controversies in cardiology: stable cad & courage pro: optimal medical therapy vs. pci syed...

Controversies in Cardiology:Stable CAD & COURAGE

Pro: Optimal Medical Therapy vs. PCI

SYED ZAHID JAMAL MDASSOC PROF NICVD

Ha ha ha ha !

Varying Degrees of CAD Lesion Severity in a Single Coronary Artery

Highly variable degrees of:• plaque formation

• luminal obstruction • inflammation

• likelihood of rupture

Is this a benign lesion Is this a benign lesion in a benign condition?in a benign condition?

Stable AnginaStable Angina

What are you lookin at?

Nature of the Problem:Severe Obstruction (Angina, No Rupture) vs Mild

Obstruction (No Angina, Likely to Rupture)

Revascularization;Anti-anginal Rx

Exertional Angina,(+) ETT

Severe FibroticPlaque

Severe obstruction, No lipid,Fibrosis, Ca++

Pharmacologic Stabilization;? Early Identification of High-risk

Plaque RuptureAcute MI,

Unstable Angina,Sudden death

Vulnerable PlaqueMinor obstruction,Eccentric plaque,

Lipid pool, Thin cap

Courtesy ofP. Stone, 2007

The Differing Fates of Coronary Stenoses of Varying Severity

• Clinical manifestations of coronary lesions behave differently based on the degree of luminal obstruction and morphology:– Lesions > 50-75% obstruction Angina;

positive stress test;

positive calcium score

– Lesions < 50% obstruction Rupture, superimposed thrombus

ACS/Death

Both types of lesions are inevitably present withinthe same stable CAD patient at any point in time

Goals of Therapy in CAD Management1. Improve anginal symptoms by optimizing myocardial O2 supply:demand

balance

Medication:Reduce HR, BP, contractility, preload

• β-blockers• Ca++ blockers• Nitrates

Enhance myocardial O2 supply• Ca++ blockers & ? Ranolazine

Revascularization (PCI or CABG)

2. Reduce/stabilize atherosclerotic plaque, reducing likelihood of rupture ACS/Cardiac death

– Aggressive statin therapy– ACE inhibitors– Aspirin ± Clopidogrel– β-blockers– Lifestyle modifications

(Courtesy of P. Stone, 2007)

* Med Management (MM), Percutaneous Coronary Intervention (PCI), Coronary Artery Bypass Grafting * Med Management (MM), Percutaneous Coronary Intervention (PCI), Coronary Artery Bypass Grafting (CABG) (CABG)

Increased Mortality with Medical Increased Mortality with Medical Management for UA/NSTEMI PatientsManagement for UA/NSTEMI Patients::

Patients with Significant CAD on Cath in the SYNERGY TrialPatients with Significant CAD on Cath in the SYNERGY Trial

Chan M, JACC Cardiovasc Int 2008

A Different Story in Stable CAD:Contrasting 1 Year Death/MI Rates: ACS,

Stable Angina, “Primary Prevention”

Wallentin L et al. Lancet 2000;356:9–16Juul-Moller S et al. Lancet 1992;340:1421–1425Shepherd J et al. N Engl J Med 1995;333:1301–1307

Poole-Wilson et al ACTION Lancet 2004;364:849-57.

Dea

th/ M

I (%

)

Months of follow up

Unstable angina/non Q wave MI (FRISC II)

16

12

8

4

0

0 2 4 6 8 10 12

Stable angina (SAPAT)

Primary Prevention (WOSCOPS)

ACTION trial (stable CAD)

Approx 1.5%Stable CAD

COURAGE 3.8%

THE PROBLEM:Major Cardiac Events Occur in Non-Target

Lesions Following Successful PCI

02468

101214161820

Year 1 Year 2 Year 3 Year 4 Year 5

Target Lesion Event

Non-target LesionEvent

HazardRate (%)

(Cutlip, et al. Circulation2004;110:1226)

Substantial number of cardiac events could be prevented if we knew how to identify them

