Myocardial Infarction In Postmenopausal Women Research Articles

Serum Vitamin Levels, Cardiovascular Disease Risk Factors, and Their Association with Depression in Korean Women: A Cross-Sectional Study of a Nationally Representative Sample.

Background and Objectives: Serum vitamin levels, cardiovascular disease risk factors, and their association with depression is a complex issue that has been the subject of much research. Therefore, we investigated the relationship between vitamin A, B9, and E levels, cardiovascular risk factors, and depression in premenopausal and menopausal South Korean women. Materials and Methods: This cross-sectional study used the 2016-2018 Korea National Health and Nutrition Examination Survey data. Depression was assessed using a questionnaire to check for symptoms of depression or the Patient Health Questionnaire-9. Blood samples were collected from the antecubital vein in the morning after an overnight fast. Covariates were defined as self-reported physician diagnoses. Well-trained medical staff performed the standard procedures. Statistical analysis was performed using the complex sample analysis method of SPSS, using two separate logistic regression models (model 1: adjusted for age; model 2: adjusted for age, marital status, smoking, and alcohol consumption). Results: A total of 3313 women aged over 20 years were enrolled. The association between vitamin A levels and depression was as follows: lower levels of vitamin A were associated with an increased risk of depression in premenopausal women in model 1 and model 2. The levels of serum vitamins E and B9 were not correlated with depression in premenopausal and postmenopausal women. In the premenopausal group, depression increased in the obesity (model 1: p = 0.037; model 2: p = 0.047) and diabetes mellitus (model 1: p = 0.010; model 2: p = 0.009) groups. The menopausal group with depression had higher rates of stroke (model 1: p = 0.017; model 2: p = 0.039) and myocardial infarction (model 1: p = 0.004; model 2: p = 0.008) than the group without depression. Conclusions: Depression is correlated with lower blood levels of vitamin A in premenopausal women. Vitamin B9 and E levels were not associated with depression independent of menopausal status. Depression is associated with obesity and diabetes mellitus in premenopausal women and with stroke and myocardial infarction in postmenopausal women.

Dyslipidemia as a risk factor for acute myocardial infarction in postmenopausal women: An observational study

Abstract Objective: This study has evaluated risk factors, especially dyslipidemia, for an acute myocardial infarction (AMI) in postmenopausal women. Materials and Methods: This was a hospital-based, observational, single-center study among 100 postmenopausal women admitted to the medicine ward with AMI. They were categorized based on lipid profile groups, viz., dyslipidemic group and non-dyslipidemic group. All clinical parameters were studied between the groups. Results: Among anthropometric profiles, in the comparison of mean height (cm), weight (kg), body mass index (BMI) (kg/m2), and waist circumference (WC) (cm) for the dyslipidemic group and non-dyslipidemic group, only WC was statistically significant (P < 0.001). Most patients were hospitalized between 6 and 12 h after the onset of symptoms. At the time of hospitalization, most patients from both groups were observed to have diabetes and hypertension with poor control of postprandial blood sugar, glycated hemoglobin, and diastolic blood pressure (DBP) (P < 0.05). The dyslipidemic group’s mean C-reactive protein was higher (P < 0.05). The comparison of mean total cholesterol, triglyceride (TG), low density lipoprotein-cholesterol in mg/dL, and TG: high density lipoprotein was significantly increased (P < 0.001), while high density lipoprotein-cholesterol (mg/dL) was significantly decreased (P < 0.001) in the dyslipidemic group. ST-segment elevation myocardial infarction is standard in both groups. The maximum patient has regional wall motion abnormality in echocardiography after day 3 of admission. Among the dyslipidemic group, ejection fraction was on the lower side, and the predominant complication was in the left ventricular failure (LVF) (P < 0.05). Conclusion: WC has a positive association with patients with AMI who have dyslipidemia and can be used as an indicator of the risk of AMI when BMI is normal. WC is a surrogate marker of abdominal fat mass (subcutaneous and intra-abdominal); increased WC is a significant component marker of metabolic syndrome and insulin resistance related to cardiovascular mortality. There was poor glycemic control and blood pressure (mainly DBP) among the dyslipidemic patients. Hypertriglyceridemia is the most common lipid abnormality, followed by hypercholesterolemia among the dyslipidemic group. LVF is the most common complication in dyslipidemic patients.

