Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina...

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Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands

Transcript of Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina...

Page 1: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Multi-vessel disease and intracoronay physiologyCombat MI 2009

Multi-vessel disease and intracoronay physiologyCombat MI 2009

Kees-joost Botman MD, PhDCatharina hospital

Eindhoven Heart InstituteThe Netherlands

Kees-joost Botman MD, PhDCatharina hospital

Eindhoven Heart InstituteThe Netherlands

Page 2: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

PCI vs CABG in multivessel disease:THE TAILORED APPROACH

For years, cardiologists and cardiac surgeons have disputed about the optimum treatment of MVD : “ Is CABG the treatment of choice ?” “ Is PCI the treatment of choice ?”

BUT......not all patients are the same !!

background considerations (1):

Page 3: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

PCI vs CABG in multivessel disease

CABG and STENTING are equally effective treatmentsto prevent death and AMI, but excess repeatedrevascularization and more angina in STENT group

IN MULTIVESSEL DISEASE:

The decision for revascularization of a particular lesionwas based upon angiography ( stenosis > 50%)

ARTS – Study:

Page 4: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

PCI vs CABG in multivessel disease

CABG and STENTING are equally effective treatmentsto prevent death and AMI, but excess repeatedrevascularization and more angina in STENT group

IN MULTIVESSEL DISEASE:

The decision for revascularization of a particular lesionwas based upon angiography ( stenosis > 50%)

SYNTAX – Study:

Page 5: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

PCI vs CABG in multivessel disease:THE TAILORED APPROACH

In patients with similar degree of anatomic disease, the most important predictor of outcome is the presence and extent of inducible ischemia (Beller,Circulation 2000):

12000 patients with MVD, similar severity of angiographic abnormalities:

MIBI negative 0.6 % per year mortality / AMI MIBI positive 7.2% per year mortality / AMI

background considerations (2)

Page 6: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

PCI vs CABG in multivessel disease:THE TAILORED APPROACH

Revascularization is warranted for functionallysignificant stenoses only

(DEFER study, Circulation, june 2001)

background considerations (3)

AND :

Page 7: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

The DEFER Study: Adverse EventsDeath, AMI, CABG and (re)PTCA

0

10

20

PTCAdeferred

PTCAperformed

PTCA anyway

6.6%

11.1%

19.5%

0.75

< 0.75

% e

ven

ts

NS

Page 8: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

The DEFER Study: Event-free Survival

0 5 100.5

0.6

0.7

0.8

0.9

1.0

FFR 0.75, PTCA deferred

FFR 0.75, PTCA performed

FFR < 0.75, PTCA performed

10 90 180 270 360

0.93

0.89

0.81

P=0.2746

P=0.0961P=0.0056

Days after Procedure

Pro

bab

ility

of

Eve

nt-

free

Su

rviv

al

Page 9: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

PCI vs CABG in multivessel diseaseTHE TAILORED APPROACH

THEREFORE:

Simply treating all patients with multivessel disease in the same way ( either CABG or PCI ) makes little sense and is a rather crude approach

TAILORED APPROACH

Split up the multivessel population in two groups depending on the functional extent of disease,by assessing the functional significance of the individual stenoses

Page 10: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

OPTIMUM TREATMENT OF MULTIVESSELDISEASE: THE TAILORED APPROACH

In many patients with multivessel disease, non-invasive testing can not indicate which of several stenoses are culprit, but.....

Fractional Flow Reserve (FFR), calculated fromcoronary pressure measurement, is an easy andaccurate index to indicate specifically which lesions are culprit and which are not

background considerations (4)

Page 11: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

• 24 def/spuit + draad

Introduction

Page 12: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

HartspierAorta Krans

slagader

100 0Pa=100 Qnormaal100

Perfusiedruk 100 mmHg

Maximale hyperaemie

Qsten/Qnorm = Pd / Pa = 0.70 (70%)

100 0Pa=100 Qstenose

ΔP 30 mmHg

Pd=70

Perfusiedruk 70 mmHg

Page 13: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

1000 X

0.014 inch

Page 14: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.
Page 15: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.
Page 16: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

OPTIMUM TREATMENT OF MULTIVESSELDISEASE: THE TAILORED APPROACH

• 150 patients with multivessel disease, ARTS and SYNTAX like characteristics (410 stenoses)

• Coronary Pressure measurement in all stenoses

• If FFR < 0.75 stenosis considered as “culprit” If FFR > 0.75 stenosis “non - culprit”

If 3 culprit lesions or 2 culprit lesions including LMCA : CABG

If 1 or 2 culprit lesion (not incl LMCA) : PCIBotman CJ et.al, JACC 2001

Page 17: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

OPTIMUM TREATMENT OF MULTIVESSELDISEASE: THE TAILORED APPROACH

In this way, the population with multivessel disease was split up in two groups, not distinguishable by the degree of angiographic abnormalities, but with different degree of functional disease.

