BACKGROUND: B-type natriuretic peptide (BNP) determination is routinely used to evaluate the severity of congestive heart failure, a possible consequence of coronary artery disease (CAD). CAD originates from vascular atherosclerotic processes and is stimulated by inflammatory events, which may also be triggered by chronic bacterial infections. AIM: To explore the effect of Helicobacter pylori infection upon systemic BNP, tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels and linear homology between cardiac peptides and H pylori. METHODS: A group of 103 consecutive patients with a diagnosis of non-ST elevation acute CAD (ACAD) and no other concomitant pathology was examined. BNP was measured by a commercial solid-phase sandwich immunoradiometric assay. H pylori infection, CagA serological status and circulating levels of IL-6 and TNF-α, were determined by ELISA assays. Amino acid sequence homology between human cardiac and H pylori peptides was investigated by Basic Local Alignment Search Tool (BLAST) analysis. RESULTS: Circulating levels of BNP and IL-6, in pg/mL (interquartile difference), among infected patients with anti-CagA serum antibodies, respectively 781 (1899) and 37.7 (137.6), were significantly increased in respect to those measured in uninfected patients, respectively 325 (655) and 7.7 (23.5), (p<0.01 and p=0.025), and, with regard to BNP alone, also in patients infected by CagA negative H pylori strains, 305 (593), (p<0.01). TNF-α levels were raised in CagA positive in respect to uninfected patients. Tropomyosin and Ca2+ transporting ATPases showed strong similarities to H pylori proteins, suggesting the existence of molecular mimicry phenomena. CONCLUSIONS: Chronic infection by H pylori expressing CagA correlates with high circulating levels of BNP and IL-6 in patients with ACAD.
Cross-sectional study: CagA-positive helicobacter pylori infection, acute coronary artery disease and systemic levels of B-type natriuretic peptide
VAIRA, BERARDINO;
2014
Abstract
BACKGROUND: B-type natriuretic peptide (BNP) determination is routinely used to evaluate the severity of congestive heart failure, a possible consequence of coronary artery disease (CAD). CAD originates from vascular atherosclerotic processes and is stimulated by inflammatory events, which may also be triggered by chronic bacterial infections. AIM: To explore the effect of Helicobacter pylori infection upon systemic BNP, tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels and linear homology between cardiac peptides and H pylori. METHODS: A group of 103 consecutive patients with a diagnosis of non-ST elevation acute CAD (ACAD) and no other concomitant pathology was examined. BNP was measured by a commercial solid-phase sandwich immunoradiometric assay. H pylori infection, CagA serological status and circulating levels of IL-6 and TNF-α, were determined by ELISA assays. Amino acid sequence homology between human cardiac and H pylori peptides was investigated by Basic Local Alignment Search Tool (BLAST) analysis. RESULTS: Circulating levels of BNP and IL-6, in pg/mL (interquartile difference), among infected patients with anti-CagA serum antibodies, respectively 781 (1899) and 37.7 (137.6), were significantly increased in respect to those measured in uninfected patients, respectively 325 (655) and 7.7 (23.5), (p<0.01 and p=0.025), and, with regard to BNP alone, also in patients infected by CagA negative H pylori strains, 305 (593), (p<0.01). TNF-α levels were raised in CagA positive in respect to uninfected patients. Tropomyosin and Ca2+ transporting ATPases showed strong similarities to H pylori proteins, suggesting the existence of molecular mimicry phenomena. CONCLUSIONS: Chronic infection by H pylori expressing CagA correlates with high circulating levels of BNP and IL-6 in patients with ACAD.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
