An acute myocardial infarction, also known as a heart attack, occurs when a blockage in one or more of the blood vessels leading to the heart muscle causes a disruption in the blood flow to the cardiac tissue. Without blood flow, oxygen cannot be delivered to the heart muscle or myocardium, and the tissue begins to die. If the lack of oxygen is prolonged, irreversible tissue death results. A typical heart attack can kill roughly one billion cells and, unfortunately, the heart is unable to replace these dead cells fast enough to recover from the damage. This initial, permanent, cell death is the precursor to the long-term effects caused by a heart attack.
Changes in Structure and Function
The American College of Sports Medicine's "Exercise Management for Persons With Chronic Diseases and Disabilities" provides a thorough explanation of the long-term effects of heart attacks on the structure and function of the heart muscle. Cardiac muscle contractions, or heart beats, are a very systematic and organized event. When a portion of the myocardium dies as a result of a heart attack, the efficiency of the cardiac system deteriorates. Dead tissue does not contract or contribute to the heart beat. The muscle loses its synchronicity, and contractions become disorganized.
The remaining cells of the heart begin to take on a different shape and tend to enlarge; this is known as hypertrophy and is the heart's attempt to counter the loss of synchronicity and organization to maintain efficiency. The enlarged cells do not contract as forcefully as normal-sized cells, and thus the ability of the heart to generate sufficient force during each contraction is hindered.
The electrical system of the heart that signals for a contraction may also become disturbed as a result of the changes in cell structure. This can lead to irregular heart rhythms, known as arrhythmias. If unable to be resolved through medication or other therapeutic means, arrhythmias generally require permanent pacemaker implantation.
Heart failure is a long-term result of the changes in muscle structure and function. For an indefinite period following a moderate heart attack, the cardiac tissue attempts to compensate for the loss of tissue by changing its structure, as noted above. This process is termed compensatory heart failure. Once these mechanisms fail, however, the heart is unable to keep up with the demands of the body, and decompensated heart failure ensues. Heart failure brings with it additional complications within the cardiovascular system beyond those incurred as a direct result of a heart attack.
The American Heart Association publishes yearly statistical information on heart attacks and heart failure in the research journal "Circulation." The 2010 publication predicts some 935,000 heart attacks in the United States in 2010 alone, which will contribute to the roughly 5.3 million Americans suffering from heart failure. There is a 20 percent one-year mortality rate for heart failure--20 percent of individuals, or one in five, diagnosed with heart failure die within one year of the initial diagnosis.
The Role of Exercise
While the tissue damage incurred during a heart attack may not be recoverable, programs such as cardiac rehabilitation, which emphasize exercising the heart muscle, can protect the remaining heart tissue and delay the onset of heart failure. In the February issue of the "Journal of Applied Physiology," Dr. Ben Esch examines the functional and structural benefits of exercise following damage to the heart muscle. Exercise increases blood flow to the heart, increases the synchronicity of contraction and, like exercising skeletal muscle, creates a stronger heart muscle. These factors slow the structural changes that heart attacks tend to cause and allow the viable tissue to remain stronger for longer.
- "ACSM's Exercise Management for Persons With Chronic Diseases and Disabilities (3rd Ed)"; J. Larry Durstine, Ph.D.; 2009
- "Circulation"; Heart Disease and Stroke Statistics - 2010 Update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee; Donald Lloyd-Jones, MD; 2010
- "Journal of Applied Physiology"; Left Ventricular Torsion and Recoil: Implications for exercise performance and cardiovascular disease; Ben Esch, Ph.D.; 2009