess durability

Re-operations

CoumadinMore durability

Bleeding

Emboliccomplications

Patient factors and preference the most important considerations


37/86

Tissue Valves


38/86

MechanicalValves


39/86

Aortic Valve Disease


40/86

Anatomy: Aortic Valve

The noncoronary leafletstraddles the central fibrous bodyoverlying the anterior leaflet ofthe mitral valve.

The conduction tissue traversesthe membranous septum betweenthe right coronary andnoncoronary leaflets.


41/86

Aortic Valve Pathology

Stenosis

bileaflet

calcifications

Insufficiency

annulus

leaflet prolapse

Both


42/86

Aortic Stenosis: Calcification


43/86

Aortic Stenosis: The Problem


44/86

AV R: Grading Aortic Stenosis

Mild aortic stenosis: area >1.5 cm2

Moderate aortic stenosis: area 1 to1.5 cm2

Severe aortic stenosis: area


45/86

Aortic Stenosis: Disease Progression

not to mention the effects of CAD


46/86

Aortic Regurgitation

Improper or inadequate coaptation of the valve leafletsduring diastole.

Allows previously ejected blood to flow retrograde into theleft ventricle.

Effective stroke volume is reduced. Unlike aortic stenosis, both volume and pressure overload

of the left ventricular chamber occurs. Volume overload secondary to regurgitant flow

Pressure overload is due to the increased wall stress Law of Laplace.

Acute overload leads to immediate decompensation andsigns of left-sided failure as left ventricular end-diastolicvolume is exceeded.

Chronic volume/pressure overload allows forcompensatory changes in left ventricular volume, leadingto eccentric hypertrophy of the chamber.


47/86

AVR: Surgery


48/86

AVR: Cribier Edwards Perc. ValveThe Future?


49/86

AVR: Tissue Valve Durability

Current Thoughts:

Young PatientsMechanical ValvesPregnancyRisk of re-opLifestyle

Middle AgeMechanicalRisk of re-opPatient preference

ElderlyTissue valvesRisk of coumadin

Influence of other comorbidities


50/86

AVR: LongTerm Survival


51/86

MitralValve Disease


52/86

MitralValve: Anatomy


53/86



54/86



55/86

Mitral Stenosis

Generally the result of rheumatic heart disease.

Very rare in the U.S. (and modern countries)

Nonrheumatic causes

Severe mitral annular and/or leaflet calcification Congenital mitral valve deformities

Malignant carcinoid syndrome

Neoplasm

Left atrial thrombus

Endocarditic vegetations

A definite history of rheumatic fever can be obtained inonly about 50% to 60% of patients; women are affectedmore often than men by a 2:1 to 3:1 ratio. Nearly alwaysacquired before age 20, rheumatic valvular diseasebecomes clinically evident one to three decades later.


56/86

Mitral Regurgitation: EtiologyMuch larger problem


57/86

Etiology: Mitral Regurgitation

Carpentier's functional classification

Type I: Leaflet motion is normal.

Type II: Due to leaflet prolapse or excessive motion.

Type III: (restricted leaflet motion) is subdivided intorestriction during diastole ("a") or systole ("b"). Type IIIb is

typically seen in patients with ischemic MR.


58/86

Functional Mitral Regurgitation

Bolling: Sem. Thor. Card. Surg. 2002

CHFNormal


59/86

MitralValve Surgery: Indications

Complications

Left atrialenlargement

PulmonaryHypertension

Atrial fib.

LV DysfxnSymptoms

Endocarditis


60/86

Mitral Repair: Annuloplasty

Reduce annulardilatation

Reduce volumeoverload

Reduceventricular stressresponse

Reverseremodeling


61/86

Mitral Repair: Leaflet Resection


62/86

MitralValve Replacement


63/86

Outcomes: Degenerative Mitral Disease

Mitral Valve Repair


64/86

Outcome: Repair vs Replacement


65/86

Survival After MVR


66/86

Survival: Repair is Better!


67/86

Mitral Repair: Sounds Great

But:

60% of Functional MR never gets addressed

>50% of all valve surgery is replacement most are mechanical

Why?

Technically difficult

Surgeon preference/bias Outcomes

?Not sure


68/86

When Fixing the Heart Doesnt Work

REPLACE IT

Transplant

Mechanical Support


69/86

Norman Shumway


70/86

Cardiac Transplantation

> 5,000 patients listed for cardiactransplantation in the U.S.*

20-30% per year die waiting

< 2500 cardiac transplantsperformed per year in theU.S.*

unchanged since 1989 despite moremarginal donors utilized

* ISHLT database


71/86

Cardiac Transplantation

2004ISHLT

189 318669

1185

2165

2720

31563380

40244186 4219

4382 4438 4356 4206 40873769

3436 3314 3219 3107

0

500

1000

1500

2000

2500

3000

3500

4000

4500

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

NumberofTran

splants

J Heart Lung Transplant 2004;23:796-803


72/86

Long-Term Functional Status


73/86

Transplant: Underlying Diagnosis

CAD 45%

Dilated CM 45%

Valvular 4%

Congenital 2%

Retransplant 2%

Misc. 2%


74/86

Transplant: Donor selection

Age


75/86

Transplant: Donor cardiectomy.


76/86

Transplantation: Implant


77/86

Transplant Rejection: A Worse Disease?

Symptoms:

AsymptomaticUnexplained arrhythmiasCongestive Heart Failure

Cardiogenic shock

vs

Infection/Sepsis

About 30% have somerejection in the first 6months


78/86

Transplant: Survival


79/86

Mechanical Assist Device


80/86

The Last Hope: Mechanical Support

Bridge to myocardial recovery

Short term

Long term

?recovery / healing Bridge to transplantation

Save the sickest patients

Make a bad candidate into a good one

? making the problem worse

Destination therapy non-transplant candidates

? chronic rejection in transplanted patients

? change age limitation for transplant listing

? can it be better than transplantation


81/86

Selection criteria forVAD

Accepted as candidate for cardiac transplantation(relative)

Absence of coagulopathy or gastrointestinal hemorrhage

Heart failure (CI 25mmHg, systolic blood pressure


82/86

Types of Mechanical Support

Short termsupport

Pulsatile

Continuous flow

Bridge totransplant

Pulsatile Continuous flow


83/86

LeftVentricular Assist Device

Inflow from the LVapex

Outflow into theascending aorta

Percutaneousdriveline attached to

power source andcontroller


84/86

Abiomed BVS 5000(i)

Easy implant/explant

Versatile

univentricular

biventriccular

Good patient support

Paracorporeal

Difficult to mobilize

patient

Aggressiveanticoagulation


85/86

LongTerm LVAD: Thoratec

Easy implant/explant

Versatile

univentricular

biventricular Good patient support

Paracorporeal

Complex initial setup

Able to mobilize patient

Anticoagulation


86/86

Total Artificial Heart: AbioCor

First Humanimplant July 2, 2001

curs de chirurgie cardiaca pt studenti

Documents