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Pulmonary embolism (PE) remains a significant cause of mortality requiring prompt diagnosis and risk stratification. This review focuses on the role of computed tomography (CT) in the risk stratification of acute PE, highlighting its impact on patient management. We will explore basic pathophysiology of pulmonary embolism (PE) and review current guidelines, which will help radiologists interpret images within a broader clinical context. This review covers key CT findings which can be used for risk stratification including indicators of right ventricular (RV) dysfunction, clot burden, clot location and left atrial volume. We will discuss the measurement of RV/LV diameter ratio as a key indicator of RV dysfunction and its limitations and challenges within various patient populations. While these parameters should be included in a radiologist's report, their predictive value for mortality depends on the patient's existing cardiopulmonary reserve and should not be interpreted in isolation., Competing Interests: Declaration of competing interest The authors have nothing to declare., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Abstract: Learning from the healthcare system's response to the COVID-19 pandemic is essential to better prepare for potential future crises. We sought to assess mortality rates for patients admitted for acute decompensated heart failure (HF) and to analyze which factors demonstrated a statistically significant correlation with this primary endpoint. We performed a retrospective analysis of patients hospitalized with a primary diagnosis of acute decompensated HF within the New York City Health and Hospitals 11-hospital system across the different COVID surge periods. Mortality information was collected in 4,405 participants (mean [SD] age 70.54 [14.44] years, 1885 [42.87%] female).The highest mortality existed in the first surge (9.02%), then improved to near prepandemic levels (3.65%) in the second (3.91%) and third surges (5.94%, p < 0.0001). In-hospital mortality inversely correlated with receipt of a COVID-19 vaccination, but had no correlation with left ventricular ejection fraction or the number of vaccination doses. Mortality for acute decompensated HF patients improved after the first surge, suggesting that hospitals adequately adapted to provide quality care. As future infectious outbreaks may occur, emergency preparedness must ensure that adequate focus and resources remain for other clinical entities, such as HF, to ensure optimal care is delivered across all areas of illness., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2024 National Association for Healthcare Quality.)

The purpose of this study is to evaluate whether early initiation of catheter-directed thrombolysis (CDT) in patients presenting with acute pulmonary embolism is associated with improved in-hospital outcomes. A retrospective cohort was extracted from the 2016-2019 National Inpatient Sample database, consisting of 21,730 weighted admissions undergoing CDT acute PE. From the time of admission, the sample was divided into early (<48 h) and late interventions (>48 h). Outcomes were measured using regression analysis and propensity score matching. No significant differences in mortality, cardiac arrest, cardiogenic shock, or intracranial hemorrhage ( p > 0.05) were found between the early and late CDT groups. Late CDT patients had a higher likelihood of receiving systemic thrombolysis (3.21 [2.18-4.74], p < 0.01), blood transfusion (1.84 [1.41-2.40], p < 0.01), intubation (1.33 [1.05-1.70], p = 0.02), discharge disposition to care facilities (1.32 [1.14-1.53], p < 0.01). and having acute kidney injury (1.42 [1.25-1.61], p < 0.01). Predictors of late intervention were older age, female sex, non-white ethnicity, non-teaching hospital admission, hospitals with higher bed sizes, and weekend admission ( p < 0.01). This study represents a comprehensive evaluation of outcomes associated with the time interval for initiating CDT, revealing reduced morbidity with early intervention. Additionally, it identifies predictors associated with delayed CDT initiation. The broader ramifications of these findings, particularly in relation to hospital resource utilization and health disparities, warrant further exploration.

