ABSTRACT
Acute hypoxic respiratory failure can be caused by severe pneumonia, cardiogenic pulmonary edema (CPE), and acute respiratory distress syndrome (ARDS). Differentiating between these causes in critically ill patients can be challenging. Lung ultrasound (LUS) evaluation of acute respiratory failure has been developed and adopted only recently. LUS offers promise as a valuable clinical tool for the diagnosis and treatment of patients with severe dyspnea and acute hypoxic respiratory failure.
Subject(s)
Lung/diagnostic imaging , Pneumonia/diagnostic imaging , Pulmonary Edema/diagnostic imaging , Respiratory Distress Syndrome/diagnostic imaging , Diagnosis, Differential , Dyspnea/etiology , Humans , UltrasonographyABSTRACT
High oestradiol (E2) and low dehydroepiandrosterone-sulfate (DHEA-S) levels are risk factors for pulmonary arterial hypertension (PAH) in men, but whether sex hormones are related to PAH in women is unknown.Post-menopausal women aged ≥55â years with PAH were matched by age and body mass index to women without cardiovascular disease. Plasma sex hormone levels were measured by immunoassay.Lower levels of DHEA-S (p<0.001) and higher levels of E2 (p=0.02) were associated with PAH. In PAH cases (n=112), lower DHEA-S levels were associated with worse haemodynamics (all p<0.01) and more right ventricular dilatation and dysfunction (both p=0.001). Lower DHEA-S levels were associated with shorter 6-min walking distance (6MWD) (p=0.01) and worse functional class (p=0.004). Each Ln(1â µg·dL-1) decrease in DHEA-S was associated with a doubling in the risk of death (hazard ratio 2.0, 95% CI 1.5-2.7; p<0.001). Higher levels of E2 were associated with shorter 6MWD (p=0.03) and worse functional class (p=0.01).High E2 and low DHEA-S levels are associated with the risk and severity of PAH in post-menopausal women. Hormonal modulation should be studied as a treatment strategy in PAH.
Subject(s)
Connective Tissue Diseases/complications , Dehydroepiandrosterone Sulfate/blood , Estradiol/blood , Heart Defects, Congenital/complications , Hypertension, Pulmonary/blood , Postmenopause/blood , Aged , Body Mass Index , Case-Control Studies , Female , Humans , Hypertension, Pulmonary/complications , Male , Middle Aged , Proportional Hazards Models , Risk Factors , Walk TestABSTRACT
5-fluorouracil (5-FU) is a key chemotherapeutic agent in the treatment of many gastrointestinal tract adenocarcinomas. Despite its proven therapeutic efficacy, 5-FU also possesses several undesired cardiac toxicities, including coronary vasospasm, coronary thrombosis, cardiomyopathy, and sudden cardiac death. This review addresses the incidence, mechanisms of action, clinical presentation, risk stratification, and management of 5-FU associated cardiotoxicity; it also highlights the importance of careful pre-administration cardiac risk stratification and close monitoring during and after drug administration.
