CARDIOLOGY GRAND ROUNDS · 1. Recognize the analytical characteristics of cardiac troponin assays....

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

C A R D I O L O G Y G R A N D R O U N D S Presentation: Troponin State of the Art: Past, Present and Future

Speaker: Yader Sandoval, MD Cardiovascular Disease Fellow Minneapolis Heart Institute® at Abbott Northwestern Hospital & Hennepin County Medical Center Research Associate Cardiac Biomarkers Trials Laboratory, Minneapolis Medical Research Foundation

Date: Monday, April 27, 2015, 7:00 – 8:00 AM Location: ANW Education Building, Watson Room

OBJECTIVES At the completion of this activity, the participants should be able to: 1. Recognize the analytical characteristics of cardiac troponin assays. 2. Describe the differences between contemporary and high-sensitivity cardiac troponin assays. 3. Describe the relation between cardiac troponin and the Universal Definition of MI with an emphasis on type 1 and 2

myocardial infarction. 4. Explain future directions of cardiac troponin.

ACCREDITATION Physicians: This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship 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 CreditTM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Nurses: 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.

Others: Individuals representing other professional disciplines may submit course materials to their respective professional associations for 1.0 hours of continuing education credit. DISCLOSURE STATEMENTS Speaker: Dr. Sandoval has declared he does not have any conflicts of interest to disclose.

Planning Committee: Dr. Michael Miedema, and Eva Zewdie have declared that they do not have any conflicts of interest associated with the planning of this activity. Dr. Robert Schwartz declared the following relationships - stockholder: Cardiomind, Interface Biologics, Aritech, DSI/Transoma, InstyMeds, Intervalve, Medtronic, Osprey Medical, Stout Medical, Tricardia LLC, CoAptus Inc, Augustine Biomedical; scientific advisory board: Abbott Laboratories, Boston Scientific, MEDRAD Inc, Thomas, McNerney & Partners, Cardiomind, Interface Biologics; options: BackBeat Medical, BioHeart, CHF Solutions; speakers bureau: Vital Images; consultant: Edwards LifeSciences.

1

Yader Sandoval, M.D.

Co-Chief Cardiovascular Disease Fellow, HCMC/ANW.

Co-Investigator, Cardiac Biomarker Trials Laboratory, MMRF.

April 27th, 2015.

MHIF Grand Rounds 2015

Disclosures

No financial relationships with industry.

2

Objectives

1. Introduction.

2. Understanding cTn assays: Analytical

characteristics.

3. Clinical correlation:

A) cTn in the emergency department.

B) Myocardial infarction.

4. New directions.

Why are we talking about this?

More than 8 million patients present annually

to the ED with acute CP.

Cardiac biomarker testing (CK-MB, cTnI and

cTnT) occurs in 16.9% of all ED visits.

28.6 million out of 169.6 million ED visits in

the United States (2009-2010).

Makam AN et al. JAMA Intern Med 2015; 175: 67-75.Hoffmann U et al. Am Heart J 2012; 163: 330-8.

3

Evolution of Cardiac Biomarkers

1950s1950s 1960s1960s 1970s1970s 1980s1980s 1990s1990s Late 1990sLate 1990s 2000s2000s TodayToday

AST

SGOT

AST

SGOTTotal CKTotal CK

CKMBLDHCKMBLDH

CKMB mass assays

CKMB mass assays

EarlycTnT cTnI

EarlycTnT cTnI

POCPOCContemporary

cTnT cTnI

Contemporary

cTnT cTnI

High sensitivity

hs-TnT

hs-cTnI

High sensitivity

hs-TnT

hs-cTnI

PAST PRESENT FUTURE *

Lewandroski KB. Clin Lab Med 2014.Ladenson JH. Clin Chem 2012.

Evolution of Cardiac Biomarkers

1950s1950s 1960s1960s 1970s1970s 1980s1980s 1990s1990s Late 1990sLate 1990s 2000s2000s TodayToday

AST

SGOT

AST

SGOTTotal CKTotal CK

CKMBLDHCKMBLDH

CKMB mass assays

CKMB mass assays

EarlycTnT cTnI

EarlycTnT cTnI

POCPOCContemporary

cTnT cTnI

Contemporary

cTnT cTnI

High sensitivity

hs-TnT

hs-cTnI

High sensitivity

hs-TnT

hs-cTnI

PAST PRESENT FUTURE *

* Please note that the the US Future is the rest of the developed world’s present.

