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
The views expressed on this blog are the author's own and do not reflect the views of their employer. Please read our full disclaimer here. Any references to clinical cases refer to patients treated at a virtual hospital, Janus General Hospital.
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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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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