Cardiovascular magnetic resonance characterization of peri-infarct zone remodeling following myocardial infarction

Abstract

BackgroundClinical studies implementing late gadolinium-enhanced (LGE) cardiovascular magnetic resonance (CMR) studies suggest that the peri-infarct zone (PIZ) contains a mixture of viable and non-viable myocytes, and is associated with greater susceptibility to ventricular tachycardia induction and adverse cardiac outcomes. However, CMR data assessing the temporal formation and functional remodeling characteristics of this complex region are limited. We intended to characterize early temporal changes in scar morphology and regional function in the PIZ.Methods and resultsCMR studies were performed at six time points up to 90 days after induction of myocardial infarction (MI) in eight minipigs with reperfused, anterior-septal infarcts. Custom signal density threshold algorithms, based on the remote myocardium, were applied to define the infarct core and PIZ region for each time point. After the initial post-MI edema subsided, the PIZ decreased by 54% from day 10 to day 90 (p = 0.04). The size of infarct scar expanded by 14% and thinned by 56% from day 3 to 12 weeks (p = 0.004 and p < 0.001, respectively). LVEDV increased from 34.7. ± 2.2 ml to 47.8 ± 3.0 ml (day3 and week12, respectively; p < 0.001). At 30 days post-MI, regional circumferential strain was increased between the infarct scar and the PIZ (-2.1 ± 0.6 and -6.8 ± 0.9, respectively;* p < 0.05).ConclusionsThe PIZ is dynamic and decreases in mass following reperfused MI. Tensile forces in the PIZ undergo changes following MI. Remodeling characteristics of the PIZ may provide mechanistic insights into the development of life-threatening arrhythmias and sudden cardiac death post-MI.

Myocardial Scar Delineation Using Diffusion Tensor Magnetic Resonance Tractography

“…These are congruent with generally accepted definitions of normal myocardium (≥1.5 mV), border zone (0.5–1.5 mV), and dense scar (≤0.5 mV) by bipolar voltage mapping 9, 31. Furthermore, these intermediate voltage and PA values are consistent with the intermediate values seen in gray‐zone LGE 2, 3, 4, 30…”

Differences in quantitative assessment of myocardial scar and gray zone by LGE-CMR imaging using established gray zone protocols

“…Additionally, respiratory artifacts or motion can lead to spatial misalignment of slices [26] increasing voxels with intermediate gray zone intensities. Finally, Schuleri et al [27] showed in a swine model that the gray zone decreased by 56 % from day 10 to day 90. The NSD method has been previously criticized for a possible overestimation of the infarct size [11,15], which may be partly due to suboptimal signal suppression of remote myocardium or image artifacts [28].…”

Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease

“…Deposition of de novo ECM is necessary to maintain structural integrity and requires the switch from inflammatory to profibrotic signaling factors (Frangogiannis, 2014). In both chronic and acute myocardial remodeling, AngII inhibits the degradation of collagen-1 and promotes the expression of FGF-2 and TGF-β1 that, in turn, promote cell growth and collagen production in the myocardium (Frangogiannis, 2014;Huang et al, 2010;Porter and Turner, 2009;Schuleri et al, 2012;Virag et al, 2007). TGF-β1 inhibits inflammation and promotes the differentiation of fibroblasts into MyoFBs, and the accumulation of dense ECM in the myocardial interstitium (Ikeuchi et al, 2004).…”

“…MMP1 and MMP9) -and collagen-1 than valves that are exposed to physiologic valve strains (10%) (Balachandran et al, 2009). MMPs and other proteases are also expressed by MyoFBs in infarct regions to break down any damaged ECM, and allow for increased fibroblast migration into the infarct region (Aisagbonhi et al, 2011;Davis and Molkentin, 2014;Schuleri et al, 2012). CFs proliferate and express increased levels of α-SMA and MMP2 in vitro after exposure to -approximately physiological -cyclic strains between 5% and 15% (Dalla Costa et al, 2010).…”