Cardiovascular disease is the leading cause of death in women. Pulmonary embolism (PE) is the third most-common cause of cardiovascular death, after myocardial infarction (MI) and stroke. We aimed to evaluate the attributes and outcomes of PE specifically in women and explore sex-based differences. We conducted a systematic review of the literature using electronic databases PubMed and Embase up to 1 April 2022 to identify studies investigating PE in women. Of the studies found, 93 studies met the eligibility criteria and were included. The risk of PE in older women (especially >40 years of age) superseded that of age-matched men, although the overall age- and sex-adjusted incidence of PE was found to be lower in women. Risk factors for PE in women included age, rheumatologic disorders, hormone replacement therapy or oral contraceptive pills, pregnancy and postpartum period, recent surgery, immobilization, trauma, increased body mass index, obesity, and heart failure. Regarding pregnancy, a relatively higher incidence of PE has been observed in the immediate postpartum period compared to the antenatal period. Women with PE tended to be older, presented more often with dyspnea, and were found to have higher NT-proBNP levels compared to men. No sex-based differences in in-hospital mortality and 30-day all-cause mortality were found. However, PE-related mortality was higher in women, particularly in hemodynamically stable patients. These differences form the basis of future research and outlets for reducing the incidence, morbidity, and mortality of PE in women.

Pulmonary embolism (PE) is the third leading cause of cardiovascular mortality. Patients with PE can present with a wide array of symptoms, ranging from mild to life threatening. The mainstay of PE treatment is anticoagulation; however, many advanced options are available for more severe patients, including catheter- directed interventions, surgical treatments, and hemodynamic support. Although different risk scores and clinical guidelines exist, the primary treating teams are frequently left uncertain on the most suitable treatment for a specific complex patient. Pulmonary Embolism Response Teams (PERT), composed of multidisciplinary experts, have emerged and been implemented in many centers and are available 24 hours a day to help guide the primary team. PERTs have changed the way complex PE patients are managed. In centers with a PERT, teams are called upon very frequently, and there is a significant increase in the use of advanced treatments for PE, although there are differences between centers based upon the center's specific PERT protocol and available capabilities. As PE is an evolving area, and more studies are necessary, PERTs around the world can help advance the field and improve the treatment offered to PE patients., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Coronavirus disease 2019 (COVID-19) is associated with a coagulopathy favouring thrombosis over bleeding that imparts a poor prognosis. Clot in transit (CIT) is considered a rare entity and the most severe form of venous thromboembolism (VTE), carrying a higher mortality than isolated pulmonary embolism (PE). The incidence of this phenomenon in patients with COVID-19 infection is unknown and likely under-recognized., Case Summary: During the peak of the COVID-19 pandemic in New York City, a 70-year-old Hispanic female presented with syncope due to a saddle PE further complicated by a highly mobile CIT. Polymerase chain reaction was positive for COVID-19 infection, however, there was no evidence of lung parenchymal involvement or hyper-inflammation. Based on consensus from a multidisciplinary team, aspiration thrombectomy was attempted to treat this extreme case of VTE, however, the patient died during the procedure., Discussion: This case raises awareness to the most catastrophic form of VTE, presenting in an early phase of COVID-19 infection without the typical hyper-inflammation and severe lung injury associated with development of COVID-related coagulopathy. It also serves to inform on the critical role echocardiography has in the comprehensive evaluation and re-evaluation of hospitalized patients with COVID-19, and the importance of a multidisciplinary organized approach in clinical decision-making for this complex and poorly understood disease and its sequelae., (© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background: Patients hospitalized for severe coronavirus disease 2019 (COVID-19) infection are at risk for in-hospital cardiac arrest (IHCA). It is unknown whether certain characteristics of cardiac arrest care and outcomes of IHCAs during the COVID-19 pandemic differed compared with a pre-COVID-19 period., Methods: All patients who experienced an IHCA at our hospital from March 1, 2020 through May 15, 2020, during the peak of the COVID-19 pandemic, and those who had an IHCA from January 1, 2019 to December 31, 2019 were identified. All patient data were extracted from our hospital's Get With The Guidelines-Resuscitation registry, a prospective hospital-based archive of IHCA data. Baseline characteristics of patients, interventions, and overall outcomes of IHCAs during the COVID-19 pandemic were compared with IHCAs in 2019, before the COVID-19 pandemic., Results: There were 125 IHCAs during a 2.5-month period at our hospital during the peak of the COVID-19 pandemic compared with 117 IHCAs in all of 2019. IHCAs during the COVID-19 pandemic occurred more often on general medicine wards than in intensive care units (46% versus 33%; 19% versus 60% in 2019; P <0.001), were overall shorter in duration (median time of 11 minutes [8.5-26.5] versus 15 minutes [7.0-20.0], P =0.001), led to fewer endotracheal intubations (52% versus 85%, P <0.001), and had overall worse survival rates (3% versus 13%; P =0.007) compared with IHCAs before the COVID-19 pandemic., Conclusions: Patients who experienced an IHCA during the COVID-19 pandemic had overall worse survival compared with those who had an IHCA before the COVID-19 pandemic. Our findings highlight important differences between these 2 time periods. Further study is needed on cardiac arrest care in patients with COVID-19.

