What event occurs when necrotic injury happens in anginal chest pain unresponsive to nitroglycerin?

In cases of anginal chest pain unresponsive to nitroglycerin, necrotic injury to the heart muscle is indicative of severe tissue damage often due to ischemia. When there is significant myocardial injury, a critical event that typically occurs is the rupture of the mitochondrial membrane.

Mitochondria are essential for cellular respiration and energy production in the form of ATP. When cardiac cells experience prolonged ischemia or necrosis, the integrity of the mitochondrial membrane is compromised. This rupture leads to impaired ATP production and the release of pro-apoptotic factors and reactive oxygen species, contributing to further cellular injury and death. The loss of mitochondrial function is a hallmark of irreversible damage often seen in myocardial infarctions.

While other options such as increased myocardial oxygen demand, coronary artery blockage, or cardiac muscle apoptosis are relevant in the context of anginal symptoms or ischemia, they do not directly describe the immediate and critical event that occurs at the cellular level in the context of necrosis. The focus on mitochondrial membrane rupture highlights the critical cellular pathophysiological change that underlies necrotic injury in heart tissue, making it the most appropriate answer for understanding the consequences of such severe cardiac events.