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Association of inflammatory gene polymorphisms with mechanical heart valve reoperation.

ABSTRACT: BACKGROUND:Various complications lead to reoperation in patients who undergo prosthetic valve replacement where inflammatory process could be involved. The goals of this study were to identify risk factors that correlate with reoperation in patients with prosthetic heart valves and to investigate the relationship between reoperation and inflammatory gene polymorphisms. RESULTS:The study included 228 patients from the EwhA-Severance Treatment Group of Warfarin. Single nucleotide polymorphisms of c-reactive protein (CRP), interferon-gamma, interleukin 1 beta, interleukin 6, interleukin 10, transforming growth factor beta 1, and tumor necrosis factor genes were genotyped by means of SNaPshot and TaqMan assays. Thirty-nine patients (17.1 %) underwent more than one heart valve operation. A threefold increased risk for heart valve reoperation was evident in homozygous variant-type (TT) carriers as compared with ancestral allele carriers of CRP rs1205. Logistic regression analysis revealed that CRP rs1205 (OR 2.68, 95 % CI 1.22-5.90, p = 0.014), valve position (mitral valve OR 2.80, 95 % CI 1.01-7.80, p = 0.048; tricuspid valve OR 9.24, 95 % CI 2.46-34.70, p = 0.001; reference: aortic valve) and time after first operation (OR 1.13, 95 % CI 1.06-1.20, p < 0.001) affected the risk of reoperation. CONCLUSIONS:Inflammatory gene polymorphisms could be a possible marker of risk for reoperation in patients with prosthetic heart valve surgery.

SUBMITTER: Lee KE

PROVIDER: S-EPMC4929098 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Association of inflammatory gene polymorphisms with mechanical heart valve reoperation.

Lee Kyung Eun KE Kim Joo Hee JH Chung Jee Eun JE Lee Gwan Yung GY Cho Yoon Jeong YJ Chang Byung Chul BC Gwak Hye Sun HS

SpringerPlus 20160630 1

<h4>Background</h4>Various complications lead to reoperation in patients who undergo prosthetic valve replacement where inflammatory process could be involved. The goals of this study were to identify risk factors that correlate with reoperation in patients with prosthetic heart valves and to investigate the relationship between reoperation and inflammatory gene polymorphisms.<h4>Results</h4>The study included 228 patients from the EwhA-Severance Treatment Group of Warfarin. Single nucleotide po ...[more]

PMID: 27386381

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Project description:ImportanceCytokine release syndrome is a complication of coronavirus disease 2019. Clinically, advanced age and cardiovascular comorbidities are the most important risk factors.ObjectiveTo determine whether clonal hematopoiesis of indeterminate potential (CHIP), an age-associated condition with excess cardiovascular risk defined as the presence of an expanded, mutated somatic blood cell clone in persons without other hematological abnormalities, may be associated with an inflammatory gene expression sensitizing monocytes to aggravated immune responses.Design, setting, and participantsThis hypothesis-generating diagnostic study examined a cohort of patients with severe degenerative aortic valve stenosis or chronic postinfarction heart failure, as well as age-matched healthy control participants. Single-cell RNA sequencing and analyses of circulating peripheral monocytes was done between 2017 and 2019 to assess the transcriptome of circulating monocytes.ExposuresSevere degenerative aortic valve stenosis or chronic postinfarction heart failure.Main outcomes and measuresCHIP-driver sequence variations in monocytes with a proinflammatory signature of genes involved in cytokine release syndrome.ResultsThe study included 8 patients with severe degenerative aortic valve stenosis, 6 with chronic postinfarction heart failure, and 3 healthy control participants. Their mean age was 75.7 (range, 54-89) years, and 6 were women. Mean CHIP-driver gene variant allele frequency was 4.2% (range, 2.5%-6.9%) for DNMT3A and 14.3% (range, 2.6%-37.4%) for TET2. Participants with DNMT3A or TET2 CHIP-driver sequence variations displayed increased expression of interleukin 1β (no CHIP-driver sequence variations, 1.6217 normalized Unique Molecular Identifiers [nUMI]; DNMT3A, 5.3956 nUMI; P < .001; TET2, 10.8216 nUMI; P < .001), the interleukin 6 receptor (no CHIP-driver sequence variations, 0.5386 nUMI; DNMT3A, 0.9162 nUMI; P < .001;TET2, 0.5738 nUMI; P < .001), as well as the NLRP3 inflammasome complex (no CHIP-driver sequence variations, 0.4797 nUMI; DNMT3A, 0.9961 nUMI; P < .001; TET2, 1.2189 nUMI; P < .001), plus upregulation of CD163 (no CHIP-driver sequence variations, 0.5239 nUMI; DNMT3A, 1.4722 nUMI; P < .001; TET2, 1.0684 nUMI; P < .001), a cellular receptor capable of mediating infection, macrophage activation syndrome, and other genes involved in cytokine response syndrome. Gene ontology term analyses of regulated genes revealed that the most significantly upregulated genes encode for leukocyte-activation and interleukin-signaling pathways in monocytes of individuals with DNMT3A (myeloid leukocyte activation: log[Q value], -50.1986; log P value, -54.5177; regulation of cytokine production: log[Q value], -21.0264; log P value, -24.1993; signaling by interleukins: log[Q value], -18.0710: log P value, -21.1597) or TET2 CHIP-driver sequence variations (immune response: log[Q value], -36.3673; log P value, -40.6864; regulation of cytokine production: log[Q value], -13.1733; log P value, -16.3463; signaling by interleukins: log[Q value], -12.6547: log P value, -15.7977).Conclusions and relevanceMonocytes of individuals who carry CHIP-driver sequence variations and have cardiovascular disease appear to be primed for excessive inflammatory responses. Further studies are warranted to address potential adverse outcomes of coronavirus disease 2019 in patients with CHIP-driver sequence variations.

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Association of inflammatory gene polymorphisms with mechanical heart valve reoperation.

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Association of inflammatory gene polymorphisms with mechanical heart valve reoperation.

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