Effect of a plant stanol ester-containing spread, placebo spread, or Mediterranean diet on estimated cardiovascular risk and lipid, inflammatory and haemostatic factors.

BACKGROUND AND AIMS: Mediterranean diet is associated with a reduced risk for cardiovascular disease (CVD). Use of plant stanols decreases low density lipoprotein cholesterol (LDL-C) concentrations. We compared the effects of the Mediterranean diet and plant stanol esters on vascular risk factors and estimated CVD (eCVD) risk. METHODS AND RESULTS: In this prospective, randomized, placebo-controlled study, 150 mildly hypercholesterolaemic subjects were randomized to Mediterranean diet, a spread containing plant stanol esters (2 g/day) or a placebo spread. Vascular risk factors were assessed every month for 4 months and the eCVD risk was calculated using the PROspective- Cardiovascular-Munster (PROCAM), Framingham, and Reynolds risk engines. Placebo had no significant effect on risk factors or eCVD risk. Mediterranean diet gradually induced a significant reduction in total cholesterol (TC), LDL-C, triglycerides, high sensitivity C-reactive protein (hsCRP), blood pressure and eCVD risk (24-32%). The plant stanol ester spread reduced (by 1 month) TC (-14%), LDL-C (-16%), hsCRP (-17%), and estimated CVD risk (26-30%). eCVD risk reduction was sustained at 4th months when the gradual Mediterranean diet eCVD risk reduction became comparable to that of the stanol group. CONCLUSIONS: Plant stanol esters yielded an early, by 1st treatment month, reduction of eCVD risk that resulted from a TC, LDL-C, and hsCRP decrease. eCVD risk reduction on the Mediterranean diet resulted from a change in several CVD risk factors and equaled that of plant stanol at 4 months. The consumption of plant stanol esters by moderately hypercholesterolaemic patients may be a useful option to reduce CVD risk in those who do not adopt a Mediterranean diet.

Atherosclerosis and osteoporosis: age-dependent degenerative processes or related entities?

Osteoporosis and atherosclerosis, two multifactorial and degenerative entities, are major public health problems. These diseases accompany the aging process and share common risk factors. Furthermore, several common pathophysiological factors have been suggested. These include similar molecular pathways involving bone and vascular mineralization, estrogen deficiency, parathyroid hormone, homocysteine, lipid oxidation products, inflammatory process, as well as vitamin D and K. Moreover, the use of statins, biphosphonates, beta-blockers and experimental dual-purpose therapies based on the biological linkage of the above entities may simultaneously benefit bone loss and vascular disease. This review considers a potential link between osteoporosis and atherosclerosis beyond aging. These common factors may lead to appropriate treatment strategies.

Smoking and aortic diseases.

Cigarette smoking is a major vascular risk factor and in this context, it is an independent risk factor for the development of aortic disease, especially the formation and growth of abdominal aortic aneurysms (AAA). Medline was searched up to January 31, 2007 for the relevant literature for this review of the mechanisms by which smoking causes aortic wall damage and its subsequent impact on the clinical manifestation of this process. Idiopathic AAAs and aortic dissection are considered, as well as other aortic diseases (eg, Takayasu, Kawasaki, Behcet and Buerger). There is evidence suggesting an abnormal homeostasis between proteolytic and antiproteolytic activity in the vascular wall during the development of AAAs, and these mechanisms can be influenced by smoking. Smoking cessation plays an important role in the management of aortic disease.

Fibrinogen: a predictor of vascular disease.

Raised plasma fibrinogen levels are associated with an increased risk of vascular events. This may be mediated by adverse effects of fibrinogen on plasma viscosity, coagulation, platelet activity, inflammation and atherogenesis. However, there is as yet no drug that specifically lowers plasma fibrinogen levels on a long-term basis. Thus, we do not have intervention trials demonstrating that lowering plasma fibrinogen levels will result in a decreased risk of vascular events. However, such a trial may never happen unless a specific agent is discovered or designed. Several drugs that are used in vascular disease prevention (e.g. lipid lowering agents and antihypertensives) may influence plasma fibrinogen levels. Whether such an additional effect accounts for variations in the benefit resulting from the use of different drugs within the same class remains to be established. The debate continues as to whether fibrinogen is just a marker of vascular risk or whether lowering its circulating levels will result in a significant decrease in clinically relevant endpoints. Whatever the case, the measurement of plasma fibrinogen levels is likely to provide a more comprehensive estimation of risk.

Platelets and vascular risk: an option for treatment.

Epidemiological studies have linked platelet hyperactivity with an increased risk of vascular events. Even more convincing is the evidence from appropriately designed clinical trials showing that antiplatelet agents decrease the risk of vascular events (e.g. myocardial infarction, MI and stroke). These findings are compatible with the known thrombotic action of platelets. A considerable limitation in platelet research is the absence of a reliable, universally accepted marker of platelet activity. Therefore, it is difficult to reliably identify the 'high risk patient' and/or evaluate the efficacy of any administered treatment other than by calculating event rates over a period of time. This review will focus on the preventive aspects of antiplatelet intervention while also briefly considering the assessment of platelet hyperactivity and the mechanisms involved in platelet-induced thrombosis.