5 year Followup of 1228 Patients Treated with Bare Metal Stents

6.75.7

7.05.6

12.4

1.41.51.32.3

18.3 Non-Target LesionEvent Rates:

• 12.4% Year 1• 37.4% Year 1-5

Classification of Natural History ofEarly Atherosclerotic Plaques

Plaque Trajectory

Histo-pathology

Progression Rate

Vascular Remodeling

Proclivity to

RuptureClinical

Manifestations

Quiescent Plaque

Small lipid core/thick cap

Minimal Compensatory Low Asymptomatic

High-risk High-risk vulnerable vulnerable plaqueplaque

Large lipid core/ thin,inflamed cap

Increased Excessive expansive

High Acute Coronary Acute Coronary SyndromeSyndrome

Stenotic Plaque

Small lipid core/very thick cap

Gradual Constrictive Low Stable Angina

(Chatzizisis, et al.JACC 2007;49:2379)

Relative Risk of Recurrent Cardiac Events with PTCA vs Medical Therapy

Meta-analysis of 6 randomized trials (n=1904)

(Bucher, et al. BMJ 2000;321:73)

Stable CAD: PCI vs ConservativeMedical Management

Meta-analysis of 11 randomized trials; N = 2950

Death

Cardiac death or MI

Nonfatal MI

CABG

PCI

Katritsis DG et al. Circulation. 2005;111:2906-12.

0 1 2

P

0.68

0.28

0.12

0.82

0.34

Risk ratio(95% Cl)

Favors PCI Favors Medical Management

Long-Term Clinical Outcome:PTCA vs Medical Management in RITA-2

(Henderson, et al. JACC 2003;42:1161)

P=NS P=NS

No difference in outcome over median of 7 years

RITA-2, 1018 patients (504 PTCA, 514 medical management)

Death Death or MI

In Patients with Chronic Angina and Stable CAD:

• We know that PCI improves angina and short-term exercise capacity, so if we don’t “fix what we see”:

1. Will we expose patients to increased risk of death/MI?2. Will angina and quality of life be worse?3. Will residual ischemia be less well treated? 4. Will patients feel they did not receive “best care”?5. What about high-risk patients—3V CAD; ↓ EF?

What Is The Concern Of Leaving Coronary Stenoses Alone?

Evidence Prior to COURAGE of Leaving Coronary Stenoses Alone

(Henderson, et al. JACC 2003;42:1161)

P=NS P=NS

No difference in outcome over median of 7 years

RITA-2, 1018 patients (504 PTCA, 514 medical management)

Death Death or MI

Stable CAD: PCI vs. Medical Management Pre-COURAGE

Meta-analysis of 11 randomized trials; N = 2950

Death

Cardiac death or MI

Nonfatal MI

CABG

PCI

Katritsis DG et al. Circulation. 2005;111:2906-12.

0 1 2

P

0.68

0.28

0.12

0.82

0.34

Risk ratio(95% Cl)

Favors PCI Favors Medical Management

COURAGE Primary EP:Survival Free of Death or MI

Years0 1 2 3 4 5 6

0.0

0.5

0.6

0.7

0.8

0.9

1.0

PCI + OMT

Optimal Medical Therapy (OMT)

Hazard ratio: 1.0595% CI (0.87-1.27)P = 0.62

7

• 2,287 Pts. Randomized to

PCI + OMT vs. OMT

• Intensive, Guideline-Driven

Medical Therapy & Lifestyle

Intervention In Both Groups

Source: Boden et al. N Engl J Med. 2007; 356:1503-16.

Optimal Medical Therapy

Pharmacologic

• Anti-platelet: aspirin; clopidogrel (c/w with established practice standards)

• Statin: simvastatin ± ezetimibe or extended-release niacin

• ACE Inhibitor or ARB: lisinopril or losartan

• Beta-blocker: long-acting metoprolol (Toprol XL®)

• Calcium channel blocker: amlodipine

• Nitrate: isosorbide 5-mononitrate

Lifestyle

• Smoking cessation

• Exercise program

• Nutrition counseling

• Weight control

Applied to Both Arms by Protocol and Case-Managed

Value of Optimal Medical Therapy:The COURAGE Trial

Death/MI Death

New ACS New MI

Compared with Optimal Medical Therapy Alone, PCI provided no incremental benefit on Death, MI, New ACS

(Boden, et al. NEJM 2007;356:1503)

