Neurocardiogenic Syncope

gering events or prodromal symptoms. The diagnosis of the non-classical form is based on the exclusion of other causes of syncope and a positive response to tilt table testing [5] . While the tilt table test is the diagnostic gold standard, pharmacologic provocation to increase sensitivity of the test is often employed. The complexity of the pathophysiology of the neurocardiogenic syncope is illustrated by the different types of syncopes as a response to tilt table test: cardioinhibitory with or without assystole, vasodepressor and mixed type [4] . Furthermore, the type of syncope can vary in the same patient from one tilt test to another. As the authors discuss, the specificity of tilt table testing is high, while the sensitivity and reproducibility varies between studies, often at an unacceptable level. Tilt table testing also has some disadvantages, such as the length of time needed to perform the test and the requirement to have a physician present, especially when provocative pharmacologic interventions are administered [1] . An easily performed and reliable adjunct to tilt table testing would be desirable and would be clinically useful. Kocabaş et al. propose a novel testing method which is based on a maximal or submaximal exercise test and the heart rate recovery following the exercise. The diagnostic measure is the heart rate recovery index, that is, the difference between the maximal heart rate at peak exercise and the heart rate 1 min after the end of the exercise, at rest. The authors have found that the heart rate recovery index was significantly greater in the neurocardioIn this issue of Cardiology , Kocabaş et al. [1] report a novel method for the diagnosis of neurocardiogenic syncope. Neurocardiogenic syncope is the most common cause of transient loss of consciousness. Other terms that have been used for this condition include vasovagal syncope, vasovagal reflex syncope and neurally mediated syncope. Neurocardiogenic syncope is a reflex response resulting in vasodilation and bradycardia. This is distinctly different from orthostatic hypotension (increase in heart rate and fall in blood pressure) and autonomic failure with a fall in blood pressure and no change in heart rate. Neurocardiogenic syncope is common in the general population. The Framingham study reports a frequency of 3–3.5%. In the study, the age of subjects ranged between 30 and 62 years at the time of the enrollment, and the follow-up time was 26 years [2] . However, the onset of neurocardiogenic syncope may be seen starting at age 13, and the number of subjects with this condition rapidly increases to a peak during the teenage years [3, 4] . A second peak is observed in subjects older than 70 years [3, 4] . The incidence cited by Kocabaş et al. underestimates the number of subjects with this condition. Neurocardiogenic syncope can be classified as ‘classical’ and ‘non-classical’ [3, 5] . The classical form is triggered by precipitating events such as fear, severe pain, emotional distress, instrumentation or prolonged standing and is associated with typical prodromal syndromes. The classical form can often be diagnosed by history. The non-classical form includes episodes without clear trigReceived: February 27, 2009 Accepted: February 27, 2009 Published online: April 9, 2009