Mekanisme Seluler dan Molekuler Cedera Miokard Tipe 2 serta Peningkatan Troponin Pasca Henti Jantung
Tinjauan Literatur
DOI:
https://doi.org/10.55606/jrik.v6i2.6676Keywords:
Cardiac Arrest, Cardiac Troponin, Ischemia Reperfusion, Oxidative Stress, Type 2 Myocardial InjuryAbstract
Cardiac arrest causes global ischemia followed by reperfusion injury, resulting in diffuse myocardial damage and cardiac troponin release. This condition is commonly associated with type 2 myocardial injury caused by an imbalance between myocardial oxygen supply and demand rather than acute coronary occlusion. This article summarizes evidence on the cellular and molecular mechanisms of type 2 myocardial injury and troponin release after cardiac arrest. A narrative literature review was conducted using articles published between 2015 and 2025 from PubMed and Google Scholar. The findings indicate that ischemia causes ATP depletion, ionic imbalance, intracellular calcium overload, and mitochondrial dysfunction. Reperfusion further aggravates myocardial injury through reactive oxygen species generation, inflammasome activation, pro-inflammatory cytokine release, apoptosis, and pyroptosis. These processes impair cardiomyocyte membrane integrity and cause structural damage, leading to troponin release. Troponin elevation may reflect reversible membrane permeability changes or irreversible cardiomyocyte injury. Therefore, high-sensitivity cardiac troponin levels should be interpreted according to pathophysiological mechanisms and clinical context to distinguish type 2 myocardial injury from myocardial infarction caused by acute coronary occlusion.
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