4

Objectives

1. Introduction.


characteristics.

3. Troponin and myocardial infarction.

4. New directions.

Troponin Assays: Understanding test results.

- Limit of blank (LoB)

- Limit of detection (LoD)

- 99th percentile upper-reference limit

(URL)

- Coefficient of variation (CV) – total

imprecision.

5




- 99th percentile upper-reference limit

(URL)


imprecision.

Smallest concentrations of a

measurand that can be reliably

measured by an analytical

procedure.

Limit of blank (LoB) – Limit of Detection (LoD)

Armbruster DA, Pry T. Clin Biochem Rev 2008

6

Case Example: Abbott Architect cTnI Assay

<0.010 ng/mLLoD

Limit of Detection

Manufacturer’s Package:

- LoD: 0.009 µg/L




- 99th percentile upper-reference limit (URL)


imprecision.

7

Cardiac Troponin and the 99th percentile URL

Thygesen et al. Third Universal Definition of MI. JACC 2012

DEFINITION OF MYOCARDIAL INFARCTION

The term acute MI should be used when there is evidence of myocardial necrosis in a

clinical setting consistent with acute myocardial ischemia. Under these conditions any

one of the following criteria meets the diagnosis for MI:

Detection of a rise and/or fall of cardiac biomarker values [preferably cTn]

with at least one value above the 99th percentile URL and with at least one of

the following:

1. Ischemic symptoms

2. New or presumed new ST-T changes or new LBBB

3. Development of pathological Q waves in the ECG

4. Imaging evidence of new loss of viable myocardium or new regional wall

motion abnormality.

5. Identification of an intracoronary thrombus by angiography or autopsy.

Case Example: Abbott Architect cTnI Assay

0.034 ng/mLNOT the 99th percentile

<0.010 ng/mLLoD

Limit of Detection

Manufacturer’s Package:

- LoD: 0.009 µg/L or ng/mL

- 99th percentile URL: 0.028 µg/L or ng/mL

- 10% CV concentration: 0.032 µg/L or ng/mL

8

Sandoval Y, Apple FS. Clin Chem 2014.

NORMALITY

Questionnaires Surrogate biomarkers Imaging Physical

examination

No patient

selection

Questionnaire

alone

Questionnaire

BP

eGFR

Imaging

29.9 ng/L

20.0 ng/L

14.4 ng/L

99th percentile URLSelection Criteria

Collinson P, Apple FS Clin Chem 2012

9

Copyright © The American College of Cardiology. All rights reserved.

SUBSTANTIAL VARIABILITY BETWEEN LABORATORIES IN TROPONIN DECISION LEVEL FOR DIAGNOSIS OF MYOCARDIAL INFARCTION AND ASSAY 99TH PERCENTILE: FINDINGS FROM THE INTERNATIONAL STUDY OF COMPARATIVE HEALTH EFFECTIVENESS WITH MEDICAL AND INVASIVE APPROACHES (ISCHEMIA) TRIAL

J Am Coll Cardiol. 2014;63(12_S). doi:10.1016/S0735-1097(14)61881-7

Significant variability exists in the cTn MI decision level used by hospital laboratories relative to the assay cTn 99th percentile.

Only one-third of labs follow the Third Universal Definition of MI. These data have important implications for the diagnosis of MI in clinical practice and adjudicating MI

endpoints in clinical trials.




- 99th percentile upper-reference limit (URL)


imprecision.

10

Total Imprecision – Coefficient of Variation (CV)

Fierdoz O. Essential laboratory knowledge for the clinician. Continuing Medical Education, [S.l.], v. 30, n. 7, p. 244-248, jun. 2012.

Total Imprecision – Coefficient of Variation (CV)

Apple FS. Clin Chem 2009

11

What is a

high-sensitivity cTn assay?

What is a high-sensitivity cTn assay?

Contemporary cTn Assay

Measure cardiac troponin

values above the LoD in

LESS than 50% of a

reference population.

High Sensitivity cTn Assay

Measure cardiac troponin

values above the LoD in

≥ 50% of a reference

population.

CV <10% at the 99th URL

12

Comparing Contemporary vs. hs-cTn Assays

Manufacturer – assay Measurable values >LoD, % CV – Total Imprecision

(according to

Manufacturer)

Abbott ARCHITECT – hs-cTnI 96% 3%

Abbott ARCHITECT – cTnI 2% 14%

Beckman Access 2 – hs-cTnI 80% 8.6%

Beckman Access 2 – cTnI 35% 14%

Siemens Dimension Vista – hs-cTnI 100% 3%

Siemens Dimension Vista - cTnI 1% 10%

Selected examples.

