The Future of Cardiovascular Imaging
2016; Lippincott Williams & Wilkins; Volume: 133; Issue: 25 Linguagem: Inglês
10.1161/circulationaha.116.023511
ISSN1524-4539
AutoresMarcelo F. Di Carli, Tal Geva, Ravin Davidoff,
Tópico(s)Cardiac Valve Diseases and Treatments
ResumoHomeCirculationVol. 133, No. 25The Future of Cardiovascular Imaging Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toSupplementary MaterialsFree AccessResearch ArticlePDF/EPUBThe Future of Cardiovascular Imaging Marcelo F. Di Carli, MD Tal Geva, and MD Ravin DavidoffMBBCh Marcelo F. Di CarliMarcelo F. Di Carli From Cardiovascular Imaging Program, Departments of Radiology and Medicine; Division of Cardiovascular Medicine, Department of Medicine; Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (MDC); Department of Cardiology, Boston Children's Hospital and Department of Pediatrics, Harvard Medical School, MA (TG); and Section of Cardiovascular Medicine, Evans Department of Medicine, Boston Medical Center, Boston University School of Medicine, MA (RD). , Tal GevaTal Geva From Cardiovascular Imaging Program, Departments of Radiology and Medicine; Division of Cardiovascular Medicine, Department of Medicine; Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (MDC); Department of Cardiology, Boston Children's Hospital and Department of Pediatrics, Harvard Medical School, MA (TG); and Section of Cardiovascular Medicine, Evans Department of Medicine, Boston Medical Center, Boston University School of Medicine, MA (RD). , and Ravin DavidoffRavin Davidoff From Cardiovascular Imaging Program, Departments of Radiology and Medicine; Division of Cardiovascular Medicine, Department of Medicine; Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (MDC); Department of Cardiology, Boston Children's Hospital and Department of Pediatrics, Harvard Medical School, MA (TG); and Section of Cardiovascular Medicine, Evans Department of Medicine, Boston Medical Center, Boston University School of Medicine, MA (RD). Originally published21 Jun 2016https://doi.org/10.1161/CIRCULATIONAHA.116.023511Circulation. 2016;133:2640–2661IntroductionOver the past 2 decades, we have witnessed an explosive expansion in the armamentarium of noninvasive and invasive imaging technologies capable of providing detailed information about the structure and function of the heart and vasculature. Many of these technologies are integrative (eg, positron emission tomography and computed tomography, positron emission tomography and MRI), thereby compounding the unique strengths of the component technologies to achieve unprecedented improvements to our ability to diagnose disease, improve patient care, and advance biomedical research. In addition, the miniaturization of imaging devices with dramatic increases in sensitivity and spatial resolution, coupled with the development of quantitative molecular imaging approaches for evaluating physiology and pathobiology at the cellular and molecular levels, provides a unique platform for a new era in diagnostic imaging. The crucial role of imaging in early phenotyping of disease, risk assessment, and management guidance is expanding rapidly in ways previously thought unrealistic.Along with clinical, molecular, and genomewide association studies, structural and functional quantitative imaging already plays a critical role in phenotyping cardiovascular disease. Unique strengths of imaging phenotyping include its ability to provide precise, organ-specific anatomic localization and quantification of disease traits, to demonstrate and quantify involvement of other organs in cardiac disease, to provide an opportunity to investigate the time course of disease-specific molecular events in vivo, and to track their response to therapy. In so doing, quantitative structural and functional imaging can provide a nuanced description of disease burden (eg, atherosclerosis, myocarditis), disease subtypes (eg, amyloidosis), and, importantly, the relationship between the specific phenotype and outcomes, thereby informing treatment strategies and allowing more personalized approaches to patient management.Our objectives for this article are to (1) provide a viewpoint regarding the evolving role of cardiovascular imaging in biomedical research and clinical practice, (2) discuss the challenges associated with clinical translation of imaging innovations and the opportunities for multimodality imaging in the changing paradigm of value-based medicine, and (3) briefly outline future challenges and opportunities including the requirements for training future generations of imaging scientists and clinical specialists. Unlike traditional reviews that provide a detailed discussion of the role of 1 or more imaging modalities in cardiovascular (CV) disease, our discussion will focus on the potential role of imaging in what we believe are key areas of the translational highway with specific examples on how structural and functional imaging may contribute to