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The Pathophysiology of Myocardial Infarction: From Coronary Occlusion to Clinical Consequence

1Coronary Supply and the Myocardial Oxygen Balance2Atherosclerotic Plaque Rupture and Coronary Thrombosis3Ischemia: Metabolic and Functional Consequences of Oxygen Deprivation4From Reversible Injury to Irreversible Cell Death5Inflammation, Healing, and Infarct Remodeling6Clinical Manifestations: ECG, Biomarkers, and Pump Dysfunction
Clinical Manifestations: ECG, Biomarkers, and Pump Dysfunction

Biomarker Release Kinetics: Troponin and CK-MB

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Troponin and CK-MB both leak from dying cells, but their kinetics differ in a way that matters clinically. Troponin has a small free pool that escapes quickly and a large bound pool that releases slowly, so it rises early but stays elevated for one to two weeks. CK-MB clears faster, returning to baseline in two to three days. That difference is why CK-MB is still used to detect a second heart attack: if troponin is already high from the first event, a new rise is hard to see, but a fresh CK-MB rise stands out. The other point is that necrosis spreads as a wavefront, so early samples can be falsely negative. That is why we draw blood serially rather than once.
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Troponin vs. CK-MB

Cardiac Troponin

  • Rises 3–6 hours after necrosis
  • Peaks ~24 hours
  • Remains elevated 7–14 days
  • Highly cardiospecific
  • Not useful for reinfarction within the elevation window

CK-MB

  • Rises 3–6 hours after necrosis
  • Peaks 12–24 hours
  • Returns to baseline in 48–72 hours
  • Less cardiospecific (skeletal muscle source)
  • Useful for detecting reinfarction

Why serial sampling matters

The wavefront of necrosis means that biomarker release is a cumulative process. A sample drawn very early may miss the rise entirely. Serial measurements at presentation and 3–6 hours later capture the kinetic curve and distinguish a true acute event from a chronic elevation.

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