Abstract
Objective. To determine serum levels of immunoglobulin M (IgM) and G (IgG) antibodies to human herpes virus type 6 (HHV-6) (anti-HHV-6) and features of clinical and morphological portrait in patients with acute decompensated heart failure (ADHF) of ischemic genesis and/or adverse left ventricular (LV) remodeling.Material and Methods. This open-label, nonrandomized, single-center, prospective trial was registered at clinicaltrials. gov (#NCT02649517) and comprised 25 patients (84% men) with ADHF and LV ejection fraction (EF) ≤ 40%. All patients underwent endomyocardial biopsy (EMB) with immunohistochemistry (IHC) analysis for the presence of HHV-6, compliment C1q, major histocompatibility complex of class II (MHC II), and B-lymphocyte antigen (CD19) as the markers of autoimmune reaction as well as the serum levels of anti-HHV-6 IgM and IgG. Serum levels of IgM and IgG were measured using enzymelinked immunosorbent assay (ELISA) with the calculation of positivity coefficient (PC) according to manufacturer instructions. The test results were interpreted as positive when PC value was greater than 0.8.Results. The endomyocardial biopsy study detected HHV-6 antigen expression in 15 (60%) out of 25 enrolled patients including 10 cases with diagnosed HHV-6-positive myocarditis and five patients with carriage of viruses. According to IHC, the autoimmune HHV-6 myocarditis was confirmed in three cases (30%). The data of ELISA (n = 18) detected anti-HHV-6 IgM in 5 patients (28%) and anti-HHV-6 IgG in 11 cases (61%). The simultaneous presence of both anti-HHV-6 IgM and IgG was detected in two patients (11%). In addition, anti-HHV-6 IgM and IgG were absent in two (11%) cases. Eight patients (44%) with HHV-6-positive myocarditis included three patients (17%) tested positive for serum anti-HHV-6 IgM, three patients (17%) tested positive for serum anti-HHV-6 IgG, and two patients (11%) who had nether anti-HHV-6 IgM nor anti-HHV-6 IgG in blood serum. Among virus carriers, one patient (20%) was tested positive for anti-HHV-6 IgM and four patients (80%) were tested positive for anti-HHV-6 IgG. The patients without HHV-6 antigen expression (n = 5, 28%) included one patient (5.6%) tested positive for anti-HHV-6 IgM and two patients (11%) tested positive for anti-HHV-6 IgG. The entire sample of patients was divided into two groups depending on the serum level of anti-HHV-6 IgM: group 1 comprised patients tested positive for anti-HHV-6 IgM (n = 5); group 2 comprised patients (n = 13) tested negative for anti-HHV-6 IgM. Clinical and instrumental parameters differed only in the duration of CHF history, which was greater in group 1 than in group 2 (11.0 [8.0; 12.0] vs. 22.5 [14.5; 75.5] months, respectively (p = 0.045). The groups did not significantly differ in the studied markers in myocardial tissue according to the results of IHC analysis. No associations were found between the severity of HHV-6 antigen expression and serum levels of anti-HHV-6 IgM and IgG.Conclusion. Patients with ADHF and/or adverse LV remodeling after complete myocardial revascularization had higher percentage of HHV-6 antigen expression whose severity was not associated with the serum levels of anti-HHV-6 IgM and IgG.
Highlights
Heart failure (HF) is a long-term chronic condition that progressively worsens with time and leads to high hospitalization rate and over 50% mortality within five years
Inclusion criteria: Acute decompensated heart failure (ADHF); LVEF ≤ 40%; medical history of ischemic heart disease (IHD); not earlier than six months after optimal surgery (PCI or/and CABG) and optimal drug treatment for HF according to ESC guidelines
Among a total of 25 patients with ADHF and/or adverse left ventricular (LV) remodeling, we identified patients (n = 15, 63%) tested positive for human herpesvirus type 6 (HHV-6) according to endomyocardial biopsy (EMB) results (Table 2)
Summary
Heart failure (HF) is a long-term chronic condition that progressively worsens with time and leads to high hospitalization rate and over 50% mortality within five years. Acute decompensated heart failure (ADHF) accounts for more than one million hospitalizations in the USA [2]. The rate of ADHF reaches 50% [3] despite the advances in coronary revascularization and optimal medical therapy [4]. Chronic myocardial ischemia causes a vicious circle, activating compensatory neurohormonal and inflammatory mechanisms [6, 7], leading to the progression of HF, and resulting in ischemic cardiomyopathy. In recent years, numerous attempts aiming to improve the outcomes in patients with HF decompensation using therapeutic approaches were unsuccessful [9] suggesting the lack of complete understanding of HF pathophysiology
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