OBJECTIVES: To identify prognostic factors that are independently predictive of in‐hospital mortality in older patients hospitalized in a medical intensive care unit (MICU). DESIGN: Prospective cohort study. SETTING: A MICU in an Italian university hospital. PARTICIPANTS: Patients aged 65 and older consecutively admitted to the MICU directly from the first‐aid unit. MEASUREMENTS: Upon admission, the following variables were examined: demographics, clinical history (diabetes mellitus, active neoplasm, cognitive impairment, immobilization, pressure ulcers, use of nutritional support, home oxygen therapy), physiopathology (Acute Physiology and Chronic Health Evaluation (APACHE) II), and cognition/function (activity of daily living (ADL), instrumental activity of daily living (IADL), Short Portable Mental Status Questionnaire (SPMSQ)). The vital status of the patient at the end of hospitalization was recorded. RESULTS: Over a period of 10 months, 659 patients were recruited (mean age ± standard deviation = 76.6 ± 7.5; 352 men and 307 women). There were 97 deaths (14.71%). The following factors proved to be significantly associated with in‐hospital mortality: old age, low body mass index (BMI) values, low values of albumin, high scores on APACHE II, functional impairment (ADL, IADL), cognitive impairment (SPMSQ), history of cognitive deterioration, history of confinement to bed, and presence of pressure ulcers. Using multivariate analysis, the following variables were independently predictive of in‐hospital mortality: lack of independence in ADLs (P < .001), moderate‐to‐severe cognitive impairment on SPMSQ (P < .001), score on APACHE II (P = .002), and low BMI values (P = .031). CONCLUSION: The prognosis of older patients hospitalized in medical intensive care units depends not only on the acute physiological impairments, but also on a series of preexisting conditions, such as loss of functional independence, severe and moderate cognitive impairment, and low BMI.

Polyunsaturated fatty acids (n-3 PUFAs) are long-chain polyunsaturated fatty acids with 18, 20 or 22 carbon atoms, which have been found able to counteract cardiovascular diseases. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in particular, have been found to produce both vaso- and cardio-protective response via modulation of membrane phospholipids thereby improving cardiac mitochondrial functions and energy production. However, antioxidant properties of n-3 PUFAs, along with their anti-inflammatory effect in both blood vessels and cardiac cells, seem to exert beneficial effects in cardiovascular impairment. In fact, dietary supplementation with n-3 PUFAs has been demonstrated to reduce oxidative stress-related mitochondrial dysfunction and endothelial cell apoptosis, an effect occurring via an increased activity of endogenous antioxidant enzymes. On the other hand, n-3 PUFAs have been shown to counteract the release of pro-inflammatory cytokines in both vascular tissues and in the myocardium, thereby restoring vascular reactivity and myocardial performance. Here we summarize the molecular mechanisms underlying the anti-oxidant and anti-inflammatory effect of n-3 PUFAs in vascular and cardiac tissues and their implication in the prevention and treatment of cardiovascular disease.

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The maintenance of physiological levels of nitric oxide (NO) produced by eNOS represents a key element for vascular endothelial homeostasis. On the other hand, NO overproduction, due to the activation of iNOS under different stress conditions, leads to endothelial dysfunction and, in the late stages, to the development of atherosclerosis. Oxidized LDLs (oxLDLs) represent the major candidates to trigger biomolecular processes accompanying endothelial dysfunction and vascular inflammation leading to atherosclerosis, though the pathophysiological mechanism still remains to be elucidated. Here, we summarize recent evidence suggesting that oxLDLs produce significant impairment in the modulation of the eNOS/iNOS machinery, downregulating eNOS via the HMGB1-TLR4-Caveolin-1 pathway. On the other hand, increased oxLDLs lead to sustained activation of the scavenger receptor LOX-1 and, subsequently, to NFkB activation, which, in turn, increases iNOS, leading to EC oxidative stress. Finally, these events are associated with reduced protective autophagic response and accelerated apoptotic EC death, which activates atherosclerotic development. Taken together, this information sheds new light on the pathophysiological mechanisms of oxLDL-related impairment of EC functionality and opens new perspectives in atherothrombosis prevention.