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Background: During the height of the coronavirus disease 2019 (COVID-19) pandemic in New York City, COVID-19 hospitalization was associated with high mortality. It is unknown how palliative care wa...

A retained intracardiac catheter fragment left in situ for 2 years was incidentally found in a patient presenting with worsening heart failure and atrial fibrillation. This case describes the diagnostic evaluation of this rare event, with successful endovascular retrieval and resolution of his symptoms. (Level of Difficulty: Advanced.), Central Illustration

Temporary mechanical circulatory support (tMCS) has become central in the treatment of refractory cardiogenic shock and can be used to bridge patients to durable MCS, heart transplant or recovery. This review will discuss contemporary data regarding bridging strategies utilizing tMCS.There has been significant growth in tMCS use recently, driven by increased familiarity with tMCS devices, and increased experience with both implantation and management. Identifying goals of therapy at the time of therapy initiation can facilitate better outcomes. The three primary goals are bridge to recovery, bridge to heart transplantation or bridge to durable left ventricular assist device. Bridging to recovery requires adequate treatment of underlying conditions and optimization of haemodynamics. Bridging to heart transplantation has become more frequent following changes to the heart allocation policy. Despite early concerns, patients bridge with tMCS, including ventricular-arterial extracorporeal membrane oxygenation, do not appear to have worse posttransplant outcomes. When bridging to durable mechanical circulatory support, tMCS can be used to enhance end-organ dysfunction and improve perioperative outcomes. In situations in which none of these goals are attainable, palliative care plays a critical role to identify patient wishes and assist with withdrawal of care when necessary.The use of tMCS, as a bridge to recovery or heart replacement therapy in patients with refractory cardiogenic shock has grown significantly over the past decade. Multiple device choices are available and must be chosen appropriately to address the specific situation and the goals of therapy.

Cardiac injury is associated with critical COVID-19, yet its etiology remains debated. To elucidate the pathogenic mechanisms of COVID-19-associated cardiac injury, we conducted a single-center prospective cohort study of 69 COVID-19 decedents. Of six cardiac histopathologic features, microthrombi was the most commonly detected (n=48, 70%). We tested associations of cardiac microthrombi with biomarkers of inflammation, cardiac injury, and fibrinolysis and with in-hospital antiplatelet therapy, therapeutic anticoagulation, and corticosteroid treatment, while adjusting for multiple clinical factors, including COVID-19 therapies. Higher peak ESR and CRP during hospitalization were independently associated with higher odds of microthrombi. Using single nuclei RNA-sequence analysis, we discovered an enrichment of pro-thrombotic/anti-fibrinolytic, extracellular matrix remodeling, and immune-potentiating signaling amongst cardiac fibroblasts in microthrombi-positive COVID-19 hearts relative to microthrombi-negative COVID-19. Non-COVID-19 non-failing hearts were used as reference controls. Our cumulative findings identify the specific transcriptomic changes in cardiac fibroblasts as salient features of COVID-19-associated cardiac microthrombi.

PERTs have emerged as a multi-disciplinary approach in the care of PE patients with intermediate and high-risk PEs. Little is known about referral patterns at PERT institutions, and whether these patterns affect quality and safety outcomes. All intermediate and high risk PE patients at our

Eosinophilic myocarditis (EM) is a rare, rapidly progressive and often fatal cause of acute heart failure. A 66 year-old male with eosinophilic pneumonia and chronic systolic heart failure presented with elevated troponin and peripheral eosinophilia. Cardiac catheterization revealed non-obstructive

Background With the increased efforts to adopt health information technology in the healthcare field, many innovative devices have emerged to improve patient care, increase efficiency, and decrease healthcare costs. A recent addition is smart glasses: web-connected glasses that can present data onto the lenses and record images or videos through a front-facing camera. Objective In this article, we review the most salient uses of smart glasses in healthcare, while also denoting their limitations including practical capabilities and patient confidentiality. Methods Using keywords including, but not limited to, ``smart glasses'', ``healthcare'', ``evaluation'', ``privacy'', and ``development'', we conducted a search on Ovid-MEDLINE, PubMed, and Google Scholar. A total of 71 studies were included in this review. Results Smart glasses have been adopted into the healthcare setting with several useful applications including, hands-free photo and video documentation, telemedicine, Electronic Health Record retrieval and input, rapid diagnostic test analysis, education, and live broadcasting. Conclusions In order for the device to gain acceptance by medical professionals, smart glasses will need to be tailored to fit the needs of medical and surgical sub-specialties. Future studies will need to qualitatively assess the benefits of smart glasses as an adjunct to the current health information technology infrastructure.

Rupture of intracranial aneurysms is the most common cause of nontraumatic subarachnoid hemorrhage, but the intricate neuroinflammatory processes which contribute to aneurysm pathophysiology are not well-understood. Mounting evidence has implicated the complement cascade in the progression of aneurysms from their formation to rupture. In this article, we identify and review studies that have sought to determine the role of the complement system in the aneurysm pathogenesis. The studies were generally conducted by immunhistological analyses on aneurysm tissue collected intraoperatively, and multiple components of the complement cascade and its modulators were identified in specific regions of the aneurysm wall. The results of the studies suggest that the complement cascade is locally upregulated and disinhibited in the perianeurysmal environment, and that it contributes to chronic as well as acute immunological damage to the aneurysm wall. In the future, understanding the mechanisms at work in complement-mediated damage is necessary to leading the development of novel therapies.