Abstract 9399: A Targeted Proteomic Approach Identifies Novel Biomarkers Associated With Risk of Myocardial Infarction in Post-Menopausal Women

Introduction: There may be unique pathways that contribute to heart disease in women. We used proteomics to evaluate the association between a panel of biomarkers and risk of incident MI in post-menopausal women and thus to inform risk prediction and potential disease biology. Methods: We analyzed 184 candidate biomarkers (Olink CVD II/III) in LOFT, a randomized trial of an osteoporosis drug in post-menopausal women. Cases and controls without prevalent CV disease were matched by age and follow-up time (123 MI cases, 123 controls). A Benjamini-Hochberg correction was applied for false discovery (adj P value <0.05). Conditional logistic regression was adjusted for the ACC/AHA pooled cohort equations (PCE). Results: 16 biomarkers assessed at baseline were associated with incident MI at the FDR threshold (Fig). After multivariable adjustment, 8 markers remained significantly associated with incident MI, including BNP (adj OR per SD 2.52, 95% CI 1.49-4.28), NT-proBNP (adj OR 2.41, 95% CI 1.43-4.08) and metalloproteinases including MMP-2 (adj OR 1.86, 95% CI 1.08-3.22) and MMP-12 (adj OR 1.55, 95% CI 1.02-2.37; Fig). Network analyses suggested these markers were overall strongly concentrated in pathways of inflammation, cellular movement and immune cell trafficking. Conclusions: A targeted proteomic approach identified markers of inflammation and immune cell trafficking as predictors of MI in post-menopausal women independent of traditional risk markers. Metalloproteinases, markers of plaque rupture and erosion, may provide insights into plaque biology and atherogenesis in women and warrant further investigation.

Matrix Metalloproteinase Mediated Type I Collagen Degradation is an Independent Predictor of Increased Risk of Acute Myocardial Infarction in Postmenopausal Women

Acute myocardial infarction (AMI) is often underdiagnosed in women. It is therefore of interest to identify biomarkers that indicate increased risk of AMI and thereby help clinicians to have additional focus on the difficult AMI diagnosis. Type I Collagen, a component of the cardiac extracellular matrix, is cleaved by matrix metalloproteinases (MMPs) generating the neo-epitope C1M. We investigated the association between serum-C1M and AMI and evaluated whether C1M is a prognostic marker for outcome following AMI. This study is based on The Prospective Epidemiological Risk Factor (PERF) Study including postmenopausal women. 316 out of 5,450 women developed AMI within the follow-up period (14 years, median). A multivariate Cox analysis assessed association between serum-C1M and AMI, and re-infaction or death subsequent to AMI. The risk of AMI increased by 18% (p = 0.03) when serum-C1M was doubled and women in the highest quartile had a 33% increased risk compared to those in the low quartiles (p = 0.025). Serum-C1M was, however not related to reinfarction or death subsequent to AMI. In this study C1M was be an independent risk factor for AMI. Measuring MMP degraded type I collagen could be useful for prediction of increased risk of AMI if replicated in other cohorts.

P3449A serum biomarker reflecting collagen type I degradation (C1M) is an independent risk factor for acute myocardial infarction in postmenopausal women: results from the PERF study

P3449A serum biomarker reflecting collagen type I degradation (C1M) is an independent risk factor for acute myocardial infarction in postmenopausal women: results from the PERF study

Pathophysiologic features of Takotsubo Cardiomyopathy: A review of the literature

Takotsubo cardiomyopathy is a newly recognized cause of chest pain mimicking a myocardial infarction in post-menopausal women. It is diagnosed based on clinical criteria established at the Mayo Clinic and imaging studies, including echocardiography, cardiac MRI, angiography, and left ventriculography. Several hypotheses have been postulated towards its etiology, with the dominant theory being cathecholamine toxicity to the myocardium in response to a stressful trigger. Pathologic investigations are limited, based mostly on autopsy findings, and represent inflammatory and fibrotic replacement of the myocardium. Here, we will address the current understanding of the disease entity of Takotsubo cardiomyopathy, its clinical mimics, and its pathophysiology.
 Ibrahim Cardiac Med J 2013; 3(1&2): 39-48

G protein-coupled estrogen receptor protects from atherosclerosis.

