Background-Diffuse myocardial fibrosis is a final end point in most cardiac diseases. It is missed by the cardiovascular magnetic resonance (CMR) late gadolinium enhancement technique. Currently, quantifying diffuse myocardial fibrosis requires invasive biopsy, with inherent risk and sampling error. We have developed a robust and noninvasive technique, equilibrium contrast CMR (EQ-CMR) to quantify diffuse fibrosis and have validated it against the current gold standard of surgical myocardial biopsy. Methods and Results-The 3 principles of EQ-CMR are a bolus of extracellular gadolinium contrast followed by continuous infusion to achieve equilibrium; a blood sample to measure blood volume of distribution (1Ϫhematocrit); and CMR to measure pre-and postequilibrium T1 (with heart rate correction). The myocardial volume of distribution is calculated, reflecting diffuse myocardial fibrosis. Clinical validation occurred in patients undergoing aortic valve replacement for aortic stenosis or myectomy in hypertrophic cardiomyopathy (nϭ18 and nϭ8, respectively). Surgical biopsies were analyzed for picrosirius red fibrosis quantification on histology. Key Words: magnetic resonance imaging Ⅲ cardiomyopathy Ⅲ imaging Ⅲ endomyocardial fibrosis Ⅲ collagen F ibrosis is a final common end point in virtually all pathological processes in human organs and tissues. In the heart, focal fibrosis (scar) as a result of myocardial infarction is the leading cause of death and heart failure in the world. 1 Cardiovascular magnetic resonance (CMR) using the late gadolinium enhancement (LGE) contrast technique is the gold standard method for its assessment. 2,3 Focal fibrosis also occurs in other diseases, including cardiomyopathy, 4 myocarditis, 5 and infiltrative diseases. 6 Scar leads to an increased volume of distribution for gadolinium and slower contrast kinetics, 7 leading to late enhancement of scar by CMR. Clinical Perspective on p 144Diffuse myocardial fibrosis is a covert process that occurs as a part of normal aging. 8 -10 It is accelerated in diseases such as hypertension, aortic stenosis, and cardiomyopathy, 11Ϫ13 where it contributes to breathlessness, heart failure, and arrhythmia. 14 -16 Unlike scar, however, it may be reversible and is a treatment target. 17,18 Currently, the only method to quantify diffuse fibrosis is invasive biopsy, which carries significant morbidity and is prone to sampling error. 19 The LGE technique cannot be used to visualize diffuse fibrosis because "normal" myocardium with diffuse fibrosis is "nulled" to highlight focal scar, thereby losing all information of any background interstitial expansion. Recently, attempts to quantify diffuse fibrosis with CMR have been made, but they have required complex kinetic modeling and have not definitively excluded confounding factors such as heart rate, body composition, and renal clearance variability. Histological validation, where present, has In this study, we describe a potentially clinically applicable, robust, noninvasive method to quantify diffuse myo...

Stratification of AL patients into three stages is possible with two readily available and reproducible tests setting the stage for more consistent and reliable cross comparisons of therapeutic outcomes.

Posttransplantation lymphoproliferative disorder (PTLD) is an uncommon but often fatal complication of solid organ transplantation that occurs in approximately 3% of patients. To determine the relative importance and relationship of potential risk factors for PTLD before transplantation (i.e., Epstein-Barr virus [EBV] serostatus of the recipient and the cytomegalovirus [CMV] sero-status of the recipient and the potential donor) and the principal risk factor after transplantation (immunosuppression with antilymphocyte antibody), we analyzed the findings for the first 381 consecutive adult nonrenal transplant recipients seen at Mayo Clinic. In the absence of the other risk factors, the incidence rate of PTLD for EBV-seronegative recipients was 24 times higher (95% confidence interval [CI]: 6.2, 89) than that for EBV-seropositive recipients. The additional risk factors of therapy with OKT3 for rejection and CMV seromismatch (i.e., a negative recipient and a positive donor) each further amplified this risk four- to sixfold. Together, all three risk factors acted synergistically to increase the incidence rate of fatal and/or CNS PTLD by a factor of 654 (CI: 368, 1,162) compared with the low incidence rate (.458 cases per 100 person years) when none of these risk factors were present. Pretransplantation determination of recipient EBV and CMV serostatus can identify a subgroup of patients whose risk for severe PTLD may preclude transplantation.