Myocardial Tissue Characterization Histological a

Authors: T A Treibel S K White J C Moon

Publish Date: 2014/01/15

Volume: 7, Issue: 3, Pages: 9254-

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Abstract

Cardiovascular magnetic resonance imaging CMR has become the gold standard not only for cardiac volume and function quantification but for a key unique strength noninvasive myocardial tissue characterization Several different techniques separately or in combination can detect and quantify early and established myocardial pathological processes permitting better diagnosis prognostication and tracking of therapy The authors will focus on the histological and pathophysiological evidence of these imaging parameters in the characterization of edema infarction scar and fibrosis In addition to laying out the strengths and weaknesses of each modality the reader will be introduced to rapid developments in T1 and T2 mapping as well as the use of contrastderived extracellular volume for quantification of diffuse fibrosisTissue characterization and measurement of fibrosis is a mainstay of clinical care in respiratory medicine nephrology and hepatology but in cardiology this has been limited to the few patients who received cardiac biopsies The emergence of cardiovascular magnetic resonance CMR is changing this Myocardial fibrosis is inherently an important clinical parameter because fibrosis represents one of the hallmarks of pathological remodeling of the myocardium 1 2 3 4 CMR has established itself over the last decade not only as the gold standard for cardiac chamber volume and function quantification but also for noninvasive myocardial tissue characterization Its strength lies in the use of multiple parameters to characterize myocardium The development of imaging parameters for the quantification of edema infarction and scar has been followed by their adoption by the CMR community for noninvasive tissue characterization in particular in acute and chronic myocardial infarction MI During an acute MI occlusion of a coronary artery territory leads to myocyte necrosis which spreads from the subendocardial to the subepicardial layers the wavefront phenomenon Without reperfusion or collateral blood supply complete necrosis of the perfusion territory distal to the occluded coronary artery ensues The total amount of myocardium at risk of necrosis is termed the areaatrisk AAR In general the resulting irreversibly injured myocardium ie chronic myocardial infarct is smaller than the AAR furthermore early reopening of the infarctrelated artery can interrupt this process and lead to salvage of myocardiumThis review will focus on the histological and pathophysiological evidence of these imaging parameters in the characterization of infarction scar and fibrosis across myocardial pathologies The majority of animal models are based on myocardial ischemia and infarction therefore large amounts of histological and pathophysiological evidence arises from the exemplar conditions of acute and chronic myocardial infarctionMagnetic resonance characteristics of protons vary between tissues depending on the configuration of atoms in the tissues These inherent differences can be exploited to generate differing signals from separate tissues T1 relaxation time longitudinal relaxation time is determined by how rapidly protons reequilibrate their spins with their environment following a radiofrequency RF pulse The native noncontrast myocardial T1 varies with water content and increases in cases of edema fibrosis or infiltration of the extracellular space eg in cardiac amyloid Inherently it embodies composite signal from both cells and interstitium and varies with measurement technique and MRI field strength Regional difference in T1 can be visualized by T1weighted MR sequences or directly estimated by T1 mapping T2 relaxation time spinspin relaxation time is determined by how rapidly the refocused transverse signal decays after a RF pulse in contrast to the rate of spin dephasing which is called T2 T2 is shorter when water is tightly bound to large molecules like collagen but longer when water is free T2weighted images emphasize tissues with long T2 or in conditions like where myocardial edema is present new T2 mapping sequences are able to quantify T2 directlyTechnical advances in T1 and T2weighted imaging have allowed invivo visualization and accurate quantification of myocardial edema a substantial feature of myocardial infarction MI with ischemic and reperfusion injury Preliminary work by Higgins et al in the 1980s in a dog infarct model showed T1 and T2 elevation in infarction 5 The observed changes were theoretically consistent with myocardial edema and correlated with the measurements of myocardial water content estimated by wetweight to dryweight ratios This early work aimed to develop noncontrast methods for diagnosing MI but overestimated infarct size It was not until a decade later that T2weighted images were clearly shown to correspond to the area at risk AAR during an acute MI rather than the eventual chronic infarct sizeIn 1993 GarciaDorado et al were the first to show in an exvivo dog model of both nonreperfused and reperfused infarction that T2weighted images represent the AAR and to confirm a tight relationship between myocardial T2 and tissue water content 6 Aletras et al then showed that invivo T2weighted images enabled measurement of the area at risk and compared well with fluorescent microspheres 7 Tilak et al reported that T2weighted images correspond to the area at risk in a canine model of nonreperfused infarcts using firstpass perfusion during coronary occlusion as reference 8 More recently Ugander et al 9 validated T2weighted and precontrast T1weighted images as measures of the AAR against wholeheart microsphere reference standardsIn humans following initial work noting that T2weighted images could be used to differentiate acute from chronic myocardial infarction 10 Berry et al 11 showed that T2weighted images in acute myocardial infarctions were transmural and had hyperintense regions in the distribution of the culprit coronary artery Friedrich et al recognized that T2weighted images could be used to image salvaged myocardium in humans 12 Carlsson et al 13 used sestamibi injected prior to acute percutaneous coronary intervention and imaged with SPECT to validate T2weighted images with regard to determination of area at risk and found excellent correlation and showed that the AAR was similar on days 1–7 post MI but then decreased over 6 months This fact alone cements the use of CMR in clinical studies and was recently confirmed by work at 3 Tesla by DallArmellina and colleagues 14 The use of T2weighted CMR has not been restricted to acute infarction but has also established itself in the diagnostic pathway for investigation and characterization of myocardial inflammation infiltration and masses This follows a pattern of myocardial tissue characterization being used and developed in infarction where large differences exist between normal and abnormal tissue and dissemination into other focal diseases particularly scar in nonischemic cardiomyopathies before use for diffuse myocardial abnormalities In a process of incremental value rather than succession technical development has followed a similar pathway with T1/T2weighted imaging followed by late gadolinium enhancement technique and more recently quantitative T1 and T2 mapping techniques These will be discussed subsequently

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