Coronary atherosclerosis and myocardial infarction in postmenopausal women have been linked to inflammation and reduced nitric oxide (NO) formation. Natural estrogen exerts protective effects on both processes, yet also displays uterotrophic activity. Here, we used genetic and pharmacologic approaches to investigate the role of the G protein-coupled estrogen receptor (GPER) in atherosclerosis. In ovary-intact mice, deletion of gper increased atherosclerosis progression, total and LDL cholesterol levels and inflammation while reducing vascular NO bioactivity, effects that were in some cases aggravated by surgical menopause. In human endothelial cells, GPER was expressed on intracellular membranes and mediated eNOS activation and NO formation, partially accounting for estrogen-mediated effects. Chronic treatment with G-1, a synthetic, highly selective small molecule agonist of GPER, reduced postmenopausal atherosclerosis and inflammation without uterotrophic effects. In summary, this study reveals an atheroprotective function of GPER and introduces selective GPER activation as a novel therapeutic approach to inhibit postmenopausal atherosclerosis and inflammation in the absence of uterotrophic activity.

Calcium supplementation increases circulating cholesterol by reducing its catabolism via GPER and TRPC1-dependent pathway in estrogen deficient women

Limited studies have addressed the effects of calcium supplementation (CaS) on serum total cholesterol (TC) in postmenopausal women and the results are inconclusive. Moreover, the potential mechanisms through which CaS regulates cholesterol metabolism in the absence of estrogen are still sealed for the limitation of human being study. Cross-sectional survey, animal and in vitro experiments were conducted to investigate the effect of CaS on endogenous cholesterol metabolism in estrogen deficiency and identify its potential mechanisms. Ovariectomized rats were used to mimic estrogen deficiency. In vitro, HepG2 cell line was exposed to estradiol and/or calcium treatment. We demonstrated that CaS significantly increased serum TC and the risk of hypercholesterolemia and myocardial infarction in postmenopausal women. Increased serum TC in estrogen deficiency was caused mainly by decreased cholesterol catabolism rather than increased synthesis. This was mediated by reduced 7α-hydroxylase resulting from increased liver intracellular Ca(2+) concentrations, reduced intracellular basal cAMP and subsequent up-regulation of SREBP-1c and SHP expression. Estrogen had a protective role in preventing CaS-induced TC increase by activating the G-protein coupled estrogen receptor, which mediated the estrogen effect through the transient receptor potential canonical 1 cation channel. CaS increases endogenous serum TC via decreasing hepatic cholesterol catabolism in estrogen deficiency. G-protein coupled estrogen receptor is shown to be a key target in mediating CaS-induced TC increase. CaS should be monitored for the prevention of serum TC increase during menopause.

Local delivery of a PKCε-activating peptide limits ischemia reperfusion injury in the aged female rat heart

Reduced efficacy of cardioprotective interventions in the aged female heart, including estrogen replacement, highlights the need for alternative therapeutics to reduce myocardial ischemia-reperfusion (I/R) injury in postmenopausal women. Here, we sought to determine the efficacy of protein kinase-Cε (PKCε)-mediated cardioprotection in the aged, estradiol-deficient rat heart. Infarct size and functional recovery were assessed in Langendorff-perfused hearts from adult (5 mo) or aged (23 mo) female Fisher 344 ovary-intact or ovariectomized (OVX) rats administered a PKCε-activator, receptor for activated C kinase (ψεRACK) prior to 47-min ischemia and 60-min reperfusion. Proteomic analysis was conducted on left ventricular mitochondrial fractions treated with ψεRACK prior to I/R, utilizing isobaric tags for relative and absolute quantitation (iTRAQ) 8plex labeling and tandem mass spectrometry. Real-time PCR was utilized to assess connexin 43 (Cx43) and RACK2 mRNA post-I/R. Greater infarct size in aged OVX (78%) vs. adult (37%) was reduced by ψεRACK (35%, P < 0.0001) and associated with greater mitochondrial PKCε localization (P < 0.0003). Proteomic analysis revealed three novel mitochondrial targets of PKCε-mediated cardioprotection with aging (P < 0.05): the antioxidant enzymes glutathione peroxidase (GPX) and MnSOD2, and heat shock protein 10. Finally, decreased levels of Cx43 and RACK2 mRNA seen with age were partially abrogated by administration of ψεRACK (P < 0.05). The mechanisms described here may represent important therapeutic candidates for the treatment of acute myocardial infarction in postmenopausal women and age-associated estradiol deficiency.