Objectives: We describe the key elements for a New York City health system to rapidly implement telecritical care consultative services to a newly created ICU during the coronavirus disease 2020 patient surge., Design: This was a rapid quality-improvement initiative using public health decrees, a HIPAA-compliant and device-agnostic telemedicine patform, and a group of out-of-state intensivist volunteers to enhance critical care support. Telecritical care volunteers initially provided on-demand consults but then shifted to round twice daily with housestaff in a 12-bed newly created ICU., Setting: A 457-bed safety net hospital in the Bronx, NY, during the pandemic., Subjects: The 12-bed newly created ICU was staffed by a telecritical care attending, a cardiology fellow, and internal medicine residents., Intervention: Prior to the intervention, the ad hoc ICU was staffed by a cardiology fellow as the attending of record, with critical care support on demand. The intervention involved twice daily rounding with an out-of-state, volunteer intensivist., Measurements and Main Results: Volunteers logged 352 encounters. Data from 26 unique encounters during the initial on-demand consult pilot study of tele-ICU support were recorded. The most common interventions were diagnostic test interpretation, ventilator management, and sedation change. The majority of housestaff felt the new tele-ICU service improved the quality of care of patients and decreased anxiety of taking care of complex patients. Likewise, the majority of volunteers expressed making significant alterations to care, and 100% believed critical care input was needed for these patients. The largest lessons learned centered around mandating the use of the telecritical care volunteers and integration into a structured format of rounding., Conclusions: The need for rapid implementation of ICUs during a major public health crisis can be challenging. Our pilot study supports the feasibility of using an out-of-state telecritical care service to support ICUs, particularly in areas where resources are limited., Competing Interests: Drs. Allison and McCurdy are advisors to the digital health company ICmed. The remaining authors have not disclosed any potential conflicts of interest., (Copyright © 2020 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.)

Background: Advances in congestive heart failure (CHF) management depend on biomarkers for monitoring disease progression and therapeutic response. During systole, intracellular Ca 2+ is released from the sarcoplasmic reticulum into the cytoplasm through type-2 ryanodine receptor/Ca 2+ release channels. In CHF, chronically elevated circulating catecholamine levels cause pathological remodeling of type-2 ryanodine receptor/Ca 2+ release channels resulting in diastolic sarcoplasmic reticulum Ca 2+ leak and decreased myocardial contractility. Similarly, skeletal muscle contraction requires sarcoplasmic reticulum Ca 2+ release through type-1 ryanodine receptors (RyR1), and chronically elevated catecholamine levels in CHF cause RyR1-mediated sarcoplasmic reticulum Ca 2+ leak, contributing to myopathy and weakness. Circulating B-lymphocytes express RyR1 and catecholamine-responsive signaling cascades, making them a potential surrogate for defects in intracellular Ca 2+ handling because of leaky RyR channels in CHF., Methods: Whole blood was collected from patients with CHF, CHF following left-ventricular assist device implant, and controls. Blood was also collected from mice with ischemic CHF, ischemic CHF+S107 (a drug that specifically reduces RyR channel Ca 2+ leak), and wild-type controls. Channel macromolecular complex was assessed by immunostaining RyR1 immunoprecipitated from lymphocyte-enriched preparations. RyR1 Ca 2+ leak was assessed using flow cytometry to measure Ca 2+ fluorescence in B-lymphocytes in the absence and presence of RyR1 agonists that empty RyR1 Ca 2+ stores within the endoplasmic reticulum., Results: Circulating B-lymphocytes from humans and mice with CHF exhibited remodeled RyR1 and decreased endoplasmic reticulum Ca 2+ stores, consistent with chronic intracellular Ca 2+ leak. This Ca 2+ leak correlated with circulating catecholamine levels. The intracellular Ca 2+ leak was significantly reduced in mice treated with the Rycal S107. Patients with CHF treated with left-ventricular assist devices exhibited a heterogeneous response., Conclusions: In CHF, B-lymphocytes exhibit remodeled leaky RyR1 channels and decreased endoplasmic reticulum Ca 2+ stores consistent with chronic intracellular Ca 2+ leak. RyR1-mediated Ca 2+ leak in B-lymphocytes assessed using flow cytometry provides a surrogate measure of intracellular Ca 2+ handling and systemic sympathetic burden, presenting a novel biomarker for monitoring response to pharmacological and mechanical CHF therapy.

