Brignole M, Menozzi C, Corbucci G, Garberoglio B, Plicchi G
Section of Arrhythmology, Ospedali Riuniti, Lavagna, Italy.
Pacing Clin Electrophysiol. 1997 Mar;20(3 Pt 2):801-5. doi: 10.1111/j.1540-8159.1997.tb03907.x.
The peak endocardial acceleration (PEA) caused by ventricular isometric contraction can be measured with an implantable microaccelerometer located inside the tip of a normal unipolar pacing lead. It has been shown that PEA correlates with myocardial contractility and the maximum rate of rise of ventricular pressure (peak dP/dt) of the left ventricle. A PEA measuring system was temporarily inserted into the apex of the right ventricle in seven patients affected by syncope of uncertain origin. Each patient subsequently underwent 60 degrees tilt testing with three different protocols: without pharmacological challenge (baseline); potentiated with sublingual trinitroglycerin (at a dose of 0.3 mg); and with isoproterenol infusion (at a dose of 3 micrograms/min). Each phase lasted 20 minutes. Syncope was induced in 1 patient during the baseline phase, in 3 patients during the trinitrin phase, and in 4 patients during the isoproterenol phase. Six patients had a negative response during the baseline phase and served as a control group. From the beginning of upright posture to the time of maximum heart rate, PEA increased by about the same amount in both positive and negative patients, but absolute values were from two- to three fold higher with isoproterenol (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 negative, positive baseline or trinitrin, and positive isoproterenol tests). At the time of syncope, PEA values fell to baseline values. PEA changes were inversely correlated with blood pressure changes and directly correlated with heart rate changes. Thus, tilt induced syncope occurred 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 PEA 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 vasovagal syncope.
由心室等容收缩引起的峰值心内膜加速度（PEA）可通过位于普通单极起搏导线尖端内部的植入式微加速度计进行测量。研究表明，PEA与心肌收缩力以及左心室压力的最大上升速率（峰值dP/dt）相关。在7例不明原因晕厥患者中，将一个PEA测量系统临时插入右心室心尖。随后，每位患者按照三种不同方案进行60度倾斜试验：无药物激发（基线）；舌下含服硝酸甘油（剂量为0.3mg）增强；异丙肾上腺素输注（剂量为3微克/分钟）。每个阶段持续20分钟。在基线阶段有1例患者诱发晕厥，硝酸甘油阶段有3例患者诱发晕厥，异丙肾上腺素阶段有4例患者诱发晕厥。6例患者在基线阶段反应阴性，作为对照组。从直立姿势开始到心率最大值时，PEA在阳性和阴性患者中升高幅度大致相同，但异丙肾上腺素作用下的绝对值高出两到三倍（阴性、阳性基线或硝酸甘油以及阳性异丙肾上腺素试验时，分别从1.2±0.5G升至1.6±0.8G，从0.8±0.2G升至1.2±0.4G，从2.8±1.8G升至3.6±1.8G）。晕厥发生时，PEA值降至基线值。PEA变化与血压变化呈负相关，与心率变化呈正相关。因此，倾斜诱发的晕厥在左心室收缩力的低水平和高水平时均会发生。自发性晕厥是否在低PEA或高PEA状态下发生仍有待确定。由于心率与PEA变化相关性良好且测量起来容易得多，所以PEA测量系统，或者一般来说基于收缩力的系统，不太可能成为用于对抗血管迷走性晕厥的设备引入的理想传感参数。
