AN IMPLANTABLE INTRACARDIAC ACCELEROMETER FOR MONITORING MYOCARDIAL-CONTRACTILITY

As the myocardium contracts isometrically, it generates vibrations tha t are transmitted throughout the heart. These vibrations can be measur ed with an implantable microaccelerometer located inside the tip of an otherwise conventional unipolar pacing lead. These vibrations are, in their audible component, responsible for the first heart sound. The a im of this study was to evaluate, in man, the clinical feasibility and reliability of intracavity sampling of Peak Endocardial Acceleration (PEA) of the first heart sound vibrations using an implantable tip mou nted accelerometer We used a unidirectional accelerometer located insi de the stimulating tip of a standard unipolar pacing lead: the sensor has a frequency response of DC to 1 kHz and a sensitivity of 5 V/G (G = 9.81 m/s(-2)). The lead was connected to an external signal amplifie r with a frequency range of 0.05-1,000 Hz and to a peak-to-peak detect or synchronized with the endocardial R wave scanning the isovolumetric contraction phase. Following standard electrophysiological studies, s ensor equipped leads were temporarily inserted in the RV of 15 patient s (68 +/- 15 years), with normal regional and global ventricular funct ion, to record PEA at rest, during AAI pacing, during VVI pacing, and during dobutamine infusion (up to 20 mu g/kg per min). PEA at baseline was 1.1 G +/- 0.5 (heart rate = 75 +/- 14 beats/min) and increased to 1.3 G +/- 0.9 (P = NS vs baseline) during AAI pacing (heart rate = 14 0 beats/min) and to 1.4 G +/- 0.5 (P = NS vs baseline) during VVI paci ng (heart rate = 140 beats/min). Dobutamine infusion increased PEA to 3.7 G +/- 1.1 (P < 0.001 vs Baseline), with a heart rate of 121 +/- 13 beats/min. In a subset of three patients, simultaneous hemodynamic RV monitoring was performed to obtain RV dP/dt(max), whose changes durin g dobutamine and pacing were ere linearly related to changes in PEA (r = 0.9; P < 0.001). In conclusion, the PEA recording can be consistent ly and safely obtained with an implantable device. Pharmacological ino tropic stimulation, but not pacing induced chronotropic stimulation, i ncreases PEA amplitude, in keeping with experimental studies, suggesti ng that PEA is an index of myocardial contractility. Acute variations in PEA are closely paralleled by changes in RV dP/dt(max), but are mai nly determined by LV events. The clinical applicability of the method using RV endocardial leads and an implantable device offers potential for diagnostic applications in the long-term monitoring of myocardial function in man.