scientific discovery, diagnosis, risk stratification, and patient management in each of those areas.Redefining the Role of Imaging Across the Continuum of Biomedical Research and Clinical PracticeTranslational ResearchThe use of imaging to study biology and uncover biomarkers of human disease provides a window through which we can phenotype disease in vivo, thereby offering an opportunity for early diagnosis of disease and assessing the potential value of novel therapies. Because the nuances of disease mechanisms and the subtleties of the responses to therapy are key to understanding and treating disease, imaging has become an essential tool for revealing pathogenic mechanisms and for developing therapeutic strategies. Importantly, many powerful imaging tools are already integrated in the continuum of patient care, which offers a unique opportunity for clinical translation. The use of imaging to study the pulmonary vasculature and right ventricular remodeling in patients with pulmonary arterial hypertension (PAH) highlights how imaging can facilitate understanding of disease mechanisms in vivo, while also providing quantitative targets for evaluating novel therapies.The remodeling of the right ventricle (RV) to the pathological changes in the pulmonary vascular bed is the major determinant of functional capacity and prognosis in PAH. Initially, sustained pressure overload leads to RV hypertrophy. This increase in mass is an adaptive response to overcome the increased afterload, reduce wall stress, and maintain RV systolic function and cardiac output. However, despite similar RV afterload and mass, some patients remain stable for many years, whereas others develop maladaptive RV hypertrophy with rapid transition to failure and clinical decompensation. Clinically, adaptive RV hypertrophy is characterized by preservation of relatively normal cardiac output, ejection fraction, RV filling pressure, and exercise capacity. Pathologically, this form of RV remodeling shows concentric hypertrophy with minimal dilatation and fibrosis. In contrast, maladaptive RV hypertrophy is characterized by a reduced cardiac output and ejection fraction, associated with elevation of RV filling pressure and reduced exercise capacity. The pathological correlates of the maladaptive phenotype include eccentric RV hypertrophy and dilatation, and increased fibrosis. Advanced cardiac imaging along with invasive hemodynamic measurements play a key role in diagnosis and risk stratification of patients with known or suspected PAH. Advanced imaging tools also offer unique quantitative insights into the underlying pathobiology of the different disease phenotypes and, in so doing, provide opportunities for early diagnosis and for monitoring response to novel therapies.RV remodeling and function in PAH patients can be accurately assessed with echocardiography,1 especially 3-dimensional (3D) imaging, and cardiac magnetic resonance (CMR) imaging2 (Figure 1). CMR is the gold standard for measuring RV function, mass, and volumes.3 CMR measurements are highly reproducible, and permit serial tracking of RV remodeling and function in clinical trials. The common features found in PAH include RV hypertrophy and increased mass with concomitant cardiomyocyte atrophy,4 which are often associated with interventricular septal flattening and leftward bowing, and diastolic dysfunction, as well. Over time, gradual RV systolic dysfunction with reduced ejection fraction and dilatation develops in decompensated patients. The use of strain imaging with speckle-tracking echocardiography, CMR tagging, or feature tracking provides opportunities for early recognition of decreased systolic function. Many noninvasive measurements of RV remodeling and function with both echocardiography and CMR are associated with clinical risk, which enhances the relevance of their use as surrogate end points in the context of treatment trials.1,2Download figureDownload PowerPointFigure 1. Noninvasive phenotyping of pulmonary and RV remodeling in pulmonary hypertension with multimodality imaging. Pulmonary vascular remodeling (Left): A, Selected cross-sectional view of a CT pulmonary angiogram demonstrating large filling defects consistent with thrombus in the right and left pulmonary arteries (arrows) and a severely dilated pulmonary artery. B, corresponding 3D volume rendered views of the same patient (images courtesy of Dr Ritu Gill, Brigham and Women's Hospital, Boston, MA). C and D, Segmentation of the intraparenchymal pulmonary vasculature reconstructed from pulmonary CT angiograms in a subject without cardiopulmonary disease (C) and in a patient with pulmonary arterial hypertension (D). The lower panels illustrate quantification of the blood volume distribution profile, demonstrating loss of smaller vessel volume in contrast to the large vessels described as vascular pruning (images courtesy of Drs Farbod Rahaghi and Raúl San José Estépar, Brigham and Women's