Abstract
BackgroundJugular venous reflux (JVR) has been reported to cause cough syncope via retrograde-transmitted venous hypertension and consequently decreased cerebral blood flow (CBF). Unmatched frequencies of JVR and cough syncope led us to postulate that there should be additional factors combined with JVR to exaggerate CBF decrement during cough, leading to syncope. The present pilot study tested the hypothesis that JVR, in addition to an increased level of plasma endothelin-1 (ET-1), a potent vasoconstrictor, is involved in the pathophysiology of cough syncope.MethodsSeventeen patients with cough syncope or pre-syncope (Mean[SD] = 74.63(12.37) years; 15 males) and 51 age/gender-matched controls received color-coded duplex ultrasonography for JVR determination and plasma ET-1 level measurements.ResultsMultivariate logistic analysis showed that the presence of both-side JVR (odds ratio [OR] = 10.77, 95% confident interval [CI] = 2.40-48.35, p = 0.0019) and plasma ET-1 > 3.43 pg/ml (OR = 14.57, 95% CI = 2.95-71.59, p = 0.001) were independently associated with the presence of cough syncope/ pre-syncope respectively. There was less incidence of cough syncope/ pre-syncope in subjects with the absence of both-side JVR and a plasma ET-1 ≦3.43 pg/ml. Presence of both side JVR and plasma ET-1 level of > 3.43 pg/ml, increased risk for cough syncope/pre-syncope (p < 0.001).ConclusionsJVR and higher plasma levels of ET-1 are associated with cough syncope/ pre-syncope. Although sample size of this study was small, we showed a synergistic effect between JVR and plasma ET-1 levels on the occurrence of cough syncope/pre-syncope. Future studies should confirm our pilot findings.
Highlights
Jugular venous reflux (JVR) has been reported to cause cough syncope via retrograde-transmitted venous hypertension and decreased cerebral blood flow (CBF)
ET-1 levels have been shown as elevated in the plasma and cerebrospinal fluid (CSF) of subarachnoid hemorrhage (SAH) patients, with the presence of elevated ET-1 levels correlating with the persistence of cerebral vasospasm [4,6,7]
Endothelial dysfunction with imbalanced releases of nitric oxide (NO) and ET-1 has been recognized in chronic obstructive pulmonary disease (COPD); those populations have been found with more frequent cough syncope [9,10]
Summary
Jugular venous reflux (JVR) has been reported to cause cough syncope via retrograde-transmitted venous hypertension and decreased cerebral blood flow (CBF). Unmatched frequencies of JVR and cough syncope led us to postulate that there should be additional factors combined with JVR to exaggerate CBF decrement during cough, leading to syncope. The present pilot study tested the hypothesis that JVR, in addition to an increased level of plasma endothelin-1 (ET-1), a potent vasoconstrictor, is involved in the pathophysiology of cough syncope. A lesser degree of compromised cerebral blood flow (CBF) may lead to pre-syncope symptoms, such as wooziness, light-headedness, nearly fainting sensation and/or visual dimming. Endothelin-1 (ET-1) is a potent vasoconstrictor peptide derived from vascular endothelial cells [3]. Endothelial dysfunction with imbalanced releases of NO and ET-1 has been recognized in chronic obstructive pulmonary disease (COPD); those populations have been found with more frequent cough syncope [9,10]
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