IMPORTANCE Current guidelines recommend ticagrelor as the preferred P2Y12 platelet inhibitor for patients with acute coronary syndrome (ACS), primarily based on a single large randomized clinical trial. The benefits and risks associated with ticagrelor vs clopidogrel in routine practice merits attention.OBJECTIVE To determine the association of ticagrelor vs clopidogrel with ischemic and hemorrhagic events in patients undergoing percutaneous coronary intervention (PCI) for ACS in clinical practice. DESIGN, SETTING, AND PARTICIPANTSA retrospective cohort study of patients with ACS who underwent PCI and received ticagrelor or clopidogrel was conducted using 2 United States electronic health record-based databases and 1 nationwide South Korean database from November 2011 to March 2019. Patients were matched using a large-scale propensity score algorithm, and the date of final follow-up was March 2019.EXPOSURES Ticagrelor vs clopidogrel. MAIN OUTCOMES AND MEASURESThe primary end point was net adverse clinical events (NACE) at 12 months, composed of ischemic events (recurrent myocardial infarction, revascularization, or ischemic stroke) and hemorrhagic events (hemorrhagic stroke or gastrointestinal bleeding). Secondary outcomes included NACE or mortality, all-cause mortality, ischemic events, hemorrhagic events, individual components of the primary outcome, and dyspnea at 12 months. The database-level hazard ratios (HRs) were pooled to calculate summary HRs by random-effects meta-analysis. RESULTSAfter propensity score matching among 31 290 propensity-matched pairs (median age group, 60-64 years; 29.3% women), 95.5% of patients took aspirin together with ticagrelor or clopidogrel. The 1-year risk of NACE was not significantly different between ticagrelor and clopidogrel (15.1% [3484/23 116 person-years] vs 14.6% [3290/22 587 person-years]; summary HR, 1.05 [95% CI, 1.00-1.10]; P = .06). There was also no significant difference in the risk of all-cause mortality (2.0% for ticagrelor vs 2.1% for clopidogrel; summary HR, 0.97 [95% CI, 0.81-1.16]; P = .74) or ischemic events (13.5% for ticagrelor vs 13.4% for clopidogrel; summary HR, 1.03 [95% CI, 0.98-1.08]; P = .32). The risks of hemorrhagic events (2.1% for ticagrelor vs 1.6% for clopidogrel; summary HR, 1.35 [95% CI, 1.13-1.61]; P = .001) and dyspnea (27.3% for ticagrelor vs 22.6% for clopidogrel; summary HR, 1.21 [95% CI, 1.17-1.26]; P < .001) were significantly higher in the ticagrelor group.CONCLUSIONS AND RELEVANCE Among patients with ACS who underwent PCI in routine clinical practice, ticagrelor, compared with clopidogrel, was not associated with significant difference in the risk of NACE at 12 months. Because the possibility of unmeasured confounders cannot be excluded, further research is needed to determine whether ticagrelor is more effective than clopidogrel in this setting.
General anesthesia (GA) can produce analgesia (loss of pain) independent of inducing loss of consciousness, but the underlying mechanisms remain unclear. We hypothesized that GA suppresses pain in part by activating supraspinal analgesic circuits. We discovered a distinct population of GABAergic neurons activated by GA in the mouse central amygdala (CeA GA neurons). In vivo calcium imaging revealed that different GA drugs activate a shared ensemble of CeA GA neurons. CeA GA neurons also possess basal activity that mostly reflect animals’ internal state rather than external stimuli. Optogenetic activation of CeA GA potently suppressed both pain-elicited reflexive and self-recuperating behaviors across sensory modalities, and abolished neuropathic pain-induced mechanical (hyper-)sensitivity. Conversely, inhibition of CeA GA activity exacerbated pain, produced strong aversion, and cancelled the analgesic effect of low-dose ketamine. CeA GA neurons have widespread inhibitory projections to numerous affective pain-processing centers. Our study points to CeA GA as a potential powerful therapeutic target for alleviating chronic pain.
Objective: This study aimed to identify the area with greatest effect using self-myofascial release technique (self-MFR) in the hamstring, suboccipital, and plantar regions. Design: Cross-sectional study. Methods: Twenty-two adult subjects were evaluated for flexibility and hamstring pain threshold after self-MFR. Based on the superficial back line, the self-MFR application areas were the suboccipital region, hamstring, and plantar regions. Self-MFR was applied to each area using a wooden pole for a total of 4 minutes. Self-MFR was applied for 3 days at the same time of day, which was randomly assigned for each subject. Treatment was applied to one area each day. The sit and reach test (SRT), active range of motion (AROM), and passive ROM (PROM) were used to determine changes in flexibility, and an algometer was used to determine pain threshold. Pre/post-self-MFR effectiveness was tested using a paired t-test. Repeated measurement was used to compare self-MFR effects in the suboccipital, hamstring, and plantar regions. Results: When the self-MFR technique was applied to the 3 areas, the SRT showed significant improvement over baseline (p<0.05). Bilateral AROM and PROM showed significant improvements (p<0.05). When the self-MFR technique was applied to the hamstring, the semimembranosus showed a significant change in pain threshold (p<0.05). Conclusions: Our findings suggest that indirect application based on the Anatomy Trains could be effective for those who need to improve muscle flexibility. Moreover, self-MFR easily alleviates myofascial pain while maintaining flexibility, and can be performed at any time and place.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.