Myocarditis in Multisystem Inflammatory Syndrome in Children Associated With Coronavirus Disease 2019.

Cardiac involvement as a complication of severe acute respiratory syndrome coronavirus 2 infection in children is a relatively new entity. We present our initial experience managing children with coronavirus disease 2019-related acute myocardial injury. The 3 patients presented here represent a spectrum of the cardiac involvement noted in children with coronavirus disease 2019-related multisystem inflammatory syndrome, including myocarditis presenting as cardiogenic shock or heart failure with biventricular dysfunction, valvulitis, coronary artery changes, and pericardial effusion.

Evaluation of the possible involvement of Ad-36-induced adipogenesis and coronary artery disease development in mediastinal adipose tissue samples.

Mediastinal fat has been suggested to be associated with cardiovascular diseases such as carotid stiffness, atherosclerosis and coronary artery calcification. We investigated the possible role of Ad-36-induced obesity in the pathogenesis of the coronary artery disease (CAD). Ad-36 DNA was investigated in the anterior mediastinal fat tissue samples of obese adults with CAD. Seventy-five obese adults with left main coronary artery (LMCA) disease, 28 non-obese adults with valvular heart diseases, and 48 healthy individuals without cardiovascular problems were included as the obese patient group (OPG), non-obese patient group (NOG) and healthy control group (HCG), respectively. We also simultaneously investigated Ad-36 antibodies by serum neutralization test (SNA), and measured leptin and adinopectin levels. Ad-36 antibodies were detected only in 10 patients (13.3%) within the 75 OPG. A statistically significant difference was detected between OPG, NOG and HCG in terms of Ad-36 antibody positivity (p>0.05). Ad-36 DNA was not detected in mediastinal tissue samples of OPG and NOP without PCR inhibitors. We suggest that Ad-36 may not have an affinity for mediastinal adipose tissue in obese patients with left main CAD and valvular heart diseases. Ad-36 antibody positivity results are not sufficient to reach a causal relationship.

Targeted gene expression analyses and immunohistology suggest a pro-proliferative state in tricuspid aortic valve-, and senescence and viral infections in bicuspid aortic valve-associated thoracic aortic aneurysms.

BACKGROUND AND AIMS: Despite the potential life-threatening consequences of thoracic aortic aneurysms (TAAs), the pathogenesis of these diseases is still poorly understood. While some aspects of TAA formation have been elucidated, the role of vascular smooth muscle cells (SMCs) in both bicuspid aortic valve (BAV)-associated and degenerative tricuspid aortic valve (TAV)-associated TAAs has not yet been fully unravelled. Thus, this work was aimed at uncovering processes in SMC biology that may contribute to TAA formation. METHODS: Using isolated SMCs and tissue samples from TAAs linked to BAV syndrome, TAV-associated degenerative TAAs and control aortas, we performed targeted mRNA expression profile analyses and conducted immunohistological analyses on aortic wall tissue sections. RESULTS: While SMC expression profiles and tissue analyses in TAV-TAAs clearly point toward a pro-proliferative state of the aortic media SMCs, BAV-TAA SMCs and tissue provide evidence for DNA damage, DNA damage response signalling as well as profound TLR-3 signalling. CONCLUSIONS: The data presented in this study emphasizes the importance of SMCs in TAA development. Furthermore, our results provide evidence that the state of SMCs in the BAV-TAA (senescent) and TAV-TAA (pro-proliferative) differs significantly. For the first time, we also present findings that may argue for the occurrence of a viral infection in BAV-TAA SMCs.

Valvular Cytomegalovirus Endocarditis.

Endocarditis is a rare presentation for cytomegalovirus (CMV) infection. We present the case of a 49-year-old man who underwent mitral and tricuspid valve replacement for valvular CMV endocarditis. The patient's past medical history was significant for human immunodeficiency virus, intravenous drug abuse, and chronic hepatitis B. During his clinical course, he was found to have tricuspid and mitral valve vegetations. After progressive valvular destruction despite antibiotic therapy, he underwent successful mitral and tricuspid valve replacement. Pathologic analysis of the culture-negative valve specimens were found to contain inclusion bodies consistent with CMV, and quantitative serum polymerase chain reaction returned a highly elevated CMV DNA count.

