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(Circulation. 2002;106:1606.)
© 2002 American Heart Association, Inc.
Clinician Update |
From the Department of Medicine, University of Pittsburgh, Pittsburgh, Pa.
Correspondence to Wishwa N. Kapoor, MD, UPMC, 200 Lothrop St, 933 West MUH, Pittsburgh, PA 15213. E-mail kapoorwn@ msx.upmc.edu
| Introduction |
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Syncope is a sudden temporary loss of consciousness associated with a loss of postural tone and spontaneous recovery not requiring electrical or chemical cardioversion. Syncope has a large differential diagnosis, is difficult to evaluate, and can be disabling. There are subsets of syncopal patients with a high risk of sudden death. The central issues in the evaluation of syncope are establishing the cause of syncope, deciding whether the patient needs to be admitted, and treating the causes of syncope effectively to reduce recurrences and potentially improve patient outcomes.
| Is It Syncope? |
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| How Often Are Causes of Syncope Established? |
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Two studies (reported in 2000 and 2001) from Europe employed diagnostic algorithms and prospective evaluation using newer diagnostic modalities. Unexplained syncope9,10 was found in 14% to 17.5% of patients. Neurally mediated syncope was the most common cause in both studies and was diagnosed in 35% to 38% of patients; psychiatric illnesses were diagnosed in up to 5.6% of the patients. These studies should be replicated in the US populations.
| Prognosis and Risk Stratification |
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A study of risk stratification used the occurrence of important cardiac arrhythmias or death in the year after presentation with syncope as an outcome.14 The 4 factors that were predictors are age
45, a history of heart failure, a history of ventricular arrhythmias, and an abnormal ECG. Patients with none of the predictors had 4% to 7% risk of this outcome as compared with 58% to 80% in patients with 3 or 4 risk factors.
The presence of underlying heart disease in patients with syncope predicts a worse prognosis. Attempts should be made to detect, define, and treat the underlying structural heart disease in syncope patients to reduce the probability of mortality and sudden death.
| Diagnostic Evaluation |
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The European Society of Cardiologys Guidelines on Management (Diagnosis and Treatment) of Syncope (Figure) provides an up-to-date recommendation on the evaluation of syncope.17 Important features of this guideline include:
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| Management |
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Treatment of patients with syncope focuses on the underlying cause of the symptom. For neurally mediated syncope, treatment can include patient education, tilt training (ie, repeated frequent tilting until the patients positive response becomes negative), pharmacological agents, and dual chamber pacing. All patients should be instructed on how to prevent episodes by avoiding triggers such as prolonged standing, heat, large meals, fasting, lack of sleep, alcohol, and dehydration. Vasodilators should be discontinued because they may increase susceptibility to vasovagal syncope. Patients should also be instructed about maneuvers that prevent loss of consciousness, to assume a supine position on premonitory symptoms, and to avoid activities that may lead to serious injury.
The effectiveness of drug therapy in preventing recurrent neurally mediated syncope is open to question.17,25 Although volume expansion with increased salt and fluid intake, moderate exercise, and tilt training are relatively safe measures, their effectiveness has not been demonstrated by randomized controlled trials. One short-term randomized trial and a large number of uncontrolled studies of ß-blockers claim effectiveness of these drugs, but several controlled trials did not show effectiveness.2628 The vasoconstrictive agent etilephrine was ineffective in a randomized European trial.29 Midodrine was shown to be beneficial in a small randomized trial when compared with no treatment, but there was no placebo arm to the study.30 A randomized trial of paroxetine showed reduced recurrences at 2 years but needs further confirmation.31
Three randomized trials have assessed permanent pacemakers.3234 In one, treatment using pacemakers with rate-drop response algorithm in patients with severe symptoms (6 or more lifetime episodes) and bradycardia on tilt testing showed 85% relative risk reduction for recurrent syncope. Another study showed that 5% of patients in the pacemaker arm experienced recurrence of syncope as compared with 61% in the no-pacemaker arm during a mean follow-up of 3.7 years. A placebo effect of the pacemaker has not been excluded in these studies. A study comparing pacemakers to atenolol showed lower recurrent rates of syncope at 2 years in the pacemaker treated group.34 Pacemakers may be a treatment option in patients with severe recurrent syncope and with a cardioinhibitory response on tilt testing. Placebo-controlled studies are needed to determine the role of pacemakers in neurally mediated syncope.
| Conclusions |
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The case presented earlier had left bundle-branch block on ECG, and thus the main factors in the differential diagnosis were arrhythmias such as complete atrioventricular block or ventricular tachycardia. The patient had an external loop event recorder placed for a month. When the patient returned for a follow-up office visit, she had not had a syncopal episode for 1 month, illustrating a common problem with the use of loop event monitoring. The patient then underwent electrophysiological testing that did not show evidence of a conduction abnormality or inducible ventricular tachycardia. An external loop event recorder was placed again, and several days later the patient had a syncopal episode with concurrent complete atrioventricular block on monitoring. She underwent a permanent pacemaker placement and has not had syncope in follow-up of more than 2 years.
| References |
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