CARDIOLOGY GRAND ROUNDS...Presentation: AHA Scientific Sessions PREVIEW Date: Monday, November 7, 2016, 7:00 – 8:00 AM Location: ANW Education Building, Watson Room Speaker: Safety

(Continued on reverse)

C A R D I O L O G Y G R A N D R O U N D S Presentation: AHA Scientific Sessions PREVIEW

Date: Monday, November 7, 2016, 7:00 – 8:00 AM Location: ANW Education Building, Watson Room Speaker: Safety of Very Early (< 3hrs) Routine Percutaneous Coronary Intervention After

Fibrinolysis in ST-segment Elevation Myocardial Infarction David M. Larson, MD, Ridgeview Medical Center & Minneapolis Heart Institute®

Clinical Trials in Cardiac Surgery: NHLBI-sponsored Trial of Postconditioning During PCI for ST-elevation Myocardial Infarction Jay H. Traverse, MD, FACC, FAHA Minneapolis Heart Institute® at Abbott Northwestern Hospital

The NHLBI TIME Trial: Role of Microvascular Obstruction in 2-Year Clinical and MRI Follow-up Jay H. Traverse, MD, FACC, FAHA Minneapolis Heart Institute® at Abbott Northwestern Hospital

OBJECTIVES At the completion of this activity, the participants should be able to:

1. Summarize emerging research that colleagues will present at upcoming national scientific meeting. 2. Synthesize ideas and input from across disciplines relevant to each presentation. 3. Recommend content revisions or areas of focus to the presenters.

ACCREDITATION Physician: This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of Allina Health and Minneapolis Heart Institute Foundation. Allina Health is accredited by the ACCME to provide continuing medical education for physicians.

Allina Health designates this live activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)TM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Nurse: This activity has been designed to meet the Minnesota Board of Nursing continuing education requirements for 1.2 hours of credit. However, the nurse is responsible for determining whether this activity meets the requirements for acceptable continuing education.

DISCLOSURE STATEMENTS Speaker(s): Drs. Sendelbach, Larson and Traverse declare that they do not have any conflicts of interest to disclose.

Planning Committee: Dr. JoEllyn Carol Moore (Abraham), MD, Dr. Alex Campbell, Dr. Kevin Harris, Rebecca Lindberg, Dr. Michael Miedema, Dr. Scott Sharkey, Eva Zewdie and Jolene Bell Makowesky have declared that they do not have any conflicts of interest associated with the planning of this activity. Dr. David Hurrell declares the following relationship – honoraria: Boston Scientific.

PLEASE SAVE A COPY OF THIS FLIER AS YOUR CERTIFICATE OF ATTENDANCE

Signature: __________________________________________________________________________ My signature verifies that I have attended the above stated number of hours of the CME activity.

Allina Health - Learning & Development - 2925 Chicago Ave - MR 10701 - Minneapolis MN 55407

Enrolling Heart Failure Studies‣ CONCERT - PI: Jay Traverse, MD

‣ NYHA II or III ischemic cardiomyopathy with LVEF<40%‣ Study product: Autologous mesenchymal stem cells plus cardiac stem cells, or Autologous mesenchymal

stem cells, or Autologous cardiac stem cells, or placebo administered by transendocardial injection ‣ 1° Endpoint: feasibility, safety, and efficacy of autologous MSCs and CSCs, alone or in combination‣ Contact: Patti Mitchell, RN, CCRC phone 612.863.6287 pager 612.654.2737

‣ SENECA – Co- PIs: Jay Traverse, MD & Kasia Hryniewicz, MD S‣ Cancer Survivors with Anthracycline-Induced Cardiomyopathy; NYHA II or III with LVEF<40% by cMRI‣ Study product: transendocardial injection Allogeneic Mesenchymal Stem Cells‣ 1° Endpoint: safety and feasibility of allo-MSCs ‣ Contact: Jane Fox RN CCRC phone: 612.863.6289 pager: 612.654.7485

‣ SMILE – PI: Peter Eckman, MD‣ Patients admitted to the hospital with the diagnosis of Acute Decompensated Heart Failure ‣ Study product: SensiVest Wearable System‣ 1° Endpoint: The rate of recurrent events of HF readmissions during follow-up period.‣ Contacts: Kelly Wilson, RN, CCRC phone 612.863.6288 pager 612.654.0993

