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The Sars coronavirus 2019 (COVID-19) pandemic has resulted in increased morbidity and mortality; however, there is limited understanding of how excess mortality is distributed among different racial and ethnic subgroups and vascular diseases., Methods: We conducted a retrospective, cross-sectional study design using data from the United States (US) Center for Disease Control (CDC) Wide Ranging Online Data for Epidemiologic Research (Wonder) database. The database contains death certificate information for all US residents by cause of death as ascertained by the treating physician. We examined the trends of excess death by vascular disease specific mortality among different racial and ethnicity subgroups. Excess deaths were defined as the difference between observed numbers of deaths in specific time periods and the expected numbers of deaths in the same time periods. We compared mortality rates during the reference period of 2018-2019 (pre-pandemic) with the study period of 2020-2021 (pandemic years). We also compared excess mortality rates among racial and ethnic subgroups (Non-Hispanic white, Non-Hispanic Black, and Hispanic individuals). Vascular disease was categorized by administrative diagnostic codes (ICD10): Vascular disease (I26, I82, I70-73, I74) and its subtypes Arterial thrombosis (I74), venous thromboembolism (I26, I82) and atherosclerotic disease (I70-73)., Results: Compared to 2018-2019, there was a 1.3 % excess mortality associated with vascular disease, a 12.2 % excess mortality due to arterial thrombosis mortality, and an 8.0 % excess mortality due to thromboembolism in 2020-2021. Black individuals demonstrated higher excess vascular mortality (6.9 %) compared to white individuals (-0.3 %) P < .001, higher excess venous thromboembolism mortality (14.1 % vs 5.1 % P = 0.002) and higher atherosclerosis mortality (2.1 % vs -2.6 % P = 0.002). Hispanics compared to white individuals had higher excess vascular mortality (5.1 % vs -0.3 % P = 0.03) and excess venous thromboembolism mortality (24.2 % vs 5.1 % P < 0.001)., Conclusion: The COVID-19 pandemic has led to a significant and persistent increase in vascular mortality. Excess mortality has disproportionately affected Black and Hispanic individuals compared to white individuals, highlighting the need for further studies to address and eliminate these health care disparities., Competing Interests: Declaration of competing interest The authors have no disclosures pertinent to this manuscript., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Cardio-oncology mortality (COM) is a complex issue that is compounded by multiple factors that transcend a depth of socioeconomic, demographic, and environmental exposures. Although metrics and indexes of vulnerability have been associated with COM, advanced methods are required to account for the intricate intertwining of associations. This cross-sectional study utilized a novel approach that combined machine learning and epidemiology to identify high-risk sociodemographic and environmental factors linked to COM in United States counties. The study consisted of 987,009 decedents from 2,717 counties, and the Classification and Regression Trees model identified 9 county socio-environmental clusters that were closely associated with COM, with a 64.1% relative increase across the spectrum. The most important variables that emerged from this study were teen birth, pre-1960 housing (lead paint indicator), area deprivation index, median household income, number of hospitals, and exposure to particulate matter air pollution. In conclusion, this study provides novel insights into the socio-environmental drivers of COM and highlights the importance of utilizing machine learning approaches to identify high-risk populations and inform targeted interventions for reducing disparities in COM., Competing Interests: Declaration of Competing Interest Dr. Dong is supported by contracts from the Cleveland Clinic Foundation, including a subcontract from Celgene Corporation. The remaining authors have no conflicts of interest to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Aneurysms complicated by rupture of the coronary arteries are exceedingly rare. Literature regarding management of mycotic aneurysms resulting in rupture is limited. Therefore, we describe