D efinitions
Myocardial infarction: An area of heart muscle is inadequately perfused
as a result of cardiac vessel occlusion resulting in ischemia, cell death,
and loss of cell constituents including enzymes into the circulation.
Electrocardiographic changes occur as a result of damaged heart tissue.
Angina: Transient disruption of adequate blood flow to a portion of heart
muscle leading to pain and a temporary shift to anaerobic glycolysis pro-
ducing pyruvate and lactate that are released into the circulation.
Aerobic glycolysis: Metabolism of glucose to pyruvate. Pyruvate in the
presence of sufficient oxygen can be metabolized to CO2 via the tricar-
boxylic acid cycle in the mitochondrion-producing NADH and FADH2,
which contribute elections through the electron transfer chain to molec-
ular oxygen producing H2O and ATP.
Anaerobic glycolysis: Metabolism of glucose to lactate in the absence of
sufficient oxygen. When oxygen is lacking, pyruvate is converted to lac-
tate, and no further oxidative pathway is available.
Electron shuttles: Enzymatic processes whereby electrons from NADH
can be transferred across the mitochondrial barrier. The glycerol 3-
phosphate shuttle uses the reduction of dihydroxyacetone phosphate to
glycerol 3-phosphate and reoxidation to transfer electrons from cytoso-
lic NADH to coenzyme Q in the electron transport chain. The malate-
aspartate shuttle uses malate and aspartate in a two-member transfer
exchange to transfer electrons from cytosolic NADH to mitochondrial
NADH (see Figures 27-2 and 27-3).
Myocardial infarction arises when perfusion of cardiac muscle is inadequate,
resulting in insufficient oxygen delivery to that portion of cardiac muscle. This
causes the affected muscle to rely on anaerobic metabolism for its energy sup-
ply with concomitant production of lactic acid. Even transient ischemia can
lead to changes in muscle tissue but prolonged ischemia leads to breakdown
of muscle cells and release of cellular proteins such as creatine kinase, lactic
acid dehydrogenase, and troponin I. Reperfusion by thrombolytic treatment
or mechanical means can restore oxygen levels and return the metabolic
processes to aerobic metabolism. A secondary consequence of reperfusion is
reperfusion injury in which the highly reduced state of injured cells meets
increased oxygen concentration and produces reactive oxygen radicals. Most
notable of these is the hydroxyl radical (OH ), which attacks tissue compo-
nents such as lipids and protein sulfhydryl groups. Myocardial infarction
causes changes in the pathways of energy generation triggered by oxygen
insufficiency in the affected heart muscle.
The glycolytic pathway for all cells under conditions of adequate tissue
oxygenation is shown in Figure 27-1. Two molecules of ATP are required to
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