Myocardial Stunning

Coastal observations along the Texas coast are valuable for many stakeholders in diverse domains. However, the management of the collected data has been limited, creating gaps in hydrological and atmospheric datasets. Among these, water and air temperature measurements are particularly crucial for water temperature predictions, especially during freeze events. These events can pose a serious threat to endangered sea turtles and economically valuable fish, which can succumb to hypothermic stunning, making them vulnerable to cold-related illness or death. Reliable and complete water and air temperature measurements are needed to provide accurate predictions of when cold-stunning events occur. To address these concerns, the focus of this paper is to describe the method used to create a complete 10-year dataset that is representative of the upper Laguna Madre, TX using multiple stations and various gap-filling methods. The raw datasets consist of a decade's worth of air and water temperature measurements within the Upper Laguna Madre from 2012 to 2022 extracted from the archives of the Texas Coastal Ocean Observation Network and the National Park Service. Large portions of data from the multiple stations were missing from the raw datasets, therefore a systematic gap-filling approach was designed and applied to create a near-continuous dataset. The proposed imputation method consists of three steps, starting with a short gap interpolation method, followed by a long gap-filling process using nearby stations, and finalized by a second short gap interpolation method. This systematic data imputation approach was evaluated by creating random artificial gaps within the original datasets, filling them using the proposed data imputation method, and assessing the viability of the proposed methods using various performance metrics. The evaluation results help to ensure the reliability of the newly imputed dataset and the effectiveness of the data imputation method. The newly created dataset is a valuable resource that transcends the local cold-stunning issue, offering viable utility for analyzing temporal variability of air and water temperatures, exploring temperature interdependencies, reducing forecasting uncertainties, and refining natural resource and weather advisory decision-making processes. The cleaned dataset with minimal gaps (<2%) is ready and convenient for artificial intelligence and machine learning applications.

Takotsubo syndrome (TTS) is a clinical condition characterized by temporary regional wall motion anomalies and dysfunction that extend beyond a single epicardial vascular distribution. Various pathophysiological mechanisms, including inflammation, microvascular dysfunction, direct catecholamine toxicity, metabolic changes, sympathetic overdrive-mediated multi-vessel epicardial spasms, and transitory ischemia may cause the observed reversible myocardial stunning. Despite the fact that TTS usually has an acute coronary syndrome-like pattern of presentation, the absence of culprit atherosclerotic coronary artery disease is often reported at coronary angiography. However, the idea that coronary artery disease (CAD) and TTS conditions are mutually exclusive has been cast into doubt by numerous recent studies suggesting that CAD may coexist in many TTS patients, with significant clinical and prognostic repercussions. Whether the relationship between CAD and TTS is a mere coincidence or a bidirectional cause-and-effect is still up for debate, and misdiagnosis of the two disorders could lead to improper patient treatment with unfavourable outcomes. Therefore, this review seeks to provide a profound understanding of the relationship between CAD and TTS by analyzing potential common underlying pathways, addressing challenges in differential diagnosis, and discussing medical and procedural techniques to treat these conditions appropriately.

Myocardial ischemia-reperfusion (IR) (stunning) injury triggers changes in the proteome and degradome of the heart. Here, we utilize quantitative proteomics and comprehensive degradomics to investigate the molecular mechanisms of IR injury in isolated rat hearts. The control group underwent aerobic perfusion, while the IR injury group underwent 20 min of ischemia and 30 min of reperfusion to induce a stunning injury. As MMP-2 activation has been shown to contribute to myocardial injury, hearts also underwent IR injury with ARP-100, an MMP-2-preferring inhibitor, to dissect the contribution of MMP-2 to IR injury. Using data-independent acquisition (DIA) and mass spectroscopy, we quantified 4468 proteins in ventricular extracts, whereby 447 proteins showed significant alterations among the three groups. We then used subtiligase-mediated N-terminomic labeling to identify more than a hundred specific cleavage sites. Among these protease substrates, 15 were identified following IR injury. We identified alterations in numerous proteins involved in mitochondrial function and metabolism following IR injury. Our findings provide valuable insights into the biochemical mechanisms of myocardial IR injury, suggesting alterations in reactive oxygen/nitrogen species handling and generation, fatty acid metabolism, mitochondrial function and metabolism, and cardiomyocyte contraction.