Hormone replacement therapy in perimenopausal women and 2-year change of carotid intima-media thickness

Kleijn, Miriam J.J. de; Bots, Michiel L.; Bak, Annette; Westendorp, I. C. D.; Planellas, Juan; Bennink, Herjan J.T. Coelingh; Witteman, Jacqueline C. M.; Grobbee, Diederick E.

doi:10.1016/s0378-5122(99)00035-3

Cited by 44 publications

(16 citation statements)

References 30 publications

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“…For the assessment of CIMT progression rates, studies were excluded when they were not placebo controlled 27,30,32,34,36,37,46,47,50,54 or when change in CIMT over time was not reported, eg, when only the differences in CIMT progression between the treatment and placebo groups were reported and not the group-specific estimates. 40 When a RCT had Ͼ1 report on CIMT progression rates, we included the report with the longest follow-up time or when the SE of the CIMT change estimate was not given. 43 Information that was retrieved from the articles included author, year of publication, type of intervention, mean age, sex, presence of cardiovascular disease, LDL and HDL levels, systolic and diastolic blood pressure levels, smoking, diabetes, hypertension, and whether a qualifying lesion was needed for enrollment.…”

Section: Estimates Of Annual Cimt Progression Ratesmentioning

confidence: 99%

Carotid Intima-Media Thickness Measurements in Intervention Studies

Bots

Evans

Riley

et al. 2003

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Background-Carotid intima-media thickness (CIMT) measurements are currently widely used in randomized controlled trials (RCTs) to study the efficacy of interventions. In designing a RCT with CIMT as a primary outcome, several ultrasound options may be considered. We discuss the various options and provide a pooled estimate of CIMT progression. In addition, we quantify the effect of these choices on the sample size for a RCT. Summary of Comment-To estimate the average CIMT progression rate, we performed a pooled analysis using CIMT progression rates of control groups from published RCTs. The pros and cons of the following ultrasound options are discussed: which arterial segments may be studied; whether near and far wall CIMT measurements should be performed; whether a single image (1 angle of interrogation) or multiple images (more angles of interrogation) should be used; whether a manual or an automated edge detection reading system should be used; and whether images should be read in a random fashion or in batches. The pooled analysis showed an annual rate of change in mean common CIMT of 0.0147 mm (95% CI, 0.0122 to 0.0173) and in mean maximum CIMT of 0.0176 mm (95% CI, 0.0149 to 0.0203). Conclusions-Given the current evidence together with our experience with recently developed ultrasound protocols, we favor the use of mean maximum CIMT rather than mean common CIMT as the primary outcome measure in RCTs designed to evaluate the efficacy of pharmacological and nonpharmacological interventions in carotid artery atherosclerosis.

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Section: Estimates Of Annual Cimt Progression Ratesmentioning

confidence: 99%

Carotid Intima-Media Thickness Measurements in Intervention Studies

Bots

Evans

Riley

et al. 2003

Stroke

Self Cite

321

112

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“…However, there are no trials with clinical endpoints to corroborate this concept. We and other workers have recently shown that HRT does not slow progression of carotid atherosclerosis in clinically healthy women [7,25]. Pooled data from randomized trials that focused mostly on bone-related outcome measures in primarily healthy women showed a non-significantly higher odds ratio for cardiovascular events in women taking HRT compared with those taking placebo [26].…”

Section: Discussionmentioning

confidence: 84%

Effect of postmenopausal hormone replacement on atherosclerosis in femoral arteries

et al. 2002

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“…Quantitative coronary angiography used in WELL-HART is a measure of symptomatic late stage atherosclerosis, whereas carotid artery wall thickness used in EPAT evaluates asymptomatic early subclinical atherosclerosis [27]. Common carotid artery IMT was used in a study of 121 perimenopausal women with a mean age of 47 years who were randomized to receive 0.625 mg of oral CEE daily and 0.15 mg of norgestrel on days 17 through 28; 1.5 mg of micronized oral 17 -estradiol daily and 0.15 mg of desogestrel on days 17 through 24, with four matched placebo pills taken on days 25 through 28; or placebo only [28]. After 2 years of treatment, women randomized to HT showed a reduction in the progression of common carotid artery IMT, compared with placebo [28].…”

Section: Discord Between Rcts and Observational Studies Of Postmenopamentioning

confidence: 99%

Postmenopausal hormone therapy and cardiovascular disease: Making sense of the evidence

Hodis¹,

Mack²

2007

Curr Cardio Risk Rep

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Controversy surrounding the cardioprotective role of postmenopausal hormone therapy continues. This controversy is fueled in part by the body of evidence that indicates a duality of hormone therapy on potential risks and benefits. The totality of evidence indicates that the effects of postmenopausal hormone therapy are affected by age, state of the target tissue, duration of therapy, and timing of initiation, according to time since menopause. This review presents evidence supporting a cardioprotective role of hormone therapy in young postmenopausal women as well as a potentially negative effect in older postmenopausal women. These data are reviewed in relation to the evidence that hormone therapy prevents new onset diabetes mellitus, and that the risks of hormone therapy are rare and even rarer in young postmenopausal women. The cardioprotective role of postmenopausal hormone therapy will only be resolved by refined research guided by the results from previous studies.

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Hormone replacement therapy in perimenopausal women and 2-year change of carotid intima-media thickness

Cited by 44 publications

References 30 publications

Carotid Intima-Media Thickness Measurements in Intervention Studies

Carotid Intima-Media Thickness Measurements in Intervention Studies

Effect of postmenopausal hormone replacement on atherosclerosis in femoral arteries

Postmenopausal hormone therapy and cardiovascular disease: Making sense of the evidence

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