a fascinating diagnosis, imaging progression and management of a ruptured mycotic coronary artery aneurysm., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Heroin use may work synergistically with human immunodeficiency virus (HIV) infection to cause greater immune dysregulation than either factor alone. Unraveling how this affects end-organ disease is key as it may play a role in the excess mortality seen in people with HIV (PWH) who use heroin despite access to care and antiretroviral therapy., Methods: This is a prospectively enrolled, cross-sectional study of adults with and without HIV who use and do not use heroin using (18)F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) to compare tissue-specific inflammation including aortic (target-to-background ratio [TBR]), splenic, and bone marrow (standardized uptake value [SUV])., Results: A total of 120 participants were enrolled. The unadjusted mean difference in aortic TBR was 0.43 between HIV-positive [HIV+] heroin+ and HIV+ heroin-negative [heroin-] (P = .02); however, among HIV-, aortic TBR was similar regardless of heroin-use status. Further, HIV-by-heroin-use status interaction was significant (P = .02), indicating that the relationship between heroin use and higher aortic TBR depended on HIV status. On the other hand, both HIV (1.54 vs 1.68; P = .04, unadjusted estimated means for HIV+ vs HIV-) and heroin use were associated with lower bone marrow SUV, although the effect of heroin depended on sex (heroin-use-by-sex interaction, P = .03). HIV-by-heroin-use interaction was not significant for splenic or bone marrow SUV., Conclusions: Aortic inflammation was greatest in PWH who use heroin, but paradoxically, bone marrow activity was the least in this group, suggesting complex and possibly divergent pathophysiology within these different end organs., Competing Interests: Potential conflicts of interest . C. O. H. has served as consultant for Theratechnologies and Gilead and has received research grant support from Gilead. N. F. has served as consultant for Gilead. G. A. M. has served as consultant for Gilead, Merck, Theratechnologies, Janssen, and GSK/ViiV and has received research grants from Gilead, Merck, Janssen, and Theratechnologies, including payment for expert testimony from Gilead (no direct relationship with Gilead, deals with lawyer only). All other authors report no potential conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed., (© The Author(s) 2022. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Objective: To investigate the patterns and demographic features of cardiovascular disease (CVD) death and subtypes myocardial infarction (MI), stroke, and heart failure in the pre-COVID-19 era (2018-2019) vs during the COVID-19 pandemic (2020-2021) in the United States., Methods: In this cross-sectional study, we used the US Multiple Cause of Death files for 2018 to 2021 to examine the trend of excess cause-specific deaths using International Classification of Diseases, Tenth Revision codes for CVD (I00 to I99), MI (I21 and I22), stroke (I60 to I69), and heart failure (I42 and I50). Our primary outcome was excess mortality from CVD and its 3 subtypes (MI, stroke, and heart failure) between prepandemic (2018-2019) and pandemic (2020-2021) years. We performed a subgroup analysis on race and month-to-month and year-to-year variation using χ 2 analysis to test statistical significance., Results: Overall, 3,598,352 CVD deaths were analyzed during the study period. There was a 6.7% excess CVD mortality, 2.5% MI mortality, and 8.5% stroke mortality during the COVID-19 pandemic (2020-2021) compared with the prepandemic era (2018-2019). Black individuals had higher excess CVD mortality (13.8%) than White individuals (5.1%; P<.001). This remained consistent across subtypes of CVD, including MI (9.6% vs 1.0%; P<.001), stroke (14.5% vs 6.9%; P<.001), and heart failure (5.1% vs -1.2%; P<.001)., Conclusion: There has been a significant rise in CVD and subtype-specific mortality during the COVID-19 pandemic that has been persistent despite 2 years since the onset of the pandemic. Excess CVD mortality has disproportionately affected Black compared with White individuals. Further studies targeting and eliminating health care disparities are necessary., (Copyright © 2022 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.)