Value of Optimal Medical Therapy:The COURAGE Trial

(Boden, et al. NEJM 2007;356:1503)

PercentWith

Angina

25

50

75

100

88 87

34 42

28

332826

Baseline 1 Year 3 Year 5 Year

Compared with Optimal Medical Therapy alone,PCI is associated with a reduction in angina, but not after 5 yrs

pNS

P<0.001P=0.02

pNS

PCI + Optimal RxOptimal Rx alone

Tertiary Outcomes: Cardiac Death/MI/ACS

Years0 1 2 3 4 5 6

PCI + OMT

OMT

Hazard ratio: 1.07CI 95% (0.91, 1.27) P = 0.60

23.5%

22.6%

10%

20%

30%

“COURAGE Enrolled Low-Risk Patients”… Huh???

•Diabetes: 34%

•Dyslipidemia: 71 %

•HTN: 67%

•Smokers: 29%

•Prior MI: 39%

•Prior Revasc: 26%

•Angina at BL: 88%

•Angina Duration: 26 mo

•Angina Freq.: 6 episodes/wk

•Multivessel CAD: 70%

•LAD disease: 68%

•Inducible Ischemia: 85%

•Stress MPI: Multiple defects 67%

•Death/MI Event Rate: 4.3%/year

COURAGE Patient Randomized to OMT Alone

Need for Subsequent Revascularization: 7 Years of F/U*

PCI + OMT OMT

Overall Need for Revascularization

21% 33%

Subsequent CABG N=77 N=81

Median Time to Revascularization†

10 months;

10.5%

10.8 months;

16.5%

*Median 4.6 years of follow-up†Median time to Repeat or 1st RevascularizationAfter ~ 11 mo, the avg. X-over from OMT to PCI was 2.8%/year over years 1-7

Freedom from CCS Angina During Follow-up & NNT to Improve Sx

Characteristic:CCS Class 0

PCI + OMT OMT NNT to improve angina in 1 pt with PCI

CLINICAL

Angina free – no.

Baseline 12% 13% ---

1 Yr *66% 58% 12.5

3 Yr *72% 67% 20

5 Yr 74% 72% 50

* The comparison between the PCI group and the medical-therapy group was significant at 1 year ( P<0.001) and 3 years (P=0.02) but not at baseline or 5 years.

SAQ Mean QOL Scores During Follow-up & NNT to Improve Sx

Characteristic PCI + OMT OMT NNT to improve SAQ QOL in 1

pt with PCI

Mean SAQ QOL Score: 0-100 Scale

Baseline 51 51 ---

1 Mo *68 62 16.7

6 Mo *75 70 20

1 Yr *76 73 33.3

2 Yr 77 76 100

*P < 0.001 between groups

COURAGE QOL Editorial Commentary

Nuclear Substudy (n=314)Nuclear Substudy (n=314)

Source: Shaw et al. J Nucl Cardiol 2006 Sep;13(5):685-98.

Rest/Stress Myocardial Perfusion Rest/Stress Myocardial Perfusion SPECT (MPS)SPECT (MPS)

• Pre-Rx Pre-Rx • Following 6-18m Randomized Following 6-18m Randomized Rx (mean 374 ± 50 days)Rx (mean 374 ± 50 days)

Documented Pre-Rx Ischemia Documented Pre-Rx Ischemia

Pre-RxTc-99m Pre-RxTc-99m sestamibi MPSsestamibi MPSPre-RxTc-99m Pre-RxTc-99m sestamibi MPSsestamibi MPS

PCI + OMTPCI + OMT(n=159)(n=159)

OMT OMT (n=155)(n=155)

Repeat MPSRepeat MPSat 6-18mat 6-18m

Repeat MPSRepeat MPSat 6-18mat 6-18m

Hypothesis: Reduction in Ischemia will be greater for Pts. Randomized to PCI+OMT than for those Randomized to OMT as Measured By Changes in Ischemic Burden by MPS at Baseline & 6-18m after Randomization

Patient Expectations AboutElective PCI for Stable CAD

• 52 consecutive patients scheduled for first elective PCI completed semi-structured questionnaire prospectively

Holmboe et al. J Gen Intern Med 2000;15:632.

Do you think the angioplasty will prevent a heart attack?

