Consumes 60-75% of all oxygen delivered to the coronary circulation.
There is regeneration throughout life with increased rate after myocardial infarction.
Regeneration is limited to viable areas and to its border zone.
There are minimal effects of normovolemic anemia, with hemoglobin levels in the range of 7.0 g/dL, on the normal coronary circulation.
Cardiac myocytes have 5 components including cell membrane and T-tubules (sarcolemma) for impulse conduction, sarcoplasmic reticulum for calcium reserve for contraction, contractile elements, mitochondria and a nucleus.
Heart muscles contain more mitochondria between myofibrils than do skeletal muscles, with 23% of cell volume vs 2%, respectively.
Has almost complete dependence on aerobic metabolism.
Cardiac muscle cells usually have one nucleus.
Ventricles contract during systole and relax during diastole.
Functional unit of cardiac muscle is the intracellular sarcomere, a arrangements of thick filaments containing myosin and thin filaments containing actin.
Sarcomeres contain the regulatory proteins troponin and tropomyosin.
Heart muscles are composed of parallel myofilaments and contraction occurs by the sliding of actin filaments between the myosin filaments towards the center of each sarcomere.
Sarcomere length ranges from 1.6-2.2 µm, depending on the state of contraction.
Shorter sarcomeres result in overlap of actin and myosin with decreased contractile force and longer sarcomeres result in enhanced ability to contract.
Ventricular dilation that occurs with diastole results in an increase in the force of contraction during systole.
When heart dilation is progressive, as in congestive heart failure, the overlap of actin and myosin filaments is reduced and contraction decreases.
Myocytes comprise 25% of heart cells but 90% of its volume because of their large size.
Other cells in the myocardium include endothelial cells and fibroblasts.
Atrial myocytes are smaller and less structured than ventricular myocytes.
Some atrial cells contain granules which contain storage sites of atrial natriuretic peptide, which is released with atrial distension.
Natriuretic peptides are also produced by ventricular cells, brain natriuretic peptide, during increased ventricular pressure and volume.
Intercalated disks functionally mediate myocytes, joining individual cells and allowing mechanical and electrical coupling.
Intercalated disks have gap junctions which allow synchronization of myocyte contractions by providing electrical coupling with passage of ions across adjacent cell membranes.
Myocyte cells have defense mechanisms to prevent injury from prolonged ischemia.
Ischemic preconditioning activates the signaling molecule epsilon form of protein kinase C (PKC-e).
Epsilon form of protein kinase C mobilizes endogenous cardiac defense mechanisms against injury and results in infarct sparing effect.
Ischemia leads to increased mitochondria Ca++ uptake, which increases permeability and leads to breakdown of mitochondrial respiration and ultimately cell death.
With preconditioning, PKC-e, prevents degeneration by phosphorylation molecules that trigger events that preserve mitochondrial function.
Mitochondria are the main energy producers of myocyte and host signaling pathways for apoptosis.
With increasing age the number of myocytes decrease, have increased connective tissue and, in some, have deposition of amyloid.
With aging the myocytes have lipofuscin deposition and basophilic degeneration.
Extensive lipofuscin deposition in an aged atrophic heart is ref2242ed to as brown atrophy, usually associated with cachectic weight loss.
The degenerative changes of the heart in old age is only rarely associated with clinical impairment.