Today’s Morning Report is presented by Dr. Freedman!
Troponin-emia 101
Background
- Compromised of three subunits: T, I, and C
- Both T and I subunits are highly-specific for cardiac tissue
- Since 1995, has emerged as the cardiac biomarker of choice
- Cardiac Specificity
- Predictable time course
- Rises above 99th percentile within 4-8 hours and remains elevated for days
- In 2009, the first high-sensitivity troponin assays were reported.
- Improved sensitivity = impaired specificity
“The Third Universal Definition of Acute Myocardial Infarction”
Some Definitions
- Ischemia
- Infarction
- ACS
99th percentile + 1 of the following
- EKG change
- Nuclear imaging defect
- Angiographic “culprit”
AMI Type 1-5
- Atheromatous plaque rupture
- Non-ACS supply/demand mismatch
- CAD +/-
- Other
Troponin-emia in High-lighted Non-ACS
- CVA, ICH, SAH
- +Troponins in ~18% of all CVA
- Mechanism unclear
- Catecholamine surge ?
- Concommitant CAD and ACS?
- Carries significantly increased mortality
- Study in progress in UK; TRELAS
- PE
- Mechanism
- RV strain?
- Hypoexmia?
- 63% of those with enlarged RV end-diastolic diameter have +troponin vs 29% of those without
- Across studies, increased short-term all-cause mortality, even among those without massive PE
- Mechanism
Chronic Troponin-ers
- ESRD
- 82% of those receiving dialysis have elevated Trop T
- Mechanism unclear
- Does not relate to GFR
- Increased afterload/Diastolic dysfunction
- Concomitant CAD?
- Clinical significance
- Increased all-cause and cardiac mortality
- Most useful for patient trends
- CHF
- For ADHF patients, those with + troponins (low-sensitivity)
- Lower SBP
- Lower EF
- Higher inpatient mortality
- For ADHF patients, those with + troponins (low-sensitivity)
- Potpourri
- 80-85% of marathoners have detectable troponins post-race
Conclusions
- New era high-sensitivity assays –> specificity for ACS falls
- Why is it important for EP’s? PCI vs Medical vs Supportive
- All-comers with + troponins
References
- Kerr G, Ray G, Wu O, Stott DJ, Langhorne P. Elevated troponin after stroke: a systematic review. Cerebrovasc Dis 2009;28:220-226.
- Jiménez D, Uresandi F, Otero R, Lobo JL, Monreal M, Martí D, Zamora J, Muriel A, Aujesky D, Yusen RD. Troponin-based risk stratification of patients with acute nonmassive pulmonary embolism: systematic review and metaanalysis. Chest 2009;136:974-982.
- Mingels A, Jacobs L, Michielsen E, Swaanenburg J, Wodzig W, van Dieijen-Visser M. Reference population and marathon runner sera assessed by highly sensitive cardiac troponin T and commercial cardiac troponin T and I assays. Clin Chem 2009;55:101-108.
- Roberts M, Hedley A, Ierino F. Understanding cardiac biomarkers in end-stage kidney disease: Frequently asked questions and the promise of clinical application. Nephrology (Carlton, Vic.) [serial online]. March 2011;16(3):251-260.
- Peacock WF 4th., De Marco T, Fonarow GC, Diercks D, Wynne, J,Apple FS, Wu AH; ADHERE Investigators. Cardiac troponin and outcome in acute heart failure. N Engl J Med 2008;358:2117-2126
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Jay Khadpe MD
- Editor in Chief of "The Original Kings of County"
- Assistant Professor of Emergency Medicine
- Assistant Residency Director
- SUNY Downstate / Kings County Hospital
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1 Comment
wendyrollerblades · October 14, 2013 at 11:10 am
thanks, joey. just anecdotally, in my brief career here, the majority of my PE patients have had mildly elevated troponins (.2-.3 @ UHB lab), which is consistent w/ your data. Also, many of my hypertensive urgency patients have also had similarly mildly elevated trops . all this to say that one must look at all causes for elevated troponins as you mentioned, and not become boxed into only ruling in/out ACS.
~thanks for the learnin’. ~wendy