Page 18: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

OPTIMUM TREATMENT OF MULTIVESSELDISEASE: THE TAILORED APPROACH

• 150 patients

• 410 stenoses: FFR measured in 360 stenoses

total occlusion in 21 vessels: culprit by definition

not able to measure: 7 stenoses

not “recognized” : 22 stenoses

259 culprit 101 not culprit

Page 19: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

OPTIMUM TREATMENT OF MULTIVESSELDISEASE: THE TAILORED APPROACH

Based upon these measurements,

87 patients qualified for CABG and

63 patients qualified for PCI

Risk factors and angiographic characteristics

were completely similar in both groups

2 vessels: n=38 1 vessel: n=25

Page 20: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Patient Characteristics 1

RISK FACTORS

CABG GROUP = 87 PTS

PCI GROUP = 63 PTS

Smoking 41.1% 49.2%

Family history 47.1% 54.0%

Hyperchol. 72.4% 63.5%

Hypertension 28.7% 28.6%

Diabetes 24.1% 23.8%

Page 21: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

CHARACTERISTICS 2

Angina Class (CCS)total no.of pts = 150

Class No. %

I 0 0 %

II 30 20%

III 60 40 %

IV 60 40 %

Page 22: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

CHARACTERISTICS 3

No.of vessels involved per patienttotal no.of pts = 150

Qty No. %

1 0 0 %

2 69 46 %

3 81 54 %

Page 23: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Angiographic characteristics of the culprit and non-culprit lesions

FFR < 0.75 FFR > 0.75

REFERENCE DIAMETER

2.97 +/- 0.63 3.11 +/- 0.77

STENOSIS PERCENTAGE

54.1 +/- 19.7 53.6 +/- 21.3

M.L.D. 1.41 +/- 0.51 1.49 +/- 0.62

Page 24: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Male,50-year-oldAngina class 2-3Positive ET

Page 25: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Intermediate branch, hyperemia pull-back

Page 26: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

LAD, hyperemia

Page 27: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

After stenting LAD

Page 28: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

LAD, after stenting

Page 29: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Adverse events at hospital discharge

CABG GROUP (N = 87) PCI GROUP (N = 63)

No. % No %

(re) CABG 1 1.2 % 0 0 %

(re) PCI 0 0 % 1 1.6 %

Infarction 1 1.2 % 1 1.6 %

Death 1 1.2 % 0 0 %

Total events 3 3.5% 2 3.2%

Page 30: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Adverse events at 2 years

CABG GROUP (N = 87) PCI GROUP (N = 63)

No. % No. %

(re) CABG 3 3.4 % 3 4.8 %

(re) PCI 7 8.1 % 7 11.2 %

Infarction 4 4.6 % 2 3.2 %

Death 2 2.3 % 0 0 %

Total events 16 18.4% 12 19.1%

Page 31: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Angina class (CCS) 1 year follow-up

CABG GROUP (N = 87) PCI GROUP (N = 63)

CLASS N % N %

I 77 88 % 54 86 %

II 10 12 % 9 14 %

III 0 0 % 0 0 %

IV 0 0 % 0 0 %

Page 32: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

Angina class (CCS) at 2-year follow-up

CABG GROUP (N = 87) PCI GROUP (N = 63)

CLASS N % N %

I 73 84 % 52 82 %

II 11 13 % 10 16 %

III 3 3 % 1 2 %

IV 0 0 % 0 0 %

Page 33: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

0

5

10

15

20

25

30

35

% M

AC

E

ARTS 1 yr ARTS 2 yr Tailored 2 yr

Incidence of MACE

CABG

PCI

Optimum Revascularization Strategy for Multivessel Disease : THE TAILORED

APPROACH

Ww3139Serruys, NEJM 2001; Botman, ESC 2002

Page 34: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

SYNTAX Subgroup MACCE Rates at 12 Months

CABG TAXUS*

Pati

en

ts (

%)

All LMN=705

LM+1VDN=138

LM IsolatedN=91

LM+2VDN=218

LM+3VDN=258

Comparisons for the LM and 3VD subgroups are observational only and hypothesis generating

3VD ( w/o LM)N=1095

* TAXUSTM Express2TM Stent SystemSource: See Glossary

Page 35: Multi-vessel disease and intracoronay physiology Combat MI 2009 Kees-joost Botman MD, PhD Catharina hospital Eindhoven Heart Institute The Netherlands.

OPTIMUM TREATMENT OF MULTIVESSEL DISEASE:

CONCLUSIONS: 1. In multivessel disease, coronary pressure measurement

is an excellent tool to identify the culprit lesion(s) by FFR < 0.75 2. In this way, patients with otherwise similar characteristics can be stratified in 2 groups, according to the functional extent of disease (“number of culprit lesions”): PCI group: one or 2 culprit lesions; CABG group: 3 or more culprit lesions)

3. PCI and CABG used in this way provide an equally effective treatment, both in terms of adverse events, repeated revascularization, and quality of life