Comprehensive Cardiovascular Magnetic Resonance Diastolic Dysfunction Grading Shows Very Good Agreement Compared With Echocardiography.

OBJECTIVES: The aims of this study were to develop a comprehensive cardiovascular magnetic resonance (CMR) approach to diastolic dysfunction (DD) grading and to evaluate the accuracy of CMR in the diagnosis of DD compared with echocardiography. BACKGROUND: Left ventricular DD is routinely assessed using echocardiography. METHODS: Consecutive clinically referred patients (n = 46; median age 59 years; interquartile range: 46 to 68 years; 33% women) underwent both conventional echocardiography and CMR. CMR diastolic transmitral velocities (E and A) and myocardial tissue velocity (e') were measured during breath-hold using a validated high-temporal resolution radial sector-wise golden-angle velocity-encoded sequence. CMR pulmonary artery pressure was estimated from 4-dimensional flow analysis of blood flow vortex duration in the pulmonary artery. CMR left atrial volume was measured using the biplane long-axis area-length method. Both CMR and echocardiographic data were used to perform blinded grading of DD according to the 2016 joint American and European recommendations. RESULTS: Grading of DD by CMR agreed with that by echocardiography in 43 of 46 cases (93%), of which 9% were normal, 2% indeterminate, 63% grade 1 DD, 4% grade 2 DD, and 15% grade 3 DD. There was a very good categorical agreement, with a weighted Cohen kappa coefficient of 0.857 (95% confidence interval: 0.73 to 1.00; p < 0.001). CONCLUSIONS: A comprehensive CMR protocol for grading DD encompassing diastolic blood and myocardial velocities, estimated pulmonary artery pressure, and left atrial volume showed very good agreement with echocardiography.

The dynamics of extracellular gadolinium-based contrast agent excretion into pleural and pericardial effusions quantified by T1 mapping cardiovascular magnetic resonance.

INTRODUCTION: Excretion of cardiovascular magnetic resonance (CMR) extracellular gadolinium-based contrast agents (GBCA) into pleural and pericardial effusions, sometimes referred to as vicarious excretion, has been described as a rare occurrence using T1-weighted imaging. However, the T1 mapping characteristics as well as presence, magnitude and dynamics of contrast excretion into these effusions is not known. AIMS: To investigate and compare the differences in T1 mapping characteristics and extracellular GBCA excretion dynamics in pleural and pericardial effusions. METHODS: Clinically referred patients with a pericardial and/or pleural effusion underwent CMR T1 mapping at 1.5 T before, and at 3 (early) and at 27 (late) minutes after administration of an extracellular GBCA (0.2 mmol/kg, gadoteric acid). Analyzed effusion characteristics were native T1, ΔR1 early and late after contrast injection, and the effusion-volume-independent early-to-late contrast concentration ratio ΔR1early/ΔR1late, where ΔR1 = 1/T1post-contrast - 1/T1native. RESULTS: Native T1 was lower in pericardial effusions (n = 69) than in pleural effusions (n = 54) (median [interquartile range], 2912 [2567-3152] vs 3148 [2692-3494] ms, p = 0.005). Pericardial and pleural effusions did not differ with regards to ΔR1early (0.05 [0.03-0.10] vs 0.07 [0.03-0.12] s- 1, p = 0.38). Compared to pleural effusions, pericardial effusions had a higher ΔR1late (0.8 [0.6-1.2] vs 0.4 [0.2-0.6] s- 1, p < 0.001) and ΔR1early/ΔR1late (0.19 [0.08-0.30] vs 0.12 [0.04-0.19], p < 0.001). CONCLUSIONS: T1 mapping shows that extracellular GBCA is excreted into pericardial and pleural effusions. Consequently, the previously used term vicarious excretion is misleading. Compared to pleural effusions, pericardial effusions had both a lower native T1, consistent with lesser relative fluid content in relation to other components such as proteins, and more prominent early excretion dynamics, which could be related to inflammation. The clinical diagnostic utility of T1 mapping to determine quantitative contrast dynamics in pericardial and pleural effusions merits further investigation.

