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High sensitivity troponin
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HIGH SENSITIVITY TROPONINS
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
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
WHAT IS ‘NORMAL’
‘Normal’ from healthy population, 1% abnormal by
chance
Below study from GP population with co-
morbidities , 99th centile 34
KNOW YOUR ASSAY
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
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’•
-
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
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
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?
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
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
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’
WHAT IS AN ACCEPTABLE ‘MISS RATE ’
WHAT HAPPENS WHEN YOU SEND THEM HOME? ‘D IRE
CONSEQUENCES’
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%
YOU CAN’T EVEN MISS SILENT INFARCTS
ED DISPOSITION-CCU
Sensitivity improves from 73% to 91% drop on
specificity form 94% to 90%
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%
ED DISPOSITION-CCU
Sensitivity similar at 3 or 6 hours compared to
previous 12 hour sampling
COMING TO HELP…
DOES THIS HELP OR HINDER?