Many Rx options; we started with fludrocortisone
Pharmacotherapy for treatment of vasovagal syncope has been extensively tested, but no medication is reliably effective. Beta-blockers are sometimes prescribed, but randomized clinical trials have failed to show a predictable benefit (SOR: A).13 Pindolol may induces less bradycardia due to intrinsic sympathomimetic activity.14
Other possible medications include midodrine, fludrocortisone, theophylline, clonidine, and serotonin reuptake inhibitors. Vasoconstrictors (such as midodrine) and fludrocortisone are more likely to be effective for patients with orthostatic hypotension than vasovagal syncope (SOR: B).15 Fludrocortisone may cause weight gain and fatigue and affect performance in athletes.
Disopyramide is a class I anti-arrhythmic agent that has additional effects of negative inotropy and a vagolytic effect. This decreases the stimulation of the carotid baroreceptors and interrupts the vagal efferent pathway. We have found this to be very useful and well-tolerated. Theoretically, though, because of its negative inotropic effect, it may decrease cardiac output enough to affect athletic performance. Initiate the drug with telemetry monitoring to detect any pro-arrhythmic electrocardiographic changes, such as torsades de pointes or QT prolongation. Prevention of the hyperdynamic cardiac contraction can trigger an abnormal baroreceptor reflex and block the efferent limb of the vagal response to counter the bradycardia and vasodepressor response.16
If pharmacotherapy is required, we generally prescribe drugs in the following sequence—first fludrocortisone, then beta-blockers, and, if these do not help, disopyramide. These should be first given in the hospital with telemetry monitoring to check for QT prolongation. If these are ineffective, try paroxetine or midodrine. In refractory cases, we may use various combinations of these drugs.
Disopyramide and a changed running strategy
Several mechanisms related to vigorous exercise played a role in our patient’s case. During exercise, she developed a very high systolic pressure with a low diastolic pressure, resulting in a high pulse pressure that possibly led to stimulation of carotid baroreceptors. Cardiac hypercontractility related to exercise was probably a contributing factor as well. Severe leg pain prior to syncope suggested involvement of a pain-mediated mechanism.
We prescribed disopyramide 150 mg twice daily for our patient. We also recommended that she do specific exercises—to strengthen her leg muscles—and modify her running strategy.
After 2 months of therapy, she resumed competitive running successfully without any further episodes of syncope. She was able to achieve a new personal record for a cross country run by running a slower pace of 6 minutes 20 seconds per mile initially and running faster only at the end of the race. She had no recurrences of syncope during 6 months of follow-up.
CorrespondenceSumit Verma, MD, Pensacola Heart Institute, 5151 N, 9th Avenue, Cardiology Consultants, Pensacola, Fl 32504; vermasumit@hotmail.com.