Ten Cate Tim J F, Van Hemel Norbert M, Verzijlbergen Johan F
Department of Nuclear Medicine, St Antonius Hospital Nieuwegein, Nieuwegein, Utrecht, The Netherlands.
Nucl Med Commun. 2009 Jun;30(6):480-4. doi: 10.1097/MNM.0b013e32832b9a45.
Myocardial perfusion defects have been shown in patients with abnormal intraventricular conduction. These defects have been ascribed to regional differences in myocardial blood flow caused by the abnormal activation. This proof of the concept study assesses the effects of abnormal electrical activation and subsequent wall motion abnormalities of the left ventricle on myocardial perfusion in a pacing model.
Fourteen patients with normal atrio-ventricular (AV) and intraventricular conduction with a right ventricular apical (RVA) pacemaker for brady-tachycardia syndrome were studied to allow for intrapatient comparison. Tc-sestamibi was injected in atrial inhibited (AAI) pacing mode allowing uptake during normal intraventricular conduction. Imaging was performed with AAI pacing and the second image was acquired directly after the first scan with AV pacing with a short AV-interval ensuring complete AV pacing with abnormal ventricular activation patterns (RVA pacing). Left ventricular ejection fraction (LVEF), wall motion score and myocardial perfusion score (SSS) were assessed with gated single photon emission computed tomography (SPECT) during normal conduction (AAI) and with RVA pacing.
Left ventricular ejection fraction was normal in all patients. During AAI, three of 14 patients showed wall motion abnormalities, mean wall motion score 0.9+/-1.8 with a mean SSS 0.6+/-1.5 increasing to 4+/-6.2 and 3.6+/-5.8 (P<0.01), respectively during RVA pacing. Wall motion abnormalities were found in the apex, inferior, inferoseptal and septal walls.
Despite a fixed amount of tracer activity in the myocardium, larger and more perfusion defects were visible during RVA pacing compared with normal conduction. The site and severity of the perfusion defects correlates with abnormal wall motion because of this pacing mode. This implies that abnormal wall motion is at least partly responsible for the apparent myocardial perfusion defects.
已有研究表明，室内传导异常的患者存在心肌灌注缺损。这些缺损被认为是由异常激动导致的心肌血流区域差异所致。本概念验证性研究评估了起搏模型中异常电激动及随后的左心室壁运动异常对心肌灌注的影响。
对14例患有缓慢性心律失常综合征且房室（AV）和室内传导正常、植入右心室心尖部（RVA）起搏器的患者进行研究，以进行患者自身对照。在心房抑制（AAI）起搏模式下注射锝- sestamibi，以便在正常室内传导期间摄取。在AAI起搏时进行成像，并在首次扫描后立即进行第二次成像，采用短AV间期的AV起搏，以确保完全的AV起搏及异常的心室激动模式（RVA起搏）。在正常传导（AAI）和RVA起搏期间，采用门控单光子发射计算机断层扫描（SPECT）评估左心室射血分数（LVEF）、壁运动评分和心肌灌注评分（SSS）。
所有患者的左心室射血分数均正常。在AAI期间，14例患者中有3例出现壁运动异常，平均壁运动评分为0.9±1.8，平均SSS为0.6±1.5，在RVA起搏期间分别增至4±6.2和3.6±5.8（P<0.01）。在心尖、下壁、下间隔和间隔壁发现壁运动异常。
尽管心肌中的示踪剂活性总量固定，但与正常传导相比，RVA起搏期间可见更大且更多的灌注缺损。由于这种起搏模式，灌注缺损的部位和严重程度与异常壁运动相关。这意味着异常壁运动至少部分导致了明显的心肌灌注缺损。
