Miscelaneas

Buenos Aires 01 de Diciembre del 2020

Following Platelets to Diagnose Myocarditis

 


Following Platelets to Diagnose Myocarditis

                                                       

                                                         A.Maier, M.Braig, K.Jakob, T.Bienert, M.Schäper, 
                                                         A.Merkle, C.Wadle,
et al. (University of Freiburg in Germany)

                                                                                 
                                                                                      
Nature Cientific Reports – 13211 - 2020

                                                                                             Traducido por: Jasper Cantrell

 

The heart is a sensitive thing, prone not just to metaphorical heartbreak, but genuine issues if not taken care of. Myocarditis is the inflammation of heart muscle, usually brought upon by toxins or viruses, and if uncontrolled, it could lead to heart failure.

Diagnosing myocarditis has been a challenge. The current standard operation is the endomyocardial biopsy, which needs an actual piece of the heart to test. By today’s standards, invasive treatments are almost archaic, and many researchers are hunting down the next diagnostic breakthrough. Researchs took of the challenge for myocarditis and hypothesized they could use platelets, a special kind of signaling agent, and MRI as a non-invasive imaging technique for myocarditis.

Platelets are clotting factors that are also involved in the inflammatory process. The group had previously found that platelets accumulated in areas of myocarditis and proposed that this could be used as a diagnostic marker. They used a special compound composed of a platelet targeted antibody connected to an iron particle. This agent would collect in inflamed areas of the heart and be identified with just an MRI.

They began with a mouse model following platelet accumulation in the heart after induction of myocarditis. They saw a strong accumulation early in the experiment (2 days post-induction), which seemed to peter off at later time points (14 and 21 days). Their signaling agent, which targeted activated platelets, could only bind to platelets early in the experiment. This observation was also seen in biopsy samples tested for method validation.

Unfortunately, the team could only speculate why their signal agent could not bind well to platelets later in their experiments. They hypothesize it is due to the targeting component of their agent, which targets activated platelets specifically. In theory, real-life myocarditis would constantly have activated platelets at the site of inflammation, but this study’s experiments induced inflammation at one point only. If true, this method might be able to identify myocarditis effectively without any invasive procedures.

One thing they could not determine was the signal difference between a heart attack and myocarditis. Both events recruit platelets, so one would have to be eliminated as a possibility id this method was used.

Conclusion: In mice, they found a time dependent involvement with higher platelet numbers in early stages of inflammation. At this stage, activated platelets can be imaged with LIBS-MPIO in molecular 3D in vivo-MRI in mice.
Activated platelets therefore represent a novel and early marker of myocarditis.