Hospital, Boston, MA). E and F, Pulmonary artery flow in a healthy subject (E) and in a patient with PAH (F) from phase-contrast MRI. The images demonstrate disruption of laminar flow and increased turbulence in PAH, and illustrate the emerging role of this technique to assess changes in pulmonary vascular hemodynamics, pulse wave velocity, and pulmonary vessel compliance noninvasively (images courtesy of Dr Yuchi Han, University of Pennsylvania, Philadelphia, PA). RV remodeling (Right): Imaging correlates of the different stages of pathological RV remodeling in the setting of PAH. G, Short-axis CMR images demonstrating RV hypertrophy and dilatation. H, Short-axis PET images demonstrating increased myocardial perfusion, and increased glucose utilization (I); short-axis pre- (J and L) and postcontrast (K and M) T1 CMR maps for quantification of interstitial fibrosis (images courtesy of Drs Ana Garcia Alvarez and Borja Ibañez, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain). N and O, postcontrast short-axis CMR images demonstrating LGE at the RV insertion points (arrows, N) and in the interventricular septum and RV free wall (arrows, O) consistent with areas of scar from RV pressure overload (images courtesy of Drs Michael Steigner and Raymond Kwong, Brigham and Women's Hospital, Boston, MA). Ao indicates aorta; CMR, cardiac magnetic resonance; CT, computed tomography; 3D, 3-dimensional; LGE, late gadolinium enhancement; LV, left ventricle; PA, pulmonary artery; PAH, pulmonary arterial hypertension; and RV, right ventricle.Quantitative imaging can also help delineate underlying molecular fingerprints of maladaptive RV remodeling in PAH.5 For example, RV ischemia, as evidenced by chest pain and reduced myocardial perfusion on radionuclide imaging6–9 and increased glucose utilization,6,8,10 reflects chronic reduction in RV perfusion resulting from decreased angiogenesis,11 capillary rarefaction,12 and potentially decreased coronary perfusion pressure in the setting of severe hypertrophy13 (Figure 1). There is also consistent evidence that mitochondrial oxidation in maladaptive RV remodeling is reduced,5 resulting in a number of metabolic changes including an increased reliance on nonoxidative glycolysis, which can be quantified by positron emission tomography (PET) imaging. Indeed, the shift from oxidative metabolism to the less efficient process of glycolysis results in a compensatory upregulation of glucose flux in RV myocytes.6,8,10 A similar shift to glycolysis away from glucose oxidation is seen in the pulmonary vessels of PAH. This correlates with an apparent increase in fatty acid metabolism, especially in the setting of severely elevated pulmonary pressure and RV dysfunction.14 However, there is a relatively increased reliance on glucose metabolism in comparison with fatty acids. Finally, increased fibrosis is a pathological hallmark of maladaptive RV remodeling. Late gadolinium enhancement (LGE)15 and potentially newer T1 mapping techniques16 with CMR can provide a quantitative measure of tissue fibrosis.Imaging is also able to provide a deeper understanding of the changes occurring in the pulmonary vasculature upstream from the RV (Figure 1). Phase-contrast MRI provides useful insights into pulmonary vascular hemodynamics, pulse wave velocity, and pulmonary vessel compliance.17 These measures can provide diagnostic information regarding pulmonary artery pressure. Importantly, noninvasive indices of pulmonary artery compliance and stiffness provide a direct physiological measure of the integrated effects of underlying abnormalities in tissue components of the pulmonary vessel wall, including the endothelium, elastin, and collagen. Normal pulmonary artery elasticity plays an important role in maintaining the normal transition from pulsatile blood flow generated by the RV to the steady flow at the capillary level. Increased pulmonary artery stiffness leads to higher RV workload and decreased function,18 and increased transmission of pulsatile force to small vessels, which can accelerate vascular injury and remodeling.19In addition, imaging can elucidate the pathophysiology of pulmonary vascular remodeling, including inflammation as a key mediator of endothelial cell activation and dysfunction,20 alterations in energy metabolism,21 and angiogenesis. As in maladaptive RV hypertrophy, pulmonary endothelial cells also show decreased mitochondrial function, reduced oxidative metabolism, and a significantly higher rate of glycolysis.21 This opens the possibility for using 18F-fluorodeoxyglucose (FDG) PET imaging potentially to evaluate endothelial cell activation and dysfunction in the pulmonary vasculature and to monitor treatment response.22,23 The FDG PET signal24 and 19F MRI25 can also be used to evaluate the inflammatory response in the pulmonary vasculature. Other imaging approaches targeting angiogenesis may also offer novel opportunities for early diagnosis and for