International journal of cardiology · 2009
Hyperoxic chemoreflex sensitivity is impaired in patients with neurocardiogenic syncope.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Meyer Christian, Rana Obaida R, Saygili Erol, Ozüyaman Burcin, Latz Katrin, Rassaf Tienush, Kelm Malte, Schauerte Patrick
Аннотация
BACKGROUND: During the development of neurocardiogenic syncope (NCS) postural dependant venous blood pooling sets off a cascade of autonomic reflexes. This causes an initial rise in sympathetic tone, which is followed by an overshoot parasympathetic activation resulting in systemic vasodilatation and/or sinus bradycardia. However, other factors like associated hyperventilation or changes in blood gas content may also contribute to syncope. Hyperoxic cardiac chemoreflex sensitivity (CHRS) is an autonomic functional test that describes the heart rate decrease in response to increases in blood oxygen content. The purpose of this study was to investigate whether CHRS is altered in NCS.
METHODS AND RESULTS: CHRS was compared in 16 NCS patients (49+/-4 yr old) vs. 16 age and gender matched controls (53+/-2 yr old). NCS was verified by clinical syncope and positive head-up tilt testing. The hyperoxic CHRS was measured by determination of the venous partial pressure of oxygen and heart rate before and after 5 min of pure oxygen inhalation. The difference of the R-R intervals before and after oxygen inhalation divided by the difference in the oxygen pressures were calculated as hyperoxic chemoreflex sensitivity [ms/mm Hg]. CHRS in the control group was 7.1+/-1.1 ms/mm Hg. By contrast, CHRS in NCS patients was significantly lower (2.8+/-1.0 ms/mm Hg; p<0.05).
CONCLUSION: Neurocardiogenic syncope is associated with decreased hyperoxic cardiac chemoreflex sensitivity possibly reflecting impaired deactivation of arterial chemoreceptors. The clinical and pathophysiologic importance of chemosensor function in neurocardiogenic syncope needs to be investigated in more detail.
METHODS AND RESULTS: CHRS was compared in 16 NCS patients (49+/-4 yr old) vs. 16 age and gender matched controls (53+/-2 yr old). NCS was verified by clinical syncope and positive head-up tilt testing. The hyperoxic CHRS was measured by determination of the venous partial pressure of oxygen and heart rate before and after 5 min of pure oxygen inhalation. The difference of the R-R intervals before and after oxygen inhalation divided by the difference in the oxygen pressures were calculated as hyperoxic chemoreflex sensitivity [ms/mm Hg]. CHRS in the control group was 7.1+/-1.1 ms/mm Hg. By contrast, CHRS in NCS patients was significantly lower (2.8+/-1.0 ms/mm Hg; p<0.05).
CONCLUSION: Neurocardiogenic syncope is associated with decreased hyperoxic cardiac chemoreflex sensitivity possibly reflecting impaired deactivation of arterial chemoreceptors. The clinical and pathophysiologic importance of chemosensor function in neurocardiogenic syncope needs to be investigated in more detail.