Comments by Dr. Calapai
Heart Disease is the number 1 killer of people in the population, and has been so for many years. Scientists and doctors have wondered why this is so, and have typically blamed the plaque phenomenon on cholesterol and fats. Studies have been ongoing for the past 40 years and have expanded into some new and exciting areas. Other contributors to inflammation and plaque include Homocysteine, Vitamin Deficiency, and Infection.
Homocysteine was discovered a few years after the cholesterol research was published, and was ignored primarily because there was no ability to make medication to control it. Its results relied on the use of simple vitamin combinations (B6, B12, Folate). Only recently has homocysteine become a major focus of medical and nutritional literature. (I'll address this in-depth in a separate newsletter).
Vitamin deficiency has received a great deal of attention in recent years, in part because of homocysteine but also in relation to free radical damage of tissues and aging.
Any of the large search engines on the internet can direct you to thousands of studies on the benefits of vitamins and minerals and how they reduce cardiovascular and cancer risk. I will also devote an entire newsletter top this topic.
Infection, at present, is the "hottest” topic in plaque research and has described some fascinating information. To make it simple, there are at least 20 or so different, common organisms that have been linked to blood vessel inflammation and the progression of disease. Most of these creatures exist in our tissues and don't create much of a stir or symptom. So, in a hidden, sneaky way, these things are starting an inflammatory process that fats and cholesterol can adhere to. They also can attach to, and colonize on, plaque that has started independently.
Take home message —- Blood testing for Vitamins, Minerals, Homocysteine and Infection is important to understand plaque risk. Ultrasound testing can help us visualize deposits in vessels, and there are various ways to change cardiovascular risk.
Stay tuned for more on risk assessment prevention and change.
Please send us a note and tell us what you'd like to see in upcoming newsletters.
Chronic Infections and the Risk of Carotid Atherosclerosis.
Background—Chronic infections have been implicated in the pathogenesis of atherosclerosis, yet from an epidemiological perspective, this concept remains controversial.
Methods and Results—The Bruneck Study is a prospective population-based survey on the pathogenesis of atherosclerosis. In 826 men and women 40 to 79 years old (1990 baseline), 5-year changes in carotid atherosclerosis were thoroughly assessed by high-resolution duplex scanning. The presence of chronic respiratory, urinary tract, dental, and other infections was ascertained by standard diagnostic criteria. Chronic infections amplified the risk of atherosclerosis development in the carotid arteries. The association was most pronounced in subjects free of carotid atherosclerosis at baseline (age-/sex-adjusted odds ratio [95% CI] for any chronic infection versus none, 4.08 [2.42 to 6.85]; P<0.0001) and applied to all types of chronic (bacterial) infections. It remained independently significant after adjustment for classic vascular risk attributes and extended to low-risk individuals free of conventional risk factors. Among subjects with chronic infections, atherosclerosis risk was highest in those with a prominent inflammatory response. Markers of systemic inflammation, such as soluble adhesion molecules and circulating bacterial endotoxin, and levels of soluble human heat-shock protein 60 and antibodies to mycobacterial heat-shock protein 65 were elevated in subjects with chronic infections and predictive of an increased risk of atherosclerosis.
Conclusions—The present study provides solid evidence for a role of common chronic infections in human atherogenesis. Induction of systemic inflammation and autoimmunity may be potential pathophysiological links.
Interactive role of infection, inflammation and traditional risk factors in atherosclerosis and coronary artery disease.
Although first suggested at the turn of the 20th century, there is a renewed interest in the infectious theory of atherosclerosis. Studies done in many laboratories around the world over the past several years have shown an association between markers of inflammation and coronary atherosclerosis with an exacerbation of the inflammatory process during acute myocardial ischemia, particularly in the early stages of reperfusion.
It is also being recognized that the traditional risk factors, such as smoking, dyslipidemia, hypertension and diabetes mellitus, do not explain the presence of coronary atherosclerosis in a large proportion of patients. We believe that in certain genetically susceptible people, infection with very common organisms, such as Chlamydia pneumoniae or cytomegalovirus, may lead to a localized infection and a chronic inflammatory reaction. Persistence of infection may relate to the degree of inflammation and severity of atherosclerosis.
Early trials with appropriate antibiotic agents in some patients with a recent history of acute myocardial infarction have led to very salutary results. If patients with an infectious basis of atherosclerosis can be identified, a directed at eradication of the offending organism may be appropriate.
