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      Correlation of Postural Blood Pressure Test and Head-Up Tilt Table Test in Patients with Vasovagal Syncope


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          Background: Vasovagal syncope is triggered by complex cerebral and cardiovascular reflex mechanisms leading to general vasodilatation and bradycardia resulting in cerebral hypoperfusion. Methods: We prospectively studied the correlation of postural blood pressure test (PBT) and head-up tilt table test (TT) in patients with recurrent vasovagal syncope. Sixty-eight patients (37 male, 52.4 ± 18.6 years) were included in the trial. They were asked to participate in a PBT and a TT. Independent samples t-test, ANOVA and Fisher’s exact test were used for statistical analysis. p values <0.05 were considered statistically significant. Results: Thirty patients (44%) showed a positive TT and thirty-four patients (50%) had a positive PBT. PBT did not show any correlation with TT, although pathophysiological mechanisms in vasovagal syncope and orthostatic hypotension are supposed to be similar. Furthermore neither TT nor PBT nor their combination had any predictive value for the patient’s risk of syncope recurrence. Conclusions: TT and PBT are not correlated with each other. Both investigations cannot predict the patient’s risk of syncope recurrence.

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          Most cited references 15

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          Pathophysiological basis of orthostatic hypotension in autonomic failure.

          In patients with autonomic failure orthostatic hypotension results from an impaired capacity to increase vascular resistance during standing. This fundamental defect leads to increased downward pooling of venous blood and a consequent reduction in stroke volume and cardiac output that exaggerates the orthostatic fall in blood pressure. The location of excessive venous blood pooling has not been established so far, but present data suggest that the abdominal compartment and perhaps leg skin vasculature are the most likely candidates. To improve the orthostatic tolerance in patients with autonomic failure, protective measures that reduce excessive orthostatic blood pooling have been developed and evaluated. These measures include physical counter-manoeuvres and abdominal compression.
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            Guidelines on management (diagnosis and treatment) of syncope--update 2004.

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              Evaluation and outcome of emergency room patients with transient loss of consciousness.

              We identified 198 patients who presented to our emergency room with transient loss of consciousness. Seizures (29 percent of patients) and vasovagal/psychogenic episodes (40 percent of patients) were the most common presumptive causes of loss of consciousness, but the cause of loss of consciousness remained uncertain even at follow-up in 11 +/- 6 months in 13 percent of the patients. The history and physical examinations were sufficient for diagnosis in 85 percent of the patients in whom a diagnosis could be established. These data guided inpatient and outpatient with potentially dangerous causes of loss of consciousness except for one patient who had pulmonary embolism. In selected patient, diagnostic tests such as blood chemistries (three patients), electrocardiograms (four patients) electroencephalograms (three patients), and Holter monitoring (four patients) provided crucial information, and CT scans identified new brain tumors in four patients with focal neurologic presentations. At the time of follow-up, 7.5 percent of patients had suffered either major morbidity or death related to the cause of the index episode of loss of consciousness. Patients with cardiac causes represented a high risk (33 percent) group for such poor outcome, whereas patients who were under age 30, or who were under age 70 and had loss of consciousness on a vasovagal/psychogenic or unknown basis, constituted a low risk (1 percent) subgroup.

                Author and article information

                S. Karger AG
                May 2007
                05 February 2007
                : 107
                : 4
                : 380-385
                Department of Cardiology, Heart Centre, University Hospital Hamburg-Eppendorf, Hamburg, Germany
                99056 Cardiology 2007;107:380–385
                © 2007 S. Karger AG, Basel

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                Figures: 1, Tables: 5, References: 30, Pages: 6
                Original Research


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