DETECTING INCIPIENT VASOVAGAL SYNCOPE - INTRAVENTRICULAR ACCELERATION

Citation
M. Brignole et al., DETECTING INCIPIENT VASOVAGAL SYNCOPE - INTRAVENTRICULAR ACCELERATION, PACE, 20(3), 1997, pp. 801-805
Citations number
5
Journal title
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
ISSN journal
01478389 → ACNP
Volume
20
Issue
3
Year of publication
1997
Part
2
Pages
801 - 805
Database
ISI
SICI code
0147-8389(1997)20:3<801:DIVS-I>2.0.ZU;2-#
Abstract
The peak endocardial acceleration (PEA) caused by ventricular isometri c contraction can be measured with an implantable microaccelerometer l ocated inside the tip of a normal unipolar pacing lead. If has been sh own that PEA correlates with myocardial contractility and the maximum rate of rise of ventricular pressure (peak dP/dt) of the left ventricl e. A PEA measuring system was temporarily inserted into the apex of th e right ventricle in seven patients affected by syncope of uncertain o rigin. Each patient subsequently underwent 60 degrees tilt testing wit h three different protocols: without pharmacological challenge (baseli ne); potentiated with sublingual trinitroglycerin (at a dose of 0.3 mg ), and with isoproterenol infusion (at a dose of 3 mu g/min). Each pha se lasted 20 minutes. Syncope was induced in I patient during the base line phase, in 3 patients during the trinitrin phase, and in 4 patient s during the isoproterenol phase. Six patients had a negative response during the baseline phase and served as a control group. From the beg inning of upright posture to the time of maximum heart rate, PEA incre ased by about the same amount in both positive and negative patients, but absolute values were from two- to three fold higher with isoproter enol (from 1.2 +/- 0.5 G to 1.6 +/- 0.8 G, from 0.8 +/- 0.2 G to 1.2 /- 0.4 G, and from 2.8 +/- 1.8 G to 3.6 +/- 1.8 G, respectively, for n egative, positive baseline or trinitrin, and positive isoproterenol te sts). At the time of syncope, PEA values fell to baseline values. PEA changes were inversely correlated with blood pressure changes and dire ctly correlated with heart rate changes. Thus, tilt induced syncope oc curred both at low and high levels of left ventricular contractility. Whether spontaneous syncopes occur at low or high PEA behavior remains to be established. Since heart rate correlates well with changes in P EA and is far easier to measure, it is unlikely that a PEA measurement system or, in general, a contractility-based system, might become an ideal sensing parameter for the introduction of devices to combat vaso vagal syncope.