monitoring response to novel therapies.Diagnosis and Risk AssessmentValvular Heart DiseaseFrom the earliest days of noninvasive imaging, valvular heart disease has been the foundation on which many technological advances have occurred. This is particularly true of echocardiography where miniaturization (allowing transesophageal, intracardiac, and intravascular imaging) and other technologies such as the development of Doppler, color flow mapping, 3D, tissue Doppler, and strain have been linked to the diagnosis, quantification, and prognostic predictors of valvular heart disease. For stenotic lesions, diagnosis and assessment of severity appeared fairly simple, but we now have a much deeper understanding of the relationship between flow and gradients and an increasing awareness of the prognosis of patients with conditions such as low flow-low gradient aortic stenosis . Individual and multicenter studies, such as Truly or Pseudo-severe Aortic Stenosis (TOPAS) and the European Multicenter Study, have provided important insights into this entity with clarity around decision making still being addressed, but with classification based on a combination of indexed stroke volume and mean transvalvular gradient.26–30 Once significant aortic stenosis is present, the diagnosis is relatively straightforward, but imaging enhances understanding of valvuloarterial interplay in which systemic arterial compliance, vascular resistance, and valvuloarterial impedance affect the left ventricle (LV). A common disease such as hypertension with aortic stenosis elevates impedance in series and, when coupled with increased aortic stiffness, accompanies aging and atherosclerosis and contributes to LV load and symptom development in an important way.31–35Advances in imaging are now allowing a deeper understanding of the pathobiology of the disease rather than merely an understanding of the hemodynamic consequences of valvular disease. One goal of multimodality imaging is to facilitate early diagnosis so as to potentially impact progression. One such agent is FDG, which has been investigated in early valvular inflammation, disease initiation, and progression.36 Aortic stenosis progression can be unpredictable but PET using 18F-fluoride as a marker of newly developing calcification has been correlated with alkaline phosphatase staining (Figure 2). Other more crude indices of calcification by computed tomography (CT) and echocardiography correlate with subsequent progression of aortic stenosis.37 These measures are now increasingly being used as end points of clinical trials. The extent of myocardial fibrosis using CMR techniques such as LGE and T1 mapping, particularly measures of extracellular volume), provides prognostic value and can be used to guide timing of intervention.38–43 Although EF may be normal despite these structural changes, sensitive functional measures of LV contractility such as strain and strain rate are now able to provide incremental prognostic information and guide timing of intervention before major morbidity and mortality occurs.44–46Download figureDownload PowerPointFigure 2. Targeted PET-CT imaging of aortic valve disease. A, Contrast-enhanced computed tomographic (CT) multiplanar reformatted views of the aortic valve and aortic root, with fused targeted images of calcium metabolism obtained with sodium fluoride (NaF) positron emission tomography (PET). B, Increased NaF uptake (arrows), reflecting active calcium deposition, despite no evidence of macroscopic calcifications on CT (images courtesy of Dr Marc Dweck, University of Edinburgh, England). LA indicates left atrium.The focus in regurgitant valvular diseases, such as mitral regurgitation, has mostly centered on regurgitant volume, the functional regurgitant orifice size, and the impact of the volume overload on chamber geometry and function in conjunction with functional capacity. Guideline recommendations for timing of intervention have been built around these relatively simple parameters but are known to be imprecise. Multimodality imaging can provide detailed 3D images of the mitral apparatus and can help us better understand potential mechanisms underlying various mitral valve disease processes. Refined strain measurement of the annulus and the leaflets themselves in the normal and disease state47,48 are advancing knowledge of the interplay between geometry and function, and the transition from an adaptive to a maladaptive or dysfunctional response, as well (Figure 3). The old concept of a mitral valve that remains constant throughout adult life is now clearly recognized as being incorrect. There is great interest in linking the genetic, hemodynamic, and functional drivers of the response of the valve, and, of possibly of greater interest, the ability to modify the maladaptive responses that occur.49 Leaflet lengthening and genetic changes in the leaflets50 allow understanding of the relationship between genotype and phenotype and will