Background: Low 25-hydroxyvitamin D levels are associated with an increased risk of cardiovascular events, but the effect of vitamin D supplementation on markers of vascular function associated with major adverse cardiovascular events is unclear., Methods and Results: We conducted a systematic review and individual participant meta-analysis to examine the effect of vitamin D supplementation on flow-mediated dilatation of the brachial artery, pulse wave velocity, augmentation index, central blood pressure, microvascular function, and reactive hyperemia index. MEDLINE, CINAHL, EMBASE, Cochrane Central Register of Controlled Trials, and http://www.ClinicalTrials.gov were searched until the end of 2016 without language restrictions. Placebo-controlled randomized trials of at least 4 weeks duration were included. Individual participant data were sought from investigators on included trials. Trial-level meta-analysis was performed using random-effects models; individual participant meta-analyses used a 2-stage analytic strategy, examining effects in prespecified subgroups. 31 trials (2751 participants) were included; 29 trials (2641 participants) contributed data to trial-level meta-analysis, and 24 trials (2051 participants) contributed to individual-participant analyses. Vitamin D3 daily dose equivalents ranged from 900 to 5000 IU; duration was 4 weeks to 12 months. Trial-level meta-analysis showed no significant effect of supplementation on macrovascular measures (flow-mediated dilatation, 0.37% [95% confidence interval, -0.23 to 0.97]; carotid-femoral pulse wave velocity, 0.00 m/s [95% confidence interval, -0.36 to 0.37]); similar results were obtained from individual participant data. Microvascular function showed a modest improvement in trial-level data only. No consistent benefit was observed in subgroup analyses or between different vitamin D analogues., Conclusions: Vitamin D supplementation had no significant effect on most markers of vascular function in this analysis., (© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.)

Adequate vitamin D levels may promote cardiovascular health by improving endothelial function and down-regulating inflammation. The objective of this pilot trial was to investigate the effects of vitamin D repletion on endothelial function and inflammation in patients with coronary artery disease (CAD). Using a double-blind placebo wait-list control design, 90 subjects with CAD and vitamin D deficiency (< 20 ng/ml) were randomized 1:1 to 50,000 IU of oral ergocalciferol or placebo weekly for 12 weeks. Endothelial function (reactive hyperemia peripheral arterial tonometry, RH-PAT), circulating adhesion molecules, and pro-inflammatory cytokines were measured at baseline and 12 weeks. The median increase in serum 25-vitamin D from baseline was 26 ± 17 ng/ml in the active group and 4 ± 8 ng/ml in the placebo group (between-group difference = 22 ng/ml, p < 0.001). The median within-subject change in RH-PAT score was 0.13 ± 0.73 with active treatment and -0.04 ± 0.63 with placebo (between-group difference = 0.17, p = 0.44). Within-group and between-group differences in intercellular adhesion molecule levels were greater with placebo (between-group difference = 6 ng/ml, p = 0.048). Vascular cell adhesion molecule levels decreased in both groups by a similar magnitude (median difference between groups = 8.5 ng/ml, p = 0.79). There was no difference between groups in magnitude of reduction in interleukin (IL)-12 (-8.6 ng/ml, p = 0.72) and interferon-gamma (0.52 ng/ml, p = 0.88). No significant differences in blood pressure, e-selectin, high-sensitivity c-reactive protein, IL-6 or the chemokine CXCL-10 were found with treatment. In conclusion, repleting vitamin D levels in subjects with CAD failed to demonstrate any benefits on surrogate markers of cardiovascular health. These results question the role of vitamin D supplementation in modifying cardiovascular disease.

