As an emerging platform technology, metabolomics offers new insights into the pathomechanisms associated with complex disease conditions, including cardiovascular diseases. It also facilitates assessing the risk of developing the disease before its clinical manifestation. For this reason, metabolomics is of growing interest for understanding the pathogenesis of acute coronary syndromes (ACS), finding new biomarkers of ACS, and its associated risk management. Metabolomics-based studies in ACS have already demonstrated immense potential for biomarker discovery and mechanistic insights by identifying metabolomic signatures (e.g., branched-chain amino acids, acylcarnitines, lysophosphatidylcholines) associated with disease progression. Herein, we discuss the various metabolomics approaches and the challenges involved in metabolic profiling, focusing on ACS. Special attention has been paid to the clinical studies of metabolomics and lipidomics in ACS, with an emphasis on ischemia/reperfusion injury.
IntroductionChronic subdural hematoma (CSDH) is one of the most encountered neurosurgical cases. CSDH is defined as the accumulation of liquified blood products in the space between the dura and the arachnoid. A reported incidence of 17.6/100,000/year has more than doubled in the past 25 years in parallel with an aging population. Surgical drainage remains the mainstay of treatment, yet it is challenged by variable recurrence risks. Less invasive embolization methods of the middle meningeal artery (EMMA) could reduce the recurrence risks. Before adopting a newer treatment (EMMA), it is prudent to establish the outcomes from surgical drainage. The purpose of this study is to assess the clinical outcome and recurrence risk in surgically treated CSDH patients in our center. MethodsA retrospective search of our surgical database was done to identify CSDH patients undergoing surgical drainage in the year 2019-2020. Demographic and clinical details were collected, and quantitative statistical analysis was performed. Peri-procedural radiographic information and follow-ups were also included as per the standard of care. ResultsA total of 102 patients (mean age: 69 years; range: 21-100 years; male: 79) with CSDH underwent surgical drainage with repeat surgery in 13.7% of the patients (n=14). Peri-procedural mortality and morbidity were 11.8%(n=12) and 19.6% (n=20), respectively. Overall, among our patient population, recurrence was seen in 22.55% (n=23). The mean total hospital stay was 10.6 days. ConclusionsOur retrospective cohort study showed an institutional CSDH recurrence risk of 22.55%, in keeping with what is reported in the literature. This baseline information is important for a Canadian setting and provides a basis for comparison for future Canadian trials.
The ‘no-reflow’ phenomenon (NRP) after primary percutaneous coronary intervention (PCI) is a serious complication among acute ST-segment elevation myocardial infarction (STEMI) patients. Herein, a comprehensive lipidomics approach was used to quantify over 300 distinct molecular species in circulating plasma from 126 patients with STEMI before and after primary PCI. Our analysis showed that three lipid classes: phosphatidylcholine (PC), alkylphosphatidylcholine (PC(O)), and sphingomyelin (SM), were significantly elevated (p < 0.05) in no-reflow patients before primary PCI. The levels of individual fatty acids and total fatty acid levels were significantly lower (p < 0.05) in no-reflow subjects after PCI. The grouping of patients based on ECG ST-segment resolution (STR) also demonstrated the same trend, confirming the possible role of these differential lipids in the setting of no-reflow. Sphingomyelin species, SM 41:1 and SM 41:2, was invariably positively correlated with corrected TIMI frame count (CTFC) at pre-PCI and post-PCI. The plasma levels of SM 42:1 exhibited an inverse association (p < 0.05) consistently with tumor necrosis factor-alpha (TNF-α) at pre-PCI and post-PCI. In conclusion, we identified plasma lipid profiles that distinguish individuals at risk of no-reflow and provided novel insights into how dyslipidemia may contribute to NRP after primary PCI.
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