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Influence of Age and Hemodynamics in Vasovagal Syncope
Quick Takes
- Cardioinhibition weakens with age, evidenced by a decrease in magnitude plus a longer duration and therefore a slower heart rate decrease and by fewer asystolic pauses.
- Vasodepression becomes more important with age and cardioinhibition less so, and basing pacing decisions on asystole only may not be ideal in the elderly.
- Assessing the relative roles of vasodepression and cardioinhibition may help avoid over-reliance on bradycardia detection while also improving the efficacy of pacing in VVS, through a re-evaluation of required hemodynamic effects.
Study Questions:
What are the age-related changes of vasodepression and cardioinhibition in tilt-induced vasovagal syncope (VVS)?
Methods:
The investigators studied 163 cases of tilt-induced VVS, evoked using the Italian protocol with blood pressure, heart rate, and video-electroencephalographic monitoring. Presyncope was excluded. Cardioinhibition was defined as the heart rate decrease before syncope; asystolic pauses (≥3 seconds) were divided into early and late asystole, i.e., beginning early enough or too late to be the major cause of loss of consciousness. The log-ratio method was used to quantify contributions of cardioinhibition and vasodepression, assessed in two 10-second periods before the onset of cardioinhibition and before syncope.
Results:
With increasing age, cardioinhibition decreased, i.e., heart rate decreased less and more slowly near syncope (p < 0.0001), while vasodepression increased. Asystolic pauses were less frequent in the older one-half of the group than the younger one-half (26% vs. 57%; p < 0.00001), but when it did, late asystole occurred more often (58% vs. 15%; p < 0.001). Differences were investigated using the Mann-Whitney U test for quantitative data and the chi-square test for count data. Spearman rank correlation was used to assess correlations.
Conclusions:
The authors reported that cardioinhibition-vasodepression balance should be considered in pacing decisions in older subjects with VVS.
Perspective:
This study reported that cardioinhibition weakens with age, evidenced by a decrease in magnitude plus a longer duration and therefore a slower heart rate decrease, and by fewer asystolic pauses. Furthermore, with increasing age, asystolic pauses started later relative to loss of consciousness. In short, asystole occurred less often with increased age, but when it did, it more often took the form of late asystole. Both effects mean that asystole was less likely to contribute to syncope in older than in younger patients. Overall, the study suggests that vasodepression becomes more important with age and cardioinhibition less so, and basing pacing decisions on asystole only may not be ideal in the elderly. Assessing the relative roles of vasodepression and cardioinhibition may help avoid over-reliance on bradycardia detection while also improving the efficacy of pacing in VVS, through a re-evaluation of required hemodynamic effects.
Clinical Topics: Arrhythmias and Clinical EP, Geriatric Cardiology, Prevention, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias
Keywords: Arrhythmias, Cardiac, Blood Pressure, Bradycardia, Electroencephalography, Geriatrics, Heart Arrest, Heart Rate, Hemodynamics, Secondary Prevention, Syncope, Syncope, Vasovagal, Unconsciousness
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