Plasma lipoprotein(a) [Lp(a)] is a quantitative genetic trait with a very broad and skewed distribution, which is largely controlled by genetic variants at the LPA locus on chromosome 6q27. Based on genetic evidence provided by studies conducted over the last two decades, Lp(a) is currently considered to be the strongest genetic risk factor for coronary heart disease (CHD). The copy number variation of kringle IV in the LPA gene has been strongly associated with both Lp(a) levels in plasma and risk of CHD, thereby fulfilling the main criterion for causality in a Mendelian randomization approach. Alleles with a low kringle IV copy number that together have a population frequency of 25–35% are associated with a doubling of the relative risk for outcomes, which is exceptional in the field of complex genetic phenotypes. The recently identified binding of oxidized phospholipids to Lp(a) is considered as one of the possible mechanisms that may explain the pathogenicity of Lp(a). Drugs that have been shown to lower Lp(a) have pleiotropic effects on other CHD risk factors, and an improvement of cardiovascular endpoints is up to now lacking. However, it has been established in a proof of principle study that lowering of very high Lp(a) by apheresis in high-risk patients with already maximally reduced low-density lipoprotein cholesterol levels can dramatically reduce major coronary events.

https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1365-2796.2012.02592.x

Lipoprotein(a): resurrected by genetics.

Hormone replacement therapy in young women with primary ovarian insufficiency and early menopause.

Background
Combined oral contraceptive (COC) use has been associated with venous thrombosis (VT) (ie, deep venous thrombosis and pulmonary embolism) The VT risk has been evaluated for many estrogen doses and progestagen types contained in COC but no comprehensive comparison involving commonly used COC is available

Objectives
To provide a comprehensive overview of the risk of venous thrombosis in women using different combined oral contraceptives

Search methods
Electronic databases (Pubmed, Embase, Web of Science, Cochrane, CINAHL, Academic Search Premier and ScienceDirect) were searched in 22 April 2013 for eligible studies, without language restrictions

Selection criteria
We selected studies including healthy women taking COC with VT as outcome

Data collection and analysis
The primary outcome of interest was a fatal or non-fatal first event of venous thrombosis with the main focus on deep venous thrombosis or pulmonary embolism Publications with at least 10 events in total were eligible The network meta-analysis was performed using an extension of frequentist random effects models for mixed multiple treatment comparisons Unadjusted relative risks with 95% confidence intervals were reportedTwo independent reviewers extracted data from selected studies

Main results
3110 publications were retrieved through a search strategy; 25 publications reporting on 26 studies were included Incidence of venous thrombosis in non-users from two included cohorts was 019 and 037 per 1 000 person years, in line with previously reported incidences of 0,16 per 1 000 person years Use of combined oral contraceptives increased the risk of venous thrombosis compared with non-use (relative risk 35, 95% confidence interval 29 to 43) The relative risk of venous thrombosis for combined oral contraceptives with 30-35 μg ethinylestradiol and gestodene, desogestrel, cyproterone acetate, or drospirenone were similar and about 50-80% higher than for combined oral contraceptives with levonorgestrel A dose related effect of ethinylestradiol was observed for gestodene, desogestrel, and levonorgestrel, with higher doses being associated with higher thrombosis risk

Authors' conclusions
All combined oral contraceptives investigated in this analysis were associated with an increased risk of venous thrombosis The effect size depended both on the progestogen used and the dose of ethinylestradiol Risk of venous thrombosis for combined oral contraceptives with 30-35 μg ethinylestradiol and gestodene, desogestrel, cyproterone acetate and drospirenone were similar, and about 50-80% higher than with levonorgestrel The combined oral contraceptive with the lowest possible dose of ethinylestradiol and good compliance should be prescribed—that is, 30 μg ethinylestradiol with levonorgestrel

Combined oral contraceptives: venous thrombosis.

Objectives To determine the risk of stroke associated with oral and transdermal routes of administration of hormone replacement therapy.

Design Population based nested case-control study. 

Setting About 400 general practices in the United Kingdom contributing to the General Practice Research Database.

Participants Cohort of all women in the database aged 50-79 years between 1 January 1987 and 31 October 2006 who were members of a practice that fulfilled predefined quality criteria and without a diagnosis of stroke before cohort entry. For each case of stroke occurring during follow-up, up to four controls were selected from among the cohort members in the risk sets defined by the case. Exposure to hormone replacement therapy (HRT) was categorised into oestrogens only, oestrogens plus progestogen, progestogen only, and tibolone. Oestrogens were further subdivided according to the route of administration (oral v transdermal) and dose (high v low).

Main outcome measures Rate ratio of stroke associated with current use of oral and transdermal HRT compared with no use. Current use was considered as a prescription whose duration included the index date.

Results There were 15 710 cases of stroke matched to 59 958 controls. The rate of stroke in the cohort was 2.85 per 1000 per year. The adjusted rate ratio of stroke associated with current use of transdermal HRT was 0.95 (95% CI 0.75 to 1.20) relative to no use. The risk of stroke was not increased with use of low oestrogen dose patches (rate ratio 0.81(0.62 to 1.05)) compared with no use, whereas the risk was increased with high dose patches (rate ratio 1.89 (1.15 to 3.11)). Current users of oral HRT had a higher rate of stroke than non-users (rate ratio 1.28 (1.15 to 1.42)) with both low dose and high dose.

Conclusions The use of transdermal HRT containing low doses of oestrogen does not seem to increase the risk of stroke. The presence of residual confounding, however, cannot be entirely excluded in the interpretation of this finding.

https://www.bmj.com/content/bmj/340/bmj.c2519.full.pdf

Transdermal and oral hormone replacement therapy and the risk of stroke: a nested case-control study

Contraceptive Hormone Use and Cardiovascular Disease

Effects of non-oral postmenopausal hormone therapy on markers of cardiovascular risk: a systematic review

Comparison of the impact of vaginal and oral administration of combined hormonal contraceptives on hepatic proteins sensitive to estrogen.

Comparative effects of a contraceptive vaginal ring delivering a nonandrogenic progestin and continuous ethinyl estradiol and a combined oral contraceptive containing levonorgestrel on hemostasis variables.

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Papers

Effects of non-oral postmenopausal hormone therapy on markers of cardiovascular risk: a systematic review

Comparison of the impact of vaginal and oral administration of combined hormonal contraceptives on hepatic proteins sensitive to estrogen.

Comparative effects of a contraceptive vaginal ring delivering a nonandrogenic progestin and continuous ethinyl estradiol and a combined oral contraceptive containing levonorgestrel on hemostasis variables.