AimsTo compare primary percutaneous coronary intervention (pPCI) and fibrinolysis in very old patients with ST-segment elevation myocardial infarction (STEMI), in whom head-to-head comparisons between both strategies are scarce.Methods and resultsPatients ≥75 years old with STEMI <6 h were randomized to pPCI or fibrinolysis. The primary endpoint was a composite of all-cause mortality, re-infarction, or disabling stroke at 30 days. The trial was prematurely stopped due to slow recruitment after enroling 266 patients (134 allocated to pPCI and 132 to fibrinolysis). Both groups were well balanced in baseline characteristics. Mean age was 81 years. The primary endpoint was reached in 25 patients in the pPCI group (18.9%) and 34 (25.4%) in the fibrinolysis arm [odds ratio (OR), 0.69; 95% confidence interval (CI) 0.38–1.23; P = 0.21]. Similarly, non-significant reductions were found in death (13.6 vs. 17.2%, P = 0.43), re-infarction (5.3 vs. 8.2%, P = 0.35), or disabling stroke (0.8 vs. 3.0%, P = 0.18). Recurrent ischaemia was less common in pPCI-treated patients (0.8 vs. 9.7%, P< 0.001). No differences were found in major bleeds. A pooled analysis with the two previous reperfusion trials performed in older patients showed an advantage of pPCI over fibrinolysis in reducing death, re-infarction, or stroke at 30 days (OR, 0.64; 95% CI 0.45–0.91).ConclusionPrimary PCI seems to be the best reperfusion therapy for STEMI even for the oldest patients. Early contemporary fibrinolytic therapy may be a safe alternative to pPCI in the elderly when this is not available.Clinicaltrials.gov # NCT00257309.

Cells translate extracellular signals to regulate processes such as differentiation, metabolism and proliferation, via transmembranar receptors. G protein-coupled receptors (GPCRs) belong to the largest family of transmembrane receptors, with over 800 members in the human species. Given the variety of key physiological functions regulated by GPCRs, these are main targets of existing drugs. During normal aging, alterations in the expression and activity of GPCRs have been observed. The central nervous system (CNS) is particularly affected by these alterations, which results in decreased brain functions, impaired neuroregeneration, and increased vulnerability to neuropathologies, such as Alzheimer’s and Parkinson diseases. GPCRs signal via heterotrimeric G proteins, such as G o , the most abundant heterotrimeric G protein in CNS. We here review age-induced effects of GPCR signaling via the G i/o subfamily at the CNS. During the aging process, a reduction in protein density is observed for almost half of the G i/o -coupled GPCRs, particularly in age-vulnerable regions such as the frontal cortex, hippocampus, substantia nigra and striatum. G i/o levels also tend to decrease with aging, particularly in regions such as the frontal cortex. Alterations in the expression and activity of GPCRs and coupled G proteins result from altered proteostasis, peroxidation of membranar lipids and age-associated neuronal degeneration and death, and have impact on aging hallmarks and age-related neuropathologies. Further, due to oligomerization of GPCRs at the membrane and their cooperative signaling, down-regulation of a specific G i/o -coupled GPCR may affect signaling and drug targeting of other types/subtypes of GPCRs with which it dimerizes. G i/o -coupled GPCRs receptorsomes are thus the focus of more effective therapeutic drugs aiming to prevent or revert the decline in brain functions and increased risk of neuropathologies at advanced ages.

In order to understand the role of the GLUTEUS MEDIUS muscle (GM) in hip joint osteoarthritis, the objective of this study was to analyze the correlation between morphometric data of GM samples with osteoarthritis scores of ipsilateral and contralateral hips in 41 patients. GM samples obtained during unilateral hip replacement surgery were used to evaluate muscle fibers in the cross-sectional area (CSA) and other features indicative for muscle aging. Clinical symptoms were assessed by the Lequesne pain score. Hip osteoarthritis was graded by the Kellgren score and by measuring the sum joint space width (sumJSW) at three different articular locations and minimal JSW in a. p. radiographs. Varying degrees of GM muscle atrophy correlated with the pain score; pain score also correlated with radiographic signs of osteoarthritis. GM CSA was significantly correlated with all radiographic signs of the contralateral hip, but only with the sumJSW in the ipsilateral hip. It can be concluded that a weak GM may be the result of ipsilateral osteoarthitis, but may especially predispose the contralateral hip to develop osteoarthritis. This can be associated with an impaired GM capacity to avoid the shock impact in the load transfer during gait. Muscle strengthening is therefore recommended.

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Nurses should use Braden Scale assessment and consider patients' characteristics and diagnoses to plan more focused preventive interventions and improve nursing care. This study could be the first step to create a preventive protocol based on institutional reality, patients' characteristics, level of risk and affected sub-scales.