Introduction: It is common to find people sent to perform a Head Up Tilt Test (HUT) who suffered a single syncope, or syncopes that occur during certain periods and never appear again. We wonder how these people are d...Introduction: It is common to find people sent to perform a Head Up Tilt Test (HUT) who suffered a single syncope, or syncopes that occur during certain periods and never appear again. We wonder how these people are different from those who have never had syncope. Methods: We found 300 patients who suffered only one (unique) or a maximum of 5 vasovagal syncopes during their life. And their HUT was positive for vasovagal dysautonomia. We compared them, with 120 healthy volunteers who have never had syncope. We try to explain how some constitutional predisposing factors act in these patients, and are associated with environmental triggers to precipitate the syncope. Results: We found differences between cases and controls in predisposing factors such as: heredity, joint hypermobility, baroreflex failure, venous compliance and some neurological diseases. Then an environmental factor acts as a trigger for syncope: prolonged standing, stress, pain and emotions, dehydration, use of certain drugs, abundant food. Conclusions: There are people with minimally expressed vasovagal dysautonomia who have an organic predisposition to present vasovagal syncopes (heredity, joint hypermobility, baroreflex failure, venous compliance, some neurological diseases, etc.). But this predisposition is not enough by itself to produce syncopes. One or more environmental factors must be added, acting as a trigger that would be the reason why these episodes are so infrequent.展开更多
文摘Introduction: It is common to find people sent to perform a Head Up Tilt Test (HUT) who suffered a single syncope, or syncopes that occur during certain periods and never appear again. We wonder how these people are different from those who have never had syncope. Methods: We found 300 patients who suffered only one (unique) or a maximum of 5 vasovagal syncopes during their life. And their HUT was positive for vasovagal dysautonomia. We compared them, with 120 healthy volunteers who have never had syncope. We try to explain how some constitutional predisposing factors act in these patients, and are associated with environmental triggers to precipitate the syncope. Results: We found differences between cases and controls in predisposing factors such as: heredity, joint hypermobility, baroreflex failure, venous compliance and some neurological diseases. Then an environmental factor acts as a trigger for syncope: prolonged standing, stress, pain and emotions, dehydration, use of certain drugs, abundant food. Conclusions: There are people with minimally expressed vasovagal dysautonomia who have an organic predisposition to present vasovagal syncopes (heredity, joint hypermobility, baroreflex failure, venous compliance, some neurological diseases, etc.). But this predisposition is not enough by itself to produce syncopes. One or more environmental factors must be added, acting as a trigger that would be the reason why these episodes are so infrequent.