increasingly be used to guide intervention in a more unique patient-centered manner. Genetic mutations are associated with mitral valve prolapse and leaflet elongation, and modifiable cell migration pathways regulated by structural molecules can limit progression of valve degeneration. Dynamic 3D imaging has enhanced our understanding of mitral leaflet adaptation to ventricular remodeling in patients with the broadly defined category of ischemic mitral regurgitation and will be a fruitful area of research in coming years.Download figureDownload PowerPointFigure 3. Patient-specific mitral leaflet strain intensities displayed at midsystole for a typical normal mitral valve (A) and for a typical organic valve with mitral regurgitation valve (B). The strain intensities color code range from dark orange for high strain to dark blue for low strain. Reprinted from Ben Zekry et al47 with permission of the publisher. Copyright © 2016, American Heart Association, Inc.Cardio-OncologyThe field of cardio-oncology, which broadly describes the CV care of patients who have cancer, has provided novel translational insights for which imaging has and will likely continue to play an important role. Targeted kinase therapy is a mainstay of cancer treatment and has been associated with both detrimental and beneficial CV effects, and has identified some common pathways for cancer and the CV system. The cardiotoxicity of trastuzumab, a monoclonal antibody to HER2, became recognized and was additive to that of anthracyclines. These findings led to an understanding of the relationship with neuregulin-1, a growth factor released from endothelial cells associated with broad beneficial effects on the heart including improvement of cardiomyocyte survival, growth and proliferation, maintenance of cardiac myofibril structure, and promotion of angiogenesis, and has stimulated trials looking at the therapeutic benefit of recombinant neuregulin.51 The identification of the role of vascular endothelial growth factor signaling pathway inhibitors in being associated with hypertension, proteinuria, and preeclampsia has opened up a new area of investigation, and noninvasive imaging has been used widely to assess the development of cardiomyopathy in small-animal models.Noninvasive imaging has been vital in the management of patients treated with cardiotoxic chemotherapeutic agents. The anthracyclines have been a central focus in this area, and the use of ejection fraction has been and today still remains a useful parameter for guiding clinical decision making. Significant decrements in ejection fraction are associated with increasing cumulative doses of anthracyclines, and although the incidence of important LV dysfunction and heart failure vary, more than half of patients exposed to therapeutic doses of anthracyclines will develop abnormalities of cardiac structure and function within 6 years.52 The interplay between efficacy of the chemotherapy regimen and toxicity needs to be carefully weighed, especially because more sensitive indices such as global longitudinal strain and biomarkers such as troponin and brain natriuretic peptide identify abnormalities that may not be predictive of future LV systolic dysfunction, let alone clinically significant heart failure.53 Although most studies have used crude indices such as LV fractional shortening, left ventricular ejection fraction, or LV size, more sensitive markers of myocardial toxicity are helpful in the experimental design of studies evaluating techniques to reduce cardiotoxicity (Figure 4). The major benefit of advances in imaging is likely to be in the assessment of analogs with lower cardiotoxicity and with agents that reduce the cardiotoxicity of well-established agents and chemotherapeutic regimens.54 Examples of this strategy include the assessment of anthracycline analogs targeting the Top2α isoenzyme, which may be less cardiotoxic, agents such as dexrazoxane,55 and an engineered bivalent neuregulin-1β, which reduces toxicity in doxorubicin-induced cardiotoxicity.56 Another area of investigation in which imaging is facilitating understanding relates to predisposing factors such as common polymorphisms in genes involved in anthracycline metabolism.57,58Download figureDownload PowerPointFigure 4. Multimodality imaging in early detection of cardiac toxicity from cancer therapy. A, Black blood short-axis CMR image showing elevated T2 signal consistent with myocardial inflammation in several segments of the LV in a patient who started anthracycline-based chemotherapy several days before and presented with palpitations and a minimally elevated cardiac troponin. B and C, Contrast CMR short-axis images from a healthy control (B) and a patient who had anthracycline therapy for sarcoma 6 years before imaging (C) demonstrating no evidence of LGE. However, the extracellular volume from T1 measurements demonstrate a higher extracellular volume of 0.35 in the anthracycline-treated