Plaque Rupture
Plaque Rupture - Related Videos
13:00
Plaque Assay: A Method to Determine Viral Titer as Plaque Forming Units (PFU)
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2023
Source: Tilde Andersson1, Rolf Lood1 1 Department of Clinical Sciences Lund, Division of Infection Medicine, Biomedical Center, Lund University, 221 00 Lund, Sweden Viruses that infect prokaryotic organisms, called bacteriophages or simply phages, were identified in the early 20th century by Twort (1) and d'Hérelle (2) independently. Phages have since been widely recognized for their therapeutic value (3) and their influence on human (4), as well as global, ecosystems (5). Current concerns have...
10:53
Plaque Assay for Murine Norovirus
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Cited by 99 •
2012
Here we describe a method to quantify infectious particles of murine norovirus (MNV), which is the only norovirus that efficiently replicates in cell culture. The plaque assay takes advantage of MNV’s tropism for murine macrophages and can be adapted for use with biological or environmental samples containing MNV.
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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Cited by 13 •
2014
Atherosclerosis is a chronic inflammatory process. This manuscript illustrates an easy to use ex vivo model to investigate fresh carotid or coronary artery plaques. The ex vivo model allows for the investigation of potential substances on the inflammatory milieu in human atherosclerotic lesions and results can be analyzed by various methods.
03:25
Quantification of Pseudovirus Particles by Plaque Assay
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2026
Source: Jamieson, T. R., et al., Detection of SARS-CoV-2 Neutralizing Antibodies using High-Throughput Fluorescent Imaging of Pseudovirus Infection. J. Vis. Exp. (2021)This video describes the virus plaque assay using coronavirus pseudovirus particles. The diluted pseudovirus is added to a monolayer of mammalian cells, followed by incubation with a methylcellulose overlay. Plaques formed by infected cells are counted visually to determine the infectious virus titer.
03:30
Assessing Rotavirus Growth Curve by Plaque Assay
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2026
Source: Kadoya, S., Sano, D. Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus. J. Vis. Exp. (2019).This video demonstrates the use of a plaque assay to assess the rotavirus growth curve. The method involves infecting host cells with diluted virus, overlaying with agarose to restrict spread, and staining to visualize plaques formed by viral replication. By counting plaque-forming units at defined time points, the resulting growth curve reveals the lag, exponential, and...
FAQs
Inflammation within an atherosclerotic plaque can weaken the fibrous cap by promoting degradation of structural proteins. This loss of structural support increases the likelihood that the cap will disrupt under circulating blood conditions. The important clinical implication is that plaque vulnerability depends not only on plaque presence, but also on the integrity of the tissue separating its lipid-rich core from blood.
Once disruption exposes the lipid-rich core to circulating blood, platelets can adhere to the damaged site and coagulation can proceed, producing a thrombus. Thrombus formation can progressively obstruct an artery or stop flow altogether. Thus, the acute danger comes from the blood response to disruption, not solely from the pre-existing plaque burden.
In a coronary artery, the resulting obstruction may cause myocardial infarction, whereas reduced or stopped blood flow in a cerebral artery may cause ischemic stroke. This distinction connects a shared vascular mechanism with different clinical syndromes. It also explains why plaque rupture matters across cardiovascular and cerebrovascular assessment rather than only in diseases affecting the heart.
Clinical risk assessment considers plaque rupture as a potential transition from an atherosclerotic lesion to an acute thrombotic event. The relevant concern is whether disruption could expose the lipid-rich core and initiate vessel-blocking thrombosis. This perspective shifts attention toward plaque vulnerability and its consequences, supporting evaluation aimed at reducing the chance that acute cardiovascular disease will develop.
Vascular imaging can contribute to clinical evaluation of plaques in the context of rupture risk. Based on the source, its relevance is to assessing vascular disease and supporting understanding of potentially dangerous plaque behavior. The specific imaging modality or measurement is not established here, so its role should be described as part of assessment rather than tied to a named technique.
Preventive treatment addresses plaque rupture in two related ways: it aims to stabilize plaques, reducing the likelihood that the protective cap will fail, and to reduce thrombosis, limiting the blood-clotting response if disruption occurs. These goals target both sides of the clinical problem, linking structural plaque stability with the downstream risk of vessel blockage.