Chronic kidney disease (CKD) is associated with high cardiovascular risk and mortality. Myeloperoxidase (MPO) has been linked to adverse events in patients with mild-moderate CKD. We sought to investigate whether MPO levels are associated with adverse outcomes in patients with CKD. We studied participants with mild to moderate CKD in the prospective chronic renal insufficiency cohort (CRIC). We followed patients for incident heart failure (HF), death, and composite outcome (myocardial infarction, incident peripheral arterial disease, cerebrovascular accident and death). A total of 3872 patients were included (2702 without CVD, 1170 with CVD). After multiple adjustments, doubling of MPO in patients with prior CAD was associated with risk of HF (HR 1.15 [1.01-1.30], P = 0.032) and mortality (HR 1.16 [1.05-1.30], P = 0.005), and composite outcome of MI, PAD, CVA and death (HR 1.12 [1.01-1.25], P = 0.031). In this cohort of patients with mild to moderate CKD and CAD, MPO levels are independently associated with incident HF, all-cause mortality, and a composite outcome., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Acute myelogenous leukemia (AML) is one of the most common leukemias experienced in adults and conveys significant morbidity and mortality. While the traditional anthracycline based treatments of AML involves cytarabine, developments in alternatives (liposomal cytarabine, fludarabine, cladribine, azacitidine, decitabine), and targeted agents (midostaurin, gilteritinib, enasidenib, ivosidenib, gemtuzumab ozogamicin, and venetoclax) exist. Multiple cardiovascular adverse events, notably pericardial toxicity, have been observed in small studies; however, to date little is known about the comparative pericardial toxicity among these newer regimens. Due to the paucity of data, we sought to investigate the reported pericardial events and mortality associated with treatments for AML. Utilizing the Food and Drug Administration (FDA) Adverse Events Reporting System (FAERS), we identified all adverse events associated with FDA approved treatments for AML (2002-2022). Pericardial events were defined as pericarditis, pericardial effusion and tamponade. We excluded any individuals with age <18 years old. Logistic regression was utilized to identify factors associated with pericardial events. Out of 94,262 reported adverse events, 675 pericardial toxicities were included (243 pericarditis, 479 tamponade). Pericardial events occurred less often in Cladribine (0.3%, P < 0.001), fludarabine (0.4%, P < 0.001), Venetoclax (0.3%, P < 0.001), enasidenib (0.3%, P value < 0.001), and ivosidenib (0.3%, P < 0.001) compared to Cytarabine (0.9%). Tamponade events occurred significantly less often in cladribine (0.1%, P < 0.001), fludarabine (0.4%, P = 0.001), enasidenib (0.1%, P = 0.006), ivosidenib (0.1%, P = 0.01), and venetoclax (0.1%, P < 0.001) compared to cytarabine 0.7%. After adjusting for age and sex, Cladribine (reporting odds ratio [ROR] 0.35 [95% CI 0.18-0.68], P = 0.008) and Fludarabine (ROR 0.65 [0.45-0.92], P = 0.03), venetoclax (ROR 0.57 [0.41-0.79], P < 0.001) remained significantly associated with lower incidence of reported pericardial events. While cytarabine has been the routinely used and/or drug of choice for induction chemotherapy for AML, alternatives like cladribine may have a greater safety profile regarding pericardial toxicities. Future studies should be directed at further investigating cardiovascular safety profiles of AML induction therapy., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Objective: Low-dose cardiac-gated chest CTs allow for simultaneous evaluation of coronary artery calcification and aortic size. We sought to evaluate the prevalence of thoracic aortic dilation (TAD) and thoracic aortic aneurysm (TAA) in a large cohort of patients undergoing coronary artery calcium (CAC) screening., Methods: We reviewed all patients from a large, prospective no-charge CAC screening program (CLARIFY, Clinicaltrials.gov NCT04075162) for whom measurements of the ascending aorta were available. TAD was defined as an ascending aortic diameter ≥4.0cm, while TAA was defined as ascending aortic diameter ≥ 4.5cm. We explored associations between patient characteristics, CAC, and the prevalence of TAD/TAA., Results: A total of 36,356 patients enrolled in the CLARIFY program underwent analysis for TAD/TAA. 3,130 patients (8.6%) had TAD and 237 (0.7%) had TAA. Patients with TAA were older (63±8 vs 59±10 years, p  < 0.001), more likely to be male (87% vs 49%, p  < 0.001), have higher BMI (32 vs 30 kg/m 2 , p  < 0.001), and 10-year atherosclerotic cardiovascular disease estimated risk (18% vs 12%, p  < 0.001). Similar differences were observed for individuals with TAD compared to individuals without TAD with respect to age (63 vs 59 years, p  < 0.001), percent male (76% vs 46%, p  < 0.001), BMI (32 vs 30 kg/m 2 , p  < 0.001), and 10-year predicted risk (17% vs 11%, p  < 0.001). CAC score was associated with prevalence of TAD (4.9% in those with CAC 0 to 16.5% in those with CAC≥400) and TAA (0.3% in those with CAC of 0 to 1.5% in those with CAC ≥400)., Conclusion: In this large, prospective study of patients undergoing no-charge CAC screening, 8.6% had TAD (≥4.0cm) and 0.7% had TAA (≥4.5cm). Our results highlight a high yield of TAD/TAA diagnosis in this targeted cohort with cardiovascular risk factors and supports the role of no-charge CAC as a population-level strategy., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Authors. Published by Elsevier B.V.)

