Vasovagal syncope is common in young adults, affecting up to 40% of subjects in this age group, with a female predominance.1 Its pathogenesis is not clear, but the main theory suggests a central role of the orthostatic venous pooling below the thorax, which leads to paradoxical activation of the cardio-neural inhibitory reflexes by the underfilled ventricles.2 We have occasionally seen dilated inferior vena cava (IVC) on echocardiograms of young patients with vasovagal syncope referred for cardiac evaluation. Since this observation could have pathophysiologic significance, we decided to design a study to measure the IVC diameter in a group of young adults with a history of vasovagal syncope.
On the basis of the results of the questionnaires distributed among medical students, we identified 53 subjects with typical vasovagal syncope or near-syncope in their medical history (mean number of episodes, 5; range, 1-23). The control group comprised 50 age- and sex-matched subjects from the same population, without any syncope or orthostatic symptoms in the past. Athletes and persons with cardiovascular disease or medications were not included in the study. The IVC diameter was assessed through echocardiography (IE33; Philips, Andover, Massachusetts). Studies were performed with subjects in the supine position by a physician unaware of subject's diagnosis. The IVC was measured in longitudinal plane from the subcostal view. Maximal end-expiratory diameter (during normal breathing) from the distal 5 cm of IVC near the cavo-atrial junction was measured. Statistical analysis was performed using Statistica 6 software (StatSoft Inc, Tulsa, Oklahoma). The unpaired t test was used for comparison of continuous variables and Fisher exact test for comparison of categorical variables. Repeated measurements of IVC size were performed in 20 subjects after 1 month, and the coefficient of repeatability was calculated as 2 standard deviations of the differences. The study was accepted by the local ethics committee, and the subjects gave informed consent.
Characteristics of the studied groups is presented in the Table. There were no significant cardiac abnormalities on echocardiography in any of the subjects. The mean IVC diameter and IVC diameter indexed for body surface area were significantly larger in subjects with vasovagal syncope than in the controls (24.6 vs 21.3 mm and 14.4 vs 12.6 mm/m2, respectively [P < .001]). The sensitivity of IVC diameter equal or above 24 mm for predicting the history of vasovagal syncope was 72% and the specificity, 82%. Intersession coefficient of repeatability for IVC size was 2.64 mm.
Our results suggest that IVC may play a role in the pathogenesis of vasovagal syncope. We propose that in healthy subjects (without volume overload, pericardial disease, and right heart abnormalities), dilated IVC may be a marker of decreased abdominal venous tone and/or increased compliance. This may lead to exaggerated abdominal venous pooling during standing and subsequently orthostatic symptoms. Our hypothesis is in accordance with the results of the study, which showed a relative increase in splanchnic (but not pelvic and leg) blood volume during tilt test in patients with syncope compared with controls.3 In another study, compression of the abdomen was more effective in preventing orthostatic symptoms than compression of the legs in patients with orthostatic intolerance,4 which may suggest a main role of the abdominal venous pool in orthostatic hypotension.
Our second observation shows that IVC diameter in young, healthy adults, without cardiac pathologic conditions, is frequently above 20 mm—commonly regarded as an upper limit of normal and a noninvasive indication of increased right atrial pressure in patients with cardiac or renal disease.5 In another study, IVC was also dilated in most competitive young athletes without heart disease.6 Thus, it seems that dilated IVC should not be used as an indicator of increased right atrial pressure in healthy young adults.
Correspondence: Dr Styczynski, Department of Internal Medicine, Hypertension and Angiology, Medical University of Warsaw, Banacha 1a, 02-097 Warsaw, Poland (firstname.lastname@example.org).
Author Contributions:Study concept and design: Styczynski and Szmigielski. Acquisition of data: Styczynski, Jaltuszewska, Kosiorowska, and Kostrzewska. Analysis and interpretation of data: Styczynski, Jaltuszewska, Kosiorowska, Kostrzewska, and Szmigielski. Drafting of the manuscript: Styczynski and Szmigielski. Critical revision of the manuscript for important intellectual content: Styczynski, Jaltuszewska, Kosiorowska, Kostrzewska, and Szmigielski. Statistical analysis: Styczynski, Jaltuszewska, Kosiorowska, Kostrzewska, and Szmigielski. Administrative, technical, and material support: Styczynski, Jaltuszewska, Kosiorowska, and Kostrzewska. Study supervision: Styczynski.
Financial Disclosure: None reported.
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