Valvular manifestations of human immunodeficiency virus infection--results from the prospective, multicenter HIV-HEART study.

BACKGROUND AND AIMS: HIV infection is associated with an elevated rate of cardiac diseases. The aim of the current study was to assess the prevalence of valvular disorders in a large population of HIV-infected patients. METHODS: We enrolled 803 adults (age 44 ± 10 years, 16.6% women) in this prospective, multicenter cohort study. All patients underwent a comprehensive two-dimensional transthoracic echocardiography examination including Doppler evaluation of valvular function. Statistical analyses were performed in respect of severity of HIV infection. RESULTS: Overall, the rate of patients with pathologic function of cardiac valves was 77.6% (N = 623). Most of these patients had signs of valvular regurgitation (N = 620; 77.2%), whereas stenoses were rare (N = 23; 2.9%). Clinically relevant valvular disorders (excluding mild stages) were seen in only 4.7% (N = 38; regurgitation: N = 36, 4.5%; stenosis: N = 3, 0.4%). Clinical stages of HIV infection, defined by the Centers for Disease Control and Prevention (CDC) classification, were associated with higher rates of valvular diseases (CDC-stage B/C versus A: 6.2 versus 2.3%, P = 0.015). However, there was no association between current CD4 cell count or virus load and the prevalence of valvular disorders (both P > 0.2). None of the patients had signs of active endocarditis in the present study. CONCLUSION: Valvular heart diseases are common in HIV-infected patients. Fortunately, most of these disorders are mild today. We found an association between the onset of valvular heart disease and clinical stages of HIV infection.

[Mesenchymal dysplasia of heart valves, cystic medianecrosis of the aorta and herpetic infection].

Histologic and immunohistochemical studies (use of antibodies for viruses of herpes simplex type 1 and 2, desmin, vimentin, SMA as well as polymerase chain reaction to DNA of viruses of herpes simplex) were made on the material of the valves taken from 1326 patients with valvular heart disease, the ascending aorta of 30 patients with aneurysm, valves of 35 deceased patients without cardiovascular pathology. As a result, expression of viruses of herpes simplex type 1 and/or 2 was found in all cases with mesenchymal dysplasia and cystic medianecrosis in endotheliocytes, fibroblasts, smooth muscle cells of valves and aorta. This indicates the role of these viruses in the pathogenesis of these diseases and their common etiology.

Detection of herpes simplex virus type 1 in rheumatic valvular tissue.

BACKGROUND: Rheumatic heart disease (RHD) is the most important sequela of rheumatic fever (RF): evidence that streptococcal infection is aetiological is prominent, but sometimes contradictory. Acute HSV-1 infection in mouse leads to carditis and valvulitis whereas recurrent infection results in inflammatory granulomatous lesions that resemble Aschoff bodies. Cells containing HSV-1 inclusions or virus infected giant cells appear similar to Anitschkow cells or Aschoff cells respectively. We hypothesized that HSV-1 infection also may be involved in RHD. METHODS: Formalin-fixed, paraffin-embedded valvular tissue samples from 32 patients with RHD were investigated for evidence of HSV-1 infection. HSV-1 antigen was detected by immunohistochemistry, using HSV-1-specific monoclonal and polyclonal antibodies. HSV-1 glycoprotein D gene sequences were amplified by nPCR, using beta-globin gene amplification in the same samples as internal control. Valvular tissue from 5 cases of sudden death and 3 cases died of neisseria meningitis without a history of valvular disease was used for comparison. HSV-1-infected lung tissue was used as positive control. RESULTS: HSV-1 antigens were detected in valvular tissues from 21 of 32 (65.6%) patients. Fifteen of these 21 (46.9% of cases), but no antigen-negative sample, were positive also for HSV DNA. Nucleotide sequence of PCR products was homologous to the targeted region of the HSV-1 glycoprotein D gene. HSV-1 antigen was present also in one case of sudden death but viral DNA was not found in any tissue sample from the comparison group. Results from reagent and positive controls were as anticipated. CONCLUSIONS: This is the first study to show the presence of HSV-1 antigen and genomic DNA in valvular tissues from patients with RHD and provides evidence for an association of HSV-1 infection with some cases of rheumatic valvular disease.