Accumulating data linking hypovitaminosis D to cardiovascular (CV) events has contributed to large increases in vitamin D testing and supplementation. To evaluate the merits of this practice, we conducted a systematic review with meta-analysis providing a framework for interpreting the literature associating hypovitaminosis D with increased CV events. Prospective studies were identified by search of MEDLINE and EMBASE from inception to January 2010, restricted to English language publications. Two authors independently extracted data and graded study quality. Pooled relative risks (RR) were calculated using a random effects model. Ten studies met criteria for review and 7 were included in meta-analysis. Pooled RR for CV events using FAIR and GOOD quality studies was 1.67 (95% confidence interval, 1.23-2.28) during an average follow-up of 11.8 years. There was evidence of significant heterogeneity across studies (Q statistics = 16.6, P = 0.01, I = 63.8%), which was eliminated after omitting 2 studies identified by sensitivity analysis (RR, 1.34 [1.08-1.67]; P for heterogeneity =0.33). When restricting analysis to GOOD quality studies (RR, 1.27 [1.04-1.56]), no significant heterogeneity was found (P = 0.602). Systematic review identified significant shortcomings in the literature, including variability in defining vitamin D status, seasonal adjustments, defining and determining CV outcomes, and the use of baseline vitamin D levels. In conclusion, a modest increased risk of CV events associated with hypovitaminosis D is tempered by significant limitations within the current literature. These findings underscore the importance of critical appraisal of the literature, looking beyond reported risk estimates before translating results into clinical practice.

Background: Atherosclerosis is an inflammatory disease in which interferon (IFN)-gamma, the signature cytokine of Th1 cells, plays a central role. We investigated whether interleukin (IL)-17, the signature cytokine of Th17 cells, is also associated with human coronary atherosclerosis., Methods and Results: Circulating IL-17 and IFN-gamma were detected in a subset of patients with coronary atherosclerosis and in referent outpatients of similar age without cardiac disease but not in young healthy individuals. IL-17 plasma levels correlated closely with those of the IL-12/IFN-gamma/CXCL10 cytokine axis but not with known Th17 inducers such as IL-1beta, IL-6, and IL-23. Both IL-17 and IFN-gamma were produced at higher levels by T cells within cultured atherosclerotic coronary arteries after polyclonal activation than within nondiseased vessels. Combinations of proinflammatory cytokines induced IFN-gamma but not IL-17 secretion. Blockade of IFN-gamma signaling increased IL-17 synthesis, whereas neutralization of IL-17 responses decreased IFN-gamma synthesis; production of both cytokines was inhibited by transforming growth factor-beta1. Approximately 10-fold fewer coronary artery-infiltrating T helper cells were IL-17 producers than IFN-gamma producers, and unexpectedly, IL-17/IFN-gamma double producers were readily detectable within the artery wall. Although IL-17 did not modulate the growth or survival of cultured vascular smooth muscle cells, IL-17 interacted cooperatively with IFN-gamma to enhance IL-6, CXCL8, and CXCL10 secretion., Conclusions: Our findings demonstrate that IL-17 is produced concomitantly with IFN-gamma by coronary artery-infiltrating T cells and that these cytokines act synergistically to induce proinflammatory responses in vascular smooth muscle cells.

