Detection of large LRP by NIRS at non-stented sites in a target artery was associated with an increased risk of future MACCE. These findings support ongoing prospective studies to further evaluate the ability of NIRS to identify vulnerable patients.

Large lipid cores similar to those recently detected by NIRS at STEMI culprit sites were frequently observed at culprit sites in patients with non-STEMI and UA. These findings support ongoing prospective trials designed to determine if NIRS can provide site-specific prediction of future acute coronary events.

Background Initial protocols for return to play cardiac testing in young competitive athletes following SARS‐CoV‐2 infection recommended cardiac troponin (cTn) to screen for cardiac involvement. This study aimed to define the diagnostic yield of cTn in athletes undergoing cardiovascular testing following SARS‐CoV‐2 infection. Methods and Results This prospective, observational cohort study from ORCCA (Outcomes Registry for Cardiac Conditions in Athletes) included collegiate athletes who underwent cTn testing as a component of return to play protocols following SARS‐CoV‐2 infection. The cTn values were stratified as undetectable, detectable but within normal limits, and abnormal (>99% percentile). The presence of probable or definite SARS‐CoV‐2 myocardial involvement was compared between those with normal versus abnormal cTn levels. A total of 3184/3685 (86%) athletes in the ORCCA database met the inclusion criteria for this study (age 20±1 years, 32% female athletes, 28% Black race). The median time from SARS‐CoV‐2 diagnosis to cTn testing was 13 days (interquartile range, 11, 18 days). The cTn levels were undetectable in 2942 athletes (92%), detectable but within normal limits in 210 athletes (7%), and abnormal in 32 athletes (1%). Of the 32 athletes with abnormal cTn testing, 19/32 (59%) underwent cardiac magnetic resonance imaging, 30/32 (94%) underwent transthoracic echocardiography, and 1/32 (3%) did not have cardiac imaging. One athlete with abnormal troponin met the criteria for definite or probable SARS‐CoV‐2 myocardial involvement. In the total cohort, 21/3184 (0.7%) had SARS‐CoV‐2 myocardial involvement, among whom 20/21 (95%) had normal troponin testing. Conclusions Abnormal cTn during routine return to play cardiac screening among competitive athletes following SARS‐CoV‐2 infection appears to have limited diagnostic utility.

Background— Neoatherosclerosis is an emerging phenomenon in which lipid-rich plaques (LRPs) develop within pre-existing stents. This study was undertaken to describe near-infrared spectroscopy (NIRS) and intravascular ultrasound findings in pre-existing stents and to compare NIRS findings in pre-existing stents, in which an increased lipid signal has been speculated to indicate neoatherosclerosis, and NIRS findings in a control group of freshly implanted stents, in which any lipid signal originates from fibroatheroma under the stent. Methods and Results— At the site of LRP detected by NIRS in a cohort of pre-existing stents, intravascular ultrasound was used to determine the presence of neointimal tissue. The lipid-core burden index and maximum lipid-core burden index in 4 mm were measured within stented segments. Findings were compared between pre-existing stents and a control group of freshly implanted stents. Among 60 pre-existing stents implanted 5.5±4.0 years earlier, NIRS detected LRP in 33%. At the site of LRP, intravascular ultrasound found no neointimal tissue in 35% of cases. NIRS findings in pre-existing stents were indistinguishable from those of freshly implanted stents (lipid-core burden index: 50±72 versus 42±58; P =0.40 and maximum lipid-core burden index in 4 mm: 156±184 versus 155±203; P =0.69). Conclusions— The detection of LRP in a pre-existing stent by NIRS alone is not reliable evidence of neoatherosclerosis, as the lipid signal may originate from fibroatheroma underlying the stent. By identifying the presence or absence of neointimal tissue at the site of LRP detected by NIRS, intravascular ultrasound may provide some insight into the potential source of the lipid signal in pre-existing stents. Registration Information— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01694368.

Background The COVID-19 pandemic caused massive disruption in usual care delivery patterns in hospitals across the USA, and highlighted long-standing inequities in health care delivery and outcomes. Its effect on hospital operations, and whether the magnitude of the effect differed for hospitals serving historically marginalized populations, is unknown. Objective To investigate the perspectives of hospital leaders on the effects of COVID-19 on their facilities’ operations and patient outcomes. Methods A survey was administered via print and electronic means to hospital leaders at 588 randomly sampled acute-care hospitals participating in Medicare’s Inpatient Prospective Payment System, fielded from November 2020 to June 2021. Summary statistics were tabulated, and responses were adjusted for sampling strategy and non-response. Results There were 203 responses to the survey (41.6%), with 20.7% of respondents representing safety-net hospitals and 19.7% representing high-minority hospitals. Over three-quarters of hospitals reported COVID testing shortages, about two-thirds reported staffing shortages, and 78.8% repurposed hospital spaces to intensive care units, with a slightly higher proportion of high-minority hospitals reporting these effects. About half of respondents felt that non-COVID inpatients received worsened quality or outcomes during peak COVID surges, and almost two-thirds reported worsened quality or outcomes for outpatient non-COVID patients as well, with few differences by hospital safety-net or minority status. Over 80% of hospitals participated in alternative payment models prior to COVID, and a third of these reported decreasing these efforts due to the pandemic, with no differences between safety-net and high-minority hospitals. Conclusions COVID-19 significantly disrupted the operations of hospitals across the USA, with hospitals serving patients in poverty and racial and ethnic minorities reporting relatively similar care disruption as non-safety-net and lower-minority hospitals. Supplementary Information The online version contains supplementary material available at 10.1007/s11606-022-08002-5.

Background Cardiogenic shock from most causes has unfavorable prognosis. Hypertrophic cardiomyopathy (HCM) can uncommonly present with apical ballooning and shock in association with sudden development of severe and unrelenting left ventricular (LV) outflow obstruction. Typical HCM phenotypic features of mild septal thickening, outflow gradients, and distinctive mitral abnormalities differentiate these patients from others with Takotsubo syndrome, who have normal mitral valves and no outflow obstruction. Methods and Results We analyzed 8 patients from our 4 HCM centers with obstructive HCM and abrupt presentation of cardiogenic shock with LV ballooning, and 6 cases reported in literature. Of 14 patients, 10 (71%) were women, aged 66±9 years, presenting with acute symptoms: LV ballooning; depressed ejection fraction (25±5%); refractory systemic hypotension; marked LV outflow tract obstruction (peak gradient, 94±28 mm Hg); and elevated troponin, but absence of atherosclerotic coronary disease. Shock was managed with intravenous administration of phenylephrine (n=6), norepinephrine (n=6), β‐blocker (n=7), and vasopressin (n=1). Mechanical circulatory support was required in 8, including intra‐aortic balloon pump (n=4), venoarterial extracorporeal membrane oxygenation (n=3), and Impella and Tandem Heart in 1 each. In refractory shock, urgent relief of obstruction by myectomy was performed in 5, and alcohol ablation in 1. All patients survived their critical illness, with full recovery of systolic function. Conclusions When cardiogenic shock and LV ballooning occur in obstructive HCM, they are marked by distinctive anatomic and physiologic features. Relief of obstruction with targeted pharmacotherapy, mechanical circulatory support, and myectomy, when necessary for refractory shock, may lead to survival and normalization of systolic function.

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