Background
Atherosclerotic cardiovascular disease (ASCVD) is a major health concern, and lipoprotein(a) (Lp(a)) is an independent risk factor. However, there is limited evidence regarding Lp(a) and the risk of ASCVD in Asian populations. This study aimed to assess the predictive value of changes in coronary artery calcification (CAC) for ASCVD risk associated with Lp(a) level.
Methods
Participants (n=2,750) were grouped according to their Lp(a) levels, and the association between Lp(a) and CAC progression was examined. CAC progression was defined as the occurrence of incident CAC or a difference ≥2.5 between the square root (√) of baseline and follow-up coronary artery calcium scores (CACSs) (Δ√transformed CACS). To adjust for differences in follow-up periods, Δ√transformed CACS was divided by the follow- up period (in years).
Results
Over an average follow-up of 3.07 years, 18.98% of participants experienced CAC progression. Those with disease progression had notably higher Lp(a) levels. Higher Lp(a) tertiles correlated with increased baseline and follow-up CACS, CAC progression (%), and Δ√transformed CACS. Even after adjustment, higher Lp(a) levels were associated with CAC progression. However, annualized Δ√transformed CACS analysis yielded no significant results.
Conclusion
This study demonstrated an association between elevated Lp(a) levels and CAC progression in a general population without ASCVD. However, longer-term follow-up studies are needed to obtain meaningful results regarding CAC progression. Further research is necessary to utilize Lp(a) level as a predictor of cardiovascular disease and to establish clinically relevant thresholds specific to the Korean population.

Background
: There are no agreement for abnormalities in serum lipid concentrations and lipoprotein(a) (Lp(a)) in patients with subclinical hypothyroidism. But there are no reports for consideration of postmenopausal state and hormone replacement therapy(HRT). Therefore, we anayzed serum Lp(a) and lipid concentrations in patients with subclinical hypothyroidism considering menopause and HRT and the correlation between serum Lp(a) level and thyroid-stimulating hormone (TSH) concentration.

Methods : We undertook this study in 99 patients with subclinical hypothyroidism (TSH>5uIU/mL) and 297 age- and sex-matched normal control. They and no abnormalities in liver and renal function, fasting blood glucose and medical and drug histories. We excluded who were receiving HRT. Serum free thyroxine, triiodothyronine, TSH were measured by radioimmune assay using commercial kits, and Lp(a), total cholesterol, TG and HDL by Latex and enzyme method, respectively.

Results : There were no significant differences of serum Lp(a), total cholesterol, LDL, TG, HDL concentrations in patients with subclinical hypothyroidism and control subjects, analyzing after dividing into men, premenopausal and postmenopausal women. In patients with subclinical hypothyroidism, there was no correlation between serum Lp(a) and TSH concentraions(r=0.06, P>0.05).

Conclusion : Considering menopause and HRT, there were no increase in serum Lp(a) and lipid concentrations in subclinical hypothyroidism. There was no correlation between serum Lp(a) and TSH concentration in patients with subclinical hypothyroidism.

Background
: Many studies to reduce serum lipoprotein(a) are done because serum lipoprotein(a) has been known to be an independent risk factor of coronary artery disease along with age, smoking, diabetes, hypertension, and hyperlipidemia. Till now, oral estrogen/androgen therapy, niacin analogue and plasmapheresis are known therapeutic methods. This study examined the relative effects of three antihyperlipidemic agents, acipimox, lovastatin, fenofibrate.

Methods : Among 70 subjects(male-19, female-51) with their serum cholesterol level of more than 240mg/dL, 56 subjects who were completed 2 months antihyperlipidemic treatment (acipimox-20, lovastatin-18, fenofibrate-18) were examined for baseline total cholesterol, HDL cholesterol, triglyceride, and lipoprotein(a) and were followed up 2 months later.

Results : Mean values of each group for acipimox, lovastatin, fenofibrate were as follows: total cholesterol (268.1±19.03, 287.1±36.42, 268.9±25.99), HDL cholesterol (43.5±10.99, 42.7±11.88, 37.9±8.20), triglyceride (226.1±165.03, 260.4±175.98, 234.3±124.33), LDL cholesterol (179.3±30.40, 192.3±41.52, 184.1±38.08), lipoprotein(a) (26.2±15.32,34.8±18.56,29.9±12.58). Mean percentile reduction of lipoprotein(a) was acipimox-41.4%(P<0.0001), lovastatin-22.2%(P<0.0001), fenofibrate-16.1%(P<0.05), and p value was less than 0.05 in the comparison of groups. Lipoprotein (a) showed no relations with age, sex, BMI, WHR, smoking, total cholesterol, HDL cholesterol, triglyceride and LDL cholesterol. After 2 months treatment, mean reduction percentages of total cholesterol was acipimox-12.2%(P<0.0001), lovastatin-17.6%(P<0.0001), fenofibrate-8.85%(P<0.05). LDL cholesterol was acipimox-16.12%(P<0.0001), lovastatin-22.89%(P<0.0001), fenofibrate-12.06% (P<0.05). Triglyceride was acipimox-17.24%(P<0.0001), lovastatin-17.39%(p<0.0001), fenofibrate-9.78%(p<0.05). HDL cholesterol was elevated in acipimox-17.24%(P<0.05), lovastatin-16.10%(P<0.05) and fenofibrate-12.06(P<0.05). In total cholesterol(P<0.05) and LDL cholesterol(P<0.05), there were significant differences among 3 groups, but not in HDL cholesterol and triglycerides.

Conclusion : In two months treatment of acipimox, lovastatin and fenofibrate in hyperlipidemic patients, lipoprotein(a), known for independent risk factor of coronary artery disease, was reduced significantly in the order of acipimox, lovastatin and fenofibrate.