Lipoprotein(a): Role in atherosclerosis and new treatment options

Atherosclerosis is a chronic process characterized by inflammation and the progressive accumulation of inflammatory cells and lipids in the blood vessel wall, resulting in narrowing of the blood vessel’s circumference. Treatment of people with dyslipidemia aims to reduce the risk of developing atherosclerotic disease and prevent major adverse cardiovascular events (MACE). The results of previous studies indicated that lipoprotein(a) (Lp(a)) is a critical causal factor in the estimated risk of developing a cardiovascular (CV) incident even after achieving desirable low-density lipoprotein (LDL) cholesterol levels. Lp(a) is a low-density lipoprotein particle, like LDL cholesterol. The levels of Lp(a) in plasma are genetically determined. Lp(a) catabolism is still controversial. The pathogenic potential of Lp(a) can be divided into three categories: promotion of plaque formation, thrombogenicity, and proinflammatory effects. Lp(a) levels above the 75th percentile reduced the risk of aortic valve stenosis and myocardial infarction, whereas higher levels (above 90th percentile) were associated with an increased risk of heart failure. However, no hypolipidemic agents have been approved for targeted use in patients with high Lp(a) levels. There are insufficient randomized controlled trials assessing CV outcomes that would support the evidence that current treatment options, which effectively lower Lp(a) levels, also effectively prevent CV event. However, according to some studies, there is strong evidence that better CV outcome is one of the benefits of such therapy. The results of ongoing clinical trials are eagerly awaited

Obesity and Vitamin D Deficiency: Trends to Promote a More Proatherogenic Cardiometabolic Risk Profile

Vitamin D deficiency is associated with cardiometabolic risk factors (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We studied 50 obese patients (body mass index [BMI]: 43.5 +/- 9.2 kg/m(2)) and 36 normal weight participants (BMI: 22.6 +/- 1.9 kg/m(2)). The prevalence of vitamin D deficiency (25-hydroxyvitamin D, 25(OH)D LT 50 nmol/L) was 88% among obese patients and 31% among nonobese individuals; 25(OH)D levels were lower in the obese group (27.3 +/- 13.7 vs 64.6 +/- 21.3 nmol/L; P LT .001). There was a negative correlation between vitamin D level and anthropometric indicators of obesity: BMI (r = -0.64; P LT .001), waist circumference (r = -0.59; P LT .001), and body fat percentage (r = -0.64; P LT .001) as well as with fasting plasma insulin (r = -0.35; P LT .001) and homeostasis model assessment of insulin resistance (r = -0.35; P LT .001). In conclusion, we observed a higher prevalence of vitamin D deficiency among obese participants and this was associated with a proatherogenic cardiometabolic risk profile

Vitamin D and Dysfunctional Adipose Tissue in Obesity

Vitamin D deficiency and dysfunctional adipose tissue are involved in the development of cardiometabolic disturbances (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We evaluated the relation between vitamin D and adipocytokines derived from adipose tissue. We studied 50 obese individuals who were classified into different subgroups according to medians of observed anthropometric parameters (body mass index, body fat percentage, waist circumference, and trunk fat mass). There was a negative correlation between vitamin D level and leptin and resistin (r = -.61, P LT .01), while a positive association with adiponectin concentrations was found (r = .7, P LT .001). Trend estimation showed that increase in vitamin D level is accompanied by intensive increase in adiponectin concentrations (growth coefficient: 12.13). In conclusion, a positive trend was established between vitamin D and the protective adipocytokine adiponectin. The clinical relevance of this relationship needs to be investigated in larger studies