MHIF Grand Rounds – AHA Preview 11/7/16

1

Safety of Very Early (<3hrs) Routine Percutaneous Coronary Intervention after Fibrinolysis in ST-segment Elevation Myocardial Infarction

David Larson, Ross Garberich, Dan Lips, Nicholas Burcke, Ivan Chavez, Scott Sharkey, Claire Donovan,

Timothy Henry

Introduction

• Primary PCI is the preferred reperfusion strategy for STEMI patients if it can be done in a timely manner

• Only 1/3 of hospitals in the US are capable of Primary PCI

• 82% of STEMI patients transferred from non-PCI hospitals for Primary PCI have Door to Balloon times > 120 minutes (ACC/NCDR) Chakrabarti, JACC 2008


2

Pinto, D. S. et al. Circulation 2006;114:2019-2025

Multivariable analysis estimating the treatment effect of reperfusion therapy with PCI or fibrinolysis based on increasing PCI-related delay

• Current ACCF/AHA guidelines recommend fibrinolysis for STEMI patients with expected delays >120mins from FMC to PCI followed by transfer to a PCI center with angiography/PCI within 3-24 hrs

“Angiography should not be performed within 2-3 hours after administration of fibrinolytictherapy” 2013 ACCF/AHA STEMI Guideline (class IIa, LOE B)

• The timing of PCI following fibrinolysis is not clear.


3

• Rationale for delaying PCI following fibrinolysis: Risk of bleeding and stroke (as seen in facilitated PCI trials)

• Pharmaco-invasive trials by design had few patients who had PCI < 2-3hrs following fibrinolysis

“High risk” STEMIPresenting to non PCI hospitals

Fibrinolytic, ASA, Antithrombin and, Clopidogrel

“Pharmaco-invasive” strategyImmediate transfer to PCI hospital

Standard Treatment

Failed reperfusion

Successful reperfusion

Transfer for Rescue PCI

Elective Angio24hrs – 2wks

Immediate or Early PCI (< 6hrs)

Pharmaco-Invasive Trials:CARESS-in-AMITRANSFER-AMINORDISTEMI


4

Pharmaco-Invasive Trials

TRANSFER-AMI

CARESS-in-AMI

NORDISTEMI

No significant differences in major bleeding

Death, Re-MI, CS,CHF 30 days

Death, Re-MI, stroke 30 days

Death, Re-MI, refractory ischemia 30 days

P=0.004

Pharmaco-Invasive Trials

Pharmacologic Regimen Time to PCI (median)

CARESS-in-AMIN=600DiMario, Lancet 2008

½ dose ReteplaseAbciximabHeparin, ASA

135 (96,175) minutes

TRANSFER-AMIN=1059Cantor, NEJM 2009

Full dose TenecteplaseHeparin or EnoxaparinClopidogrel, ASA

3.9 (3.1,4.2) hrs

NORDISTEMIN=266Bohmer, JACC 2009

Full dose TenecteplaseEnoxaparinClopidogrel, ASA

162 (137,189)minutes

MHI Level 1N=867Larson, EHJ 2011

½ dose Tenecteplase, UFH, Clopidogrel, ASA

86 (70,108) minutes


5

• Assessment of reperfusion prior to angiography may not be accurate based on clinical and ECG criteria alone.

• Recent meta-analysis data suggested lower recurrent ischemia in pharmaco-invasive treated patients undergoing angiography < 4 hrs


6

Objective

• To analyze data in the Level 1 data base to compare clinical outcomes related to timing of angiography/PCI following fibrinolysis in transferred patients with expected delays to PCI.

• Hypothesis: There is not an increase in adverse clinical outcomes (death, reinfarction, stroke or bleeding) associated with very early angiography/PCI following fibrinolysis.


7

Methods

• The Minneapolis Heart Institute Level 1 MI program is a regional STEMI system with a standardized protocol where patients transferred from spoke hospitals with expected delays of > 90 minsto PCI receive pharmaco-invasive therapy: which includes ½ dose Fibrinolytic, UFH, ASA and Clopidogrel (or Ticagrelor) with transfer for immediate PCI.

