Helicobacter cinaedi (H. cinaedi) is a Gram-negative curved motile rod that causes bloodstream or enteric infections. It was suggested that H. cinaedi was involved in the progression of atherosclerosis. We aimed to investigate the presence of H. cinaedi DNA using a nested-polymerase chain reaction (PCR) in atheroma plaques from patients with atherosclerosis-induced vascular diseases. A total of 129 patients diagnosed with valvular heart disease due to atherosclerosis and 146 patients with non-atherosclerotic post-stenotic dilatation were included as the patient and the control groups, respectively. The ATCC BA847 H. cinaedi strain was used as the positive control for the nested-PCR method. We investigated H. cinaedi DNA in our study groups using the nested-PCR method and detected only six H. cinaedi DNA (4.65%) in the 129 atherosclerotic patient group. We detected significant difference between patient and control groups with respect to the presence of H. cinaedi on the basis of Fischer’s exact test (p = 0.010) by univariate analysis. Age (OR: 1.042, p = 0.016), total cholesterol (≥200 mg/dL) (OR: 1.849, p = 0.0001), and high-density lipoprotein (≥50 mg/dL) (OR: 0.745, p = 0.039) levels were detected as independent variables for the risk of atherosclerosis development in the patient group. The presence of H. cinaedi was not detected as an independent variable in a multivariate analysis. Previous studies suggested that H. cinaedi-induced oral infections might translocate to vascular tissue and induce chronic inflammation in the aorta, which subsequently may lead to atherosclerotic plaque formation. In conclusion, we could not suggest that there is a causal relationship between H. cinaedi and the development of atherosclerosis. However, age (OR: 1.042), total cholesterol (≥200 mg/dL, OR: 1.849), and high-density lipoprotein (≥50 mg/dL, OR: 0.745, as protective) levels have a significant role in the pathogenesis of atherosclerosis development. We also suggest that the presence of H. cinaedi may contribute to the risk of atherosclerosis development due to the univariate comparison result.