Effects of exercise training on autonomic dysfunction management in an experimental model of menopause and myocardial infarction

The aim of this study was to investigate the effects of exercise training on cardiovascular autonomic dysfunction in ovariectomized rats submitted to myocardial infarction. Female Wistar rats were divided into the following ovariectomized groups: sedentary ovariectomized (SO), trained ovariectomized (TO), sedentary ovariectomized infarcted (SOI), and trained ovariectomized infarcted (TOI). Trained groups were submitted to an exercise training protocol on a treadmill (8 wk). Arterial baroreflex sensitivity was evaluated by heart rate responses to arterial pressure changes, and cardiopulmonary baroreflex sensitivity was tested by bradycardic and hypotension responses to serotonin injection. Vagal and sympathetic effects were calculated by pharmacological blockade. Arterial pressure was reduced in the TO in comparison with the SO group and increased in the TOI in relation to the SOI group. Exercise training improved the baroreflex sensitivity in both the TO and TOI groups. The TOI group displayed improvement in cardiopulmonary reflex sensitivity compared with the SOI group at the 16 microg/kg serotonin dose. Exercise training enhanced the vagal effect in both the TO (45%) and TOI (46%) animals compared with the SO and SOI animals and reduced the sympathetic effect in the TOI (38%) in comparison with the SOI animals. Significant correlations were obtained between bradycardic baroreflex responses and vagal (r = -0.7, P < 0.005) and sympathetic (r = 0.7, P < 0.001) effects. These results indicate that exercise training in ovariectomized rats submitted to myocardial infarction improves resting hemodynamic status and reflex control of the circulation, which may be due to an increase in the vagal component. This suggests a homeostatic role for exercise training in reducing the autonomic impairment of myocardial infarction in postmenopausal women.

Association of Polymorphism of Estrogen Receptor-.ALPHA. Gene with Circulating Levels of Adiponectin in Postmenopausal Women with Type 2 Diabetes

Menopause is a risk factor for cardiovascular disease (CVD) in women because of the reduction in endogenous estrogen. Recently, single nucleotide polymorphisms (SNPs) of the estrogen receptor alpha (ESR-1) gene (c.454-397T>C) associated with the prognosis of myocardial infarction in postmenopausal women were identified; however, the mechanism by which genetic variation of ESR-1 contributes to the pathogenesis of CVD is unknown. Circulating levels of adipokines and inflammatory cytokines predict CVD risk; hence, this study aimed to investigate whether ESR-1 genotypes (c.454-397T>C) might influence circulating levels of adipokines and inflammatory cytokines in postmenopausal women with type 2 diabetes. Sixty-three postmenopausal women with type 2 diabetes were recruited. Serum levels of adiponectin, resistin, interleukin-6 (IL-6), and high-sensitive C-reactive protein (hs-CRP) were determined. The genotype of ESR-1 was closely associated with serum adiponectin, which was decreased in subjects with the T allele and was lowest in those with the T/T genotype. Multiple logistic regression analysis revealed independent contribution of the homozygote for the T allele to low serum levels of adiponectin. The T allele of the c.454-397T>C SNP of ESR-1 is associated with low serum levels of adiponectin, which may lead to a high risk of CVD in postmenopausal women.

INCONSISTENT APPLICATION OF DIAGNOSTIC CRITERIA LEADING TO UNDERTREATMENT OF OSTEOPOROSIS IN POSTMENOPAUSAL WOMEN.

