Cardiac Enzymes & BioMarkers 101

Editor’s Note:

One of the strongest aspects of this blog is that it represents real-time issues as they occur in my life/arena or to others in either my clinical circle, or my family and friends. In this case, the point of this refresher article is to help and assist the latter in terms of understanding some of the myriad of questions that present when a loved one goes to the emergency room with a suspected myocardial infarction.

That being the case, a lot of things are thrown at you at once. The first most pressing is obviously the welfare of your family member that may or may not have had a heart attack. So the immediate fear of course is death or the prolonged agony that goes with the uncertainty what’s in front of you.

This blog is a reflection of all of our lives so bear with me as I deal with mine. 🙂

Once immediate risk of sudden death from a heart attack is further in the distance, the following questions always come to the foreground:

  • Did my loved one have a heart attack?
    • Chest pain or shortness of breath is not the only way to evaluate whether or not someone has- or is having a heart attack. Typically an EKG will indicate the possibility of a heart attack – but it may not be entirely conclusive.  Another way to assess damage to the heart is by measuring cardiac enzymes are biomarkers. That is a topic of this particular post – and explanations as well as charts are listed below to help in that assessment.
  • How serious is the heart attack?
    • We always hear the expression a “massive heart attack”but that tends to be an emotional and misleading statement that people attribute to something they really don’t understand. There are very definable ways to measure myocardial (heart) function or lack thereof:
      • The ejection fraction is an excellent measurement of myocardial contractility and is measured as a percentage of blood that is ejected by the heart with each beat. A normal ejection fraction in an adult would be 60 to 70%. Most of the patients that I see however, are in the 40 to 50% range, and I only really worry if that range covers or is lower than 35%.
  • How do you know they had a heart attack?
    • When interpreting whether or not a patient has had a heart attack is typically a combination of various lab and test results that lead to diagnosis of myocardial infarction. The EKG, cardiac enzymes, transesophageal echocardiogram, ultrasound, thallium stress test, and most definitively a cardiac catheterization – will help paint the full picture.
  • How much damage was done?
    • The initial assessment of heart function is not necessarily a valid predictor of how much damage was done and/or how well the heart will recover. That will depend on the overall health of the patient, which vessels of the heart may or may not be blocked, if there is collateral flow (other tiny blood vessels feeding the heart muscle past the point of where the major artery is obstructed), or if there are any other existing problems (co-morbidities) such as aortic valve disease or mitral valve disease.
  • What is the treatment plan to help repair or stabilize the heart?
    • Depending on what the mechanism of injury was, the most common treatment plans are as follows:
      • No surgical intervention treat with
        • Medications- beta-blockers, aspirin, statins, ACE inhibitors, blood thinners (warfarin or platelet inhibitors).
        • modifications and diet, lifestyle, exercise.
      • Surgical interventions are more invasive, riskier and may include:
        • PCI – percutaneous coronary intervention (heart catheterization with dye injected into the coronaries to assess coronary flow to the myocardium as well as right and left ventricle performance. In ejection fraction will be calculated during this phase.
        • TEE– transesophageal echocardiogram-where a probe was placed into the esophagus and the function of the heart is evaluated.
        • Cardiac ultrasound-this is the least risky and least invasive of these three diagnostic procedures, and will render very accurate and important information regarding heart function.
        • Open heart surgery.
  • How dangerous is this treatment plan – in other words is it worth the risk?
    • The risk of any treatment plan depends on the following:
      • The skill of your physician
      • The resources available at this hospital
      • The general health of the patient.  The following is a list of factors that may create an increased risk to the patient.
        • Age
        • Family history of cardiac disease
        • Smoking or tobacco
        • Alcohol use
        • Diabetes
        • Obesity
        • Previous stroke and or carotid disease
        • Lung function
        • Liver function
        • Kidney function
        • Peripheral Vascular Disease
  • What is the prognosis? (Will they live- and if so how long and with what quality of life?)
    • That’s for another time …

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Cardiac enzymes ― also known as cardiac biomarkers ― include myoglobin, troponin and creatine kinase.

Historically, lactate dehydrogenase, or LDH, was also used but is non-specific. Cardiac enzymes are released into the circulation when myocardial necrosis occurs, as seen in myocardial infarction.

Myoglobin

Myoglobin is released into circulation with any damage to muscle tissue, including myocardial necrosis. Because skeletal muscle contains myoglobin, this measurement is quite nonspecific for MIs. The benefit in myoglobin is that a detectable increase is seen only 30 minutes after injury occurs, unlike in troponin and creatine kinase, which can take between 3 and 4 hours.

Troponin

The enzymes troponin I and troponin T are normal proteins that are important in the contractile apparatus of the cardiac myocyte. The proteins are released into the circulation between 3 and 4 hours after myocardial infarction and remain detectable for 10 days following. This long half-life allows for the late diagnosis of MI but makes it difficult to detect re-infarction, as can occur in acute stent thrombosis after percutaneous coronary intervention, or PCI. There are a number causes for troponin elevation not related to myocardial infarction; however, troponin elevation is much more sensitive than myoglobin and even creatine kinase.

Creatine kinase (CK)

Creatine kinase ― also known as creatine phosphokinase, or CPK ― is a muscle enzyme that exists as isoenzymes. The MB type is specific to myocardial cells, whereas MM and BB are specific to skeletal muscle and brain tissue, respectively. The CK level increases approximately 3 to 4 hours after MI and remains elevated for 3 to 4 days. This makes it useful for detecting re-infarction in the window of 4 to 10 days after the initial insult; troponin remains elevated for 10 days, making it less useful for this purpose.

Troponin normal values:footnote1

CK-MB (creatine kinase-myocardial band) normal values:footnote1

  • 0–3 micrograms per liter (mcg/L)

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