Local Cardiologist Publishes Book on Inflammation and Heart Attacks Dr. Richard Frink, Principal Investigator of the Heart Research Foundation of Sacramento, has recently published his findings in his new book Inflammatory Atherosclerosis: Characteristics of the Injurious Agent. Dr. Frink has concluded, based on evidence gained from the study of many post-mortem hearts, that atherosclerosis is caused by a single infectious organism, producing inflammation and destruction of tissue in the wall of the artery. However, the specific organism has not yet been identified and further research is continuing. Recent newspaper articles, quoting research studies from Boston, have emphasized the value of testing the blood for C Reactive Protein (CRP) in patients suspected of having or developing heart attacks. The CRP is a method for detecting the presence of inflammation in the body and becomes elevated in any condition associated with inflammation. Since atherosclerosis is an inflammatory disease, the CRP is used as a means of identifying persons who have active atherosclerosis and are at high risk of heart attack. For example, the CRP is a more accurate predictor of heart attack than is the blood cholesterol. The CRP has proven to be a major advance and is very useful in the management of heart patients, but it is not specific for atherosclerosis and does not identify the agent or the organism responsible for causing the inflammation. Dr. Frink's work goes beyond the CRP to focus on the cause of the inflammation, particularly an infectious organism. Dr. Frink explains how atherosclerosis develops. The organism appears to reside within one of the white blood cells in a dormant, inactive state, entering the artery wall through an area where the artery lining has been injured. The artery lining is injured by smoking, high cholesterol, high blood pressure and other risk factors. Once in the artery wall, the organism is able to evade normal body defenses and set up shop, establishing an initial focus of the disease, or the beginning of the plaque. If there are multiple areas of injury, multiple but separate plaques are formed. The organism alters cholesterol metabolism and the transfer of blood lipids across the artery wall resulting in the build-up of cholesterol. This explains why plaques are high in cholesterol and lipids. Dr. Frink theorizes cholesterol is retained to serve as an energy source for the purpose of fueling replication, growth and expansion of the organism. In other words, cholesterol or other lipids are required in the life cycle of this organism. Giving the patient cholesterol lowering drugs such as statins are beneficial in reducing inflammation because, Dr. Frink reasons, the organism no longer has an energy source, forcing it to return to a dormant state. As a result plaque growth is halted or severely reduced and heart attacks and other forms of coronary disease are reduced. Microscopic examination of the artery wall shows the disease, once established, grows in both a longitudinal and circumferential direction from a central focus, consistent with a spreading infectious organism. Adjacent plaques tend to fuse together, producing extensive disease of a given artery. As the organism expands and grows, it first stimulates the growth of excessive scar tissue, but then, in the fullness of time, proceeds to destroy this same scar tissue, forming what is called the atheroma. This is the origin of the term athero-sclerosis. An atheroma is basically a tiny pocket of destroyed tissue that has the consistency of toothpaste. This semi-solid material can be squeezed from the wall of the artery into the channel of the artery and carried downstream to the heart muscle. An atheroma is similar to a bacterial abscess in that both contain destroyed tissue and both spontaneously rupture and drain their contents. The important consideration here is an atheroma drains its contents directly into the coronary circulation, the most important blood supply in the body, whereas a bacterial abscess drains its contents to the skin surface or into a body cavity. The destroyed tissue in an atheroma contains potent chemical agents and toxins derived from the breakdown of plaque tissue. It is easy to understand how such material, draining directly into the coronary circulation, has the potential to do more damage than if such material drained onto the skin surface. Sudden rupture of an atheroma explains how heart pains and heart attacks can occur without warning in patients that were apparently healthy moments before. At the present time most doctors believe heart attacks are caused by a blood clot that blocks blood flow in one of the coronary arteries. Blocking or obstructing blood flow in a coronary artery causes a portion of the heart muscle supplied by that artery to die, causing a heart attack. The medical term for the effects of obstructed blood flow is called ischemia. Dr. Frink agrees that some heart attacks are caused by ischemia due to clots obstructing blood flow, but not all. Plaque toxins alone, without obstruction of blood flow, can also cause heart attacks and explains how heart attacks can occur in people who have normal or near normal coronary arteries on the coronary angiogram. Doctors who are puzzled by heart attacks in patients who do not have obstruction to blood flow, must now take into account the potential effect of plaque toxins in the management of their heart patients. If an infectious organism is identified as the cause of atherosclerosis, an antibiotic or a vaccine may be developed to usse in the treatment of atherosclerosis to prevent heart attacks. It may be possible to cure atherosclerosis in the future. In the meantime all preventive efforts should be aimed at reducing the blood cholesterol and all other risk factors to create unfavorable conditions for the organism. Finding ways to neutralize plaque toxins and reducing toxic injury will greatly improve treatments and survival in the patient with heart attacks and other types of coronary heart disease. Dr. Frink's book can be reviewed at the Heart Research Foundation web site: http://www.hrfsac.org. New National Patient Safety Goals Take Effect January 1 for all Joint Accredited Organizations Effective January 1, accredited health care organizations across the United States will be required to focus attention on a series of specific actions to prevent medical mistakes. These actions will help to avoid confusion in identifying patients, miscommunication among caregivers, wrong-site surgery, unsafe use of infusion pumps, medication mix-ups, and problems with equipment alarm systems. The required actions are set forth in new National Patient Safety Goals that were developed by the Joint Commission on Accreditation of Healthcare Organizations, the not-for-profit safety and quality evaluator for nearly 17,000 health care organizations. The Joint Commission believes that taking these simple, proven steps will have major impacts in reducing the frequency of devastating medical errors that affect thousands of patients each year. The know-how to prevent these errors exists, says Dennis S. O'Leary, MD, president, JCAHO. We now need to focus on making sure that health care organizations are actually taking these preventive steps. The six National Patient Safety Goals include 11 required actions for all accredited organizations that provide care relevant to the Goals. The expected actions include, among others: Making sure medicines are given to the right patient before giving medicines. Using a room number to identify a patient is not sufficient. Reading back medical orders given over the phone. This reduces the likelihood of miscommunications or misunderstandings. Standardizing abbreviations or symbols are used in providing care. For example, when "u" is handwritten to indicate units, it can often look like a zero and lead to incorrect medication dosages. Removing certain concentrated medications from patient care units. If administered accidentally, these medications can be deadly. Marking the site where surgery is to be performed, e.g., the left foot, and involving the patient in the process. This reduces the risk that surgery will be performed accidentally on the wrong side of the patient. Testing clinical alarm systems and assuring that clinical alarms can be heard at a distance and over the din of background noise. Assuring that all intravenous infusion pumps have free-flow protection. This reduces the risk that patients will inadvertently receive medication overdoses. An expert panel of doctors, nurses and patient safety leaders helped the Joint Commission formulate its 2002 National Patient Safety Goals and the related evidence-based requirements. The Joint Commission intends to issue new or revised National Patient Safety Goals and requirements every year. Aggregate data on organization compliance with the requirements will be published by the Joint Commission at the conclusion of 2003. Individual organization performance data will become available approximately one year later.