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...

Though rare in incidence, chylothorax can lead to significant morbidity and mortality. Its occurrence corresponds to increased mortality following esophagectomy. Leakage of chyle and lymph leads to significant loss of essential proteins, immunoglobulins, fat, vitamins, electrolytes and water. The presence of chylomicrons and a triglyceride level >110 mg/dl in the aspirated pleural fluid confirms the diagnosis of chylothorax. Identifying the aetiology using different diagnostic tests is important in planning treatment. While therapeutic thoracentesis provides relief from respiratory symptoms, the nutritional deficiency will continue to persist or deteriorate unless definitive therapeutic measures are instituted to stop leakage of chyle into the pleural space. Definitive therapy consists of obliteration and prevention of recurrence of chylothorax. Aggressive surgical therapy is recommended for post-traumatic or post-surgical chylothorax.

Background-The mechanisms that sustain ventricular fibrillation (VF) in the human heart remain unclear. Experimental models have demonstrated either a periodic source (mother rotor) or multiple wavelets as the mechanism underlying VF. The aim of this study was to map electrical activity from the entire ventricular epicardium of human hearts to establish the relative roles of these mechanisms in sustaining early human VF. Methods and Results-In 10 patients undergoing cardiac surgery, VF was induced by burst pacing, and 20 to 40 seconds of epicardial activity was sampled (1 kHz) with a sock containing 256 unipolar contact electrodes connected to a UnEmap system. Signals were interpolated from the electrode sites to a fine regular grid (100ϫ100 points), and dominant frequencies (DFs) were calculated with a fast Fourier transform with a moving 4096-ms window (10-ms increments). Epicardial phase was calculated at each grid point with the Hilbert transform, and phase singularities and activation wavefronts were identified at 10-ms intervals. Early human VF was sustained by large coherent wavefronts punctuated by periods of disorganized wavelet behavior. The initial fitted DF intercept was 5.11Ϯ0.25 (meanϮSE) Hz (PϽ0.0001), and DF increased at a rate of 0.018Ϯ0.005 Hz/s (PϽ0.01) during VF, whereas combinations of homogeneous, heterogeneous, static, and mobile DF domains were observed for each of the patients. Epicardial reentry was present in all fibrillating hearts, typically with low numbers of phase singularities. In some cases, persistent phase singularities interacted with multiple complex wavelets; in other cases, VF was driven at times by a single reentrant wave that swept the entire epicardium for several cycles. Conclusions-Our data support both the mother rotor and multiple wavelet mechanisms of VF, which do not appear to be mutually exclusive in the human heart. (Circulation. 2006;114:536-542.)