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. Author manuscript; available in PMC: 2016 Jun 5.
Published in final edited form as: Circ Res. 2015 Jun 5;116(12):2005–2019. doi: 10.1161/CIRCRESAHA.116.304679

Figure 6. Functional remodeling of cardiac innervation in an experimental infarct model and humans with post-infarct cardiomyopathy.

Figure 6

Innervation patterns of the mammalian heart are altered following myocardial infarction. Left upper panel: polar maps of global epicardial activation recovery intervals (ARIs) recorded from a control and an infarcted porcine heart at baseline (BL), and during stimulation of the right, left, and bilateral stellate ganglion (RSG, LSG, & BSG, respectively). The focal region of myocardial infarction in the antero-apical left ventricle is indicated by the dashed circle in bottom row. The altered pattern of ARI distribution in the infarcted heart extends beyond the region of focal myocardial infarction. Right upper panel: graphical representation of the regional responses of the porcine heart to stimulation of RSG, LSG, and BSG in control and infarcted hearts respectively. The anterior and posterior predominance of RSG and LSG stimulations respectively, are completely lost following infarction. Left lower panel: ARIs recorded from a patient with ischemic cardiomopathy and a large antero-apical scar. The location of the recording multi-electrode catheter on fluoroscopy in the right and left anterior oblique (RAO and LAO, respectively) projections; and the corresponding electroanatomic map are shown. On the electroanatomic map, the purple regions indicate tissue with normal voltage (non-scar tissue), while the dense grey regions represent dense scar. All other colors represent border zones (tissue with voltage ≥0.5 mV but ≤1.5 mV). Right lower panel: The degree of change in ARI from baseline in response to direct (isoproterenol) and indirect reflex-mediated (nitroprusside) sympathetic stimulation in cardiomyopathic and normal hearts is shown. With isoproterenol, ARI shortening is exaggerated in CM-NL (normal voltage regions in cardiomyopathic hearts) and CM-scar (scarred tissue) regions of the cardiomyopathic heart. Border zone regions are slightly less responsive to isopreterenol. With nitroprusside, CM-NL and CM-Scar zones paradoxically demonstrate ARI increase compared with the border zone regions. These observations, when compared to normal hearts, indicate the severe degree of adrenergic nerve dysfunction in human hearts with ischemic cardiomyopathy. AICD=automatic internal cardioverter defibrillator lead, CS=coronary sinus electrode, RV= right ventricular lead