Acute haemodynamic effects of AV-synchronous pacemaker stimulation in patients with congestive heart failure and left bundle branch block.

INTRODUCTION: The therapeutical limits of drug and surgical therapy for severe chronic heart failure make the research for adjunctive treatment options necessary. After the positive effects of AV-synchronous pacemaker stimulation in patients with dilatative cardiomyopathy and 1st degree AV-block, this study was to evaluate the benefit of transient pacemaker stimulation in patients with dilated cardiomyopathy and left bundle branch block. METHODS AND PATIENTS: 19 patients (14 male, 5 female, age 60 +/- 8 yrs) were included in the study. Inclusion criteria were congestive heart failure, stage NYHA III or greater and left bundle branch block. Transient stimulation of the myocardium was applied via two electrodes (right atrium and right ventricle) in VDD mode, whereby a series of AV-delay-times between 80 and 180 ms was tested. Thermodilution was used to determine cardiac output, pulmonary capillary pressure and pulmonary arterial pressure. RESULTS: In 16 patients, pacemaker stimulation led to a significant increase of cardiac output (3.8 +/- 0.5 l/min to 4.6 +/- 0.5 l/min; p < 0.002), cardiac index (1.90 +/- 0.20 l/min/m2 to 2.3 +/- 0.2 l/min/m2; p < 0.002) and of stroke volume (51 +/- 8 ml to 62 +/- 6 ml; p < 0.002) as well as a significant reduction of mean pulmonary capillary pressure (19 +/- 1 mmHg to 15 +/- 1 mmHg; p < 0.01). The mean pulmonary arterial pressure remained unchanged. Three patients did not benefit from the treatment. CONCLUSION: AV-sequential pacemaker-stimulation (right ventricular electrode placement) can be a valuable adjunctive therapy in selected patients with late stage congestive heart failure and left bundle branch block.

Prevalence of Helicobacter pylori infection in coronary artery disease and effect of its eradication on coronary lumen reduction after percutaneous coronary angioplasty.

BACKGROUND: Gastric infection caused by Helicobacter pylori has recently been associated with increased risk of coronary artery disease. AIM: To: 1) determine seroprevalence of Helicobacter pylori and its cytotoxin associated gene A in patients with/without coronary artery disease (group A), 2) assess influence of Helicobacter pylori eradication on coronary artery lumen reduction after percutaneous coronary angioplasty (group B) and 3) determine influence of Helicobacter pylori eradication on plasma cytokines, lipids and coagulation factors in patients subjected to percutaneous coronary angioplasty (group B). PATIENTS AND METHODS: Group A included 100 patients with coronary artery disease (subgroup 1) and 100 patients without (subgroup II). For Helicobacter pylori seroprevalence, plasma anti-Helicobacter pylori and anti-cytotoxin associated gene A IgG were examined. Group B included 40 patients with significant single-vessel coronary arterial disease and Helicobacter pylori infection confirmed by 13C-urea breath test and serologically using anti-Helicobacter pylori and anti-cytotoxin associated gene A IgG. Six months after percutaneous coronary angioplasty and triple anti-Helicobacter pylori therapy, the Helicobacter pylori status reassessed by urea breath test was negative in all but two patients of subgroup I subjected to Helicobacter pylori therapy. Coronary angiography and laboratory tests were repeated in both subgroups of group B included in the trial and reduction in coronary artery lumen in these subgroups was compared to baseline after percutaneous coronary angioplasty considered as 100%. RESULTS: Helicobacter pylori seropositivity reached 81.5% of coronary artery disease (subgroup I) and was significantly higher than that in controls without coronary artery disease (subgroup II) (51%), the odds ratio being 4.3 for Helicobacter pylori in coronary artery disease. Cytotoxin associated gene A IgG detection was also significantly higher (47.3%) in coronary artery disease than in controls (28%) giving the odds ratio about 2.3. Mean coronary artery lumen reduction in patients undergoing percutaneous coronary angioplasty + Helicobacter pylori eradication therapy (subgroup I) was significantly (p<0.05) smaller compared to percutaneous coronary angioplasty + placebo-treated subgroup II (22% vs 41%). CONCLUSIONS: 1) There is a significant link between coronary artery disease and infection with Helicobacter pylori, especially expressing CagA proteins, 2) Helicobacter pylori eradication significantly attenuates reduction in coronary artery lumen in coronary artery disease patients after percutaneous coronary angioplasty possibly by elimination of chronic inflammation and decline in proinflammatory cytokine release, and 3) Infection of Chlamydia pneumoniae in these percutaneous coronary angioplasty patients is not affected by eradication therapy.