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Creatine kinase (CK) is a critical enzyme involved in cellular energy metabolism, catalyzing the reversible transfer of a phosphate group from ATP to creatine.[1] This reaction plays a crucial role in tissues with high and fluctuating energy demands, including skeletal muscle, cardiac muscle, and the brain. CK exists in tissue-specific isoenzymatic forms: CK-MM (muscle), CK-BB (brain), and CK-MB (a hybrid of muscle and brain subunits), which can be measured to assess tissue injury. Among these, CK-MB has historically served as a key biomarker for detecting myocardial infarction, due to its relative abundance in cardiac muscle. Although cardiac troponins have largely supplanted CK-MB in routine clinical practice, CK-MB retains diagnostic relevance in certain contexts, such as suspected reinfarction or when troponin assays are not available. The isoenzymes of CK are dimers of either type B or M polypeptide chains. The BB isoenzyme is found in the central nervous system, whereas the MM isoenzyme is a principal component in adult skeletal muscles.[2] The myocardium has 15% CK-MB isoenzyme and 85% CK-MM.[3] Skeletal muscles contain about 1% to 3% of CK-MB.[4]

Clearance of CK from Blood or Plasma CK and its isoenzymes are inactivated in the lymph through proteolysis.[5] Abnormal liver function or renal function does not affect the clearance of CK in a significant manner, and CK is not excreted in the urine.[6] Hypothyroidism retards the clearance of CK.[7] CK-MB levels can also be elevated in the circulation in the absence of acute myocardial infarction.[8] This elevation is due to increased amounts of B subunit production in injured skeletal muscle, as it does during fetal development; ontogeny recapitulates phylogeny.[9] Rhabdomyolysis, intense exercise, and trauma result in transient elevation of CK and CK-MB; CK-MB is present in skeletal muscles as well, albeit in lesser concentrations.[10] Chronic skeletal muscle disorders, such as autoimmune myopathies and inflammatory myopathy, can result in persistently high CK-MB levels in the plasma due to ongoing injury and repair.[11][12] Damage to the myocardium releases CK-MB, and since the myocardium contains the largest percentage of CK-MB, patients with rapidly rising and falling CK-MB exceeding the reference range of normal should be considered as having acute myocardial infarction until proven otherwise.[13]

Enhancing healthcare team outcomes in CK-MB testing requires coordinated interprofessional collaboration to ensure appropriate use aligned with current evidence and clinical relevance. While CK-MB was historically used in the evaluation of myocardial injury, its role has been limited by the emergence of more sensitive biomarkers. However, CK-MB may still be used in specific clinical situations, such as detecting perioperative myocardial injury in cardiac surgery or reinfarction within a short time frame after the initial event. Physicians and advanced practitioners are responsible for determining when CK-MB testing is clinically appropriate, taking into account patient history and current guidelines. Nurses support this process by ensuring accurate test ordering and proper sample handling during pre-analytical phases, and by communicating test results efficiently. Laboratory technologists ensure analytical accuracy through adherence to validated protocols and quality management procedures. Pharmacists may contribute by assessing medications that could influence CK-MB levels or clinical interpretation. Effective communication among all team members, adherence to ethical responsibilities, and a shared understanding of CK-MB's utility and limitations are essential for coordinated patient care. This interprofessional approach helps minimize unnecessary testing, supports clinical decision-making in select patient populations, and promotes optimal resource utilization while maintaining patient safety and care quality.