These prospective data indicate a significant increase in the relative risk of hypertension with each unit decrease of flow-mediated dilation that is independent of age and baseline systolic and diastolic pressure values. This could suggest that an impaired endothelial vasomotor function precedes and predicts the future development of hypertension in postmenopausal women.
OBJECTIVE -Both postmenopausal state and diabetes are associated with endothelial dysfunction and are well-known risk factors for atherosclerosis. However, the relationship of endothelium-dependent vasodilation and diabetes has never been prospectively evaluated. This study provided the opportunity to assess the association between endothelial vasodilation function and the incidence of diabetes in a cohort of apparently healthy postmenopausal women.RESEARCH DESIGN AND METHODS -We conducted a prospective cohort study that began in 1997 with 840 apparently healthy, nonobese, postmenopausal women, aged 53 Ϯ 6 years, initially with normal glucose tolerance at the oral glucose tolerance test. All participants were followed up for a mean period of 3.9 Ϯ 0.7 years (range 0.5-6.9). Endothelial function was measured as flow-mediated dilation (FMD) of the brachial artery, using high-resolution ultrasound.RESULTS -There were no significant differences in demographic, blood pressure, and biochemical profiles among each tertile group at baseline or at follow-up review. During follow-up, 102 women developed type 2 diabetes. The adjusted relative risk (RR) for women with FMD Յ4.3 (lowest tertile) was 5.87 (95% CI 4.34 -8.10) versus women with FMD Ն5.6 (highest tertile reference). Each 1-unit decrease of FMD was associated with a significant 32% (22-48%) increase in the multiple-adjusted RR of incident diabetes.CONCLUSIONS -These prospective data indicate a significant increase in the RR of diabetes with each unit decrease of FMD. This could suggest that an impaired endothelial function may play a fundamental role in diabetogenesis in postmenopausal women. Diabetes Care 28:702-707, 2005P ostmenopause is a physiological condition known to be associated with endothelial dysfunction. It is due to a lack of estrogen that is typical in this phase of a woman's life (1,2). There is considerable evidence that the impairment of endothelial function is a predicting factor in the development of atherosclerosis (3).Type 2 diabetes represents a very important public health problem in all industrialized countries, mainly in the U.S. (4,5), that involves conspicuous cardiovascular consequences and high costs in terms of mortality, morbidity, and financial resources (6). Endothelial dysfunction is a very frequent occurrence among diabetic patients (7-10).Because endothelial dysfunction is also present in nondiabetic postmenopausal women (1,2), it is not clear whether endothelial dysfunction is a consequence or rather the cause of diabetes, thus preceding its onset. Although there are both references relating to the fact that endothelial dysfunction may precede insulin resistance (11,12) and unique recent work concerning the relationship between the spillover markers of endothelial dysfunction and incident diabetes (13), a clear relationship between endothelium-dependent vasodilation and diabetes has, to our knowledge, never been demonstrated. This study provided the opportunity to prospectively assess the association between endothelial vasodi...
Introduction Cardiovascular diseases (CVD) and Cancer (C), the most important causes of mortality worldwide. share many risk factors and common pathophysiological processes such as chronic inflammation and unfavorable cardio–metabolic profile. Progress in oncological treatments improved the survival of oncological patients (Pt) but have increased the likelihood of short– and long–term CV cardiovascular complications. The multidisciplinary collaboration between cardiologist and onco–hematologists is the task of Cardioncology, an emerging new sub–specialization of clinical cardiology that often make available personalized treatment with a favorable outcome also in clinically complex patients. Here we present a case of severe acute heart failure in a woman with advanced breast C (BC). Clinical Case 2021 April: 55–year–old woman with G3 BC, (ER 0%PgR 0%,Ki6770%HER2+) (T4N3M1), (chest wall and liver) on well tolerated treatment with Docetaxel X 6 and continuous double antiHER2 block (Trastuzumab + Pertuzumab) X 4 and steroids as ancillary therapy. After about 6 months of therapy a lower airways infection occurred and acute congestive heart failure (HF) with severe left ventricular systolic dysfunction (LVEF 25%) ensued requiring hospitalization in the ICU, where newly detected type II diabetes was diagnosed. Appropriate HF therapy with insulin and anticoagulant was established and congestive clinical state resolved. On outpatient basis B–Blocker and anti–RAAS therapy was titrated switching to empagliflozin. About 7 months after discharge, we registered the full recovery up to a normalization of systolic function (LVEF 55%) and the disappearance of the intraventricular thrombus. For progression of C, pt underwent chemotherapy with Capecitabine at metronomic and in October 2022 after cardio–oncological collegial discussion, anti–HER2 therapy resumed. Paz started Trastuzumab–Emtansine, well tolerated with substantial stability of the clinical picture (NYHA I–II) and instrumental and echocardiographic evaluation (LVEF 65%). Conclusions This clinical case reaffirms that close collaboration between cardiologist and oncologist is fundamental for the successful management of complex patients and surveillance must also extend during (and after) treatment. It also demonstrates that an early diagnosis and an "evidence–based" cardiological therapy can allow the recovery of the cardio–toxic effect of anti–HER2 drugs and may allow to resume the therapy successfully.
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