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Cardiac Pacing for Prevention of Recurrent Vasovagal Syncope

David G. Benditt, MD; Mark Petersen, MRCP; Keith G. Lurie, MD; Blair P. Grubb, MD; and Richard Sutton, DSc Med
[+] Article and Author Information

From the University of Minnesota, Minneapolis, Minnesota; Chelsea and Westminster Hospital and Royal Brompton National Heart and Lung Hospital, London, United Kingdom; and the Medical College of Ohio, Toledo, Ohio. Requests for Reprints: David G. Benditt, MD, University of Minnesota Hospital, Box 341 UMHC, Minneapolis, MN 55455. Acknowledgments: The authors thank Barry L.S. Detloff for technical assistance and Wendy Markuson and Stephanie Colbert for manuscript preparation. Drs. Benditt and Sutton currently hold consulting relationships with pacemaker manufacturers.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1995;122(3):204-209. doi:10.7326/0003-4819-122-3-199502010-00008
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Purpose: To review the status of cardiac pacing for the treatment of patients with recurrent vasovagal syncope.

Data Sources: A MEDLINE search for English- and French-language articles published between 1980 and 1994 about cardiac pacing for prevention or treatment of vasovagal syncope. The term cardiac pacing was used in conjunction with the terms vasovagal, neurally mediated, or neurocardiogenic syncope, but not with the term carotid sinus hypersensitivity.

Study Selection: Case reports and series from peer-reviewed journals were selected if they documented the presence of vasovagal syncope and assessed pacing effectiveness using tilt-table testing, clinical follow-up, or both. Four case reports and four series met these criteria.

Data Extraction: Findings were summarized individually. Statistical analysis of combined data was inappropriate given differences among studies in patient selection, testing, and follow-up.

Results: Pacing may be useful in selected patients with predominantly cardioinhibitory vasovagal responses. Pacing alone may eliminate symptoms in 25% of these patients and may prevent abrupt cardiovascular collapse in others (such as those in whom syncope occurs with minimal or no premonitory sensation). However, interpretation of most available reports has been limited both by the uncertainty associated with using the tilt-table technique to assess pacing effectiveness and by relatively short-term follow-up.

Conclusions: The usefulness of cardiac pacing for patients with recurrent vasovagal syncope remains only partly understood. Randomized controlled trials are needed for this and other aspects of the treatment of this condition. Additionally, substantial room remains for innovation both in earlier recognition of imminent vasovagal syncope by implantable devices and in specifically designing cardiac pacing algorithms for treatment of this condition.

Figures

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Figure 1.
Heart rate and blood pressure (Finapres plethysmographic technique) for each cardiac cycle.Top.[18]Bottom.[18][18]

One-minute intervals are indicated along the abscissa. Left-hand arrows indicate the initiation of tilt, and right-hand arrows indicate return to supine position. Type 2A cardioinhibitory vasovagal syncope as categorized by the Vasovagal International Study group . The heart rate increases initially and then decreases abruptly. Blood pressure also increases initially but begins to decrease before heart rate does, thereby contributing substantially to the development of symptomatic hypotension. Type 2B cardioinhibitory vasovagal syncope as categorized by the Vasovagal International Study group . The heart rate initially increases and later decreases abruptly. Blood pressure decreases as a direct result of the decrease in heart rate (this is a relatively “pure” form of cardioinhibitory response). Figure adapted from Sutton and colleagues with permission.

Grahic Jump Location
Grahic Jump Location
Figure 2.
The potential value of cardiac pacing for moderating decrease in blood pressure and for extending the period before syncope in a patient whose cardioinhibitory vasovagal syncope was reproducible by 60-degree head-up tilt-table testing.Top.Bottom.

In both panels, heart rate and blood pressure (Finapres plethysmographic technique) are recorded for each cardiac cycle at slow speed. One-minute intervals are indicated by the marks along the abscissa. Baseline, untreated state. Heart rate and blood pressure initially increase when tilt is begun (left-hand arrow). Approximately 15.5 minutes into the procedure, abrupt bradycardia (right-hand arrow) is associated with hypotension and syncope (*). The brief overall duration of hypotension is due to the need to return the patient immediately to the supine position. After placement of a dual-chamber pacemaker in the same patient. The pacemaker is triggered by a heart rate of less than 45 beats/min and responds by pacing at 90 beats/min (note the relatively fixed rate at the right side of the figure and the occasional irregularities due to premature beats). Once again, onset of tilt (left-hand arrow) is associated with an increase in heart rate and blood pressure. Abrupt onset of bradycardia (right-hand arrow, approximately 3 minutes into the tilt) triggers pacing. After onset of pacing, the rate of decrease in blood pressure is reduced. Although presyncopal symptoms are present, pacing is associated with prolonged tolerance to upright tilt despite systemic hypotension. Supine posture was restored without the occurrence of frank syncope.

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