WORLD DEVELOPMENT REPORT 2024 - Economic Growth in Middle-Income Countries.
update 11.pptx
1.
2. When is it safe to do a stress test?
It would usually be safe to perform a stress test in the following
situations:
Cardiology Consultation can be considered for:
– Any patient with a down trending troponin above the normal range of 19 pg/ml, prior to
stress
– Unsure what type of stress test is most appropriate
– Active chest pain with unclear cardiovascular stability
Do not perform a stress test on a patient with active
chest pain and a rising troponin.
Active Chest Pain
No Active Chest Pain* or
Resolved Chest Pain*
*if clinically indicated
• Ruled-out troponins and clinically
stable (no aortic dissection, no
acute PE, no severe aortic stenosis,
etc.)
• Indeterminent troponins
• Ruled-out troponins
3. How to Select Imaging
Stress Test Decision Algorithm:
Consider ETT/Echo for: can exercise/
walk on treadmill, BMI < 40
Consider Nuc Med Perfusion for: Prior
MI, Obesity, Hx of AF or Arrhythmia
Consider Dobutamine Stress for: Lung
Disease, no Arrhythmia, inability to
exercise
CTCA Algorithm:
Renal function (GFR ≥ 30)
Able to get HR ≤ 65 (w/ or w/o beta-
blocker)
Normal sinus rhythm
No known CAD
No IV contrast allergy
4. Take Home Message
• Lower level of detection leads to:
– Higher confidence and quicker rule-outs
– More “false positives” for ACS evaluation that make clinical assessment critically important
• Acute MI is defined by labs and clinical changes, not just labs alone. Serial measurement of troponin is
important.
• Do not order Troponin test routinely unless you have a compelling clinical reason (concern for
ACS/NSTEMI) to do so.
• Utilize stress testing or imaging in patients with no active chest pain and/or non-rising troponins.
• Proper MiChart documentation of the cause of an elevated troponin (myocardial injury due to , NSTEMI,
or type 2 myocardial infarction) is critical.
5. Troponins first described
by Ebashi et al. (1963)
Clinical use of cardiac-specific TnT in AMI
Katus et al. (1984)
Troponins increased the diagnosis rate of AMI approximately 15%*
Kavsak P et al. The impact of the ESC/ACC redefinition of myocardial infarction and new sensitive troponin assays on the frequency of acute
myocardial infarction. Am Heart J 2006;152:118–25.
6. Sarcomere
• Cardiomyocytes are composed of tubular myofibrils, which consist of repeating sections of
sarcomeres
• Sarcomeres are the fundamental contractile unit (between two Z-lines)
• They are composed of long fibrous protein filaments (thick = myosin / thin = actin) that slide
past each other when a muscle contracts/relaxes
Microscopic anatomy of cardiac muscle
7. • Cardiac-specific troponin (cTn) is a heteromeric protein complex located along the thin
filaments of myofibrils
• Regulators of muscle contraction
• 3 distinct gene products cTnC binds calcium
cTnT attaches to tropomyosin on thin filaments
cTnI inhibits actomyosin ATPase.
Jaffe AS, Vasile VC, Milone M, et al. Diseased skeletal muscle: a noncardiac source of increased circulating
concentrations of cardiac troponin T. J Am Coll Cardiol. 2011 Oct 18;58(17): 1819-24.
Troponin protein
complex
8. Troponin detection – potential mechanisms of injury?
Cardiomyocyte
troponin
release
Type I/II
ischaemia
Increased
wall stress
Oxidative
stress
Altered Ca2+
handling
Inflammatory
cytokines
Neurohormonal
activations
Necrosis
Apoptosis
Normal myocyte
turnover
Proteolytic Tn
degradation products
Increased cellular
permeability
Formation and release of
membranous blebs
9. • cTnI and cTnT have unique N-terminal amino acid sequences specific antibody
immuno-assays.
• The original first generation TnT assay consisted of capture and detection antibodies
sandwich complex.
• The capture antibody was cardiac specific, but the detection antibody cross-reacted with
skeletal muscle TnT
• In 1997, a second-generation assay using cardiac specific capture and detection
antibodies was introduced with no cross-reaction with skeletal TnT.
• A newer third-generation assay with similar specificity is now available using the same
cardiac-specific antibodies and substituting recombinant human cardiac TnT as the
material standard
c-Tn assays