Because this is a retrospective cohort study of prognosis, it is subject to all of the limitations of such studies. Particularly, the prognosis of CAD could depend on therapeutic strategies selected by physicians. We observed, however, that there were no group differences in the frequency of coronary interventions performed during the follow-up (Table 3) and that the frequency of regular (3-blocking therapy was greater in group R. Thus, the adverse prognosis in patients with LF rise was not attributable to the insufficient implementation of effective therapies. canadianfamilypharmacy
It is unclear whether LF rise is involved in the pathophysiologic mechanism of death in patients with CAD or is merely characteristic of patients with poor prognosis. We observed that the LF rise is associated only with an increased risk for cardiac death but not for noncardiac death. Also, a survival analysis only for stroke death (n = 6) revealed no association of LF rise (data are not shown). Given that the causes of cardiac death in this study were acute myocardial infarction and sudden cardiac death, the LF rise may be associated with the progression of CAD or an increased susceptibility to fatal arrhythmia.
In the present study, we assessed HRV and its postural response under paced breathing, which may have affected the LF and its postural response. The use of paced breathing improves the accuracy of the assessment of cardiac vagal modulation through better separation of the LF and HF in frequency domain and through controlling the nonautonomic effects of respiratory frequency and tidal volume on the HF. However, in a previous study we observed that paced breathing reduced the LF with patients in the supine and tilt positions by 31% and 36%, respectively, and hence the postural LF response by a similar percentage. Thus, the results of our study, particularly the definition of groups by postural LF response, may be applicable only to HRV measures assessed under paced breathing.
Finally, we did not perform ambulatory electrocardiography in our patients. Although we observed that LF rise is a powerful predictor of cardiac mortality in patients with CAD, we were unable to examine whether our method is advantageous over long-term HRV analysis with ambulatory electrocardiography.
This study demonstrates that the postural response of HRV predicts the prognosis for stable patients with CAD. In particular, increased postural LF response (LF rise) is associated with an increased risk for cardiac death during long-term follow-up. The LF rise may reflect exaggerated ^-adrenergic activation and/or impaired cardiac vagal response in postural heart rate regulation. This study seems to add new evidence for the important involvement of autonomic nervous system function in the pathophysiology of CAD.