Background Despite the known significant morbidity and mortality associated with cardiovascular disease and peripheral vascular disease (PVD), contemporary data describing racial demographics in PVD mortality are scarce. Methods and Results Using the multiple causes of death file from the Centers for Disease Control and Prevention's Wide-Ranging Online Data for Epidemiologic Research, we analyzed the trends of age-adjusted mortality (AAMR) for PVD and its subtypes (aortic aneurysm/dissection, arterial thrombosis, venous thrombosis/disease, pulmonary embolism), by race and sex between 1999 and 2019. Of the 17 826 871 deaths attributed to cardiovascular disease, a total of 888 187 (5.0%) PVD deaths were analyzed during the study period (12.4% Black, 85.6% White). Between 1999 and 2019, AAMR for PVD decreased by 52% (24.8-11.8 per 100 000 people) in the overall population. Despite a decrease in the overall mortality across all race and sex groups, Black men and Black women continued to have higher mortality for PVD (1.5×), aortic dissection (1.8×), arterial thrombosis (1.3×), and venous thrombosis/disease (2.0×) mortality compared with White men and White women in 2019. While there was a 53% decrease in PVD among White individuals (AAMR 24.5-11.5 per 100 000), there was only a 43% decrease (30.0-17.1) in PVD AAMR in Black individuals between 1999 and 2019. The ratio of PVD AAMR increased from 1.2 (1999) to 1.5 (2019) in Black men/White men and from to 1.3 (1999) to 1.5 (2019) in Black women/White women. Similar trends were noted in aortic dissection (Black men/White men, 1.2-1.8; and Black women/White women, 1.5-1.7), arterial thrombosis (Black men/White men, 1.0-1.3; and Black women/White women, 0.9-1.3), and venous thrombosis/disease (Black men/White men, 1.7-1.8; and Black women/White women, 1.7-2.0). Conclusions In this retrospective review of death certificate data in the United States, we demonstrate continued significant disparities between Black and White populations in PVD mortality and its subtypes. Future studies should investigate etiologies and social determinants of PVD mortality.

Cardiac allograft vasculopathy (CAV) is the leading cause of long-term graft dysfunction in patients with heart transplantation and is linked with significant morbidity and mortality. Currently, the gold standard for diagnosing CAV is coronary imaging with intravascular ultrasound during traditional invasive coronary angiography. Invasive imaging, however, carries increased procedural risk and expense to patients in addition to requiring an experienced interventionalist. With the improvements in non-invasive cardiac imaging modalities such as transthoracic echocardiography, computed tomography, magnetic resonance imaging and positron emission tomography, an alternative non-invasive imaging approach for the early detection of CAV may be feasible. In this systematic review, we explored the literature to investigate the utility of non-invasive imaging in diagnosis of CAV in >3000 patients across 49 studies. We also discuss the strengths and weaknesses for each imaging modality. Overall, all 4 imaging modalities show good to excellent accuracy for identifying CAV with significant variations across studies. Majority of the studies compared non-invasive imaging with invasive coronary angiography without intravascular imaging. In summary, non-invasive imaging modalities offer an alternative approach to invasive coronary imaging for CAV. Future studies should investigate longitudinal non-invasive protocols in low-risk patients after heart transplantation., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Competing Interests: Declaration of Competing Interest All authors have no disclosures. This article is not under consideration or publication elsewhere. The publication is approved by all authors and all authors are responsible for the work that has been carried out.

