BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.