Disorders of perfusion of the heart muscle are broadly divided according to their severity into:
- Stable angina
- Acute coronary syndrome, which is further subdivided into:
1. Unstable angina
2. Myocardial infarction
Like all body tissues, the heart needs a continuous oxygen-carrying blood supply to function, and for the cells to maintain their metabolism. Cells eventually die without it.
The degree of tolerance to oxygen deficiency varies widely according to the type of tissue. At the extremes of the spectrum lie the nerve cells (neurons) and bone cells (osteocytes).
Neural tissue can’t tolerate oxygen deficiency after 5 minutes, while bone tissue can handle a few hours without irreversible tissue damage. It usually depends on the rate of metabolism of tissues. A factory that produces large amounts of products per hour is more quickly affected by the cessation of its raw materials supplies.
Heart muscle cells are also sensitive to oxygen deficiency, and its effect takes less than 30 minutes to produce an irreversible injury and death to the muscle cells.
How does it happen?
Unstable angina is a supply-demand mismatch of the heart, which means that there are either physiological or pathological conditions that affected the heart, leading to increased oxygen demands. Such conditions range from mild fever to severe valve diseases. This can also be coupled with other health problems that cause the heart muscle’s blood supply to deteriorate. Since oxygen is carried by red blood cells -the better name is red blood corpuscles as they are not “true” cells- through their hemoglobin, which is an oxygen-carrying iron-containing protein. Such conditions include anemia, hypotension, or any other disease affecting breathing or the oxygenation of blood.
Another important mechanism is what is called plaque disruption. When fats are deposited in a gradual manner causing the narrowing of the heart’s blood vessels, they produce stable angina. It increases in severity over a long time and takes years to produce typical symptoms. Such plaques of fat are covered by a layer of the lining of the mentioned blood vessels. In some cases, this cover or “cap” is thin or “unstable” that it becomes liable to rupture, releasing the fatty plaques into the lumen of the blood vessel. This is a catastrophic event because while the cap itself has a smooth surface, it prevents the blood from clotting in the vessel’s wall when released. The cap is ruptured, the smooth surface becomes rough, and clotting occurs, rapidly disrupting the heart’s blood supply. The greatest anticoagulant of the body is the unmatched smoothness of the interior of blood vessels.
An important thing to note here, however, is that muscle cell death does not occur in unstable angina like heart attacks. That’s because the vessel is not completely obstructed but leaves a small portion that allows the cells just to live until it is obliterated.