• Prospective registry data from the Level 1 database was analyzed to compare clinical outcomes related to the timing of PCI following fibrinolysis. (5 groups):

< 60, 61-90, 91-120, 121-180 and > 180 minutes

• Zone 1: (primary PCI) ASA

UFH

Clopidogrel or Ticagrelor

PCI

• Zone 2: (pharmaco-invasive PCI) ASA

UFH

Clopidogrel or Ticagrelor

½ TNK

PCI

MHI Level 1 STEMI System


8

Patient Population (01/01 – 12/15)

Total STEMI pts transferred

N=3,451

pPCI2,584

PI PCI867

< 60 minN=86

61-90 minN=412

91-120 minN=244

121-180 minN=105

>180 minN=20

Time from Lytic to Angiography/PCI

86

412

244

105

200

50

100

150

200

250

300

350

400

450

< 60 min 61-90 min 91-120 min 121-180 min > 180 min

12%

2%

10%

28%

48%


9

Baseline characteristics

≤ 60 min

(n=86)

61 – 90 min

(n=412)

91 – 120 min

(n=244)

121 – 180 min

(n=105)

> 180 mins

(n=20)

P‐Value for

Trend

Age, Mean (SD) 62.8 ± 12.9 62.6 ± 13.7 63.9 ± 12.8 64.4 ± 12.7 68.8 ± 13.5 0.026

Patients ≥ 75, (%) 13 (15.1) 97 (23.5) 61 (25.0) 24 (22.9) 6 (30.0) 0.19

Male, (%) 60 (69.8) 301 (73.1) 185 (75.8) 69 (65.7) 13 (65.0) 0.50

Hypertension, (%) 43 (50.0) 236 (57.3) 142 (58.2) 63 (60.0) 13 (65.0) 0.16

Hyperlipidemia, (%) 41 (48.2) 227 (56.6) 127 (54.3) 64 (62.8) 7 (36.8) 0.55

Diabetes, (%) 12 (14.0) 69 (16.8) 39 (16.1) 25 (23.8) 3 (15.0) 0.20

Current Smoker, (%) 26 (30.2) 92 (22.3) 71 (29.2) 28 (26.7) 5 (25.0) 0.58

History of MI, (%) 18 (20.9) 67 (16.3) 48 (19.7) 22 (21.0) 8 (40.0) 0.094

History of PCI, (%) 20 (23.3) 68 (16.5) 43 (17.6) 27 (25.7) 5 (25.0) 0.27

History of CABG, (%) 5 (5.9) 21 (5.1) 19 (7.8) 4 (3.8) 2 (10.0) 0.66

Cardiogenic Shock,

(%)5 (5.8) 30 (7.3) 16 (6.6) 12 (11.4) 0 (0) 0.58

Cardiac Arrest, (%) 7 (8.1) 24 (5.8) 8 (3.3) 13 (12.4) 0 (0) 0.84

Anterior MI, (%) 30 (36.1) 159 (38.7) 90 (37.0) 30 (29.1) 6 (30.0) 0.16

Killip Class 2‐4, (%) 8 (9.3) 49 (11.9) 30 (12.3) 20 (19.2) 0 (0) 0.29

Pharmacoinvasive

(n=867)

Primary PCI

(n=2584) P‐Value

Age, Mean (SD) 63.3 ± 13.3 62.5 ± 14.1 0.12

Patients ≥ 75, (%) 201 (23.2) 583 (22.6) 0.71

Male, (%) 628 (72.4) 1852 (71.7) 0.67

Hypertension, (%) 497 (57.3) 1481 (57.8) 0.80

Hyperlipidemia, (%) 466 (55.4) 1381 (54.7) 0.70

Diabetes, (%) 148 (17.1) 461 (18.0) 0.57

Current Smoker, (%) 222 (25.6) 652 (25.4) 0.87

History of MI, (%) 163 (18.8) 519 (20.2) 0.36

History of PCI, (%) 163 (18.8) 542 (21.1) 0.15

History of CABG, (%) 51 (5.9) 167 (6.5) 0.53

Cardiogenic Shock, (%) 63 (7.3) 228 (8.8) 0.15

Cardiac Arrest, (%) 52 (6.0) 315 (12.2) <0.001

Anterior MI, (%) 315 (36.6) 859 (33.7) 0.12

Killip Class 2‐4, (%) 107 (12.4) 332 (12.9) 0.72


10

Results

• Median door to lytic was 29 (20,42) minutes

• Median Lytic to balloon was 86 (70,180) minutes

• Lytic to balloon < 3 hrs in 98%, < 2hrs in 86% of patients

• Pre-PCI TIMI 2/3 flow occurred in 71%

0

10

20

30

40

50

60

70

80

90

< 60 min 61-90 min 91-120 min 121-180 min > 180 min No lytic

P=0.043

Pre-PCI TIMI 2/3 Flow

perc

ent


11

Clinical Outcomes

≤ 60 min

(n=86)

