Objectives: The purposes of the present study were to: 1) determine whether fibrinogen (Fg) is the plasma protein responsible for spontaneous echo contrast (SEC), and 2) investigate modulators of SEC.
Background: Spontaneous echo contrast has been linked to the development of thromboemboli. The blood products and their interaction responsible for SEC formation have not been fully elucidated.
Methods: Blood echogenicity was examined with the use of quantitative videodensitometry over a controlled range of flow velocities in an in vitro model. Human blood samples were analyzed in a manner to methodically eliminate individual blood components from whole blood to determine which components are responsible for the formation of SEC.
Results: The videodensity (VD) of whole blood was found to be flow-dependent, with higher VD at lower flow rates, and correlated with visually dense SEC. The following blood products produced faint VD values: washed red blood cells (wRBCs), platelet-depleted plasma, Fg, defibrinated plasma, wRBCs plus defibrinated plasma, and physiologic saline. The VD of wRBCs increased incrementally as increasing concentrations of Fg were added. At each hematocrit (Hct) range, as Fg concentration increased, the SEC became denser, and the VD level also increased until a plateau level was reached that was distinct for each Hct. The addition of sialic acid, which inhibits RBC-RBC aggregation, decreased the amount of SEC, even in the presence of Fg.
Conclusion: These results demonstrated that Fg-mediated RBC aggregation may be responsible for SEC generation. Furthermore, a unique stoichiometric relationship exists between Fg and RBC concentrations that is necessary for blood echogenicity.
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http://dx.doi.org/10.1016/s0735-1097(02)02898-x | DOI Listing |
Rev Cardiovasc Med
November 2024
Children's Heart Institute, UT Health McGovern Medical School, Houston, TX 77030, USA.
This review addresses the diagnosis and management of ventricular septal defects (VSDs). The VSDs are classified on the basis of their size, their number, and their location in the ventricular septum. Natural history of VSDs includes spontaneous closure, development of pulmonary hypertension, onset of infundibular obstruction, and progression to aortic insufficiency.
View Article and Find Full Text PDFCureus
October 2024
Cardiovascular, University of Baghdad, Baghdad, IRQ.
Spontaneous coronary artery dissection (SCAD) is a significant cause of acute coronary syndrome, myocardial infarction, arrhythmia, and sudden death, particularly in young women and individuals with few conventional atherosclerotic risk factors, necessitating a high degree of suspicion. The most common risk factors for SCAD include atherosclerosis, females in the peripartum period, autoimmune inflammatory diseases, and connective tissue diseases. We present an unusual case of a young man who was initially suspected of having myocarditis, but cardiac magnetic resonance (CMR) revealed an ischemic pattern in late gadolinium enhancement.
View Article and Find Full Text PDFBMC Cardiovasc Disord
November 2024
Tianjin Key laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211, China.
CJC Open
October 2024
Department of Cardiology, Govind Ballabh Pant Institute of Post Graduate Medical Education and Research, Delhi, India.
Am J Epidemiol
November 2024
Curtin School of Population Health, Curtin University, Perth, Kent Street, Bentley, Western Australia 6102, Australia.
A few studies investigated critical periods of temperature and the risks of stillbirth and preterm birth. This study aimed to identify critical periods of composite biothermal stress (Universal Thermal Climate Index, UTCI) for stillbirth and spontaneous preterm birth (sPTB). From the Midwives Notification System, 415,271 singleton births between 1st January 2000 and 31st December 2015 were linked to spatiotemporal UTCI in Western Australia.
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