The heart is similar to the skeletal muscles in that it too faces glucose deprivation when calcium and vitamin D supplies are inadequate. Like the skeletal muscles, it can utilize both fat and sugar as fuel, and it uses the same GLUT4 peptide to usher the glucose across the cell walls . As long as the fat cells in the rest of the body are able to release a steady stream of triglycerides into the blood stream, the heart can simply use these for most of its energy needs. But it is likely that, especially after a high-carb, low-fat meal, there will be intervals when the heart is fuel deficient.
I propose that the heart adopts two different coping mechanisms: (1) grow bigger, and (2) develop its own "private" supply of nutrients, in the form of fat deposits. By becoming enlarged, the heart is using the strategy of "strength in numbers." Imagine that six children are competing against three adults in a tug-of-war. The children may win, even though they are weaker, simply because there are more of them. Likewise, the heart, by increasing the number of muscle cells, may be able to beat as strongly as a smaller heart, but each independent muscle cell carries a lesser burden, and therefore can get by on a reduced fuel supply.
The second strategy, creating an internal supply of fats, begins with fatty deposits in the linings of the arteries supplying the heart, known familiarly as arteriosclerosis. These deposits, with time, become "hardened," i.e, associated with calcium deposits; calcium that has been hoarded by the fat cells over the years, just as is done in the abdominal fat cells. The calcium is hoarded because it enables the fat cells to absorb glucose and convert it into fats. As a further strategy, the heart develops a layer of "pericardial fat,"  fatty deposits, typically just outside of the major arteries feeding into the heart. These deposits supply additional fats directly to the heart, to supplement those lining the artery walls.
One problem with encasing the heart with fats is that it becomes susceptible to bacterial infection. The highly oxygenated blood, coming directly from the lungs, may easily become contaminated with bacteria that have entered the body through the lungs. These bacteria may find it attractive to feed off of the fatty deposits lining the arterial walls. As a consequence, cholesterol must infiltrate the artery walls, as a first line of defense in the immune system, to attack the bacteria (Details) . The cholesterol also draws upon white blood cells to assist in the battle. Furthermore, the fat cells encasing the heart, as contrasted with fat cells elsewhere in the body, are especially primed to release cytokines , which are also infection-fighting agents. Thus the presence of fat in the heart's arterial walls and encasing the heart is associated with high levels of cholesterol and cytokines in the blood.