The relative contributions of myocardial perfusion, blood volume and extracellular volume to native T1 and native T2 at rest and during adenosine stress in normal physiology.

BACKGROUND: Both ischemic and non-ischemic heart disease can cause disturbances in the myocardial blood volume (MBV), myocardial perfusion and the myocardial extracellular volume fraction (ECV). Recent studies suggest that native myocardial T1 mapping can detect changes in MBV during adenosine stress without the use of contrast agents. Furthermore, native T2 mapping could also potentially be used to quantify changes in myocardial perfusion and/or MBV. Therefore, the aim of this study was to explore the relative contributions of myocardial perfusion, MBV and ECV to native T1 and native T2 at rest and during adenosine stress in normal physiology. METHODS: Healthy subjects (n = 41, 26 ± 5 years, 51% females) underwent 1.5 T cardiovascular magnetic resonance (CMR) scanning. Quantitative myocardial perfusion [ml/min/g] and MBV [%] maps were computed from first pass perfusion imaging at adenosine stress (140 microg/kg/min infusion) and rest following an intravenous contrast bolus (0.05 mmol/kg, gadobutrol). Native T1 and T2 maps were acquired before and during adenosine stress. T1 maps at rest and stress were also acquired following a 0.2 mmol/kg cumulative intravenous contrast dose, rendering rest and stress ECV maps [%]. Myocardial T1, T2, perfusion, MBV and ECV values were measured by delineating a region of interest in the midmural third of the myocardium. RESULTS: During adenosine stress, there was an increase in myocardial native T1, native T2, perfusion, MBV, and ECV (p ≤ 0.001 for all). Myocardial perfusion, MBV and ECV all correlated with both native T1 and native T2, respectively (R2 = 0.35 to 0.61, p < 0.001 for all). Multivariate linear regression revealed that ECV and perfusion together best explained the change in native T2 (ECV beta 0.21, p = 0.02, perfusion beta 0.66, p < 0.001, model R2 = 0.64, p < 0.001), and native T1 (ECV beta 0.50, p < 0.001, perfusion beta 0.43, p < 0.001, model R2 = 0.69, p < 0.001). CONCLUSIONS: Myocardial native T1, native T2, perfusion, MBV, and ECV all increase during adenosine stress. Changes in myocardial native T1 and T2 during adenosine stress in normal physiology can largely be explained by the combined changes in myocardial perfusion and ECV. TRIAL REGISTRATION: Clinicaltrials.gov identifier NCT02723747. Registered March 16, 2016.

Pneumatic tube transport affects platelet function measured by multiplate electrode aggregometry.

Multiple electrode aggregometry (MEA) is used to measure platelet function. Pneumatic tube transport systems (PTS) for delivery of patient samples to a central laboratory are often used to reduce turnaround time for vital analyses. We evaluated the effects of PTS transport on platelet function as measured by MEA. Duplicate samples were collected from 58 individuals. One sample was sent using PTS and the other was carried by personnel to the lab. Platelet function was measured by means of a Multiplate® analyzer using the ADP test, ASPI test, COL test, RISTO test and TRAP test. Samples transported using PTS showed a reduction of AUC-values of up to a 100% of the average as compared to samples carried by personnel and a majority showed reductions of AUC-values greater than 20% of the average. Bias±95% limits of agreement for the ADP test were 26±56% of the average. Bias±95% limits of agreement for the ASPI test were 16±58% of the average. Bias±95% limits of agreement for the COL test were 20±54% of the average. Bias±95% limits of agreement for the RISTO were 14±79% of the average. Bias±95% limits of agreement for the TRAP test were 19±45% of the average. We conclude that PTS transport affect platelet activity as measured by MEA. We advise against clinical decisions regarding platelet function on the basis of samples sent by PTS in our hospital settings.