Key result
Border-zone intramyocardial adiposity is ~8% higher in sheep with inducible post-MI VT.
Why the study?
Collagen was considered the principal structural substrate of VT after MI, even though post-MI myocardial adiposity is well recognized histologically. The effects of intramyocardial adiposity compared with collagen on electrophysiological properties, connexin43 expression, and VT induction after MI were investigated.
Does intramyocardial adiposity correlate with altered electrophysiological properties and ventricular tachycardia induction after myocardial infarction in a sheep model?
Does intramyocardial adiposity correlate with altered electrophysiological properties and ventricular tachycardia induction after myocardial infarction in a sheep model?
Answers are grounded in this paper and cite their sources.
Intramyocardial adiposity, rather than just collagen, significantly alters electrophysiological properties and increases the propensity for ventricular tachycardia after myocardial infarction.
Background— Collagen has been attributed as the principal structural substrate of ventricular tachycardia (VT) after myocardial infarction (MI), even though adiposity of myocardium after MI is well recognized histologically. We investigated the effects of intramyocardial adiposity compared with collagen on electrophysiological properties, connexin43 expression, and VT induction after MI. Methods and Results— Simultaneous left ventricular plunge-needle, noncontact mapping was performed in sheep without MI (MI−; n=5), with MI and inducible VT (MI+VT+; n=7), and with MI and no inducible VT (MI+VT−; n=8). Histological intramyocardial quantity of adipose and collagen and degree of discontinuity were coregistered with electrophysiological parameters (MI+; 290 specimens). Additional assessment of connexin43 expression was performed. Left ventricular scar contained a body mass–independent abundance of adipocytes (adipose:collagen=0.8). Increased adipose density and discontinuity contributed to a greater inverse correlation ( r ) with conduction velocity ( r for adipose=0.39, r for discontinuity=0.45, r for collagen=0.26) and electrogram amplitude ( r for adipose=0.73, r for contiguity=0.77, r for collagen=0.68) compared with collagen. Collagen density was similar between the MI+ groups ( P >0.29). However, the MI+VT+ group demonstrated a significant (all P ≤0.01) increase in adipose (8%) and discontinuity (qualitative) and decrease in conduction velocity (13%) and electrogram amplitude (21%) at MI borders compared with the MI+VT− group. In scar, myocytes adjacent to fibrofatty interfaces demonstrated increased connexin43 lateralization. A gradient increase in adipose was observed at sites that supported preferential presystolic VT activation and exhibited attenuation of excitation wavelength ( P <0.001). Conclusions— Intramyocardial adiposity, in association with myocardial discontinuity within left ventricular scar borders, is a significant factor associated with altered electrophysiological properties, aberrant connexin43 expression, and increased propensity for VT after MI.
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Pouliopoulos et al. (2013) studied Ventricular tachycardia after myocardial infarction (n=20). Intramyocardial adiposity vs. Intramyocardial collagen / MI without inducible VT was evaluated on Electrophysiological properties (conduction velocity and electrogram amplitude), connexin43 expression, and VT induction (p=<=0.01). Intramyocardial adiposity was 8% higher at MI borders in sheep with inducible VT vs no VT, with 13% lower conduction velocity and 21% lower electrogram amplitude.
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