High sensitivity troponin

1. HIGH SENSITIVITY
TROPONINS

2. WHAT ARE TROPONINS?
 Cardiac regulating protein controlling Ca mediated interaction between
actin & myosin-not an enzyme!
 Troponin-Tropomyosin complex – 3 subunits : T,I,C
 Troponin I not found outside heart muscle – highly specific
 Troponin T also expressed in skeletal muscle - differentiated from
skeletal isoforms by monoclonal antibodies
 Raised in myocardial injury of any mechanism, initial cytosolic loss,
more sustained with contractile apparatus destruction

3. WHAT ARE HS TROPONINS?
 ‘When troponin was a lousy assay it was a great test, now that it is a great
assay it is a lousy test’-Robert Jesse
 ‘Low specificity troponins’ –Joe Lex
 Can detect <1g of myocardial necrosis (microscopic zone)
 Old test-99th centile at limits of detection

5. WHAT IS ‘NORMAL’
 ‘Normal’ from healthy population, 1% abnormal by chance
 Below study from GP population with co-morbidities , 99th centile
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7. KNOW YOUR ASSAY

8. WHY DO WE NEED THEM?
 Clinician ‘Gestalt’
• http://intensivecarenetwork.com/heart-stress-body
• Character of pain-no change to PTP, radiation to left arm, no change in
PTP, RF-no change, asking doctors on likelihood scale-poor
 ECG-Too insensitive, 28 % but 97% specific

9. INTERPRETATION OF HS
 Always in clinical context
 Significant change rise/fall
• Increase in >20% if 1st troponin elevated (European
Society of Cardiology)
• Better evidence with delta value of 10
• No clear evidence of % rise if troponins ‘normal’
•
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11. UTILITY OF HST FOR ED
PHYSICIANS
1) Disposition
• Home-safely and quickly
• Studies largely confined to low risk
patients
• CCU
2) Treat patients
• Not much utility except home/ward quicker

12. DISPOSITION-IMPORTANT FOR
THE PATIENT AND NEAT
 Bayley et al. The financial burden of emergency department
congestion and hospital crowding for chest pain patients awaiting
admission. Ann Emerge Med 2005: 45; 110-7
 Pines et al. The association between emergency department
crowding and adverse cardiovascular outcomes in patients with chest
pain. Acad emerge Med 2009 Jun 22

13. NUMERATORS VS
DENOMINATORS
 ED physicians
• Work with denominators/uncertainty
• We are very proficient with working with numerators
 Ward physicians
• Work with numerators
• What happens when we ask them to work with denominators?

15. ED DISPOSITION-HOME-
MOST ‘LOW RISK’
 1635 patients, 30d follow up for MACE
• Non ischaemic ECG, TIMI 0, neg 0 & 2/24 troponin, 0% MACE
with sens 100%, spec 23.1, NPV 100%
• As above with TIMI 0 or 1, 0.8% MACE, sens 99.2, spec 48.7, NPV
99.7
• Allowed early discharge in 40% of suspected ACS presentations

16. ED DISPOSITION-HOME
 Results
• Swedish study, Mean age 55
• 61% (8883) had hs-TnT <5ng/L
• 39 had MI and 2 died at 1/12, 15 of whom had no ECG changes
• If Hs TnT<5 with no ECG changes, absolute MI risk 0.17, no
difference in death at 12/12 between discharged & admitted

18. ED DISPOSITION-HOME
 Strategy to maximize advantage of lower detection rate
• 703 patients, 28% had TnT <3ng/L at presentation (less than
detection threshold)
• Overall MI rate 19%
• No MI at 1/12 in undetectable cohort
 Authors-’Pending further validation studies’

19. WHAT IS AN ACCEPTABLE
‘MISS RATE’

20. WHAT HAPPE NS WHE N YOU SE ND THE M
HOME ? ‘ DIRE CONSE QUE NCES’
 They die! ?
• 10689 patients, 17% ACS, 2% sent home=2% miss rate, death rate
doubled c/w hospitalized if ‘risk adjusted’ but absolute risk the same
(but confidence interval wide and includes 1)
• Readmission hospitalized 17%, not hospitalized 72%

21. YOU CAN’T EVEN MISS
SILENT INFARCTS

22. ED DISPOSITION-CCU
 Sensitivity improves from 73% to 91% drop on specificity form
94% to 90%

23. ED DISPOSITION-CCU
 Reichlin, T et al. Early Diagnosis of Myocardial infarction with
sensitive cardiac troponin assays. N Engl J Med 2009: 361:858-67
• Multicentre study, 718 patients
• AUC at 3/24 93% vs 76%

24. ED DISPOSITION-CCU
 Sensitivity similar at 3 or 6 hours compared to previous 12 hour
sampling

25. COMING TO HELP…

26. DOES THIS HELP OR
HINDER?