Yes 75%

Do you think the angioplasty will help you live longer?

Yes 71%

Recent Mid-America Heart Institute Patient PCI Survey

• One million PCI procedures per year

• Majority elective• Prospective survey of 350

elective PCI patients with stable CAD @ MAHI between 1/06-10/07

• Focus: are pt. perspectives of PCI benefit aligned with current evidence?

• John H. Lee, MD et al: 2008 AHA Scientific Sessions, November 12, 2008

Patient Perceived Benefitsof Elective PCI

66

31

4242

71

33

0

10

20

30

40

50

60

70

80

90

100

Emergent? Prevent HeartAttack?

Extend LifeSpan?

Saved Life? NormalizeStress test?

DecreasesAngina?

Pe

rce

nt

Alternate Therapies Offered

1813

68

0

10

20

30

40

50

60

70

80

90

100

Medical Therapy CABG None

Pe

rce

nt

For Patients Undergoing Elective Coronary Angiography for Chronic Angina:

• 13 RCTs in 7,605 patients (including BARI-2D) show no difference in death, MI, stroke or other “hard” endpoints between PCI and OMT

• An initial course of OMT preserves the option for PCI if medical therapy fails (only 16.5% of COURAGE OMT patients “crossed over” to PCI within 1 year)

• Over a full 7-year follow-up period, 2/3 of all OMT patients never required even a 1st PCI procedure

Why The Evidence Supports OMT as the Initial Approach to

Stable CAD Management


• There is better angina relief with PCI over 1-3 years• There is better QOL with PCI over 1-2 years• The subsequent need for revascularization in the 1st year

is lower in PCI than OMT patients• OMT is a safe & viable option for most patients, and for

those who may not be good candidates for PCI (frailty; CKD; multiple co-morbidities; treacherous anatomy, etc.)

• OMT as an initial approach preserves PCI as a subsequent option for symptom/QOL relief, if needed

Where Does COURAGE Give Us Clarity of Management?


• Is OMT as good as PCI + OMT in patients with impaired LV systolic function (EF < 40%)?

• Do patients with high-grade 3-vessel CAD fare as well with OMT vs. PCI + OMT, esp. with EF < 40%?

• Does stenosis severity (≥ 90% vs. 70%-80%) alter PCI vs. OMT outcomes, and does defining coronary anatomy in all patients aid clinical decision-making?

• Is it important to delineate the presence or absence of high-risk inducible ischemia in all patients?

Where Do the Results of COURAGE Still Leave Uncertainty?

• CAD manifestations in an individual patient are due both to:– Flow-limiting obstructions (angina, + stress test, + Ca++

score)– Minor obstructions with high-risk vulnerable plaque

(ACS, death)– Catheter-based treatment directed only at flow-limiting

obstructions will do little to reduce the burden of CAD events precipitated by olaque rupture of non-flow-limiting stenoses

Selective Management Strategies Focusing on Obstructive and Non-Obstructive CAD

Summary and Conclusions

• Non-obstructive high-risk plaque:– Difficult to identify/predict natural history at this time– Aggressive systemic pharmacologic therapy stabilizes

vulnerable plaque and thereby reduces mortality and morbidity

• Statins, ACE-inhibitors, ? Niacin– Ultimately, risk stratification (and local intervention) of

individual lesions may be possible



• Flow-limiting Obstructive CAD:– Optimal Medical Therapy is a viable & defendable initial

management strategy and is supported by existing ACC/AHA Clinical Practice Guidelines

– Revascularization is appropriate in patients with severe angina symptoms (or who have failed medical Rx), or in those who have substantial ischemic jeopardy

– Revascularization may be more effective than medications to:• reduce angina• increase exercise capacity• decrease subsequent revascularization procedures• but not to improve mortality, reduce MI, or other CV events.



Occluded Artery Trial (OAT)

Presented atPresented atThe American Heart Association The American Heart Association

Scientific Session 2006Scientific Session 2006

OAT TrialOAT TrialOAT TrialOAT Trial

OAT Trial: Background

• The goal of the trial was to evaluate percutaneous The goal of the trial was to evaluate percutaneous coronary intervention (PCI) compared with coronary intervention (PCI) compared with medical therapy among stable, high-risk patients medical therapy among stable, high-risk patients with persistent total occlusion of the infarct-related with persistent total occlusion of the infarct-related artery post-myocardial infarction (MI).artery post-myocardial infarction (MI).

