Periodontal disease (PD) is generated by microorganisms. These microbes can enter the general circulation causing a bacteraemia. The result can be adverse systemic effects, which could promote conditions such as cardiovascular disease. Level A evidence supports that PD is independently associated with arterial disease. PD is a common chronic condition affecting the majority of Americans 30 years of age and older. Atherosclerosis remains the largest cause of death and disability. Studies indicate that the adverse cardiovascular effects from PD are due to a few putative or high-risk bacteria: Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola or Fusobacterium nucleatum. There are three accepted essential elements in the pathogenesis of atherosclerosis: lipoprotein serum concentration, endothelial permeability and binding of lipoproteins in the arterial intima. There is scientific evidence that PD caused by the high-risk pathogens can influence the pathogenesis triad in an adverse manner. With this appreciation, it is reasonable to state PD, due to high-risk pathogens, is a contributory cause of atherosclerosis. Distinguishing this type of PD as causal provides a significant opportunity to reduce arterial disease.

Heart disease is the primary cause of death in the United States. Fortunately, intervention measures can reduce the risk of cardiovascular disease (CVD) after a patient has been accurately assessed. Atherosclerotic disease, one of the driving forces behind CVD, is not always detected by traditional risk assessment. Carotid intima-media thickness (CIMT), as measured by B-mode ultrasound, is a surrogate marker for atherosclerosis and can be used to detect an accelerated disease process and subclinical disease. Advantages of CIMT are that it is noninvasive, relatively inexpensive, and can be repeatedly performed with no adverse effects on the patient. Carotid intima-media thickness is associated with CVD and is an independent predictor of stroke and myocardial infarction. Therefore, CIMT is valuable for clarifying CVD risk, particularly for patients with intermediate risk by conventional risk assessment. Screening for subclinical disease even in low-risk patients may have benefit, especially for those with a family history of premature CVD or those with any of the National Cholesterol Education Program risk factors. The detection of subclinical atherosclerosis allows the physician to implement prevention efforts prior to a devastating CVD event and to investigate possible reasons for increased arterial thickening, such as an occult underlying insulin-resistant condition or residual lipid risk markers. Treatment with several types of drugs has been demonstrated to halt the progression or even reduce CIMT. Carotid intima-media thickness is currently limited by the lack of standardized protocols that may affect reproducibility from measure to measure. Efforts to draft a standardized protocol are underway by the Society of Atherosclerosis Imaging and Prevention that will address this issue. Carotid intima-media thickness provides a valuable tool for physicians to clarify the CVD risk of their patients. Practical implications of CIMT for everyday clinical practice are addressed.

IntroductionThe aim of the study was to examine changes in carotid intima-media thickness (CIMT) and carotid plaque morphology in patients receiving multifactorial cardiovascular disease (CVD) risk factor management in a community-based prevention clinic. Quantitative changes in CIMT and qualitative changes in carotid plaque morphology may be measured non-invasively by ultrasound.Material and methodsThis is a retrospective study on a cohort of 324 patients who received multifactorial cardiovascular risk reduction treatment at a community prevention clinic. All patients received lipid-lowering medications (statin, niacin, and/or ezetimibe) and lifestyle modification. All patients underwent at least one follow-up CIMT measurement after starting their regimen. Annual biomarker, CIMT, and plaque measurements were analyzed for associations with CVD risk reduction treatment.ResultsMedian time to last CIMT was 3.0 years. Compared to baseline, follow-up analysis of all treatment groups at 2 years showed a 52.7% decrease in max CIMT, a 3.0% decrease in mean CIMT, and an 87.0% decrease in the difference between max and mean CIMT (p < 0.001). Plaque composition changes occurred, including a decrease in lipid-rich plaques of 78.4% within the first 2 years (p < 0.001). After the first 2 years, CIMT and lipid-rich plaques continued to decline at reduced rates.ConclusionIn a cohort of patients receiving comprehensive CVD risk reduction therapy, delipidation of subclinical carotid plaque and reductions in CIMT predominantly occurred within 2 years, and correlated with changes in traditional biomarkers. These observations, generated from existing clinical data, provide unique insight into the longitudinal on-treatment changes in carotid plaque.

Cardiovascular disease (CVD) is the leading cause of death and disability in the United States. Although current therapies can reduce the risk for CVD, they are only given to patients who are considered to be at risk, and are therefore only beneficial if a patient's risk is accurately predicted before he or she sustains a cardiovascular (CV) event. Unfortunately, even relatively accurate risk factor analyses, such as the Reynolds Risk Score algorithm, fail to identify some patients who will sustain a CV event within 10 years. In contrast, the presence of an atheroma is an absolute predictor for the potential of an atherothrombotic event to occur, and it is therefore reasonable to anchor clinical decisions based on this knowledge. Carotid intima-media thickness (CIMT) testing via B-mode ultrasound is a safe, simple, and inexpensive method for evaluating CV risk by measuring the combined thickness of the intimal and medial layers of the arterial wall. Use of CIMT testing can also detect marked thickening of the arterial wall, possibly indicating plaques or atheromas that are associated with accelerated atherosclerotic disease and increased risk for coronary artery disease, myocardial infarction, and stroke. These characteristics make CIMT a practical supplemental method that physicians can use when making decisions. Moreover, the ability of CIMT testing to identify and quantify atherosclerotic disease has led to the adoption of CIMT as a surrogate endpoint in clinical trials, allowing the efficacy of new drugs to be assessed much more rapidly than would be possible by focusing solely on CV event or mortality rates. To date, several trials have provided evidence to indicate that some CVD therapies slow, stop, or reverse the progression of CIMT. Although many of these studies show that changes in CIMT predict future CV events, the value of CIMT testing in CVD risk assessment is still vigorously debated. In this article, we clarify the utility of CIMT testing for risk classification and reexamine its usefulness as a method for assessing therapeutic efficacy.

The formation of an atheroma begins when lipoproteins become trapped in the intima. Entrapped lipoproteins become oxidized and activate the innate immune system. This immunity represents the primary association between lipids and inflammation. When the trapping continues, the link between lipids and inflammation becomes chronic and detrimental, resulting in atherosclerosis. When entrapment ceases, the association between lipids and inflammation is temporary and healthy, and the atherogenic process halts. Therefore, the link between lipids and inflammation depends upon lipoprotein retention in the intima. The entrapment is due to electrostatic forces uniting apolipoprotein B to polysaccharide chains on intimal proteoglycans. The genetic transformation of contractile smooth muscle cells in the media into migratory secretory smooth muscle cells produces the intimal proteoglycans. The protein, platelet-derived growth factor produced by activated platelets, is the primary stimulus for this genetic change. Oxidative stress is the main stimulus to activate platelets. Therefore, minimizing oxidative stress would significantly reduce the retention of lipoproteins. Less entrapment decreases the association between lipids and inflammation. More importantly, it would halt atherogenesis. This review will analyze oxidative stress as the critical link between lipids, inflammation, and the pathogenesis of atherosclerosis. Through this perspective, we will discuss stopping oxidative stress to disrupt a harmful association between lipids and inflammation. Numerous therapeutic options will be discussed to mitigate oxidative stress. This paper will add a new meaning to the Morse code distress signal SOS-stopping oxidative stress.