61 – 90 min

(n=412)

91 – 120 min

(n=244)

121 – 180 min

(n=105)

180 mins

(n=20)

P‐Value for

Trend

Total with

Lytics

(n=869)

Zone 1/2

Patients

without Lytics

(n=2584)

P‐Value

TIMI Bleed During

Intervention, (%)9 (10.5) 34 (8.3) 23 (9.4) 6 (5.7) 2 (10.0) 0.54 74 (8.6) 258 (10.0) 0.20

TIMI Major Bleed

During

Intervention, (%)

0 (0) 11(2.7) 3 (1.2) 2 (1.9) 0 (0) 0.80 16 (1.9) 67 (2.6) 0.21

Death in‐

hospital, (%)4 (4.7) 14 (3.4) 6 (2.5) 9 (8.6) 0 (0) 0.47 33 (3.8) 154 (6.0) 0.015

Death at 30 days,

(%)4 (4.7) 14 (3.4) 9 (3.7) 9 (8.6) 0 (0) 0.33 36 (4.2) 176 (6.8) 0.005

Reinfarction at 30

days, (%)1 (1.1) 2 (0.5) 3 (1.2) 1 (1.0) 1 (5.0) 0.23 8 (0.9) 36 (1.4) 0.29

Stroke at 30 days,

(%)1 (1.1) 8 (1.9) 3 (1.2) 0 (0) 0 (0) 0.21 12 (1.4) 21 (0.8) 0.14

MACE at 30 days,

(%)6 (7.0) 24 (5.8) 14 (5.7) 10 (9.5) 1 (5.0) 0.56 55 (6.3) 224 (8.7) 0.030

Bleeding

Per

cent

P=0.20

10.5

8.3

9.4

5.7

10 10

0

2.7

1.2

1.9

0

2.6

0

2

4

6

8

10

12


Any bleeding Major bleeding


12

Stroke

1.1

1.9

1.2

0 0

0.8

0

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6

1.8

2


P=0.14

perc

ent

Hemorrhagic Stroke

0

1

2

0 0

3

0

0.5

1

1.5

2

2.5

3

3.5


0.8%

0.1%

0.1%

P=0.16


13

Reinfarction – 30 days

1.1

0.5

1.2

1

1.51.4

0

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6


perc

ent

P=0.29

Mortality – 30 days

4.7

3.4 3.7

8.6

0

6.8

0

1

2

3

4

5

6

7

8

9

10


perc

ent

P=0.33 P=0.005


14

Survival Stratified by time from lytic to PCI

Log rank test = 0.043

Conclusions

• Delaying angiography for 3-24 hours following FL may not be necessary and may result in delays to reperfusion in patients who fail to reperfuse.

• Pre-PCI TIMI 2-3 flow was higher in PI treated patients, but decreased as time from FL to angiography/PCI became longer.

• Despite a significantly longer D2B, PI patients had decreased mortality (p=0.002), although this likely was influenced by less pre-PCI cardiac arrest.

• Very early PCI (< 3 hours) following FL in patients with expected delays to PCI is safe without increased bleeding or MACE.


15

Thank you


1

Jay H. Traverse, MDPrincipal Investigator, TIME Study

Minneapolis Heart Institute at Abbott Northwestern Hospital

University of Minnesota Medical School

Cardiovascular Cell Therapy Research Network (CCTRN)

2016 Scientific Sessions of the AHA

The NHLBI TIME Trial:Role of Microvascular Obstruction in 2‐Year Clinical and MRI Follow‐up

Rationale for TIME• Optimal timing for cell delivery post‐AMI was not known and had not been directly tested in a prospective clinical trial.

• Biochemical and structural changes in myocardium and bone marrow in the first week (cytokines, inflammation, ROS) may create optimal window for cell delivery.

• Almost all BMC trials delivered cells ≤7 days post‐AMI.

o REPAIR‐AMI subgroup suggested later delivery preferable to earlier

• LateTIME showed no benefit when BMCs delivered 2‐3 weeks post‐MI.