• The goal of the trial was to evaluate percutaneous The goal of the trial was to evaluate percutaneous coronary intervention (PCI) compared with coronary intervention (PCI) compared with medical therapy among stable, high-risk patients medical therapy among stable, high-risk patients with persistent total occlusion of the infarct-related with persistent total occlusion of the infarct-related artery post-myocardial infarction (MI).artery post-myocardial infarction (MI).

Presented at AHA 2006Presented at AHA 2006Presented at AHA 2006Presented at AHA 2006

OAT Trial: Hypothesis

• A strategy of routine PCI for total occlusion of the A strategy of routine PCI for total occlusion of the infarct-related artery 3-28 days after acute MI infarct-related artery 3-28 days after acute MI would reduce the occurrence of the composite of would reduce the occurrence of the composite of death, reinfarction, or New York Heart Association death, reinfarction, or New York Heart Association (NYHA) class IV heart failure.(NYHA) class IV heart failure.

• A strategy of routine PCI for total occlusion of the A strategy of routine PCI for total occlusion of the infarct-related artery 3-28 days after acute MI infarct-related artery 3-28 days after acute MI would reduce the occurrence of the composite of would reduce the occurrence of the composite of death, reinfarction, or New York Heart Association death, reinfarction, or New York Heart Association (NYHA) class IV heart failure.(NYHA) class IV heart failure.


OAT Trial: Study Design

Primary Endpoints: Death, MI, or NYHA class IV heart failurePrimary Endpoints: Death, MI, or NYHA class IV heart failure Primary Endpoints: Death, MI, or NYHA class IV heart failurePrimary Endpoints: Death, MI, or NYHA class IV heart failure

PCI with stentingPCI with stentingn=1082n=1082

PCI with stentingPCI with stentingn=1082n=1082

Medical TherapyMedical Therapyn=1084n=1084

Medical TherapyMedical Therapyn=1084n=1084

2166 patients with angiography on day 3-28 post-MI with evidence of total occlusion of the infarct-2166 patients with angiography on day 3-28 post-MI with evidence of total occlusion of the infarct-related artery with poor or absent antegrade flow (TIMI flow grade 0 or 1); and met a criterion for related artery with poor or absent antegrade flow (TIMI flow grade 0 or 1); and met a criterion for increased risk, defined as ejection fraction <50%, proximal occlusion of a major epicardial vessel increased risk, defined as ejection fraction <50%, proximal occlusion of a major epicardial vessel

with a large risk region, or bothwith a large risk region, or bothExclusions: NYHA class III or IV heart failure, shock , serum creatinine concentration >2.5 mg/dl, Exclusions: NYHA class III or IV heart failure, shock , serum creatinine concentration >2.5 mg/dl,

angiographically significant left main or three-vessel coronary artery disease, angina at rest, or severe ischemia angiographically significant left main or three-vessel coronary artery disease, angina at rest, or severe ischemia on stress testing.on stress testing.

Randomized.Randomized.22% female, mean age 59 years, mean follow-up 3 years, mean EF 48% at baseline22% female, mean age 59 years, mean follow-up 3 years, mean EF 48% at baseline

Concomitant medications: Aspirin, anticoagulation if indicated, ACE inhibitors, beta-blockers, Concomitant medications: Aspirin, anticoagulation if indicated, ACE inhibitors, beta-blockers, and lipid-lowering therapy, unless contraindicatedand lipid-lowering therapy, unless contraindicated

2166 patients with angiography on day 3-28 post-MI with evidence of total occlusion of the infarct-2166 patients with angiography on day 3-28 post-MI with evidence of total occlusion of the infarct-related artery with poor or absent antegrade flow (TIMI flow grade 0 or 1); and met a criterion for related artery with poor or absent antegrade flow (TIMI flow grade 0 or 1); and met a criterion for increased risk, defined as ejection fraction <50%, proximal occlusion of a major epicardial vessel increased risk, defined as ejection fraction <50%, proximal occlusion of a major epicardial vessel

with a large risk region, or bothwith a large risk region, or bothExclusions: NYHA class III or IV heart failure, shock , serum creatinine concentration >2.5 mg/dl, Exclusions: NYHA class III or IV heart failure, shock , serum creatinine concentration >2.5 mg/dl,

angiographically significant left main or three-vessel coronary artery disease, angina at rest, or severe ischemia angiographically significant left main or three-vessel coronary artery disease, angina at rest, or severe ischemia on stress testing.on stress testing.