Aims: Heart failure (HF) is one of the leading causes of cardiovascular morbidity and mortality in the ever-growing population of patients with chronic kidney disease (CKD). There is a need to enhance early prediction to initiate treatment in CKD. We sought to study the feasibility of a multi-variable biomarker approach to predict incident HF risk in CKD., Methods and Results: We examined 3182 adults enrolled in the Chronic Renal Insufficiency Cohort (CRIC) without prevalent HF who underwent serum/plasma assays for 11 blood biomarkers at baseline visit (B-type natriuretic peptide [BNP], CXC motif chemokine ligand 12, fibrinogen, fractalkine, high-sensitivity C-reactive protein, myeloperoxidase, high-sensitivity troponin T (hsTnT), fibroblast growth factor 23 [FGF23], neutrophil gelatinase-associated lipocalin, fetuin A, aldosterone). The population was randomly divided into derivation (n = 1629) and validation (n = 1553) cohorts. Biomarkers that were associated with HF after adjustment for established HF risk factors were combined into an overall biomarker score (number of biomarkers above the Youden's index cut-off value). Cox regression was used to explore the predictive role of a biomarker panel to predict incident HF. A total of 411 patients developed incident HF at a median follow-up of 7 years. In the derivation cohort, four biomarkers were associated with HF (BNP, FGF23, fibrinogen, hsTnT). In a model combining all four biomarkers, BNP (hazard ratio [HR] 2.96 [95% confidence interval 2.14-4.09]), FGF23 (HR 1.74 [1.30-2.32]), fibrinogen (HR 2.40 [1.74-3.30]), and hsTnT (HR 2.89 [2.06-4.04]) were associated with incident HF. The incidence of HF increased with the biomarker score, to a similar degree in both derivation and validation cohorts: from 2.0% in score of 0% to 46.6% in score of 4 in the derivation cohort to 2.4% in score of 0% to 43.5% in score of 4 in the validation cohort. A model incorporating biomarkers in addition to clinical factors reclassified risk in 601 (19%) participants (352 [11%] participants to higher risk and 249 [8%] to lower risk) compared with clinical risk model alone (net reclassification improvement of 0.16)., Conclusion: A basic panel of four blood biomarkers (BNP, FGF23, fibrinogen, and hsTnT) can be used as a standalone score to predict incident HF in patients with CKD allowing early identification of patients at high-risk for HF. Addition of biomarker score to clinical risk model modestly reclassifies HF risk and slightly improves discrimination., (© 2022 European Society of Cardiology.)

Patients with chronic kidney disease (CKD) are at increased risk for stroke. High-sensitivity troponin (hsTP), a marker of myocardial injury, has been associated with stroke risk in patients without CKD, but whether this applies to patients with CKD is not known. We assessed whether hsTP levels is associated with incident stroke in patients with mild-to-moderate CKD without a history of stroke enrolled in the Chronic Renal Insufficiency Cohort. Patients were followed for incident stroke, and the association with hsTP was assessed. A total of 3477 patients without prior stroke were included in this investigation. Over a median follow-up of 7.3 years, 101 (2.8%) patients had an incident stroke. Baseline hsTP was associated with a 9-year risk of stroke (quartile 1: 1.8%, quartile 2: 3.8%, quartile 3: 4.9%, quartile 4: 7.3%; P < .001). After adjusting for traditional stroke risk factors, patients in the fourth quartile (hazard ratio: 2.52, 95% CI: 1.10-5.76, P = .021) had higher risk of stroke when compared with the lowest quartile of hsTP. In conclusion, hsTP levels are associated with increased risk of incident stroke in patients with mild to moderate CKD, and this association remains significant despite the adjustment for traditional risk factors and CKD.

