Abstract 16024: Elevated Bacterial Levels Measured by 16s rRNA PCR Correlate With Worsening Clinical Markers in Congestive Heart Failure
Background: It is well established that patients with CHF have increased inflammatory markers such as TNF, IL-6 and CRP. These changes are prognostic on EF, progression to higher NYHA class and death. However, the physiological mechanisms that underlie the increased inflammation in CHF patients remain unresolved. In CHF, elevated vascular pressures in the pulmonary and gut microcirculation can lead to increased bacterial translocation, which in turn can activate the immune system. We hypothesized that subclinical bacteria modulates the immune response observed with CHF and correlate with severity of CHF.
Methods: We studied 50 patients recruited from our cardiology and advanced heart failure clinics. Patients with active infections were excluded. A hybridization capture probe to selectively reduce interference from human DNA and PCR were used to detect DNA from the bacterial 16S rRNA gene. This method detects bacteria that do not grow in culture including partially degraded bacteria within circulating immune cells. Inflammatory markers were measured to study whether bacterial and cytokine levels correlate with various clinical parameters including NYHA class, EF and filling pressures.
Results: We found that patients with NYHA class III-IV symptoms have significantly higher bacterial levels, IL-6 and CRP compared to patients with NYHA class I-II symptoms. Patients with EF less than 25% have significantly higher bacterial levels and TNF than patients with EF greater than 25%.
We also found that bacterial levels, IL6, TNF and CRP are positively correlated with NYHA class, lower EF, CVP, admission for CHF, RV dysfunction and elevated pulmonary artery pressure.
Conclusions: Our results show that bacterial levels measured by 16s ribosomal RNA PCR correlate with increased cytokine production and clinical markers of CHF. These findings suggest that subclinical bacteria and immune activation may serve as potential clinical targets in worsening heart failure.
Author Disclosures: J. Weisbrot: None. T.S. Parker: None. S.D. Saal: None. D.M. Levine: None. S. Qui: None. E.M. Horn: None.
- © 2014 by American Heart Association, Inc.