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Opening Lecture – Cardiovascular protection in women

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Opening Lecture Cardiovascular protection in women
Genazzani A.R.

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THE RISK OF VENOUS THROMBOEMBOLISM ASSOCIATED WITH THE USE OF TRANEXAMIC ACID AND OTHER DRUGS USED TO TREAT MENORRHAGIA: A CASE-CONTROL STUDY USING THE GENERAL PRACTICE RESEARCH DATABASE.

BJOG. 2009 Jan;116(1):91-7.

Sundström A, Seaman H, Kieler H, Alfredsson L.

OBJECTIVE: To assess whether use of tranexamic acid is associated with an increased risk of venous thromboembolism (VTE). DESIGN: Nested case-control study. SETTING: Database study using the General Practice Research Database for the years 1992-1998. POPULATION: Women aged 15-49 years with a diagnosis of menorrhagia. METHODS: Multivariate conditional logistic regression was used to estimate the risk for VTE associated with different drug treatments for menorrhagia, adjusting for confounders. MAIN OUTCOME MEASURES: Adjusted odds ratios with 95% CI. RESULTS: A total of 134 cases of VTE and 552 matched controls were identified. Recent use of tranexamic acid was scarce, yielding an adjusted odds ratio for VTE of 3.20 (95% CI 0.65-15.78). The use of mefenamic acid (ORadj 5.54 [95% CI 2.13-14.40]) or norethisterone (ORadj 2.41 [95% CI 1.00-5.78]) was associated with an increased risk of VTE, as was a recent–in relation to menorrhagia–diagnosis of anaemia or a haemoglobin value <11.5 g/dl (ORadj 2.23 [95% CI 1.02-4.86]). CONCLUSIONS: We found that tranexamic acid was associated with an increased risk of VTE, although the risk estimate did not reach statistical significance. Increased risks of VTE associated with other treatments for menorrhagia were observed. The increased risk of VTE observed with a diagnosis of anaemia–a proxy for more severe menorrhagia–suggests that menorrhagia could be a prothrombotic condition. The observed association between VTE, tranexamic acid and other treatments for menorrhagia may thus partly be explained by confounding by indication. The possibility that menorrhagia is itself a risk factor for VTE merits further investigation

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A LIFETIME OF ALDOSTERONE EXCESS: LONG-TERM CONSEQUENCES OF ALTERED REGULATION OF ALDOSTERONE PRODUCTION FOR CARDIOVASCULAR FUNCTION.

Endocr Rev. 2008 Apr;29(2):133-54.
Connell JM, MacKenzie SM, Freel EM, Fraser R, Davies E.

Up to 15% of patients with essential hypertension have inappropriate regulation of aldosterone; although only a minority have distinct adrenal tumors, recent evidence shows that mineralocorticoid receptor activation contributes to the age-related blood pressure rise and illustrates the importance of aldosterone in determining cardiovascular risk. Aldosterone also has a major role in progression and outcome of ischemic heart disease. These data highlight the need to understand better the regulation of aldosterone synthesis and its action. more

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USE OF ALENDRONATE AND RISK OF INCIDENT ATRIAL FIBRILLATION IN WOMEN.

Arch Intern Med. 2008 Apr 28;168(8):826-31.
Heckbert SR, Li G, Cummings SR, Smith NL, Psaty BM.

BACKGROUND: A recent publication from the HORIZON (Health Outcomes and Reduced Incidence With Zoledronic Acid Once Yearly) trial in women with postmenopausal osteoporosis reported a higher risk of serious atrial fibrillation (AF) in zoledronic acid recipients than in placebo recipients. This adverse effect was unexpected and had not been recognized previously. more

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ESTROGEN-ENHANCED GENE EXPRESSION OF LIPOPROTEIN LIPASE IN HEART IS ANTAGONIZED BY PROGESTERONE.

Endocrinology. 2008 Feb;149(2):711-6.
Liu D, Deschamps A, Korach KS, Murphy E.

Although estrogen has effects on the heart, little is known regarding which genes in the heart are directly responsive to estrogen. We have shown previously that lipoprotein lipase (LPL) expression was increased in female hearts compared with male hearts. To test whether LPL gene expression in heart is regulated by estrogen, we perfused mouse hearts from ovariectomized females with 100 nM 17beta-estradiol or vehicle for 2 h, after which hearts were frozen, and RNA was isolated. The SYBR green real-time PCR method was used to detect LPL gene expression. We found that addition of 17beta-estradiol to hearts from ovariectomized females resulted in a significant increase in LPL mRNA. This estrogen effect on LPL gene expression in mouse heart can be blocked by the estrogen receptor (ER) antagonist ICI 182,780 or by progesterone. We also identified a potential estrogen receptor element (ERE) enhancer sequence located in the first intron of the mouse LPL gene. The potential ERE sequence was linked to a TATA-luciferase (LUC) reporter plasmid in HeLa cells. Both ERalpha and ERbeta stimulated strong activity on the heterologous promoter reporter in Hela cells upon estrogen addition. Both ERalpha and ERbeta activities on the LPL ERE reporter were abrogated by the ER antagonist ICI 182,780. Progesterone also dose dependently inhibited the estrogen-mediated increase in LPL ERE reporter activity. These results show that heart LPL is an estrogen-responsive gene exhibiting an intronic regulatory sequence.

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