Elevated Homocysteine Levels in Patients with Slow Coronary Flow: Relationship with Helicobacter pylori Infection

Background and objective:  Elevation of plasma homocysteine (Hcy) level has been implicated in the pathogenesis of slow coronary flow (SCF) as it can severely disturb vascular endothelial function. Helicobacter pylori chronically infect the human stomach and causes malabsorption of vitamin B12 and folate in food, leading ultimately to an increase in circulating Hcy levels. Methods:  Forty-three patients with angiographically proven SCF (group I) were enrolled in this study; 43 cases with normal coronary flow pattern (group II) served as controls. Fasting plasma levels of Hcy, vitamin B12, and folate were measured in all subjects. Presence of H. pylori infection was defined as positive 14 C urea breath test. Coronary flow patterns for each major epicardial coronary artery were determined with the Thrombolysis in Myocardial Infarction (TIMI) frame count method. Results:  Mean TIMI frame count was 46.3 ± 8.7 in group I and 24.3 ± 2.9 in Group II (p = .0001). Vitamin B12 levels were similar, whereas folate levels were dramatically reduced in group I compared to group II (13.2 ± 4.3 vs. 17.1 ± 5.2, p = .0001). Plasma Hcy levels were significantly higher in group I compared to group II (13.4 ± 5.6 vs. 7.9 ± 2.5, p = .0001) as was the prevalence of H. pylori infection (90.7% in group I vs. 58.1% in group II, p = .001). Hcy levels were elevated (11.7 ± 5.3 vs. 7.5 ± 2.7, p = .0001) and folate levels were reduced (13.9 ± 4.7 vs. 18.6 ± 4.9, p = .0001) in patients with H. pylori infection, while vitamin B12 levels were similar in patients with and without H. pylori infection. Correlation analysis revealed a significant negative correlation between plasma folate and Hcy levels and also between folate levels and mean TIMI frame counts (r = –.33, p = .002 vs. r = –.33, p = .003). Moreover, there was a significant positive correlation between plasma Hcy levels and mean TIMI frame counts (r = .66, p = .0001). In addition, the folate level was the only significant determinant of the variance of Hcy in multiple regression analysis (r = –.21, p = .03). Conclusion:  Our data showed that plasma folate levels were decreased and plasma Hcy levels were increased in patients with SCF compared to controls. Also, the prevalence of H. pylori infection was increased in patients with SCF. These findings suggest that elevated levels of plasma Hcy, possibly caused by H. pylori infection, and/or a possible disturbance in its metabolism may play a role in the pathogenesis of SCF.