Abstract
BackgroundDiagnosis of viral myocarditis is difficult by clinical criteria but facilitated by detection of inflammation and viral genomes in endomyocardial biopsies. Parvovirus B19 (B19V) targets endothelial cells where viral nucleic acid is exclusively detected in the heart. Microparticles (MPs) are released after cell damage or activation of specific cells. We aimed to investigate whether circulating endothelial MPs (EMPs) in human and experimental models of myocarditis are associated with B19V myocarditis.MethodsMPs were investigated in patients with myocarditis (n = 54), divided into two groups: B19V+ (n = 23) and B19V- (n = 31) and compared with healthy controls (HCTR, n = 25). MPs were also investigated in B19V transgenic mice (B19V-NS1+) and mice infected with coxsackievirus B3 (CVB3). MPs were analyzed with fluorescent activated cell sorting (FACS).ResultsIn human samples, EMP subpopulation patterns were significantly different in B19V+ compared to B19V- and HCTR (p<0.001), with an increase of apoptotic but not activated EMPs. Other MPs such as platelet- (PMPs) leukocyte-(LMPs) and monocyte-derived MPs (MMPs) showed less specific patterns. Significantly different levels of EMPs were observed in transgenic B19V-NS1+ mice compared with CVB3-infected mice (p<0.001).ConclusionEMP subpopulations are different in B19V+ myocarditis in humans and transgenic B19V mice reflecting vascular damage. EMP profiles might permit differentiation between endothelial-cell-mediated diseases like myocardial B19V infection and other causes of myocarditis.
Highlights
Myocarditis is a non-ischemic inflammatory heart disease, which is potentially leading to severe heart failure and death [1,2]
MPs were investigated in B19V transgenic mice (B19V-NS1+) and mice infected with coxsackievirus B3 (CVB3)
endothelial MPs (EMPs) subpopulation patterns were significantly different in B19V+ compared to B19V- and healthy controls (HCTR) (p
Summary
Myocarditis is a non-ischemic inflammatory heart disease, which is potentially leading to severe heart failure and death [1,2]. It has been shown that cardiac endothelial cells (ECs) but not myocytes are the B19V-specific targets providing expression of the blood-group P-antigen serving as a cellular receptor for B19V [14] allowing persistence of B19V in ECs leading to endothelial cell apoptosis [15] EMPs are released from cellular membranes during cell activation and apoptosis [16] and predict flowmediated dilatation, cardiovascular events in rheumatoid arthritis [17] with endothelial dysfunction, predicts outcomes in acute coronary syndromes [18] and allow differentiating peripartal cardiomyopathy from normal pregnancy and other causes of heart failure [19] It is unknown whether EMPs can differentiate among inflammatory cardiac diseases. We aimed to investigate whether circulating endothelial MPs (EMPs) in human and experimental models of myocarditis are associated with B19V myocarditis
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call