The Role of Estrogen Therapy as a Protective Factor for Alzheimer's Disease and Dementia in Postmenopausal Women: A Comprehensive Review of the Literature.

The complete cessation of menstruation for 12 months with associated vasomotor symptoms is termed menopause. Apart from playing a role in reproduction, estrogen significantly affects the central nervous system (CNS). Population-based studies highlighted a substantial difference in the prevalence of dementia between men and women, with Alzheimer-associated dementia being more prevalent in women, indicating that estrogen deficiency might be a risk factor for neurodegenerative diseases. Patients with dementia experience a progressive decline in neurocognitive function, beginning with short-term memory loss that progresses to long-term memory loss and the inability to perform everyday activities, leading ultimately to death. There is currently no cure for dementia, so preventing or slowing the disease's progression is paramount. Accordingly, researchers have widely studied the role of estrogen as a neuroprotective agent. Estrogen prevents dementia by augmenting Hippocampal and prefrontal cortex function, reducing neuroinflammation, preventing degradation of estrogen receptors, decreasing oxidative damage to the brain, and increasing cholinergic and serotonergic function. According to the window phase hypothesis, estrogen's effect on preventing dementia is more pronounced if therapy is started early, during the first five years of menopause. Other studies like The Woman's Health Initiative Memory Study (WHIMS) showed unfavorable effects of estrogen on the brain. This review aims to establish an understanding of the currently available data on estrogen's effect on neurodegeneration, namely, dementia and Alzheimer's disease.

Readmission Risk Factors and Heart Failure With Preserved Ejection Fraction.

CONTEXT: Cases of heart failure with preserved ejection fraction (HFpEF) exacerbations continue to affect patients' quality of life and cause significant financial burden on our healthcare system. OBJECTIVE: To identify risk factors for readmission in patients discharged with a diagnosis of HFpEF. METHODS: Electronic health records of patients over 18 years of age with a primary diagnosis of HFpEF treated between August 1, 2017 and March 1, 2018 in a community hospital were retrospectively reviewed. The study population included patients with HFpEF greater than 40% who were screened but did not qualify for the ongoing CONNECT- HF trial being conducted by Duke Clinical Research. To be included, subjects had to fall into 1 of 2 classifications (NYHA Class II-IV or ACC/AHA Stage B-D) and have a life expectancy greater than 6 months. Patients were excluded if they had terminal illness other than HF, a prior heart transplant or were on a transplant list, a current or planned placement of a left ventricular assist device, chronic kidney disease requiring hemodialysis, inability to use mobile applications, or inability to participate in longitudinal follow up. Readmission rate was analyzed at 30 and 90 days along with patients' demographics and associated comorbidities, including peripheral vascular disease, anemia, pulmonary hypertension, arrythmia, and valvular heart disease. Patients were risk stratified using the LACE index readmission score and the Charlson comorbidity index. RESULTS: Of the 492 cases of HFpEF identified during the 7-month study period, 212 patients were included. The majority of patients were women (126; 59.4%), had a median body mass index above 30 kg/m2 (123; 58%), and had pulmonary hypertension (94; 44.3%), anemia (146; 68.8%), and arrhythmia (101, 47.6%). Forty-five (21.2%) patients were readmitted for HFpEF within 90 days of initial discharge; 32 of those (71.1%) were readmitted within 30 days of initial discharge. Patients with higher LACE and Charlson comorbidity index scores were more likely to be readmitted within 90 days. Peripheral vascular disease (P=.002), tricuspid regurgitation (P=.001), pulmonary hypertension (P=.049), and anemia (P=.029) were risk factors associated with readmissions. Use of ACEi/ARBs (P=.017) was associated with fewer readmissions. CONCLUSION: Anemia, peripheral vascular disease, pulmonary hypertension, and valvular heart disease are not only postulated mechanisms of HFpEF, but also important risk factors for readmission. These study findings affirm the need for continued research of the pathophysiology and associated comorbidities of the HFpEF population to improve quality of life and lower healthcare costs.

Zieve's Syndrome Presenting With Severe Hypertriglyceridemia.

Zieve's syndrome (ZS) is a rare disease characterized by a triad of hemolytic anemia, cholestatic jaundice, and transient hyperlipidemia seen in patients with alcoholic steatohepatitis. We report a case of ZS with severe hypertriglyceridemia. Among the reported cases of ZS in English literature, we believe this is the first case of the syndrome presenting with severe hypertriglyceridemia requiring plasmapheresis.

The Unusual Suspect: Gadobenate-Dimeglumine Induced Kounis Syndrome.

A myocardial bridge has traditionally been considered a benign condition characterized by an atypical intramyocardial route of a segment of one of the major coronary arteries. However, the clinical complications of myocardial bridges can be dangerous. These potential complications include acute coronary syndromes, arrhythmias, ventricular dysfunction, and sudden death. Myocardial bridges are suspected to be adjuvant of Kounis syndrome, which is defined as an acute coronary syndrome caused by an allergic reaction. Due to high epidemiologic prevalence, clinical suspicion of a myocardial bridge should be considered in atypical and typical presentations of chest pain, especially in patients with low-risk factors for atherosclerotic disease. A male in their late 30's presented with non-ST elevation myocardial infarction suspected to be secondary to Kounis syndrome after gadobenate dimeglumine contrast media was used for an imaging study. His clinical presentation was further complicated when he was found to have a mid-left anterior descending coronary artery myocardial bridge.