Apple FS, Collinson PO. Clin Chem 2012.Apple FS, Ler R, Murakami MM. Clin Chem 2012.

Impact of Analytical Variation on MI Diagnosis

Sandoval Y, Smith SW, Schulz KM, Murakami MM, Love SA, Nicholson J, Apple FS. Clin Chem 2015.

13

Objectives

1. Introduction.


characteristics.

3. Troponin: Clinical correlation – Part I

cTn in the emergency department.

4. New directions.

EMERGENCY PHYSICIANS CARDIOLOGISTS

DX. SPECIFICITYEMPHASIS ON ACS

NEGATIVE PREDICTIVE VALUEED OVERCROWDING

Can’t miss ACS.

Not another “trop leak” please…

14

Chest Pain in the ED – US Data >8 million patients present annually to the ED with acute CP.

2 – 10% are diagnosed with ACS.

Cost in excess of $8 billion.

Unnecessary hospitalization and testing.

Current strategies often require hospital admission from 24-36

hours in most US hospitals (>90%) and include serial ECGs and

biomarker measurements, observation and some of functional

testing to exclude myocardial ischemia.

Hoffmann U et al. AHJ 2012

Limitations of Contemporary cTn Assays

Delays in Excluding Disease

Delays in rule-out interferes with

evaluation of alternative

diagnoses and contributes to

expensive overcrowding in the

ED (~ increased in medical

errors, public health problem).

Delays in Diagnosing Disease

Delays in rule-in hold back

prompt use of evidence-

based therapies.

Delayed increase of circulating levels for 3-4 hours, often requiring

sampling for 6-12 hours.

Reichlin et al. Arch Intern Med 2012.

15

Symptoms Suggestive of ACS

Non cardiac diagnosis

Treatment as indicated by alternative diagnosis.

Chronic stable angina

ACC/AHA Guidelines for Chronic Stable

Angina.

Possible ACS

Non-diagnostic ECG and normal initial biomarkers

Observe, serial ECGs, cardiac

biomarkers

If negative

Study to provoke ischemia or detect

anatomic CAD

If negative

Outpatient follow up

If positive

Admit to hospital

If positive

Admit to hospital

Consider MPI to identify rest

ischemia

If negative

Outpatient Follow Up

If positive

Admit to hospital

Definite ACS

Guidelines for NSTEMI/UA

Guidelines for STEMI

Amsterdam EA et al. Testing of low-risk patients presenting to the emergency department with chest pain. Circulation 2010.

Symptoms Suggestive of ACS

Non cardiac diagnosis

Treatment as indicated by alternative diagnosis.

Chronic stable angina

ACC/AHA Guidelines for Chronic Stable

Angina.

Possible ACS

Non-diagnostic ECG and normal initial biomarkers

Observe, serial ECGs, cardiac

biomarkers

If negative

Study to provoke ischemia or detect

anatomic CAD

If negative

Outpatient follow up

If positive

Admit to hospital

If positive

Admit to hospital

Consider MPI to identify rest

ischemia

If negative

Outpatient Follow Up

If positive

Admit to hospital

Definite ACS

Guidelines for NSTEMI/UA

Guidelines for STEMI

Amsterdam EA et al. Testing of low-risk patients presenting to the emergency department with chest pain. Circulation 2010.

16

Rule-out Strategies

Use of

undetectable

hs-cTn levels.

(Below <LoD or

<LoB)

Accelerated Serial

hs-cTn sampling

(0h and 1-3h)

Hs-cTn in

combination with

a risk score

(ADPs)

Rule-out strategies with hs-cTn: Using LoD/LoB

Author - Journal - Year cTn Assay Cutoff value used % qualifying for

strategy

NPV

Body R et al.

JACC 2011

Roche

hs-cTnT

<3 ng/L

(LoB)

195 out of 703

(28%)

99.4%

(6 month)

Bandstein N et al.

JACC 2014

Roche

hs-cTnT

<5 ng/L

(LoD)

8,907 out of 14,636.

(61%)

NPV for MI:

99.8% (30 d)

99.4% (1 year)

NPV for death:

100% (30 d)

99.6% (1 year)

Thelin J et al.

