Is local myocardial contractility related to endocardial acceleration signals detected by a transvenous pacing lead?
The availability of sensors monitoring cardiac function parameters may offer many interesting new applications in cardiac pacing. A microaccelerometer sensor (BEST, Biomechanical Endocardial Sorin Transducer) located at the tip of a pacing lead (PL) has been developed by Sorin Biomedica. The signal detected by the accelerometer, peak endocardial acceleration (PEA), was shown to reflect cardiac contractility and to be related to the dP/dt signal. Whether the PEA detected by the BEST sensor in different cardiac locations is the expression of local acceleration forces or reflects the whole heart contractility has not yet been demonstrated in humans. Endocardial acceleration and PEA were evaluated in five patients (4 males, 1 female, mean age 68 years) who underwent cardiac catheterization. Sinus rhythm was present in four patients and chronic atrial fibrillation was present in one. The BEST PL was introduced through the left subclavian vein and PEA signals were recorded: (1) at the apex of the right ventricle (RV), (2) within the coronary sinus (CS), (3) at the right atrial appendage (RAA), and (4) floating in the right atrium. The PEA signals were recorded simultaneously with surface ECG, intracardiac electrograms, and RV pressure. At each recording site, PEA signals with significant amplitude were always recorded during the preejection period, during the isovolumic contraction phase, independently of the recording site and cardiac rhythm. The PEA amplitude was higher in the RV (mean value 1.32 g) and it decreased in the RAA and CS (0.75 and 0.45 g, respectively). The same behavior of PEA was observed during sinus rhythm or atrial fibrillation. The amplitude and the timing of the PEA signals detected by the BEST accelerometer were independent of the recording site and atrial rhythm; they appeared to be strictly related to the global ventricular contractility. These results suggest that the BEST could be used either as an effective sensor in closed loop pacing systems, or primarily as a diagnostic hemodynamic sensor.
Bongiorni
M G
MG
CNR-CREAS Clinical Physiology Institute, Pisa, Italy. mgb@nsifc.ifc.pi.cnr.it
Soldati
E
E
Arena
G
G
Quirino
G
G
Vernazza
F
F
Bernasconi
A
A
Garberoglio
B
B
D000054:Acceleration; D000368:Aged; D001281:Atrial Fibrillation / Q000503:physiopathology; D016280:Atrial Function, Right; D006328:Cardiac Catheterization; D002304:Cardiac Pacing, Artificial / Q000379:methods; D002306:Cardiac Volume; D002908:Chronic Disease; D003331:Coronary Vessels; D004562:Electrocardiography; D004582:Electronics, Medical / Q000295:instrumentation*; D005260:Female; D005500:Follow-Up Studies; D006321:Heart / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D010138:Pacemaker, Artificial; D012815:Signal Processing, Computer-Assisted / Q000295:instrumentation; D016276:Ventricular Function; D016278:Ventricular Function, Right; D017725:Ventricular Pressure