22


2

• Study Aim: assess the effect of autologous BMCs and timing of delivery at Day3 vs. Day7 post MI on measures of LV function

• Target Population: 120 patients w/first anterior MI, reperfused by PCI + stent, with residual LV dysfunction (EF≤45%)

• Treatment: 150 x 106 autologous BMCs or placebo (2:1) delivered by intracoronary infusion (Stop Flow)

• Primary Endpoints: change in global and regional LV function from baseline to 6 months by cardiac MRI

• Secondary Endpoints: change in infarct size and LV volumes

• Prespecified long‐term (2‐years) clinical and MRI F/U.

3

TIME Study Design

4

Results for both infarct zone and border zone wall motion were also not significant by therapy group for 3 days, 7 days, or overall.

6‐month LVEF Results of TIME


3

Two-Year Results of TIME

5

85 patients (BMC=58; Placebo=27) completedstipulated 2-year clinical and MRI Follow-up.

- ICD implants (n=10)- Death (n=3)- Lost to Follow-up (n=7)- MRI contraindications (n=15)

Change in LV Ejection Fraction

45.9 50.3 49.8 48.746.9 51.6 50 51.60

10

20

30

40

50

60

70

Day 3 6 months 1 year 2 year

BMCPlacebo


4

Change in Infarct Size (g)

8

0

10

20

30

40

50

60

70

80


BMC

Placebo

0.0

20.0

40.0

60.0

80.0

100.0

120.0


BMC

Placebo

Change in LV End-Diastolic Volume Index (ml / m2)


5

A B C

Figure 1. Infarct sizing and microvascular obstruction (MVO). Panel A: Short axis view with endo-and epicardial borders. Infarct (arrows) in the antero-, mid and infero-septal regions with microvascular obstruction (*) noted . Panel B: Quantification of infarct tissue based upon the intensity of the myocardium [minus the MVO(*)] using 5 standard deviations from the mean intensity to define infarcted myocardium, Panel C: Total infarct size including the MVO region

* *

Prognostic Importance of MVO

*MVO (late) measured 20-mins post-gadoliniumwas identified in 47 /107 baseline (Day 3) MRIs

10

Baseline Data Stratified by MVO

MVO (n=47) No MVO (n=60) P-value

AGE 55.2 58.3 0.120Female (n) 14/15 1/15 0.001Infarct Size (g) 52.8 34.9 0.001Peak CK (IU/ml) 3925 2439 0.0001LVEF (%) 43.1 46.6 0.078LVEDVI (ml/m2) 80.2 71.1 0.006LVESVI (ml/m2) 46.0 38.4 0.005


6

11

‐0.1

6.1

‐5

0

5

10

15

20

MVO present(n=47)

MVO absent(n=60)

17.8 6.811.6

‐0.5‐5

0

5

10

15

20

25

30

35

40

MVO present(n=47)

MVO absent(n=60)

LVEDVI

LVESVI

LVEF

Effect of MVO on Changes in LVEF and Volumes at 6-months

Change in LV Ejection Fraction

0

10

20

30

40

50

60

70

Baseline (MVO=47, NoMVO=60)

6 months (MVO=47, NoMVO=60)

2 years (MVO=34, NoMVO=49)

MVO

No MVO


7

Change in Infarct Size (g)

0

10

20

30

40

50

60

70

80

90




MVO

No MVO

0

10

20

30

40

50

60

70

80

90




MVO

No MVO

Change in LVESVI (ml / m2)


8

Conclusions• Intracoronary delivery of autologous BMCs 3 or 7 days following STEMI did not improve LV function or attenuate LV remodeling at 6 months.

• LV function, volumes and infarct size remain stable between 6 months and 2‐years.

• The presence of MVO is associated with significant reductions in the recovery of LV function, greater adverse LV remodeling and increased need for ICD implants.

15


1

Jay H. Traverse, MDPrincipal Investigator

Minneapolis Heart Institute at Abbott Northwestern Hospital

University of Minnesota Medical School

2016 Scientific Sessions of the AHA

NHLBI‐sponsored Trial of Postconditioning During PCI for ST‐elevation Myocardial

Infarction

BACKGROUND

Reperfusion injury may significantly contribute toinfarct size in setting of STEMI.

Interventions to reduce I/R injury must bedelivered at time of reperfusion.

Modification of reperfusion by postconditioningmay significantly reduce infarct size.

Previous Postconditioning trials from Europe and Asia have demonstrated inconsistent findings ofbenefit during STEMI.


