Molecular biological research at fatal consequences of viral myocarditis

Анотація

Introduction. Diagnosis of viral myocarditis, based on the evidence base, is still one of the key problems of the heart disease. The presence of morphological features of the inflammatory process makes it possible to confirm the diagnosis of myocarditis, but, at the same time, the absence of these features is not sufficient to remove this diagnosis. In routine postmortem study of deaths in multidisciplinary (non-infectious) hospital myocarditis is stated as a cause of death in 0.2-0.4% of all the autopsies. Mortality in myocarditis depends on the severity of the underlying disease, premorbid background, age and sex composition of the patients. According to different authors, it is very different and ranges from 0.03 to 26%.The aim of the work was to carry out histological and molecular biological studies postmortem material for confirming the etiologic role of herpesviruses with fatal consequences of infectious myocarditis during the observation period 2015-2016 years. Material & methods. The material of pathological heart, vascular endothelium, nerve ganglia, kidneys, liver and pancreas were investigated. Viral antigen detection was performed by fluorescent antibody technique with specific sera labeled with FITC (Dako Corporation, Carpinteria, CA) and detection of the viral genome by PCR (in SYNEVO Laboratory). Morphological studies have been conducted in the post-mortem offices of the Kharkov clinical hospitals. Detection of viral genome was performed by PCR using certified commercial kits for detection of nucleotide sequences of herpesviruses «HSV I, II-EPh», «VZV-FL», «EBV-EPh», «CMV-EPh», «HHV VI-Eph», («AmpliSens»). Diagnosis was made in «real time» using modern six-channel thermocycler «Rotor Gene 6000» (Qiagen, Germany). The first group consisted of 19 people who died from infectious myocarditis (group 1). The second group (group 2) consisted of 22 dead from complications of other cardiovascular disease. Pathoanatomical material of 11 people was used as a control group. Death in this group occurred as a result of traumatic injuries. The average age of those groups was 31 ± 3,8 years. All groups were matched by sex and age. Results & discussion. It has been found, that DNA HSV1,2 turned out in infectious myocarditis group and in the group with the same frequency cardiovascular disease. Whereas DNA HHV6 and CMV appeared in infectious myocarditis group 6-7 times more often. Noteworthy the DNA VZV finding of a significant percentage of myocardial tissue samples of the dead from group 1 in relation to other groups. According to our data, which coincides with the tendency of foreign research, the proportion of finding enteroviruses, compared with herpesviruses, is insignificant in all the groups. In all of the dead of the main group (infectious myocarditis) herpes viruses have been detected in several organs simultaneously. Also infarction hypertension virus is most often in the liver, pancreas and nerve ganglia. Thus, when HSV was expected in the nerve ganglia, kidney and vascular endothelium, the detection of a relatively high percentage of hypertension HHV6, CMV and, especially, VZV was quite unexpected in the pancreas and liver tissues. Detection of different herpes viruses in various organs confirms the pantropism of viruses of this family. And the persistence of the virus in one of the bodies makes it possible to its participation in the etiopathogenesis of infectious myocarditis. Conclusion. In deceased patients with viral myocarditis HHV6 and CMV, VZV and EBV are most often found in the myocardial tissue. In all of the dead of the main group (infectious myocarditis) herpes viruses have been detected in several organs simultaneously. Also infarction hypertension virus is most often in the liver, pancreas and nerve ganglia. In the group with infectious myocarditis 3-4 viruses and 5 or more viruses appeared significantly more often in comparison with the group with cardiovascular disease in two and 4,5 times, respectively. This may increase the virulence of the various representatives of herpesviruses from general cell receptors.