Rickards A F, Bombardini T, Corbucci G, Plicchi G
Royal Brompton Hospital, London, United Kingdom.
Pacing Clin Electrophysiol. 1996 Dec;19(12 Pt 1):2066-71. doi: 10.1111/j.1540-8159.1996.tb03280.x.
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 electrophysiological 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 micrograms/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 = 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/dtmax, 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 of myocardial contractility. Acute variations in PEA are closely paralleled by changes in RV dP/dtmax, 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.
当心肌进行等长收缩时，会产生传遍整个心脏的振动。这些振动可用置于传统单极起搏导线尖端内部的植入式微型加速度计进行测量。这些振动的可听成分构成了第一心音。本研究的目的是评估在人体中，使用植入式尖端安装加速度计对第一心音振动的峰值心内膜加速度（PEA）进行心腔内采样的临床可行性和可靠性。我们使用了一个位于标准单极起搏导线刺激尖端内部的单向加速度计：该传感器的频率响应为直流至1千赫兹，灵敏度为5毫伏/克（1克 = 9.81米/秒²）。该导线连接到一个频率范围为0.05 - 1000赫兹的外部信号放大器，并连接到一个与心内膜R波同步的峰峰值检测器，以扫描等容收缩期。在进行标准电生理研究后，将配备传感器的导线临时插入15名患者（年龄68 ± 15岁）的右心室，这些患者的局部和整体心室功能正常，以记录静息时、AAI起搏期间、VVI起搏期间以及多巴酚丁胺输注期间（最高20微克/千克每分钟）的PEA。基线时PEA为1.1克 ± 0.5（心率 = 75 ± 14次/分钟），在AAI起搏期间（心率 = 140次/分钟）增加到1.3克 ± 0.9（与基线相比P = 无显著性差异），在VVI起搏期间（心率 = 140次/分钟）增加到1.4克 ± 0.5（与基线相比P = 无显著性差异）。多巴酚丁胺输注使PEA增加到3.7克 ± 1.1（与基线相比P < 0.001），心率为121 ± 13次/分钟。在三名患者的亚组中，同时进行了右心室血流动力学监测以获取右心室dP/dtmax，其在多巴酚丁胺和起搏期间的变化与PEA的变化呈线性相关（r = 0.9；P < 0.001）。总之，使用植入式装置能够持续且安全地获取PEA记录。与实验研究一致，药物性变力刺激而非起搏诱导的变时刺激会增加PEA幅度，这表明PEA是心肌收缩力的一个指标。PEA的急性变化与右心室dP/dtmax的变化密切平行，但主要由左心室事件决定。使用右心室心内膜导线和植入式装置的该方法在人体心肌功能长期监测的诊断应用中具有潜力。
