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Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of myocardial infarction that most frequently affects younger women, making it an important cause of morbidity and mortality within these demographics. The evolution of intracoronary imaging, improved diagnosis with coronary angiography, and ongoing research efforts and attention via social media, has led to increasing recognition of this previously underdiagnosed condition. In this review, we provide a summary of the current body of knowledge, as well as focused updates on the pathogenesis of SCAD, insights on genetic susceptibility, contemporary diagnostic tools, and immediate, short- and long-term management., (© 2024 The Authors. Clinical Cardiology published by Wiley Periodicals, LLC.)

Spontaneous coronary artery dissection (SCAD) is a condition that leads to tearing of the coronary vessel wall in the absence of trauma, iatrogenic injury, or atherosclerosis. SCAD is an important cause of myocardial infarction in young women, leading to significant cardiovascular morbidity and mortality. Within cohorts of women aged around 50 years on average, who experience acute coronary syndrome, the prevalence of SCAD is 22.5%- 35%. Over the past decade, SCAD research has expanded rapidly, leading to improved understanding of this condition. In this review, we provide a summary of the current body of knowledge, highlight areas of ongoing research, and identify existing knowledge gaps. Specifically, we provide a focused update on the pathogenesis of SCAD, including genetic and associated conditions, clinical presentation and diagnosis, prognosis, and short-term and long-term management. Highlighted areas include the following: insights from recent genome-wide association studies; intracoronary imaging for the diagnosis of SCAD; the role of cardiac computed tomography angiography to assess for vessel healing; revascularization strategies and challenges; cardiogenic shock in SCAD; and the increasingly recognized burden of anxiety, depression, and posttraumatic stress disorder among SCAD patients., (© 2024 The Authors.)

Background: Despite historically being considered a channelopathy, subtle structural changes have been reported in Brugada syndrome (BrS) on histopathology and cardiac magnetic resonance (CMR) imaging. It is not known if these structural changes progress over time., Objective: The study sought to assess if structural changes in BrS evolve over time with serial CMR assessment and to investigate the utility of parametric mapping techniques to identify diffuse fibrosis in BrS., Methods: Patients with a diagnosis of BrS based on international guidelines and normal CMR at least 3 years prior to the study period were invited to undergo repeat CMR. CMR images were analyzed de novo and compared at baseline and follow-up., Results: Eighteen patients with BrS (72% men; mean age at follow-up 47.4 ± 8.9 years) underwent serial CMR with an average of 5.0 ± 1.7 years between scans. No patients had late gadolinium enhancement (LGE) on baseline CMR, but 4 (22%) developed LGE on follow-up, typically localized to the right ventricular (RV) side of the basal septum. RV end-systolic volume increased over time ( P = .04) and was associated with a trend toward reduction in RV ejection fraction ( P = .07). Four patients showed a reduction in RV ejection fraction >10%. There was no evidence of diffuse myocardial fibrosis observed on parametric mapping., Conclusions: Structural changes may evolve over time with development of focal fibrosis, evidenced by LGE on CMR in a significant proportion of patients with BrS. These findings have implications for our understanding of the pathological substrate in BrS and the longitudinal evaluation of patients with BrS., (© 2022 Heart Rhythm Society. Published by Elsevier Inc.)

Functional magnetic resonance imaging (fMRI) was used to measure activity in human somatosensory cortex and to test for cross-digit suppression. Subjects received stimulation (vibration of varying amplitudes) to the right thumb (target) with or without concurrent stimulation of the right middle finger (mask). Subjects were less sensitive to target stimulation (psychophysical detection thresholds were higher) when target and mask digits were stimulated concurrently compared with when the target was stimulated in isolation. fMRI voxels in a region of the left postcentral gyrus each responded when either digit was stimulated. A regression model (called a forward model) was used to separate the fMRI measurements from these voxels into two hypothetical channels, each of which responded selectively to only one of the two digits. For the channel tuned to the target digit, responses in the left postcentral gyrus increased with target stimulus amplitude but were suppressed by concurrent stimulation to the mask digit, evident as a shift in the gain of the response functions. For the channel tuned to the mask digit, a constant baseline response was evoked for all target amplitudes when the mask was absent and responses decreased with increasing target amplitude when the mask was concurrently presented. A computational model based on divisive normalization provided a good fit to the measurements for both mask-absent and target + mask stimulation. We conclude that the normalization model can explain cross-digit suppression in human somatosensory cortex, supporting the hypothesis that normalization is a canonical neural computation., (Copyright © 2015 the American Physiological Society.)