Background: People with HIV (PWH) experience increased systemic inflammation and monocyte activation, leading to increased risk of cardiovascular events (death, stroke, and myocardial infarction) and higher coronary artery calcium scores (CACs). Vitamins D and K2 have significant anti-inflammatory effects; in addition, vitamin K2 is involved in preventing vascular calcifications in the general population. The roles of vitamins D and K in increased coronary calcifications in successfully treated PWH is less understood., Methods: We prospectively recruited 237 PWH on antiretroviral treatment (ART) and 67 healthy controls. CACs were derived from noncontrast chest computed tomography (CT) and levels of 25-hydroxyvitamin D (vitamin D) and inactive vitamin K-dependent dephosphorylated-uncarboxylated matrix Gla protein (dp-uc MGP, marker of vitamin K deficiency) were measured in plasma during a fasting state. The relationship between inflammation markers, dp-uc MGP, and vitamin D on CACs were estimated using zero-inflated negative binomial regression. Adjusted models included 25(OH)D, MGP, sex, race, age, and markers of inflammation or monocyte activation., Results: Overall, controls had lower median age (45.8 vs. 48.8; P = 0.03), a larger proportion of female individuals (55.2 vs. 23.6%; P < 0.0001), and nonwhite (33.8 vs. 70%; P < 0.0001). Among PWH, less than 1% had detectable viral load and the median CD4+ cell count was 682 (IQR: 473.00-899.00). 62.17% of the participants had zero CACs and 51.32% were vitamin D-deficient (<20 ng/ml). There was no difference in detectable CACs (P = 0.19) or dp-uc MGP (P = 0.42) between PWH and controls. In adjusted models, PWH with nonzero CACs have three times greater expected CAC burden compared with controls. Every 1% increase in MGP (worse K status) decreases the probability of having CACs equal to zero by 21.33% (P = 0.01). Evidence suggests that the effects of 25(OH)D and MGP are inflammation-mediated, specifically through sVCAM, TNF-αRI, and TNF-αRII., Conclusion: Vitamin K deficiency is a modifiable preventive factor against coronary calcification in PWH. Further research should determine whether vitamin K supplementation would reduce systemic inflammation, vascular calcification, and risk of cardiovascular events in PWH., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Chronic systemic inflammation is associated with an increased risk of heart failure (HF). We sought to determine the association between biomarkers of systemic inflammation interleukin (IL)-6, IL-2, tumor necrosis factor alpha (TNF-α), and C-reactive protein (CRP) with those of HF and its subtypes. We hypothesize that inflammatory biomarkers IL-6, IL-2, TNF-α, and CRP are associated with HF and its subtypes. We included participants from the Multi-Ethnic Study of Atherosclerosis (a prospective population-based cohort study [2000 to 2002]), without a history of HF, and with available baseline inflammatory biomarkers. We explored the association of IL-6, IL-2, TNF-α, and CRP with incident HF, HF with reduced ejection fraction (left ventricular ejection fraction [LVEF] <40%, HFrEF), HF with midrange EF (LVEF 40% to 50%, HFmrEF), and HF with preserved ejection fraction (LVEF >50%, HFpEF). Among 6,814 participants, 195 developed HF over 10.9 years (56 HFrEF, 30 HFmrEF, and 57 HFpEF). In the models adjusted for clinical risk factors of HF, IL-6 (hazard ratio [HR] 1.33 per doubling; 95% confidence interval [CI] 1.10 to 1.60), TNF-α (HR 2.49 per doubling; 95% CI 1.18 to 5.28), and CRP (HR 1.18 per doubling; 95% CI 1.06 to 1.30) were associated with all HF, and IL-6 (HR 1.51 per doubling; 95% CI 1.09 to 2.10) and CRP (HR 1.21 per doubling; 95% CI: 1.01 to 1.45) were associated with incident HFpEF, whereas none of the examined biomarkers were associated with HFmrEF or HFrEF. In conclusion, inflammatory biomarkers (IL-6, TNF-α, and CRP) are independently associated with incident HF. IL-6 and CRP are associated with incident HFpEF but not HFrEF or HFmrEF. These findings suggest that activation of the IL-6/CRP pathway (as cause, consequence, or epiphenomenon) may be unique to HFpEF., Competing Interests: Disclosures The authors have no conflicts of interest to declare. This manuscript was prepared using MESA Research Materials obtained from the National Heart, Lung, and Blood Institute Biologic Specimen and Data Repository Information Coordinating Center and does not necessarily reflect the opinions or views of MESA or the National Heart, Lung, and Blood Institute., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Despite a rising prevalence of chronic inflammatory disease (CID), the recent trends in cardiovascular disease (CVD) mortality of patients with CID is scarce. In this study, we investigated patterns of CVD mortality in systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), and rheumatoid arthritis (RA) compared with the general population., Methods: We used the 1999 to 2019 