Unveiling the evolving landscape of stroke care costs: A time-driven analysis.

INTRODUCTION: Stroke is a common cause of mortality in the United States. However, the economic burden of stroke on the healthcare system is not well known. In this study, we aim to calculate the annual cumulative and per-patient cost of stroke. METHODS: We conducted a retrospective analysis of Nationwide Emergency Department Sample (NEDS). We calculate annual trends in cost for stroke patients from 2006 to 2019. A multivariate linear regression with patient characteristics (e.g. age, sex, Charlson Comorbidity Index) as covariates was used to identify factors for higher costs. RESULTS: In this study time-period, 2,998,237 stroke patients presented to the ED and 2,481,171 (83 %) were admitted. From 2006 to 2019, the cumulative ED cost increased by a factor of 7.0 from 0.49 ± 0.03 to 3.91 ± 0.16 billion dollars (p < 0.001). The cumulative inpatient (IP) cost increased by a factor of 2.7 from 14.42 ± 0.78 to 37.06 ± 2.26 billion dollars (p < 0.001. Per-patient ED charges increased by a factor of 3.0 from 1950 ± 64 to 7818 ± 260 dollars (p < 0.001). Per-patient IP charges increased by 89 % from 40.22 +/- 1.12 to 76.06 ± 3.18 thousand dollars (p < 0.001). CONCLUSION: Strokes place an increasing financial burden on the US healthcare system. Certain patient demographics including age, male gender, more comorbidities, and insurance type were significantly associated with increased cost of care.

The validity and applications of the analgesia nociception index: a narrative review.

Pain refers to the subjective, unpleasant experience that is related to illness or injury. In contrast to pain, nociception refers to the physiological neural processing of noxious stimuli, such as intra-operative surgical stimuli. One novel device, the Analgesia Nociception Index (ANI), aims to objectively measure intra-operative nociception by analyzing the heart rate variability in patients undergoing surgery. Through this method of nociceptive monitoring, the ANI device aims to provide an objective, continuous evaluation of patient comfort levels and allow anesthesiologists to better manage surgical stress and patient analgesia, perhaps with even better efficacy than current practices used to assess nociception. Additionally, ANI may have clinical application in settings outside of the operating room, such as in the intensive care unit. In this narrative review, we compiled and summarized the findings of many studies that have investigated ANI's validity and applications in different clinical settings. Currently, the literature appears mostly supportive of ANI's ability to detect nociception in both surgical and non-surgical settings. However, the ability for ANI to provide clinical benefits, such as decreased intra-operative opioid use, post-operative opioid use, and post-operative pain compared to standard practices appear controversial. Because of the wide variety of methodology, clinical settings, patient populations, and limitations in these studies, more investigation of ANI is needed before any firm conclusions can be drawn on its clinical benefits.

Age-dependent Lamin changes induce cardiac dysfunction via dysregulation of cardiac transcriptional programs.

As we age, structural changes contribute to progressive decline in organ function, which in the heart act through poorly characterized mechanisms. Taking advantage of the short lifespan and conserved cardiac proteome of the fruit fly, we found that cardiomyocytes exhibit progressive loss of Lamin C (mammalian Lamin A/C homologue) with age, coincident with decreasing nuclear size and increasing nuclear stiffness. Premature genetic reduction of Lamin C phenocopies aging's effects on the nucleus, and subsequently decreases heart contractility and sarcomere organization. Surprisingly, Lamin C reduction downregulates myogenic transcription factors and cytoskeletal regulators, possibly via reduced chromatin accessibility. Subsequently, we find a role for cardiac transcription factors in regulating adult heart contractility and show that maintenance of Lamin C, and cardiac transcription factor expression, prevents age-dependent cardiac decline. Our findings are conserved in aged non-human primates and mice, demonstrating that age-dependent nuclear remodeling is a major mechanism contributing to cardiac dysfunction.