An Implantable Intracardiac Accelerometer for Monitoring Myocardial Contractility

As the myocardium contracts isometrically, it generates vibrations that are transmitted throughout the heart. These vibrations can be measured 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 aim 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 mounted accelerometer. We used a unidirectional accelerometer located inside 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 mV/G (G - 9.81 m/s^?2). The lead was connected to an external signal amplifier with a frequency range of 0.05–1,000 Hz and to a peak-to-peak detector synchronized with the endocardial R wave scanning the isovolumetric contraction phase. Following standard electro-physiological studies, sensor equipped leads were temporarily inserted in the RV of 15 patients (68 ± 15 years), with normal regional and global ventricular function, to record PEA at rest, during AAI pacing, during VVI pacing, and during dobutamine infusion (up to 20 |mg/kg per min). PEA at baseline was 1.1 G ± 0.5 (heart rate = 75 ± 14 beats/rain) and increased to 1.3 G ± 0.9 (P = NS vs baseline) during AAI pacing (heart rate = 140 beats/min) and to 1.4 G ± 0.5 (P = NS vs baseline) during VVI pacing (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 during dobutamine and pacing were linearly related to changes in PEA (r = 0.9; P < 0.001). In conclusion, the PEA recording can be consistently and safely obtained with an implantable device. Pharmacological inotropic stimulation, but not pacing induced chronotropic stimulation, increases PEA amplitude, in keeping with experimental studies, suggesting that PEA is an index ofmyocardial contractility. Acute variations in PEA are closely paralleled by changes in R V dP/dt_max, but are mainly 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.     

Transthoracic Sensor for Noninvasive Assessment of Left Ventricular Contractility: Validation in A Minipig Model of Chronic Heart Failure

Background: Invasively measured left ventricular (LV) dP/dt is the accepted standard for measuring acute and chronic directional changes in LV contractility. Recently, we developed a noninvasive force sensor based on an accelerometer positioned on the chest, which measures the vibrations generated by isovolumic myocardial contraction. The aim of this paper was to compare noninvasive (accelerometer) versus invasive (LV dP/dt) indices of myocardial contractility in a chronic minipig model of pacing‐induced heart failure (HF). Comparative assessment was performed both at rest and following dobutamine infusion. Methods: In adult male minipigs (n = 6), LV contractility was simultaneously assessed both invasively (LV dP/dt, Millar catheter) and noninvasively (accelerometer) at rest and following dobutamine (up to 7.5 mcg/kg/min), both before and after development of HF by pacing the LV at 180 beats/min for 3 weeks. Results: Invasive and noninvasive assessments were obtained in 24 conditions (12 at rest and 12 after dobutamine infusion). Sensor‐based cardiac force changes were significantly related to positive peak LV dP/dt_max changes following dobutamine infusion both in normal (r = 0.88, P < 0.001) and failing heart (r = 0.89, P < 0.001). The force‐frequency relation showed a tight correlation between invasive and noninvasive assessment (r = 0.68, P = 0.02). Conclusions: The force‐frequency relation can be assessed noninvasively by a transthoracic sensor based on an accelerometer. The method can efficiently detect the development of resting dysfunction and the contractile reserve at different HF steps, with potential for wearable HF monitoring. (PACE 2010; 795–803)     

Short-term cardiac adaptation to severe haemodilution: an echocardiographic study in normal and hypertensive subjects

In order to avoid transfusion risks and optimize blood bankresources, in recent years many blood sparing techniques havebeen proposed, including severe haemodilution. The aim of thisstudy is to assess the pattern of normal haemodynamic and cardiacadaptation to severe haemodilution in patients undergoing majororthopaedic surgery and refusing blood transfusions for religiousreasons (the patients were Jehovah's Witnesses). Two-dimensionally guided M-mode echocardiograms were performedat baseline and 4 days after major orthopaedic surgery in 26Jehovah's Witnesses (age 61±11 years), with normal regionaland global baseline left ventricular function and no valvulardisease. Left ventricular (LV) volumes were estimated by usingthe Teichholz formula. From the latter, we calculated ejectionfraction and stroke volume, cardiac output (stroke volumex heartrate), and total peripheral resistance estimated as mean arterialpressure by cuff sphygmomanometer x 80/cardiac output. On thebasis of LV mass (ASE-cube corrected by Devereux), two groupswere identified: non-hypertrophic (LV mass index <110 g.m^–2 in women and <130g. m^–2 in males) and hypertrophic. In the 19 patients without LV hypertrophy, haemoglobin decreasedfrom 13.5±1.6 (mean ± standard deviation) g. dl^–1(at baseline) to 8.7 ± 1.3 post-operation (P<0.01),and peripheral vascular resistances fell from 2131 ±450 to 1278±310 (dyne. s. cm^–5) (P<0.01). Therewas an increase in heart rate (from 68±9 to 87±9beats. min^–1, P<0.01) and cardiac output (from 3.8±0.7 to 6.7 ±1.41 min^–1, P<0.01), witha rise in ejection fraction (from 62 ± 5 to 66 ±6%, P<0.01) and a decrease in relative wall thickness (from0.42 ± 0.03 to 0.35 ± 0.04, P<0.01). In theseven hypertensive hypertrophic patients, haemoglobin went from12.4 ± 1 (at baseline) to 8.4 ± 1.5 post-operation(P<0.01) and peripheral vascular resistances fell from 2551± 845 to 1363 ± 413 (P<0.01). There was anincrease in heart rate (+38%) and cardiac output (+46%) comparableto that found in non-hypertrophic patients, but with no significantvariation in LV relative wall thickness (from 0.50 ±0.08 to 0.48 ± 0.05, P=ns) and no increase in ejectionfraction (from 62 ±8 to 62.3 ±9%, P=ns). Therewas an inverse correlation between haemoglobin levels and LVcardiac output in both the normal (r= - 0.74; P<0.01) andthe hypertrophic (r= -0.63, P<0.05) group. In conclusion, severe haemodilution induces a high output statewith a fall in peripheral vascular resistance. This haemodynamicadaptation is accompanied by an eccentric remodelling in normal,but not in hypertrophic, hearts. In normal patients, but muchless so in the hypertrophic ones, LV geometry is a dynamic variablewhich can be profoundly modified by a few days of severe haemodilutionand can thus significantly contribute to the overall adaptationto altered haemodynamics.