Troponins: The Heart of Cardiac Diagnostics

Troponins are a big deal in medicine, especially when it comes to diagnosing heart attacks. Let’s break down the basics of troponins, how they work in the body, and how we detect them in the lab.

What Are Troponins? Troponins are proteins involved in muscle contraction, found in both skeletal and cardiac muscle. They’re part of the troponin-tropomyosin complex, which helps regulate muscle contraction by interacting with actin and myosin.

There are three types of troponins:

Troponin C (TnC) – Binds to calcium, triggering muscle contraction. Troponin I (TnI) – Inhibits muscle contraction in the absence of calcium. Troponin T (TnT) – Anchors the troponin complex to the muscle fiber.

For cardiac diagnostics, we focus on cardiac-specific troponins: Troponin I (cTnI) and Troponin T (cTnT). These versions are unique to the heart muscle, making them incredibly important markers for detecting cardiac injury. When the heart is damaged, like during a heart attack, these cardiac-specific troponins are released into the bloodstream, signaling that heart cells are in distress.

Why Are Troponins Important? Elevated troponin levels are a key indicator of myocardial injury (damage to the heart muscle), most often associated with acute coronary syndrome (ACS), which includes heart attacks. When heart cells are damaged due to ischemia (lack of oxygen), they break open, and troponins leak into the blood.

Troponin tests are the gold standard for diagnosing heart attacks because they are sensitive (they detect even small amounts of damage) and specific (they’re associated with cardiac tissue, not other types of damage).

This specificity is very important because in the ED a panic attacks and even gastric reflux can present very similarly to heart attacks. The lab is crucial to making sure we catch the cases that even the most experienced clinicians miss!

How Are Troponins Detected in the Lab? The process of measuring troponins in the lab is highly standardized and involves several steps, starting with blood collection and ending with immunoassay analysis:

Blood Collection and Processing:

Troponin tests are typically done using either the green top (heparin) or lavender top (EDTA) tubes, depending on the lab. These tubes prevent blood from clotting, allowing for plasma testing. Which is faster than allowing the blood to clot (serum testing). Speed here is important for obvious reasons. (Technically both plasma and serum can and are used to measure troponins, but plasma testing is more common because it allows for quicker processing—there’s no need to wait for the blood to clot.)

After collection, the sample is centrifuged to separate the plasma from the blood cells and transferred to a sample cup for testing by Immunoassay which involves specific antibodies designed to bind to cardiac-specific troponins (either cTnI or cTnT). When these antibodies bind to troponin in the blood sample, they trigger a signal (usually via chemiluminescence or fluorescence) that can be measured. The strength of the signal corresponds to the amount of troponin present in the blood. This value is then compared to a reference range.

Each lab sets a reference range based on the assay, but in general, elevated levels of troponins suggest myocardial damage. The rise and fall pattern of troponin levels is key in diagnosing a heart attack—you’re not just looking for elevated levels, but how they change over time.

Timing: Troponins typically rise within 3-6 hours after a cardiac event, peak at 12-24 hours, and can remain elevated for days. This pattern helps clinicians confirm the presence and extent of cardiac injury.

Other Markers for Myocardial Infarction In addition to troponins, other markers may be measured for myocardial infarction (MI), though they’ve largely been replaced by troponins due to their higher sensitivity and specificity:

Creatine Kinase-MB (CK-MB):

CK-MB is an enzyme found in heart muscle and was used widely before troponins became standard. CK-MB rises and falls more quickly than troponins, which can be useful in detecting a reinfarction shortly after a heart attack. Many old school cardiologist swear by this marker!

Myoglobin:

Myoglobin is a small oxygen-binding protein that rises rapidly after muscle damage, but because it’s also found in skeletal muscle, it’s not specific to the heart. However, it can be an early marker for cardiac damage due to its rapid rise.

BNP/NT-proBNP:

These markers are released by the heart in response to stretching from heart failure. While not specific for heart attacks, elevated BNP levels can help differentiate between heart failure and other causes of similar symptoms, such as shortness of breath. More on this in a future post!

Feel free to drop any questions or thoughts below! Let’s chat about how these tests have changed modern cardiology and what’s next in cardiac biomarker research!

No comments yet!

Mainlined Science

!mainlined_science@mander.xyz

Create post

Welcome, welcome, welcome!

This community is here to share the passion of science with anyone and everyone. We have a special interest in longevity science, but all STEM fields are appreciated. This is a place to share and discuss these topics in a respectful and open minded manner.

Rules

  1. No spam
  2. If posting articles ALWAYS include source material
  3. Be kind

What’s with the name?

Like Mariella, we should all aim to mainline science at least five times a day.

Who are we? We are a normie that has a lot of freetime and a wicked smaaht postdoc.

What do we want? To share info from the scientific world with an emphasis in longevity science.

What’s longevity science? This is the arm of science that looks into ways to promote a healthy and extended lifespan.

Wait, immortality? Nah. While that would be dope, immortality isn’t necessarily the end goal. In terms of total lifespan we are a relatively long lived species, however, most people spend their older years living with debilitating age related conditions and diseases. Let’s say Person A lives to be 96 years of age, but they spent twenty of those years bedridden. Whereas Person B lived to be 88 and was perfectly healthy up to the last minute before dying from a stroke. I’d argue that Person B had a healthier lifespan. Obviously, this is a very nuanced concept to breeze through, but the goal of this field is to find ways to extend our ability to live healthy lives without age related declines. Eventually the hope is for total lifespan to also increase, but for now living longer in good health is the real marker of longevity.

Now what? Have a fun topic you wanna discuss or learn more about? Make a post! Afraid you don’t know enough to post or ask questions? Pffft! Ask away! Above all, you do you. And be kind.

Community stats

  • 5

    Monthly active users

  • 19

    Posts

  • 15

    Comments