multiple causes of death files from the national center for health statistics to analyze patterns and trends of proportionate CVD mortality in CID compared with the general population., Results: We analyzed a total of 11,154 CVD deaths in IBD, 58,337 CVD deaths in RA, 6227 CVD deaths in SLE, and 17,826,871 CVD deaths in the general population. Between 1999 and 2019, we found that proportionate CVD mortality decreased significantly in the IBD group (25% to 16%), RA group (34% to 25%), and the general population (41% to 31%), but did not change for the SLE group (15% to 15%). Patients with SLE who died of CVD were approximately 10 years younger compared with CVD decedents with RA, IBD, or general population. The White population had higher proportionate CVD mortality than African American (IBD [19% vs 16%-18%] and SLE [14%-16% vs 12-14%], respectively)., Conclusions: This study identifies current trends in CVD mortality in the CID population and elucidates current demographics in CVD mortality in CID. Although proportionate CVD mortality decreased in the general population, and in patients with RA and IBD, there was no change among patients with SLE. Further studies are needed to elucidate these differences., Competing Interests: The authors declare no conflict of interest., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Accurate identification of left ventricular masses (LVM) can be challenging, and if incorrect, may have devastating consequences. While transthoracic echocardiography is often the first test to identify intracardiac masses, cardiac MRI (CMRI) allows for better anatomical definition and tissue characterisation. We present a case of a 51-year-old man who presented with 4 weeks of shortness of breath, found on echocardiogram to have severely reduced LV function and a 2.5×4.0 cm LVM with a hypolucent/cystic core. Due to the unusual appearance, CMRI was required for confirmation of an LV thrombus. This case highlights the importance of multimodality imaging in the discovery and identification of LVM., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

When pericardial fluid accumulates and exceed the reserve volume of the pericardium or when the pericardium becomes scarred and inelastic, one of three pericardial compressive syndromes may ensue, namely, cardiac tamponade (CT), characterised by the accumulation of pericardial fluid under pressure; constrictive pericarditis (CP), the result of scarring and loss of the normal elasticity of the pericardial sac; and effusive-constrictive pericarditis (ECP), characterised by the concurrence of a tense pericardial effusion and constriction of the heart by the visceral pericardium. Although relatively uncommon, prevalence estimates vary widely and depend on the nature of the cohorts studied, the methods used to diagnose ECP and the manner in which ECP is defined. Most cases of ECP are idiopathic, reflecting the frequency of idiopathic pericardial disease in general, and other causes include radiation, malignancy, chemotherapy, infection and postsurgical/iatrogenic pericardial disease. The diagnosis of ECP often becomes apparent when pericardiocentesis fails to decrease the right atrial pressure by 50% or to a level below 10 mm Hg. Important non-invasive diagnostic modalities include echocardiography, cardiac magnetic resonance and, to a lesser extent, cardiac CT. In cases with clear evidence of pericardial inflammation, a trial of an anti-inflammatory regimen is warranted. A complete pericardiectomy should be reserved for refractory symptoms or clinical evidence of chronic CP., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Venoarterial (VA) extracorporeal membrane oxygenation (ECMO) support is an increasingly used temporizing therapy for patients with refractory cardiogenic shock. Contrast-enhanced echocardiography plays a critical role in the diagnosis and management of diseases that precipitate severe cardiac failure. In this case report, we describe a previously healthy 60-year-old woman who presented with dyspnea on exertion, and whose hospital course was complicated by ventricular fibrillation, emergent coronary artery bypass surgery (CABG), and ECMO support. Her contrast-enhanced ECMO images demonstrated a unique pattern of opacification of three of the four cardiac chambers, which led to a diagnosis of severe aortic insufficiency., (© 2020 Wiley Periodicals LLC.)

