Ventricular muscarinic receptor remodeling in patients with and without primary ventricular fibrillation. An imaging study

Background

Vagal innervation modulates the electrical stability of the left ventricle (LV) during ischemia. Thus, abnormal parasympathetic activity in myocardial infarction (MI) patients with primary ventricular fibrillation (FV) can account for their arrhythmic disorders. We evaluated LV muscarinic receptor density (B _max) after MI in patients with (FV_G, n?=?11) or without (nFV_G, n?=?12) primary FV.

Methods and Results

The B _max was measured by positron emission tomography and the specific antagonist ¹¹C]methylquinuclidinyl benzilate (¹¹C]MQNB) in 23 patients 39?±?19?days post-MI, and 10 volunteers. Myocardial damage was quantified by delayed contrast-enhanced magnetic resonance imaging. Three short-axis slices per subject were analyzed and six time-activity curves per slice were fitted to a 3-compartment ligand-receptor model. The B _max in remote regions of the 23 patients (67?±?36?pmol/mL?·?tissue; n?=?139) was higher than in normal regions of volunteers (33?±?16?pmol/mL?·?tissue; n?=?171; P?=?.01). Receptor density in remote regions was similarly upregulated in nFV_G (69?±?31?pmol/mL?·?tissue, n?=?73) and FV_G (66?±?40?pmol/mL?·?tissue, n?=?66; P?=?.72). In damaged regions, the B _max was reduced in both patient groups (44?pmol/mL?·?tissue).

Conclusions

Chronically infarcted patients with or without primary FV share similar patterns of ventricular muscarinic receptor remodeling, characterized by receptor upregulation, in remote non-damaged territories.