Methods: CBF was measured with the 133-Xenon method in 12 patients (coronary artery diesease: N = 8; previous myocardits: N = 4) with implanted pacemakers (DDD-mode: N = 7; WI-mode: N = 5) during control conditions at a heart rate of 50 to 70 ppm (A). Regulation of CBF was tested by the 5 % carbon dioxide inhalation test which normally induces a marked CBF increase due to the arterial hypercapnia (B). In addition, CBF was measured during cardiac pacing at a heart rate of 120 to 130 ppm (C).
Results: Measurements were performed during normotension and arterial normoxia. Mean values of CBF in group A, B and C were 70 ± 7, 94 ± 10 and 68 ± 8 ml/100 g/min, respectively. In group B a uniform, significant increase of CBF was observed in all patients (p ≤ 0.01). In group C different CBF-responses were found: a slight CBF increase of 5 % (n = 4), a distinct CBF increase of 15 to 20 % (n = 2), no changes of CBF (n = 5), a CBF reduction of 18 % (n = 1).
Conclusions: A significant CBF increase during rapid pacing indicates an impairment of CBF regulation. We suggest that the analysis of brain perfusion with the CO2 inhalation test and during increased heart rate will indentify the patients with permanent pacemakers who had neurological symptoms due to cerebrovascular dysfunction. Basic heart rate was elevated from 50 to 80 ppm in patients with a distinct CBF-increase during the rapid pacing test. Then, neurological symptoms were not observed during a 18 month follow-up in those patients.