Randomized.Randomized.22% female, mean age 59 years, mean follow-up 3 years, mean EF 48% at baseline22% female, mean age 59 years, mean follow-up 3 years, mean EF 48% at baseline

Concomitant medications: Aspirin, anticoagulation if indicated, ACE inhibitors, beta-blockers, Concomitant medications: Aspirin, anticoagulation if indicated, ACE inhibitors, beta-blockers, and lipid-lowering therapy, unless contraindicatedand lipid-lowering therapy, unless contraindicated


OAT Trial: Primary Endpoint

17.2%15.6%

0%

5%

10%

15%

20%

PCI Medical Therapy

17.2%15.6%

0%

5%

10%

15%

20%

PCI Medical Therapy

• The primary The primary endpoint of death, endpoint of death,

reinfarction, or reinfarction, or NYHA class IV NYHA class IV

heart failure heart failure occurred in 17.2% occurred in 17.2%

of the PCI group of the PCI group and 15.6% of the and 15.6% of the medical therapy medical therapy

group ([HR] 1.16, group ([HR] 1.16, p=0.20). p=0.20).

Primary Endpoint of death, reinfarction, NYHA Primary Endpoint of death, reinfarction, NYHA class IV heart failure (% patients)class IV heart failure (% patients)

Hazard Ratio 1.16, p=0.20Hazard Ratio 1.16, p=0.20


OAT Trial: Primary Component Endpoints

• Total reinfarction trended Total reinfarction trended higher in the PCI group (7.0% higher in the PCI group (7.0% vs. 5.3%, HR 1.36, p=0.13), as vs. 5.3%, HR 1.36, p=0.13), as

did nonfatal reinfarction (6.9% did nonfatal reinfarction (6.9% vs. 5.0%, HR 1.44, p=0.08).vs. 5.0%, HR 1.44, p=0.08).

• Repeated elevation of cardiac Repeated elevation of cardiac biomarkers within 48 hours of biomarkers within 48 hours of

randomization occurred randomization occurred significantly more frequently significantly more frequently

in the PCI group (10.0% vs. in the PCI group (10.0% vs. 3.3%, p<0.001).3.3%, p<0.001).

• There was no difference in the There was no difference in the individual endpoints of death individual endpoints of death

(9.1% for PCI vs. 9.4% for (9.1% for PCI vs. 9.4% for medical therapy, p=0.83) or medical therapy, p=0.83) or NYHA class IV heart failure NYHA class IV heart failure

(4.4% vs. 4.5%, p=0.92) (4.4% vs. 4.5%, p=0.92) between the treatment groups.between the treatment groups.

Primary Component Endpoints (% patients)Primary Component Endpoints (% patients)

7.0 6.9

10.09.1

4.45.3 5.0

3.3

9.4

4.5

0

3

6

9

12

15

PCI Medical Therapy

7.0 6.9

10.09.1

4.45.3 5.0

3.3

9.4

4.5

0

3

6

9

12

15

PCI Medical Therapy

TotalTotalReinfarctionReinfarction


% p

atie

nts

% p

atie

nts

NonfatalNonfatalReinfarctionReinfarction

DeathDeathRepeated Repeated ↑ ↑ of Cardiacof Cardiac

BiomarkersBiomarkers

NYHA Class NYHA Class IV Heart IV Heart FailureFailure

p=0.13p=0.13p=0.13p=0.13 p=0.08p=0.08p=0.08p=0.08

p<0.001p<0.001p<0.001p<0.001p=0.83p=0.83p=0.83p=0.83

p=0.92p=0.92p=0.92p=0.92

OAT Trial: Summary

• Among stable, high-risk patients with persistent total Among stable, high-risk patients with persistent total occlusion of the infarct-related artery post-MI, performance occlusion of the infarct-related artery post-MI, performance of PCI 3-28 days post-MI was not associated with a of PCI 3-28 days post-MI was not associated with a difference in the composite of death, reinfarction, or NYHA difference in the composite of death, reinfarction, or NYHA class IV heart failure through a mean follow-up of 3 years class IV heart failure through a mean follow-up of 3 years compared with medical therapy.compared with medical therapy.

