Which mechanism best explains the pathogenesis of myocardial injury after reperfusion, evidenced by elevated CK-MB and troponin I?

Which mechanism best explains the pathogenesis of myocardial injury after reperfusion, evidenced by elevated CK-MB and troponin I?

• A. Protease inactivation by cytoplasmic free calcium ions
• B. Membrane lipid peroxidation
• C. Liquefactive necrosis of the myocardium
• D. Formation of apoptotic bodies

Answer: (B)

Reperfusion injury is driven by oxidative stress: when blood flow returns to ischemic myocardium, a burst of reactive oxygen species forms and attacks cell membranes. This lipid peroxidation damages the sarcolemma and mitochondrial membranes, increasing membrane permeability, disrupting ion homeostasis (especially calcium), and triggering progressive cellular injury and necrosis. The release of intracellular enzymes like CK‑MB and troponin I into the blood reflects this myocyte membrane breakdown and death. Membrane lipid peroxidation best explains the mechanism behind the observed enzyme elevation after reperfusion. Other mechanisms described—apoptotic bodies from programmed cell death, liquefactive necrosis typical of certain brain injuries, or protease inactivation by calcium—do not capture the principal acute process driving reperfusion-associated myocardial injury.

Reperfusion injury is driven by oxidative stress: when blood flow returns to ischemic myocardium, a burst of reactive oxygen species forms and attacks cell membranes. This lipid peroxidation damages the sarcolemma and mitochondrial membranes, increasing membrane permeability, disrupting ion homeostasis (especially calcium), and triggering progressive cellular injury and necrosis. The release of intracellular enzymes like CK‑MB and troponin I into the blood reflects this myocyte membrane breakdown and death. Membrane lipid peroxidation best explains the mechanism behind the observed enzyme elevation after reperfusion. Other mechanisms described—apoptotic bodies from programmed cell death, liquefactive necrosis typical of certain brain injuries, or protease inactivation by calcium—do not capture the principal acute process driving reperfusion-associated myocardial injury.