Key result
NSVT-derived sympathetic gain closely correlates with Valsalva-derived gain, indicating analogous arterial pressure recovery.
Why the study?
Sympathetic baroreflex gain can be calculated from sympathetic nerve activity but this method is not available in practice, prompting evaluation of alternative non-invasive methods.
Does NSVT-derived sympathetic gain correlate with Valsalva manoeuvre-derived sympathetic gain in subjects without significant cardiovascular disease?
Observational (n=25)
Does NSVT-derived sympathetic gain correlate with Valsalva manoeuvre-derived sympathetic gain in subjects without significant cardiovascular disease?
Sympathetically mediated arterial pressure recovery following paced NSVT correlates closely with that following Valsalva manoeuvre, suggesting NSVT-derived indices may be useful for assessing baroreflex sensitivity in patients with implanted antiarrhythmic devices.
Answers are grounded in this paper and cite their sources.
NSVT- or VM-derived sympathetic gain correlates closely; leaves open non-invasive baroreflex assessment pending larger validation studies.
AIMS: Abnormalities of the sympathetic baroreflex regulation are documented in various diseases. The recording of sympathetic nerve activity allows for the calculation of baroreflex gain but this is not available in practice. A non-invasive method based on blood pressure during the late phases of Valsalva manoeuvre (VM) was proposed. Sympathetic gain could be calculated from the pressure fluctuations following ventricular extrasystole or non-sustained ventricular tachycardia (NSVT). METHODS AND RESULTS: We assessed both indices in 25 subjects with no significant cardiovascular disease. VM was performed at 40 mmHg for 12 s. Paced NSVT consisted of five to six cycles. The sympathetic gains were determined based on the recovery of mean arterial pressure (MAP, mmHg/s). The maximum slope of five consecutive MAP elevations occurring within a 15-cycle period after NSVT was calculated. This MAP turbulence slope (MAP(TS)) was expressed in mmHg/cycle. Five patients were excluded because of unacceptable VM. VM-derived sympathetic gain (SBRS(vals)) and the NSVT-derived gain (SBRS(NSVT)) correlated closely (R = 0.86, P < 0.001). Their mean difference was 3.2 +/- 4.8 mmHg. Both SBRS(vals) and SBRS(NSVT) correlated closely with MAP(TS) (R = 0.77, P < 0.001 and R = 0.86, P < 0.001, respectively). CONCLUSION: The sympathetically mediated arterial pressure recovery is an analogous process following both VM and NSVT. SBRS(NSVT) or MAP(TS) may be useful in the assessment of patients with implanted antiarrhythmic devices.
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Makai et al. (2010) conducted an observational in No significant cardiovascular disease (n=25). Non-sustained ventricular tachycardia (NSVT)-derived sympathetic gain vs. Valsalva manoeuvre (VM)-derived sympathetic gain was evaluated on Correlation between VM-derived sympathetic gain (SBRS(vals)) and NSVT-derived gain (SBRS(NSVT)) (R = 0.86, p=< 0.001). NSVT-derived sympathetic gain correlated closely with Valsalva-derived sympathetic gain (R = 0.86, P < 0.001), indicating analogous sympathetically mediated arterial pressure recovery.
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