well that is kind of a misnomer. sure the heart can survive long time producing it's own atp but it will probably stop beating earlier and getting it back to normal is almost impossible.

"During ischemia, succinate, a citric acid cycle (CAC) intermediate, accumulates in mammalian hearts as it cannot be oxidised by the mitochondrial respiratory chain9. Upon reoxygenation, succinate oxidation fuels an overproduction of mitochondrial reactive oxygen species (ROS), causing extensive cardiac damage9. This arises when electrons from succinate oxidation by complex II are forced backwards through complex I by a high mitochondrial proton-motive force. This process is known as reverse electron transfer (RET) and is favoured when ATP generation by the ATP synthase is low10,11. At the flavin site of complex I electrons can react with molecular oxygen, forming superoxide, which is converted further to H2O2. Succinate is thus a major cause of oxidative damage in the mammalian heart after I/R. "