Background Although the incidence of hip and vertebral fractures due to osteoporosis surpasses the incidence of breast cancer, stroke, and myocardial infarction in postmenopausal women, the reported screening rates for osteoporosis with DEXA scan have been less than half of those reported for breast cancer screening. The low rate of osteoporosis screening occurs despite reimbursement by Medicare. In this report, we examine the association of Dexascan T-scores with osteoporosis treatment. Methods The Better Osteoporosis Knowledge and Screening Study (BONES) is a quality improvement initiative that includes 13 residency clinics. We report results from the first six sites. Enrolled women were at least 67 years of age (to ensure Medicare coverage over the last 2 years) with at least one prior visit to the participating clinic. Participants answered a 77-item survey and viewed an educational video on osteoporosis. Baseline chart reviews of all participating patients were done to document prior screening. Descriptive statistics were compiled. Bivariate analyses were performed regarding actual osteoporosis treatment with bisphosphonates, PTH, or calcitonin as the outcome. Results In a preliminary analysis of 122 charts, 31 women had the diagnosis of osteoporosis, yet only 23 had received a DEXA scan. Only 15 met diagnostic criteria by DEXA scan. Regarding treatment, of the 28 women who had been prescribed osteoporosis medications, 10 had T scores ≤ −2.5; 3 had T scores −2.0 to −2.4; 4 had T scores −1.9 to −1.5, and 1 had a T score ≤ −1.0. The remaining 10 (36%) receiving treatment had no evidence of DEXA scan, and only 4 of the 10 had a diagnosis of osteoporosis documented in the chart. Age, income, prior education, comorbidities, and history of fractures did not significantly predict diagnosis or treatment or in any T score group. The only statistically significant associations of treatment were white race (p = .05) and prior conversation about osteoporosis with their physician (p = .005). Conclusion Our preliminary data suggest that physicians are applying and interpreting diagnostic criteria for osteoporosis inconsistently and basing decisions to treat osteoporosis on factors that are not readily apparent or documented.

Issue Highlights

HomeCirculationVol. 113, No. 16Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published25 Apr 2006https://doi.org/10.1161/circ.113.16.1921Circulation. 2006;113:1921NON–TRANSFERRIN-BOUND IRON AND RISK OF CORONARY HEART DISEASE IN POSTMENOPAUSAL WOMEN, by van der A et al.The parallel rise in both body iron stores and vascular risk in women after menopause led to the ‘iron overload‘ theory of coronary heart disease (CHD). Epidemiological studies relating serum ferritin levels to CHD risk have yielded inconsistent results, however. In this issue of Circulation, van der A and colleagues evaluated a community-based sample of postmenopausal women to test the hypothesis that a labile iron component associated with non--transferrin-bound iron (NTBI) might be more suitable for relating to CHD risk. The investigators noted that women in the highest NTBI tertile had a statistically significant 53% lower risk of acute myocardial infarction and a nonsignificant 16% lower risk of CHD compared with those in the lowest tertile in multivariable analyses. Similar results were obtained for serum iron, transferrin saturation, and serum ferritin. These observations do not support the presence of an excess risk of CHD or myocardial infarction in postmenopausal women with relatively higher levels of NTBI or other measures of iron overload. See p 1942.STEM CELL MOBILIZATION INDUCED BY SUBCUTANEOUS GRANULOCYTE-COLONY STIMULATING FACTOR TO IMPROVE CARDIAC REGENERATION AFTER ACUTE ST-ELEVATION MYOCARDIAL INFARCTION: RESULT OF THE DOUBLE-BLIND, RANDOMIZED, PLACEBO-CONTROLLED STEM CELLS IN MYOCARDIAL INFACTION (STEMMI) TRIAL, by Ripa et al.Percutaneous coronary revascularization procedures restore coronary flow quickly in patients with acute ST-elevation myocardial infarction, and yet there is often some degree of myocardial necrosis resulting in left ventricular dysfunction. To prevent adverse ventricular remodeling, efforts have been devoted to determining the therapeutic efficacy of bone-marrow–derived stem cells in preserving ventricular function. These cells have been isolated ex vivo and infused into the coronary artery or have been stimulated to exit the bone marrow to home to sites of myocardial injury by the administration of granulocyte-colony stimulating factor (G-CSF). Early open-label studies have demonstrated the safety and potential efficacy of G-CSF. In this issue of Circulation, Ripa et al present data from the STEM cells in Myocardial Infarction (STEMMI) Trial. This is the first report of a randomized, double-blind, placebo-controlled trial of G-CSF in patients with ST-elevation myocardial infarction and successful percutaneous revascularization. See p 1983.MACROPHAGE METALLOELASTASE ACCELERATES THE PROGRESSION OF ATHEROSCLEROSIS IN TRANSGENIC RABBITS, by Liang et al.In this issue of Circulation, Liang et al used a novel approach involving the generation of transgenic rabbits to study the role of the macrophage metalloelastase (matrix metalloproteinase [MMP]-12) in atherosclerosis. Their results indicate that MMP-12 causes media destruction and pseudoaneurysm formation and accelerates plaque growth in an animal model that more closely resembles atherosclerosis in humans. This transgenic rabbit model may offer new insights into the roles of MMPs in extracellular matrix remodelling and cellular migration in atherosclerotic lesion formation that may challenge some prior conclusions based on mouse models. See p 1993.Visit http://circ.ahajournals.org:Cardiology Patient PageSyncope. See p e715.Images in Cardiovascular MedicineNatural Tissue Engineering Inside a Ventricular Septum Defect Occluder. See p e718. Download figureDownload PowerPointTransition From Left Ventricular Hypertrophy to Massive Fibrosis in the Cardiac Variant of Fabry Disease. See p e720.External Carotid Artery--Internal Jugular Vein Fistula: A Complication of Internal Jugular Cannulation. See p e722.CorrespondenceSee p e724. Previous Back to top Next FiguresReferencesRelatedDetails April 25, 2006Vol 113, Issue 16 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.113.16.1921 Originally publishedApril 25, 2006 PDF download Advertisement

