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Imaging of Cardiovascular Disease
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
Aleksandra Kalinowska, Lawrence W. Dobrucki
Perfusion in the myocardium is a precisely controlled process, regulated by vessels and the endothelium. Any dysfunctions, such as vasoconstriction from acetylcholine and not enough nitric oxide release, are early signs of coronary artery disease (CAD). Coronary arteries have autoregulation that normalizes blood flow and oxygen supply by reducing resistance in the distal perfusion beds. However, when stenosis exceeds 85%–90% of the diameter of the lumen, the autoregulation becomes insufficient and resting blood flow is decreased, initiating the ischemic cascade (Salerno and Beller 2009).
Future directions in stroke treatment
Published in Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees, Stroke in Practice, 2017
Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees
The goal of these strategies is to maintain tissue viability in the very early phase of ischaemic stroke with a view to increasing the tissue that can be salvaged once reperfusion occurs. The ideal agent for this purpose would be easy to administer (ideally by paramedics in a pre-hospital setting) and have a low toxicity profile, as patients with stroke mimics would inevitably be treated on occasion. No such treatment exists at present, although intravenous magnesium sulphate has shown some promise in this context and remains under evaluation. Magnesium slows neuronal calcium influx (a process involved in the ischaemic cascade that culminates in cell death) and may induce local cerebral microcirculatory changes after ischaemic stroke. It is generally well tolerated and has been used in the management of preeclampsia for many years. Following some encouraging pilot studies, a phase 3 trial of pre-hospital magnesium treatment is underway.1
Neurology and Non-Traumatic Spinal Imaging
Published in Gareth Lewis, Hiten Patel, Sachin Modi, Shahid Hussain, On Call Radiology, 2015
Gareth Lewis, Hiten Patel, Sachin Modi, Shahid Hussain
An understanding of the pathophysiology of ischaemic stoke is necessary to appreciate the corresponding imaging findings. Cell hypoxia causes an ‘ischaemic cascade’, initially resulting in cytotoxic oedema. Vasogenic oedema occurs within 4–6 hours. Due to collateralisation, the result is a core of necrosis surrounded by cells that are potentially viable if perfusion is restored; the latter region is referred to as the penumbra. As infarction matures, cell death results in encephalomalacia with secondary volume loss.
Segmental myocardial viability by echocardiography at rest
Published in Scandinavian Cardiovascular Journal, 2023
Marlene Iversen Halvorsrød, Anders Thorstensen, Gabriel Kiss, Asbjørn Støylen
Different mechanisms for PSS have been suggested. One theory is that PSS is a mix between passive recoil and active contraction [13,14], another suggestion is that PSS may be recoil after elongation due to traction from neighbor myocardial cells and thus mainly a passive phenomenon, but also a marker of preserved elasticity [37]. From a physiological aspect, it is not possible to describe the phenomena solely as either active or passive, as the mechanism differs with the level and duration of ischemia. In 1984, Brutsaert [38] described three factors that controlled the relaxation: (1) load (2) inactivation and (3) uniformity. In the present study, we studied chronic infarctions, and all three factors are affected. Early in the ischemic cascade the load and the inactivation are altered due to reduced reuptake of Ca2+ in SERCA-pump due to hypoxia, later the load is reduced due to prolonged reduced systolic function and relative myocardial loading. As ischemia is regional, the physiological uniformity also is disturbed, leading to a reduced ability to relax. This may explain why PSS is more prominent in acute infarctions than in chronic infarctions as in this material. According to our hypothesis, we wanted to evaluate PSS as an additional resting viability marker. Some studies have shown that resting echocardiography with this addition is sufficient for viability testing [21], while others conclude that stress testing by dobutamine is needed [22,37]. In our study, however, PSS did not increase sensitivity for viability.
Gallic acid attenuates cerebral ischemia/re-perfusion-induced blood–brain barrier injury by modifying polarization of microglia
Published in Journal of Immunotoxicology, 2022
Yang Qu, Lin Wang, Yanfang Mao
Cerebrovascular disease is a common frequently-occurring pathology. The complexity of the pathologies present, and the underlying mechanisms for their development after cerebral ischemia determines the difficulty of treatment. Finding new and effective drugs that could block or reduce the cerebral ischemic cascade are an intense focus of research. Studies have shown that within a few hours after cerebral ischemia, an inflammatory response occurs immediately, and microglia are activated (Xu et al. 2020). The role of microglia in this response to cerebral ischemia is complex; it is believed that microglial activation leads to increased release of nitric oxide, oxygen free radicals, and other toxic substances, all which act to damage neurons (Jiang et al. 2020). As activation of microglia continues for a few weeks after ischemia, it would seem that interventions against this second type of brain injury (i.e., caused by inflammatory reactions) should become an additional target for the developers of neuroprotective drugs.
Predictive serum biomarkers of patients with cerebral infarction
Published in Neurological Research, 2022
Yan Kong, Yu-qing Feng, Ya-ting Lu, Shi-sui Feng, Zheng Huang, Qian-yi Wang, Hui-min Huang, Xue Ling, Zhi-heng Su, Yue Guo
Arachidonic acid (AA) is a type of unsaturated fatty acid that has the widest distribution and highest content in the human body. It is the precursor of many important active cardiovascular and cerebrovascular substances in the human body. A variety of AA metabolites that are regulated by AA metabolism genes are related to the formation of atherosclerotic plaques and the pathogenesis of cerebral infarction. The metabolism of AA is always dynamic, and once its balance is destroyed, atherosclerosis and cerebral infarction occur. AA is involved in three metabolic pathways: cyclooxygenase, lipoxygenase, and cytochrome P450 (CYP) [24,25]. Among these, the third metabolic pathway, CYP cyclooxygenase, catalyzes AA into epoxyeicosatrienoic acids (EETs), which has functions of anti-inflammation, lowering of blood pressure, attenuation of ischemia-reperfusion injury of the myocardium, and reduction of the infarct area of the myocardium and brain tissue [26]. Cerebral inflammation plays a crucial role in the pathophysiology of ischemic stroke and involves all stages of the ischemic cascade [27]. We showed that the level of 5,6-epoxy-8,11,14-eicosatrienoic acid in the serum of patients with cerebral infarction was significantly higher than that of the control group. We hypothesized that AA is converted into EET under the catalysis of the CYP2 enzyme to a greater degree with the occurrence of cerebral inflammation during cerebral infarction. Therefore, AA metabolism dysfunction may be another pathogenesis of cerebral infarction. Patients with cerebral infarction may be treated by stabilizing AA metabolism.