Abstract 5789: Increased Left Ventricular Myocardial Vagal Innervation After Myocardial Infarction: A New Paradigm?
Despite the major role of parasympathetic innervation in cardiac regulation and its proved alterations under several pathophysiological conditions, the impact of acute myocardial infarction (AMI) on left ventricular (LV) muscarinic receptors concentration (Bmax) has not yet been established in vivo. We estimated LV Bmax by Positron Emission Tomography (PET) with [11C] methylquinuclidinyl benzilate ([11C] MQNB, a specific antagonist) in 11 patients with AMI and 8 healthy volunteers. The extent of myocardial damage was quantified by delayed contrast-enhanced Magnetic Resonance (MR) images. The study was carried out 30 – 45 days after AMI and three short-axis slices in matched PET and MR images were analyzed. A simplified two injection PET protocol (tracer injection and coinjection) was used. [11C] MQNB time-activity curves were obtained in six regions per slice and fitted to a three compartments ligand-receptor model. Four class of myocardial regions were considered: normal (in volunteers); remote: supplied by healthy or by <70% of diameter reduction arteries and without MR signs of damage; potentially damaged: supplied by infarct-related or >70% diameter reduction arteries; damaged: with myocardial damage. Bmax in remote regions of patients (65.5±29.9 pmol/ml. tissue; n=86) was higher than in normal regions from volunteers (31.6±18.2; n=116; p<0.01). Bmax in potentially damaged (54.5±28.9; n=100) and damaged (42.3±21; n=58) regions was reduced (p<0.05) compared with remote, but higher than in normal regions from volunteers. LV muscarinic receptors are upregulated in remote, non-damaged myocardium of patients with AMI. This study suggests that muscarinic receptor density fall down in damaged tissue as characterized by MR imaging, but it remains however above normal values.