Common Genetic Variation in the Prothrombin Gene, Hormone Therapy, and Incident Nonfatal Myocardial Infarction in Postmenopausal Women

Genetic variants in coagulation factors are associated with myocardial infarction and may modify the association between hormone therapy and cardiovascular disease risk. This study assessed whether common variation in the prothrombin gene was associated with incident nonfatal myocardial infarction in postmenopausal women and whether this association differed according to current estrogen use. Eight variants representing 98% of common prothrombin variants were selected using publicly available genomic variation data. These variants and the functional G20210A variant were genotyped and used to infer haplotypes in a population-based Washington State case-control study of postmenopausal Caucasian women (1995-1999; 273 cases and 788 controls). Women carrying a nonsynonymous polymorphism in exon 6 (C5467T) had an increased risk of myocardial infarction (for each additional copy, relative to women with one fewer copy, odds ratio = 1.4, 95% confidence interval: 1.0, 1.8). Prothrombin haplotypes were also associated with myocardial infarction (with minimal adjustment, global p = 0.056; with full adjustment, p = 0.034). Associations between haplotypes and myocardial infarction were similar among users of hormone therapy and nonusers (global p = 0.61), though statistical power was limited. These preliminary results suggest that common genetic variants in the prothrombin gene or other variants in linkage disequilibrium are associated with myocardial infarction in postmenopausal women.

Total Abdominal Hysterectomy May Be a Risk Factor for Acute Myocardial Infarction in Postmenopausal Women: An Age-Matched, Case-Controlled Retrospective Analysis

Total Abdominal Hysterectomy May Be a Risk Factor for Acute Myocardial Infarction in Postmenopausal Women: An Age-Matched, Case-Controlled Retrospective Analysis

Total Abdominal Hysterectomy May Be a Risk Factor for Acute Myocardial Infarction in Postmenopausal Women: An Age-Matched, Case-Controlled Retrospective Analysis

Objective: To investigate the risk factors for acute myocardial infarction (AMI) in postmenopausal women in comparison to age-matched controls by retrospective analysis. Methods: This study was conducted retrospectively on 105 postmenopausal women who were diagnosed and treated for AMI in our hospital in comparison with age-matched women who had received health testing and screening. The odds ratios for six factors were calculated. The factors were hypertension, hyperlipidemia, diabetes mellitus (DM), smoking, obesity, and total abdominal hysterectomy. Results: Among 105 subjects in whom AMI occurred, smoking was the highest risk factor for AMI. Hyperlipidemia and diabetes were the next most common risk factors for AMI. Eighteen subjects (17.1%) had a past history of total abdominal hysterectomy. The odds ratio for hysterectomy and AMI was 3.591. Conclusions: Smoking may be the highest risk factor for AMI in postmenopausal women. Total abdominal hysterectomy was also identified to be the risk factor for A...