Eur Heart J ACC 2014.

Roche

hs-cTnT

<5 ng/L

(LoD)

160 out of 478

(33%)

NPV for NSTEMI:

100%

NPV for ACS/UA:

94%

17

Rule-out strategies with hs-cTn: Serial Sampling

Author - Journal - Year Total

patients

cTn Assay Sampling

algorithm

% qualifying for

strategy

NPV

Reichlin T et al.

CMAJ 2015

n=1320

(APACE)

Roche

hs-cTnT

0h and 1h 786 out of 1320

59.5%

NPV AMI: 99.9%

Rubini Gimenez et al.

AJM 2015

n=1811 Abbott

hs-cTnI

0h and 1h 50.5% 99.6%

Reichlin T et al.

Arch Int Med 2012

DC=436

VC=436

Roche

hs-cTnT

0h and 1h 259 out of 436

60%

100%

Reichlin et al.

AJM 2015

N=1665

DC=1148

VC=517

Roche

hs-cTnT

0h and 2h DC=60%

VC=78%

99.9%

99.5%

Thelin J et al.

Eur H J ACC 2014

n=478 Roche

hs-cTnT

Oh and 3-4h 309 out of 478

65%

NPV ACS: 91%

NPV NSTEMI: 99%

2011 ESC GuidelinesA rapid rule-out protocol (0h and 3h) is

recommended when highly sensitive troponin

tests are available (Class I – LOE: B).

Eur Heart J 2011; 32: 2999-3054.

18

Rule-out strategies hs-cTn: Accelerated Diagnostic Protocols (ADPs)

Author - Journal -

Year

Total

patients

cTn

Assay

Protocol % qualifying

for strategy

NPV

Cullen L et al.

JACC 2013

ADAPT=1635

APACE=909

Abbott

hs-cTnI

0h and 2h

TIMI ≤1, nL ECG, nL

hs-cTnI (<99th URL)

ADAPT=41.5%

APACE=38.6%

NPV MACE*

ADAPT= 99.7%

APACE= 99.7%

Carlton EW et al.

Heart 2015

N=960 Roche

hs-cTnT

TRUST ADP

Low Risk: Goldman ≤1

Non-ischemic ECG

Single hs-cTnT < 99th

URL (14 ng/L)

382 of 960

(39.8%)

99.7%

* Cullen et al. MACE (30‐days): death (excluding clearly noncardiac, cardiac arrest, acute MI, emergency revascularization procedure, cardiogenic shock, ventricular arrhythmia requiring intervention and high‐degree AV block requiring intervention.

Regardless of the achieved NPV, cTn should always be used in conjunction with full clinical assessment, including patient history and exam, and 12-lead ECG.

Reichlin T et al. CMAJ 2015

19

Distinguishing between acute and chronic cTn elevations: DELTA TROPONIN

Korley F, Jaffe AS. JACC 2013Keller T et al. JAMA 2011

Reichlin T et al. Circulation 2011

20

Objectives

1. Introduction.


characteristics.

3. Troponin: Clinical correlation – Part II

Myocardial infarction.

4. New directions.

Non ST-Elevation MI

ST-Elevation MIUnstable Angina

ACS

Classical Acute Coronary Syndromes (ACS) Classification.

21

2014 NSTEMI Guidelines

STE/ACS

NSTE/ACSUA/ACS

ACS MI

MI is not synonymous with

ACS (plaque disruption with

thrombosis), since ischemia

can occur via a number of

other mechanisms.

ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations.Newby K et al. JACC 2012

22

Myocardial Injury vs. Myocardial Infarction

Type 1 vs. Type 2 MI

Thygesen. Circulation 2012.

Thygesen K et al. Third Universal Definition of MI. JACC 2012

23

MI subtypes

• Spontaneous MI (atherosclerotic plaque rupture) (>1x URL)Type 1

• MI secondary to an ischemic imbalance. (>1x URL)Type 2

• MI resulting in death when biomarker values are unavailable.Type 3

• MI related to PCI (>5x URL)Type 4A

• MI related to stent thrombosis.Type 4B

• MI related to CABG (>10x URL)Type 5

Thygesen. Circulation 2012.

T5MI

T2MI T1MI

T4MI

T3MI

MI is not synonymous with ACS (plaque disruption with

thrombosis), since ischemia can occur via a number of other

mechanisms.

ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations.Newby K et al. JACC 2012

24

Type 2 MI Frequency Based on Total MI Denominator

1.6 2 3 4.5 5

10.2 10

2629.6

36.6

62.1

71.2

0

10

20

30

40

50

60

70

80

Sandoval et al. JACC 2014

25

T2MI Frequency

Definition

Adjudication Studied Population

cTn Assay and utilized cutoff value

Sandoval et al. JACC 2014

Mortality in Type 1 vs. Type 2 MI

Author -

Journal

Total N Type 1 MI Type 2 MI Follow up P value

Sandoval et al.

Eur Heart J ESC

2014.

1112 7.6% 11.4% 180 days 0.4

* Post DC

Saaby et al. Am

J Med 2014.

3762 26%

In-hospital: 7%

30d: 9%

1y: 17%

49%

In-hospital: 19%

30d: 24%

1y: 44%

2.1 years <0.001

Bonaca et al.

Circulation 2012.

13608 8.3% 7.3% 180 days NR

26

MI Subtypes in Clinical Practice

TYPE 1 MI

ACC/AHA Guidelines Focused

on STE/ACS and NSTE/ACS.

ACS – directed therapies.

Possible revascularization

NSTE/ACS: conservative vs.

early strategies.

STE/ACS: revascularization

TYPE 2 MI

No guidelines exist.

Treat underlying etiology / correct

underlying trigger.

If underlying fixed CAD contributing,

consider ASA and statins.

If related to underlying CAD, consider

additional invasive or non-invasive

imaging and consider outpatient

follow up.

Sandoval et al JACC 2014

What will happen when

high-sensitivity troponin

assays are approved for clinical

use in the US?

27

MI Frequency: cTnI vs. hs-cTnI

Sandoval Y, Smith SW, Schulz KM, Murakami MM, Love SA, Nicholson J, Apple FS. Clin Chem 2015; 61: 657-63.

Adjudication Method by

Assay – Total n=310

99th percentile

URL (ng/L)

MI

n (%)

Type 1

n (%)

Type 2

n (%)

MIs adjudicated using

contemporary assay

30 43

(14%)

14

(4.5%)

29

(9.4%)


hs-cTnI

26 33

(11%)

11

(3.5%)

22

(7.1%)


hs-cTnI with GS cutoffs

F:16; M:34 32

(10%)

10

(3.2%)

22

(7.1%)

127 (41%) had at least 1 value above the sex-specific 99th percentile.

Most common etiologies are not related to primary myocardial ischemia.

Reichlin T et al. AJM 2012

Roche hs-cTnT (n=1124)

AMI: 18% (198) 22% (242)New AMI: n=35, Type 1 MI

* e.g. myocarditis, SCM, acute HF, tachyarrhythmias.

cTnT >99th URL: 22%

hs-cTnT >99th URL: 36%

*

28

Reichlin T et al. AJM 2012

Total N = 1124

Moderate Large MI (+ cTnT and + hs-cTnT) = 198

Small MIs (only + hs)= 44

30m CV Mortality

No MI: 2.6%

Small MIs: 13.5%

Mod-Large MIs: 17.9%

Moderate – Large AMIDetected with Both cTnI and hs-cTnT) (n=198)

Small AMI(Detected with only hs-cTnT)(n=44)

P value

Coronary angiography within 30-days

77% 50% <0.001

Revascularizationwithin 30-days

68% 36% <0.001

Those undergoingcoronary angiography.

Moderate – Large AMIDetected with Both cTnI and hs-cTnT) (n=198)

Small AMI(Detected with only hs-cTnT)(n=22)

P value

Stenosis <75% 2% 0% 0.6

Stenosis 75-95% 16% 25% 0.34

Stenosis 95-99% 35% 69% 0.01

Stenosis 100% 47% 6% 0.002Reichlin T et al. AJM 2012

29

SWEDEHEART

2009-2012

Study Population

48,594 patients

Group 1

hs-cTnT <6 ng/L

5,790 patients

(11.9%)

Group 2

hs-cTnT 6-13 ng/L

6,491 patients

(13.4%)

Group 3

hs-cTnT 14-49 ng/L

10,476 patients

(21.6%)

Group 4

hs-cTnT ≥50 ng/L

25,837 patients

(53.2%)

1-YEAR

MORTALITY

Most would have had a negative cTnT using old assay

Most would have a positive cTnT even suing the old cTnT assay

Melki D et al. JACC 2015; 65: 1655-64.

