Background: Accurate synchronization between magnetic resonance imaging data acquisition and a subject's cardiac activity ("triggering") is essential for reducing image artifacts but conventional, contact-based methods for this task are limited by several factors, including preparation time, patient inconvenience, and susceptibility to signal degradation. The purpose of this work is to evaluate the performance of a new contact-free triggering method developed with the aim to eventually replace conventional methods in non-cardiac imaging applications. In this study, the method's performance is evaluated in the context of 7 Tesla non-enhanced angiography of the lower extremities.
Methods: Our main contribution is a basic algorithm capable of estimating in real-time the phase of the cardiac cycle from reflection photoplethysmography signals obtained from skin color variations of the forehead recorded with a video camera. Instead of finding the algorithm's parameters heuristically, they were optimized using videos of the forehead as well as electrocardiography and pulse oximetry signals that were recorded from eight healthy volunteers in and outside the scanner, with and without active radio frequency and gradient coils. Based on the video characteristics, synthetic signals were generated and the "best available" values of an objective function were determined using mathematical optimization. The performance of the proposed method with optimized algorithm parameters was evaluated by applying it to the recorded videos and comparing the computed triggers to those of contact-based methods. Additionally, the method was evaluated by using its triggers for acquiring images from a healthy volunteer and comparing the result to images obtained using pulse oximetry triggering.
Results: During evaluation of the videos recorded inside the bore with active radio frequency and gradient coils, the pulse oximeter triggers were labeled in 62.5% as "potentially usable" for cardiac triggering, the electrocardiography triggers in 12.5%, and the proposed method's triggers in 62.5%. Evaluation of the angiography images demonstrated that under appropriate conditions the method is feasible to produce an image quality comparable to pulse oximetry.
Conclusion: We conclude that cardiac triggering using the proposed method is technically feasible. However, for improved reliability the signal-to-noise ratio of the videos will have to be addressed by either replacing the camera sensor, improving the illumination, or by use of additional signal filtering techniques.
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http://dx.doi.org/10.1186/s12938-016-0245-3 | DOI Listing |
Compr Physiol
February 2025
Physiology and Behavior Laboratory, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland.
Glucagon-like peptide-1 (GLP-1), a hormone released from enteroendocrine cells in the distal small and large intestines in response to nutrients and other stimuli, not only controls eating and insulin release, but is also involved in drinking control as well as renal and cardiovascular functions. Moreover, GLP-1 functions as a central nervous system peptide transmitter, produced by preproglucagon (PPG) neurons in the hindbrain. Intestinal GLP-1 inhibits eating by activating vagal sensory neurons directly, via GLP-1 receptors (GLP-1Rs), but presumably also indirectly, by triggering the release of serotonin from enterochromaffin cells.
View Article and Find Full Text PDFACS Biomater Sci Eng
January 2025
Central Laboratory, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong 510910, China.
Myocardial infarction (MI), a severe cardiovascular condition, is typically triggered by coronary artery disease, resulting in ischemic damage and the subsequent necrosis of the myocardium. Macrophages, known for their remarkable plasticity, are capable of exhibiting a range of phenotypes and functions as they react to diverse stimuli within their local microenvironment. In recent years, there has been an increasing number of studies on the regulation of macrophage behavior based on tissue engineering strategies, and its regulatory mechanisms deserve further investigation.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Université de Tours, Inserm UMR1327 ISCHEMIA Membrane Signalling and Inflammation in reperfusion injuries, Tours, France.
Pathological left ventricular remodeling is a complex process following an acute myocardial infarction, leading to architectural disorganization of the cardiac tissue. This phenomenon is characterized by sterile inflammation and the exaggerated development of fibrotic tissue, which is non-contractile and poorly conductive, responsible for organ dysfunction and heart failure. At present, specific therapies are lacking for both prevention and treatment of this condition, and no biomarkers are currently validated to identify at-risk patients.
View Article and Find Full Text PDFSemin Thromb Hemost
January 2025
of Medicine, Universita degli Studi di Padova Scuola di Medicina e Chirurgia, Padova, Italy.
Anti-platelet factor 4 (PF4) antibody-mediated disorders are a heterogenous group of diseases characterized by the presence of highly pathogenic immunoglobulins G directed against PF4 and/or PF4/heparin complexes. These antibodies are able to activate platelets, neutrophils and monocytes, thus resulting in thrombocytopenia and a hypercoagulable state. Five different forms of anti-PF4 antibody-mediated disorders have been identified: i) classic heparin-induced thrombocytopenia (cHIT) mediated by heparin and certain polyanionic drugs; ii) autoimmune HIT (aHIT) characterized by the presence of anti-PFA/polyanion antibodies that can strongly activate platelets even in the absence of heparin; iii) spontaneous HIT (spHIT) characterized by thrombocytopenia and thrombosis without proximate exposure to heparin, with two subtypes: (a) post-total knee arthroplasty, and cardiac surgery using cardiopulmonary bypass or extracorporeal membrane oxygenation, and (b) post-infections; iv) vaccine-induced immune thrombotic thrombocytopenia (VITT) characterized by thrombocytopenia, arterial and venous thrombosis, or secondary hemorrhage after receiving adenoviral vector vaccines for COVID-19; v) VITT-like disorders triggered by adenoviral infections.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Department of Cardiovascular Medicine, The University of Tokyo, Bunkyo-ku, Japan. (H. Yagi, H.A., Q.L., A.S.-K., M.U., H.K., R.M., A.S., S.O., H.T., Norifumi Takeda, I.K.).
Background: Marfan syndrome (MFS) is an inherited disorder caused by mutations in the gene encoding fibrillin-1, a matrix component of extracellular microfibrils. The main cause of morbidity and mortality in MFS is thoracic aortic aneurysm and dissection, but the underlying mechanisms remain undetermined.
Methods: To elucidate the role of endothelial XOR (xanthine oxidoreductase)-derived reactive oxygen species in aortic aneurysm progression, we inhibited in vivo function of XOR either by endothelial cell (EC)-specific disruption of the gene or by systemic administration of an XOR inhibitor febuxostat in MFS mice harboring the missense mutation p.
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