Objective: Chronic pulmonary regurgitation (PR) has deleterious effects on right ventricular (RV) function in repaired tetralogy of Fallot (ToF). However, there are little data regarding right ventricular outflow tract (RVOT) contractile dysfunction in response to chronic PR and on both RV and LV volumes and function., Methods: We retrospectively identified consecutive patients with PR who were referred for magnetic resonance imaging quantification of "free PR" detected on echocardiography between 2003 and 2008. Patients had ToF and a transannular patch procedure (n = 30, 25.1 ± 1.2 years) or PR resulting from valvar pulmonary stenosis treated with surgical or percutaneous valvotomy (n = 30, 26.6 ± 1.8 years)., Results: The ToF and the PS groups were well matched for age at scan, age at repair surgery in ToF or initial valvotomy in PS, duration of exposure to PR, body surface area, heart rate, PR fraction, net forward pulmonary artery flow, and main and branch pulmonary artery dimensions. Severe PR fractions were identified in both groups (ToF: 40% ± 1% vs PS: 37% ± 2%, P = .2). Indexed RV and LV end-diastolic volumes were similar for both ToF and PS groups (RV end-diastolic volume index: 137 ± 6 mL/m(2) vs 128 ± 5 mL/m(2), P = .2, and LV end-diastolic volume index: 72 ± 2 mL/m(2) vs 67 ± 2 mL/m(2), P = .1, respectively). RV mass was also similar between groups (95 ± 5 g vs 81 ± 6 g, respectively, P = .08). However, indexed RV and LV end-systolic volumes were consistently higher in ToF when compared with PS (RV end-systolic volume index: 70 ± 5 mL/m(2) vs 54 ± 3 mL/m(2), P < .01, and LV end-systolic volume index: 29 ± 1 mL/m(2) vs 22 ± 1 mL/m(2), P < .01, respectively). These changes were reflected in lower biventricular systolic function in patients with ToF when compared with PS (RV ejection fraction: 52% ± 1.5% vs 59% ± 1%, P < .001, and LV ejection fraction: 61% ± 1% vs 67 ± 1%, P < .001, respectively). Although RV transannular plane systolic excursion was not significantly different between the groups (P = .86), the RV outflow tract was considered contractile in only 50% of patients with ToF compared with 93% of patients with PS (P = .0004). RV volumes and function were similar when only patients with contractile RV outflow tracts were compared., Conclusions: RV outflow tract patch dysfunction in repaired ToF is responsible for higher end-systolic volumes and thus lower global measures of ventricular systolic function. These findings were not evident in cases of PS treated with valvotomy with comparable amount of PR. These observations highlight the importance of the initial repair surgery in ToF for late outcomes., (Copyright © 2012 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.)

We measured cortical activity with functional magnetic resonance imaging to probe the involvement of early visual cortex in visual short-term memory and visual attention. In four experimental tasks, human subjects viewed two visual stimuli separated by a variable delay period. The tasks placed differential demands on short-term memory and attention, but the stimuli were visually identical until after the delay period. Early visual cortex exhibited sustained responses throughout the delay when subjects performed attention-demanding tasks, but delay-period activity was not distinguishable from zero when subjects performed a task that required short-term memory. This dissociation reveals different computational mechanisms underlying the two processes.

Possible hemifield differences in texture segregation were investigated for both simple (Fourier, linear) and complex (non-Fourier, second-order) texture channels. There was only a very small lower-field advantage for texture segregation, consistent with the notion that the major processing in texture segregation is quite low level, perhaps V1. Complex-channel tasks do not show larger hemifield asymmetries than do simple-channel tasks, which suggests that the processes in complex texture channels are not higher level than those in simple.