patient in comparison with a volume of 0.26 in the healthy control. (Images in A through E are courtesy of Dr Tomas Neilan, Massachusetts General Hospital, Boston, MA.) F and G, 2D echocardiographic images of a patient with breast cancer obtained before and after chemotherapy. There was normal LVEF prechemotherapy and 12 months after chemotherapy. Global longitudinal strain was normal at baseline but reduced 3 months after chemotherapy (images courtesy of Dr Thomas Marwick, Menzies Institute for Clinical Research, University of Tasmania, Australia). ANT indicates anterior; ANT_SEPT, anteroseptal; CMR, cardiac magnetic resonance; INF, inferior; LAT, lateral; LGE, late gadolinium enhancement; LV, left ventricle; LVEF, left ventricular ejection fraction; POST, posterior; and Sept, septal.Much work remains to establish the role of biomarkers and imaging in defining the cut points for heightened monitoring and adjusting potentially curative chemotherapy. Highly sensitive markers may raise undue concern and potentially lower the likelihood of a cancer cure. It will be important that investigators use common language to define adverse events in this arena and the Common Technology Criteria for Adverse Events is currently recognized as being that standard.59Left Ventricular HypertrophyEarly identification of disease constitutes an important goal of medicine in general and the role of CV imaging as a tool to achieve this goal is unfolding before our eyes. One example of this is the assessment of patients with left ventricular hypertrophy (LVH). Characterization of the genotype-phenotype relationship has been an active area of investigation in numerous areas, particularly in hypertrophic cardiomyopathy, which is caused by mutations in genes encoding sarcomere proteins. In advanced stages of disease, specific morphological subtypes are associated with certain genetic mutations and outcome.60–63 The ability to associate early, subclinical stages of disease before the development of LVH64 with specific sarcomere mutations provides an opportunity for interventions that could change the course of the disease. Morphological observations such as multiple crypts, anterior mitral leaflet elongation, and small LV cavity dimension in combination may prove useful in relating to genotype (Figure 5). These findings can and should be coupled with other imaging assessment, such as abnormalities in energy metabolism,65 diastolic dysfunction,66 T1 mapping assessment of extracellular volume expansion,67 and myocardial fibrosis.68 The clinical advances described have been coupled with basic and animal work showing early increases in extracellular matrix in the mouse model and increased type 1 collagen formation in humans, confirming that structural changes occur early in the disease. The pathway to fibrosis in hypertrophic cardiomyopathy is thus not merely a consequence of pressure overload and myocardial ischemia, as previously thought, but, at least in part, an intrinsic component of the disease itself. Research in this area is likely to provide opportunities for disease modification and changes in the genetically linked progression of disease.Download figureDownload PowerPointFigure 5. Advanced CMR imaging for phenoptyping patients with HCM. A, Cardiac structural and functional parameters shown to have significant independent association with the presence of sarcomere gene mutations in subclinical hypertrophic cardiomyopathy. B, Receiver operating characteristics (ROC) curve containing the 4 parameters and using patient classification according to study criteria for inclusion of carriers and controls as a reference, showed an area under the curve (AUC) of 0.85. C, In this case–control study, the authors used a 2×2 contingency table to calculate the percentage of rulings that agreed with genetic diagnosis and obtained a sensitivity of 75% (95% confidence interval [CI], 64–84) and specificity, 84% (95% CI, 73–91). AMVL indicates anterior mitral valve leaflet; CMR, cardiac magnetic resonance; FD, fractal dimension; G+LVH−, genotype positive, left ventricular hypertrophy negative; HCM, hypertrophic cardiomyopathy; and LVESViR, left ventricular end-systolic volume adjusted for age, body surface area, and sex. Reprinted from Captur et al64 with permission of the publisher. Copyright © 2014, American Heart Association, Inc.In other diseases associated with LVH, T1 mapping with CMR has now been used to differentiate different causes of LVH. For example, in patients with Anderson-Fabry disease, there appears to be a unique pattern in comparison with healthy controls and other patients with LVH from causes such as hypertension, aortic stenosis, hypertrophic cardiomyopathy, and amyloid light-chain amyloidosis.69 This will be a fruitful area of investigation because the prognostic impact of LVH varies widely based on etiology and the pattern of hypertrophy and remodeli
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