95 (1.6%) 158 (2.4%) 1,078 (10.3%) 4,422 (17.1%)

Groups stratified

according to maximum

hs-cTnT value during

hospitalization.

Group 3: Increased hs-cTnT (previously negative cTnT)

MEDICATIONS ADMISSION MEDICATIONS DISCHARGE

ASPIRIN (%) 52% 71%

PY212 RECEPTOR BLOCKER (%) 15% 39%

BETA-BLOCKER (%) 56% 77%

STATIN (%) 49% 69%

ACEI-ARB (%) 51% 66%

GROUP 3:

- Diagnosis at discharge: ACS (62%)

- MI (18%)

- UA (44%)

Coronary angiography: 4,808 (46%)

- 1 – 2 vessel disease: 2,222 (46%)

- Left main or 3V disease: 1,194 (25%)

Revascularization:

- PCI: 2421 (23% all or 50% CA)

- CABG: 411 (4% all or 8.5% CA)

Melki D et al. JACC 2015; 65: 1655-64.

30

Validation phase (reported ≥0.20 ng/mL) (Total n=1038)

Implementation phase (reported 0≥0.05 ng/mL) (Total n=1054)

Mills NL et al. JAMA 2011; 305: 1210‐1216.

Validation

Implementation

Objectives

1. Introduction.


characteristics.

3. Troponin: Clinical correlation

4. New directions.

31

Patients presenting with symptoms suggesting ACS

Measure hs-cTn

hs-cTnI <LoD

Calcium score, median: 0

Any CAD: 11%

Stenosis >50%: 0%

Stenosis >70%: 0%

Between LoD and

99th percentile


Any CAD: 58%

Stenosis >50%: 19%

Stenosis >70%: 13%

hs-cTnI ≥99th

percentile


Any CAD: 83%

Stenosis >50%: 75%

Stenosis >70%: 58%

hs-cTn and cCTA: ROMICAT II

Januzzi JL et al. Am Heart J 2015; 169: 572-578.

hs-cTnI as a Predictor of Vascular Events in Primary Prevention: Impact of Statin Therapy

JUPITER trial (Rosuvastatin 20 mg daily vs. Placebo).

Without known CVD, DM, LDL <130 mg/dL

12,596 (73%) with baseline samples available.

Primary endpoint:

1st major vascular event defined as the composite of non

fatal MI, non-fatal stroke, hospitalization for UA, arterial

revascularization or death from CV causes.

Everett BM, Zeller T, Glynn RJ, Ridker PM, Blankenberg S. Circulation 2015 [In press]

32


ARCHITECT STAT hs-cTnI assay.

Median hs-cTnI: 3.4 ng/L

92% had concentrations > LoD (1.9 ng/L)




33

Tertiles Rosuvastatin Placebo

hs-cTnI N events/

N at risk

Incidence

Rate

N events/

N at risk

Incidence

Rate

ARR

1 18 / 2058 0.42 30 / 2028 0.71 0.30

2 34 / 2286 0.68 55 / 2246 1.13 0.44

3 56 / 2147 1.17 111 / 2191 2.29 1.12


Lowest tertile hs-cTnI: 5-year NNT of 67

Highest tertile hs-cTnT: 5-year NNT of 18

Rosuvastatin offered similar relative reductions of risk of major vascular events across baseline hs-cTnI levels.

In the highest category baseline cTnI, rosuvastatin was associated with the most substantial reduction in absolute risk of CV events and therefore the lowest NNT.


34

TAKE-HOME POINTS1. Understanding and mastering basic cTn concepts

NOW (prior to the introduction of high-sensitivity cTn

assays) is critical.

2. LoD – 99th percentile URL – CV (imprecision)

3. Rule-out and rule-in strategies. Delta troponin.

4. Type 1 vs. Type 2 MI.

5. Future: Complementary approaches (e.g. cardiac CT,

cardiac MRI) in selected cohorts.

6. Future: Prevention.

Thank you for your attention.

Acknowledgements:

- Fred S. Apple, PhD.

- Stephen W. Smith, M.D.

- All the staff, research associates, and co-investigators at

the (CBTL),

MMRF.

CARDIOLOGY GRAND ROUNDS · 1. Recognize the analytical characteristics of cardiac troponin assays....

Documents

Transcript of CARDIOLOGY GRAND ROUNDS · 1. Recognize the analytical characteristics of cardiac troponin assays....