High sensitivity troponin

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?