Hormone replacement therapy and risk of acute myocardial infarction in postmenopausal women with diabetes mellitus

Use of estrogen with or without progesterone (hormone replacement therapy [HRT]) was shown in numerous observational studies to substantially reduce risk of coronary heart disease (CHD) morbidity and mortality in postmenopausal women.1 The largest of these, The Nurses Health Study, revealed a graded benefit with greater risk reduction in subjects with increased baseline risk.2 Two large randomized controlled trials, the Heart and Estrogen/progestin Replacement Study and the Women’s Health Initiative, reported lack of cardiovascular benefit with HRT in postmenopausal women with and without prior CHD.3–5 Despite the large numbers of patients studied, there are little data about the potential benefit of HRT in women with diabetes mellitus, a subgroup at very high risk of cardiovascular morbidity and mortality. Diabetes approximately quadruples the risk of CHD in women6,7 and about 5% of postmenopausal women have diabetes.8 A 1999 study found that HRT was used by 17% of postmenopausal women with diabetes mellitus in the United States (compared with 39% of those without diabetes).9 The pathophysiology of diabetic cardiovascular risk is multifactorial, and little is known about how HRT modulates cardiovascular risk. This study explores whether current HRT modulated the risk of acute myocardial infarction (AMI) in postmenopausal women with diabetes mellitus.

Hormone Therapy and In-Hospital Survival After Myocardial Infarction in Postmenopausal Women

Although postmenopausal hormone therapy (HRT) commonly is used in hope of preventing coronary heart disease, the effect of HRT on case fatality of myocardial infarction has never been studied. We evaluated HRT as a predictor of survival after MI in postmenopausal women. The present study was performed with 114 724 women of age >/=55 years with confirmed myocardial infarction who presented between April 1998 and January 2000 to 1 of 1674 hospitals participating in the National Registry of Myocardial Infarction-3. Presenting characteristics, treatment, and clinical outcome data were obtained by chart review. At time of hospitalization, 7353 (6.4%) women reported current use of HRT, defined as use of estrogen, progestin, or estrogen/progestin for reasons other than contraception. Unadjusted mortality was 7.4% in users of HRT and 16.2% in nonusers (odds ratio 0.41, 95% confidence interval 0.36 to 0.43). After adjustments were made for prior medical history, clinical characteristics, treatments received in-hospital, and likelihood of receiving HRT, HRT remained associated with an improved rate of survival (odds ratio 0.65, 95% confidence interval 0.59 to 0.72). Significant association of HRT with decreased mortality after myocardial infarction was observed in all age strata. Postmenopausal HRT appears to be associated with reduced mortality after myocardial infarction. This finding could be caused by therapeutic effect of HRT, selection and adherence bias, or some combination of both.

Hormone therapy and the risk of stroke after acute myocardial infarction in postmenopausal women

OBJECTIVESWe examined the association of hormone therapy (HRT) with hemorrhagic and ischemic stroke among postmenopausal women with acute myocardial infarction (AMI).BACKGROUNDHemorrhagic and ischemic strokes are common complications of AMI, and women are at increased risk for hemorrhagic stroke after thrombolytic therapy. This risk may be related to female hormones.METHODSUsing data from the National Registry of Myocardial Infarction-3, we studied 114,724 women age 55 years or older admitted to the hospital for AMI, of whom 7,353 reported HRT use on admission. We determined rates of in-hospital hemorrhagic and ischemic stroke stratified by HRT use and estimated the independent association of HRT with each stroke type using multivariable logistic regression.RESULTSThe HRT users were younger than non-users, had fewer risk factors for stroke including diabetes and prior stroke, and received more pharmacologic and invasive therapy including cardiac catheterization. A total of 2,152 (1.9%) in-hospital strokes occurred, with 442 (0.4%) hemorrhagic, 1,017 (0.9%) ischemic and 693 (0.6%) unspecified. Among HRT users and non-users, the rates of hemorrhagic stroke (0.40% vs. 0.42%, p = 1.00) and ischemic stroke (0.80% vs. 0.96%, p = 0.11) were similar. Among 13,328 women who received thrombolytic therapy, the rate of hemorrhagic stroke was not significantly different for users and non-users (1.6% vs. 2.1%, p = 0.22). After adjustment for baseline and treatment differences, HRT was not associated with hemorrhagic (odds ratio [OR], 0.88; 95% confidence intervals [CI], 0.58 to 1.35) or ischemic stroke (OR, 0.89; CI, 0.66 to 1.18).CONCLUSIONSAcute myocardial infarction is a high-risk setting for stroke among postmenopausal women, but HRT does not appear to modify that risk. Clinicians should not alter their approach to thrombolytic therapy based on HRT use.

Hormone replacement therapy, prothrombotic mutations, and the risk of innocent nonfatal myocardial infarction in postmenopausal women

Hormone replacement therapy, prothrombotic mutations, and the risk of innocent nonfatal myocardial infarction in postmenopausal women