2

Contribution of Lethal Reperfusion Injury to Final Infarct Size

Yellon DM, Hausenloy DJ. N Engl J Med 2007;357:1121-1135.

Postconditioning

“The application of brief periods ofischemia during the initial phase of reperfusion.”


3

Mechanisms of Postconditioning• Activation of sarcolemmalG‐protein‐coupled receptors.

• Activation of RISK Pathway

• Inhibition of GSK3increasesthreshold for MPTP opening

Heusch Circ 2008;118:1919

How do brief periods of reperfusion and ischemia result in myocardial

protection?

Hypotheses:

1.) Repeated occlusions maintain acidosis to keep MPTP from opening.

2.) Delivery of O2 during reperfusion promotes ROS formation which activates kinases through redox signaling.

Cohen MV, Basic Res Cardiol 2008


4

Consequences of MPTP Opening

• Collapse of the mitochondrial‐membrane potential

• ATP depletion

• Increased ROS production

•Matrix swelling ‐ rupture of outer mitochondrial membrane

• Release of cytochrome c into cytosol resulting in caspase activationand apoptosis.

Minneapolis Heart Institute: Preliminary Experience

N Ischemic time (hrs)

Age CK (IU) LVEF (%)

PosC 22 4.5 61±3 1987±281 53±2

Control 21 4.5 56±3 2335±434 45±3

Traverse JH. Et al. Post Conditioning reduces infarct size and improves LV function during acute myocardial infarction. Circulation 2006;114:II‐344


5

HYPOTHESIS

The inconsistent finding of benefit in previous trialsarises from issues of patient selection that may renderPostconditioning ineffective.

These include: Prolonged ischemic times (> 6 hrs.) Collateral blood flow Occurrence of limited reperfusion (TIMI flow > 0) Failure to exclude patients with pre‐infarction

angina.

Trial Design

We designed a single‐center trial funded by theNHLBI to definitively answer if postconditioningreduces infarct size and increases myocardialsalvage by using an optimized patient population of STEMI patients presenting for primary PCI.

Ischemic times between 1 and 6 hours 100% occlusion of major epicardial artery Exclusion of patients with PIA and collaterals cMRI measurements of infarct size and salvage


6

Trial Design (Cont)

STEMI patients admitted directly to cardiac catheterization laboratory as part of LEVEL 1Program.

First STEMI with 100% occlusion of major artery.

Consent obtained following initial angiography.

Verbal consent followed by full informed consentwithin 24 hrs. (n=90).

Emergency Waiver of Consent for remaining patients(BRANY IRB).

Trial Design (Cont)

Postconditiong Protocol: Four, 30‐sec inflation / deflations upon

immediate restoration of flow by guidewire. Thrombectomy mandated after PC protocol. Cardiac MRI performed 1 – 3 days post PCI and

again at 3 and 12‐months.

Primary Endpoints: Infarct size and Myocardial Salvage (AAR‐IS)/AAR

and MVO between PostC and Control group.


7

Baseline Data

POSTCON (n= 55) CONTROL (n= 49) P‐ValueAGE (years) 58.0 58.2 0.65 Male (%) 89 79 0.38Ischemic Time (mins) 143 153 0.70Infarct Artery (%) 0.44

‐ LAD 49 38 ‐ CX 6 11 ‐ RCA 45 51

Thrombectomy (%) 27 41 0.14GP IIB IIIA (%) 46 40 0.54DES (%) 100 91Peak CKMB (IU/ml) 131 159 0.71LVEF(echo)‐Day1 (%) 50.0 ± 10.0 50.2± 10.4 0.95


8

Safety Data

• 1 Death – CVA 3 months post‐PCI (Control)

– All other patients remain alive

• Acute Stent Thrombosis – PostC Group

• TVR – 8 months post‐PCI – PostC Group

0

10

20

30

40

50

60

70

0 100 200 300 400 500 600

Scar (g)

Peak CKMB

Control

PostConditioning


9

Final Results

To be presented next Monday, November 14th

2:40 PM at the AHA Scientific Sessions

“Clinical Trials in Cardiac Surgery”

Documents

CARDIOLOGY GRAND ROUNDS...Presentation: AHA Scientific Sessions PREVIEW Date: Monday, November 7, 2016, 7:00 – 8:00 AM Location: ANW Education Building, Watson Room Speaker: Safety