Towards accurate and precise T1 and extracellular volume mapping in the myocardium: a guide to current pitfalls and their solutions

Mapping of the longitudinal relaxation time (T1) and extracellular volume (ECV) offers a means of identifying pathological changes in myocardial tissue, including diffuse changes that may be invisible to existing T1-weighted methods. This technique has recently shown strong clinical utility for pathologies such as Anderson- Fabry disease and amyloidosis and has generated clinical interest as a possible means of detecting small changes in diffuse fibrosis; however, scatter in T1 and ECV estimates offers challenges for detecting these changes, and bias limits comparisons between sites and vendors. There are several technical and physiological pitfalls that influence the accuracy (bias) and precision (repeatability) of T1 and ECV mapping methods. The goal of this review is to describe the most significant of these, and detail current solutions, in order to aid scientists and clinicians to maximise the utility of T1 mapping in their clinical or research setting. A detailed summary of technical and physiological factors, issues relating to contrast agents, and specific disease-related issues is provided, along with some considerations on the future directions of the field. Towards accurate and precise T1 and extracellular volume mapping in the myocardium: a guide to current pitfalls and their solutions. Available from: https://www.researchgate.net/publication/317548806_Towards_accurate_and_precise_T1_and_extracellular_volume_mapping_in_the_myocardium_a_guide_to_current_pitfalls_and_their_solutions [accessed Jun 13, 2017]

Heart Failure–Induced Skeletal Muscle Wasting

Purpose of Review: Heart failure (HF) is a structural or functional cardiac abnormality which leads to failure of the heart to deliver oxygen commensurately with the requirements of the tissues and it may progress to a generalized wasting of skeletal muscle, fat tissue, and bone tissue (cardiac cachexia). Clinically, dyspnea, fatigue, and exercise intolerance are some typical signs and symptoms that characterize HF patients. This review focused on the phenotypic characteristics of HF-induced skeletal myopathy as well as the mechanisms of muscle wasting due to HF and highlighted possible therapeutic strategies for skeletal muscle wasting in HF. Recent Findings: The impaired exercise capacity of those patients is not attributed to the reduced blood flow in the exercising muscles, but rather to abnormal metabolic responses, myocyte apoptosis and atrophy of skeletal muscle. Specifically, the development of skeletal muscle wasting in chronic HF is characterized by structural, metabolic, and functional abnormalities in skeletal muscle and may be a result not only of reduced physical activity, but also of metabolic or hormonal derangements that favour catabolism over anabolism. In particular, abnormal energy metabolism, mitochondrial dysfunction, transition of myofibers from type I to type II, muscle atrophy, and reduction in muscular strength are included in skeletal muscle abnormalities which play a central role in the decreased exercise capacity of HF patients. Summary: Skeletal muscle alterations and exercise intolerance observed in HF are reversible by exercise training, since it is the only demonstrated intervention able to improve skeletal muscle metabolism, growth factor activity, and functional capacity and to reverse peripheral abnormalities. © 2020, Springer Science+Business Media, LLC, part of Springer Nature

Decreased atrioventricular plane displacement after acute myocardial infarction yields a concomitant decrease in stroke volume

Acute myocardial infarction (AMI) can progress to heart failure, which has a poor prognosis. Normally, 60% of stroke volume (SV) is attributed to the longitudinal ventricular shortening and lengthening evident in the atrioventricular plane displacement (AVPD) during the cardiac cycle, but there is no information on how the relationship changes between SV and AVPD before and after AMI. Therefore, the aim of this study was to determine how SV depends on AVPD before and after AMI in two swine models. Serial cardiac magnetic resonance imaging was carried out before and 1-2 h after AMI in a microembolization model (n = 12) and an ischemia-reperfusion model (n = 14). A subset of pigs (n = 7) were additionally imaged at 24 h and at 7 days. Cine and late gadolinium enhancement images were analyzed for cardiac function, AVPD measurements and infarct size estimation, respectively. AVPD decreased (P < 0.05) in all myocardial regions after AMI, with a concomitant SV decrease (P < 0.001). The ischemia-reperfusion model affected SV to a higher degree and had a larger AVPD decrease than the microembolization model (-29 ± 14% vs. -15 ± 18%; P < 0.05). Wall thickening decreased in infarcted areas (P < 0.001), and A-wave AVPD remained unchanged (P = 0.93) whereas E-wave AVPD decreased (P < 0.001) after AMI. We conclude that AVPD is coupled to SV independent of infarct type but likely to a greater degree in ischemia-reperfusion infarcts compared with microembolization infarcts. AMI reduces diastolic early filling AVPD but not AVPD from atrial contraction. These findings shed light on the physiological significance of atrioventricular plane motion when assessing acute and subacute myocardial infarction.NEW & NOTEWORTHY The link between cardiac longitudinal motion, measured as atrioventricular plane displacement (AVPD), and stroke volume (SV) is investigated in swine after acute myocardial infarction (AMI). This cardiac magnetic resonance study demonstrates a close coupling between AVPD and SV before and after AMI in an experimental setting and demonstrates that this connection is present in ischemia-reperfusion and microembolization infarcts, acutely and during the first week. Furthermore, AVPD is equally and persistently depressed in infarcted and remote myocardium after AMI

Prophylactic antibiotic treatment in severe acute ischemic stroke: the Antimicrobial chemopRrophylaxis for Ischemic STrokE In MaceDonIa–Thrace Study (ARISTEIDIS)

Infections represent a leading cause of mortality in patients with acute ischemic stroke, but it is unclear whether prophylactic antibiotic treatment improves the outcome. We aimed to evaluate the effects of this treatment on infection incidence and short-term mortality. This was a pragmatic, prospective multicenter real-world analysis of previously independent consecutive patients with acute ischemic stroke who were >18 years, and who had at admission National Institutes of Health Stroke Scale (NIHSS) >11. Patients with infection at admission or during the preceding month, with axillary temperature at admission >37 °C, with chronic inflammatory diseases or under treatment with corticosteroids were excluded from the study. Among 110 patients (44.5 % males, 80.2 ± 6.8 years), 31 (28.2 %) received prophylactic antibiotic treatment, mostly cefuroxime (n = 21). Prophylactic antibiotic treatment was administered to 51.4 % of patients who developed infection, and to 16.4 % of patients who did not (p < 0.001). Independent predictors of infection were NIHSS at admission [relative risk (RR) 1.16, 95 % confidence interval (CI) 1.08–1.26, p < 0.001] and prophylactic antibiotic treatment (RR 5.84, 95 % CI 2.03–16.79, p < 0.001). The proportion of patients who received prophylactic antibiotic treatment did not differ between patients who died during hospitalization and those discharged, or between patients who died during hospitalization or during follow-up and those who were alive 3 months after discharge. Prophylactic administration of antibiotics in patients with severe acute ischemic stroke is associated with an increased risk of infection during hospitalization, and does not affect short-term mortality risk. © 2016, SIMI