Inflammation is associated with the pathogenesis of coronary atherosclerosis, although the mechanisms remain unclear. We investigated whether cytokine secretion by innate immune responses could contribute to the production of proarteriosclerotic Th1-type cytokines in human coronary atherosclerosis. Cytokines were measured by ELISA in the plasma of patients with coronary atherosclerosis undergoing cardiac catheterization. IL-18 was detected in all subjects, whereas a subset of patients demonstrated a coordinated induction of other IFN-gamma-related cytokines. Specifically, elevated plasma levels of IL-12 correlated with that of IFN-gamma and IFN-gamma-inducible chemokines, defining an IFN-gamma axis that was activated independently of IL-6 or C-reactive protein. Systemic inflammation triggered by cardiopulmonary bypass increased plasma levels of the IFN-gamma axis, but not that of IL-18. Activation of the IFN-gamma axis was not associated with acute coronary syndromes, but portended increased morbidity and mortality after 1-year follow-up. IL-12 and IL-18, but not other monokines, elicited secretion of IFN-gamma and IFN-gamma-inducible chemokines in human atherosclerotic coronary arteries maintained in organ culture. T cells were the principal source of IFN-gamma in response to IL-12/IL-18 within the arterial wall. This inflammatory response did not require, but was synergistic with and primed for TCR signals. IL-12/IL-18-stimulated T cells displayed a cytokine-producing, nonproliferating, and noncytolytic phenotype, consistent with previous descriptions of lymphocytes in stable plaques. In contrast to cognate stimuli, IL-12/IL-18-dependent IFN-gamma secretion was prevented by a p38 MAPK inhibitor and not by cyclosporine. In conclusion, circulating IL-12 may provide a mechanistic link between inflammation and Th1-type cytokine production in coronary atherosclerosis.

Control of hypertension is well established for the primary prevention of stroke. Prior studies, on the other hand, conflict over whether hypertension remains a risk factor for recurrent stroke and if blood pressure reduction is associated with better outcomes in this subset of patients. We review current evidence regarding the role of BP lowering for primary and secondary prevention of stroke. Current evidence amassed from both primary and secondary prevention trials demonstrate that BP reduction is a crucial common element in overall reduction of stroke risk.

Objectives: The aim of this study was to assess the prognostic importance of left ventricular ejection fraction (LVEF) in stable outpatients with heart failure (HF)., Background: Although LVEF is an accepted prognostic indicator of prognosis in HF patients, the relationship of LVEF and mortality across the full spectrum of LVEF is incompletely understood., Methods: We examined the association of LVEF and outcomes among 7,788 stable HF patients enrolled in the Digitalis Investigation Group trial., Results: During mean follow-up of 37 months, mortality was substantial in all LVEF groups (range, LVEF 55%, 23.5%). Among patients with LVEF 45% both before (LVEF 46% to 55%: 23.3%; LVEF > 55%: 23.5%; p = 0.25), and after multivariable adjustment (LVEF 46% to 55%: HR 0.92, 95% CI 0.77 to 1.10; LVEF > 55%: HR 0.88, 95% CI 0.71 to 1.09; LVEF 36% to 45%: referent). Patients with lower LVEF were at increased absolute risk of death due to arrhythmia and worsening HF, but these were leading causes of death in all LVEF groups., Conclusions: Among HF patients in sinus rhythm, higher LVEFs were associated with a linear decrease in mortality up to an LVEF of 45%. However, increases above 45% were not associated with further reductions in mortality.

Hepatic impairment can alter the pharmacokinetic profiles of cardiovascular drugs, which can lead to unwanted toxicity. In the presence of cirrhosis, portosystemic shunting occurs and cytochrome P450 activity is reduced. Impaired oxygen uptake caused by changes in the liver's sinusoids, as proposed by the oxygen limitation theory, may also explain the alteration of drug metabolism seen in cirrhosis. With congestive heart failure, sinusoidal congestion and hypoperfusion of the liver are seen. Similar to cirrhosis, the common pathway for hepatic damage in congestive heart failure seems to be liver hypoxia, which may explain the disease's effect on drug metabolism. Since routine hepatic function tests do not always relate to the liver's ability to eliminate drugs, existing guidelines for dosing cardiovascular drugs in patients with hepatic impairment are limited. This article provides guidance for dosing cardiovascular drugs in cirrhotic and heart failure patients based on available research data. Altered drug metabolism, especially in congestive heart failure, tends to be overlooked or not realized in clinical practice. Therefore, further research is needed in congestive heart failure to better elucidate safe prescribing patterns.