The HF was assessed with the same method and the same conditions as were used in a previous study in which we observed the strong correlation between the HF and the level of cardiac vagal tone as assessed by pharmacologic autonomic blockades. In the present study, however, we also observed that a decreased HF had no significant association with the risk for cardiac death and that its predictive power for noncardiac death disappeared after adjustment for cardiovascular risk factors and CAD severity. Cardiac vagal dysfunction may be associated with adverse medical conditions that have a poor prognosis, but this association could be the consequence of, at least in part, coexisting cardiovascular risks and/or disease severity.
Possible Mechanisms for Postural LF Rise
As to the autonomic neural mechanisms underlying the postural response of LF (ie, LF rise), we need to consider complex interactions between the following two factors: ^-adrenergic activation; and cardiac vagal withdrawal. canadian health and care mall
There is convincing evidence indicating the important involvement of ^-adrenergic sympathetic activation in the postural increase in LF. Studies have reported that the LF, particularly its normalized power, increases with the patient in the upright position and that the increase is suppressed by (3-blockade. In the present study, we observed that when the patients were grouped by postural LF response at baseline, those showing an LF rise (group R) were more frequently treated by (3-blockers during the follow-up (Table 5) and that the difference in cardiac mortality among the groups was enhanced after excluding those patients regularly treated by (3-blockers. Although the mean R-R interval at baseline was not short in group R, one may speculate that patients showing an LF rise may have presented clinical conditions in which (3-blocking therapy was beneficial and that (3-blocker therapy may have moderated the harmful effects of the LF rise. These speculations are consistent with the hypothesis that the LF rise reflects the exaggerated postural (3-adrenergic activation, which could lead to an adverse prognosis in stable patients with CAD.