• Despite no reduction in the composite endpoint, PCI was Despite no reduction in the composite endpoint, PCI was associated with a trend toward higher rates of reinfarction associated with a trend toward higher rates of reinfarction compared with medication therapy.compared with medication therapy.

• Among stable, high-risk patients with persistent total Among stable, high-risk patients with persistent total occlusion of the infarct-related artery post-MI, performance occlusion of the infarct-related artery post-MI, performance of PCI 3-28 days post-MI was not associated with a of PCI 3-28 days post-MI was not associated with a difference in the composite of death, reinfarction, or NYHA difference in the composite of death, reinfarction, or NYHA class IV heart failure through a mean follow-up of 3 years class IV heart failure through a mean follow-up of 3 years compared with medical therapy.compared with medical therapy.

• Despite no reduction in the composite endpoint, PCI was Despite no reduction in the composite endpoint, PCI was associated with a trend toward higher rates of reinfarction associated with a trend toward higher rates of reinfarction compared with medication therapy.compared with medication therapy.


OAT Trial: Summary (cont.)

• The reinfarctions were not only procedural-related infarcts The reinfarctions were not only procedural-related infarcts (i.e., early procedural enzymatic leaks), but true ST elevation (i.e., early procedural enzymatic leaks), but true ST elevation reinfarctions that accumulated throughout follow-up.reinfarctions that accumulated throughout follow-up.

• One explanation for the trend toward an increase in One explanation for the trend toward an increase in reinfarctions with PCI may be embolization resulting in reinfarctions with PCI may be embolization resulting in myocardial damage and impaired collateral flow.myocardial damage and impaired collateral flow.

• Presence of persistent total occlusion remains a problem for Presence of persistent total occlusion remains a problem for a sizeable cohort of patients for whom suitable treatment is a sizeable cohort of patients for whom suitable treatment is lacking.lacking.

• The reinfarctions were not only procedural-related infarcts The reinfarctions were not only procedural-related infarcts (i.e., early procedural enzymatic leaks), but true ST elevation (i.e., early procedural enzymatic leaks), but true ST elevation reinfarctions that accumulated throughout follow-up.reinfarctions that accumulated throughout follow-up.

• One explanation for the trend toward an increase in One explanation for the trend toward an increase in reinfarctions with PCI may be embolization resulting in reinfarctions with PCI may be embolization resulting in myocardial damage and impaired collateral flow.myocardial damage and impaired collateral flow.

• Presence of persistent total occlusion remains a problem for Presence of persistent total occlusion remains a problem for a sizeable cohort of patients for whom suitable treatment is a sizeable cohort of patients for whom suitable treatment is lacking.lacking.


OAT Trial: Summary (cont.)

• Early reperfusion therapy, the goal of ST elevation MI Early reperfusion therapy, the goal of ST elevation MI treatment, with either primary PCI or thrombolysis, is treatment, with either primary PCI or thrombolysis, is not indicated for patients who present late, often with not indicated for patients who present late, often with persistent total occlusion.persistent total occlusion.

• The present study, the largest randomized trial to The present study, the largest randomized trial to date in this population, does not support the use of date in this population, does not support the use of late PCI for stable but persistent total occlusion.late PCI for stable but persistent total occlusion.

• Early reperfusion therapy, the goal of ST elevation MI Early reperfusion therapy, the goal of ST elevation MI treatment, with either primary PCI or thrombolysis, is treatment, with either primary PCI or thrombolysis, is not indicated for patients who present late, often with not indicated for patients who present late, often with persistent total occlusion.persistent total occlusion.

• The present study, the largest randomized trial to The present study, the largest randomized trial to date in this population, does not support the use of date in this population, does not support the use of late PCI for stable but persistent total occlusion.late PCI for stable but persistent total occlusion.


Dang, HE IS DRUNK

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