Patients with chronic kidney disease (CKD) are at increased risk for peripheral arterial disease (PAD). A novel biomarker to accurately and reliably predict new onset PAD in high risk patients is needed. High sensitivity troponin (HsTP) is a new assay which allows detection of very low troponin levels with high precision. We sought to explore the association between HsTP and risk of PAD in CKD. The Chronic Renal Insufficiency Cohort (CRIC) is a prospective cohort of 3,939 individuals with mild to moderate CKD using age related criteria for glomerular filtration rate. High sensitivity troponin T was measured at study enrollment. Patients with previous history of PAD or coronary artery disease were excluded. Patients were followed for new-onset adjudicated PAD, and the association between HsTP and incident PAD was examined. A total of 2,909 participants free of PAD and coronary artery disease at enrollment were included in this analysis. Over a mean follow up 7.4 years [interquartile ranges 5.8 to 8.5] years, 79 (2.7%) patients developed PAD. The 3-, 6-, and 9-year incidence of PAD was 1.00%, 2.03%, and 2.72%, respectively. At 9 years, the cumulative rates of PAD increased with HsTP (Quartile 1: 0.3%, Quartile 2: 2.4%, Quartile 3: 3.7%, Quartile 4: 10.7%; p <0.001). After adjusting for clinical risk factors of PAD, patients in the third quartile (Hazards ratio 5.89, 95% confidence interval: 1.31 to 26.47, p = 0.021) and fourth quartile of HsTP (Hazards ratio 10.24, 95% confidence interval 2.23 to 47.08, p = 0.003) had higher risk of PAD compared with lowest quartile of HsTP. HsTP had good discrimination of PAD at 3 years (area under the curve [AUC] 0.76), 6 years (AUC 0.79) and 9 years (AUC 0.80). Addition of HsTP to Framingham risk score improved model discrimination of PAD. In conclusion, in patients with mild-moderate CKD, HsTP levels are associated with and predictive of risk of incident PAD. This association remains significant despite adjustment for traditional PAD risk factors and chronic kidney disease., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Patients with chronic kidney disease (CKD) are at an increased risk of atrial fibrillation (AF). There is a need for novel biomarkers to reliably and accurately predict AF in this population. High-sensitivity troponin (HsTP) allows the detection of low troponin concentrations. The utility of HsTP for evaluating the risk of AF in CKD has not been established., Objective: We sought to explore the association between HsTP and the risk of incident AF in CKD., Methods: The Chronic Renal Insufficiency Cohort is a prospective cohort of 3939 individuals with mild to moderate CKD. HsTP was measured at study enrollment. Patients with a history of AF were excluded. Patients were followed for new-onset AF, and the association between HsTP and incident AF was examined using the Cox regression model., Results: A total of 3217 participants were included. Over a median follow-up period of 7.1 years (interquartile range 5.0-8.4 years), 252 patients developed new-onset AF (12 events per 1000 person-years of follow-up). The incidence of new-onset AF was 2.46%, 7.06%, and 11.5% at 3, 6, and 9 years, respectively. Compared with the lowest quartile of HsTP, patients in the third quartile of HsTP (hazard ratio 2.40; 95% confidence interval 1.58-3.65; P < .001) and the fourth quartile of HsTP (hazard ratio 4.43; 95% confidence interval 2.98-6.59; P < .001) had a higher incidence of AF., Conclusion: HsTP levels are associated with an increased risk of AF in patients with mild to moderate CKD. This association remains significant despite adjustment for traditional AF risk factors and chronic renal disease., (Copyright © 2019 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

While the classical apical ballooning takotsubo cardiomyopathy (TC) was first reported in the 1990s, the rarer mid-ventricular and basal variants were not formally recognized until recently and they remain poorly understood. In this case report, we describe a 67-year-old woman who, during her hospitalization for a subarachnoid hemorrhage and subsequent readmission, experienced multiple complications, each of which resulted in a different variant of TC. To our knowledge, this is the first report of a single patient developing all three variants of TC., (© 2019 Wiley Periodicals, Inc.)

Orthostatic hypotension has a vast differential that has been previously described throughout the literature. However, baroreceptor failure as a sequela of head and neck radiation is not often recognised as an important cause of dramatic haemodynamic variability. As a result, individuals suffering from baroreceptor failure likely have been undertreated. Herein, we report a case of a patient with a history of radiation to the neck for squamous cell carcinoma of the tongue and resultant baroreceptor failure resulting in syncope., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Objective: We aimed to determine whether the severity of inhalation injury evokes an immune response measurable at the systemic level and to further characterize the balance of systemic pro- and anti-inflammation early after burn and inhalation injury., Background: Previously, we reported that the pulmonary inflammatory response is enhanced with worse grades of inhalation injury and that those who die of injuries have a blunted pulmonary immune profile compared with survivors., Methods: From August 2007 to June 2011, bronchoscopy was performed on 80 patients admitted to the burn intensive care unit when smoke inhalation was suspected. Of these, inhalation injury was graded into 1 of 5 categories (0, 1, 2, 3, and 4), with grade 0 being the absence of visible injury and grade 4 corresponding to massive injury. Plasma was collected at the time of bronchoscopy and analyzed for 28 immunomodulating proteins via multiplex bead array or enzyme-linked immunosorbent assay., Results: The concentrations of several plasma immune mediators were increased with worse inhalation injury severity, even after adjusting for age and % total body surface area (TBSA) burn. These included interleukin (IL)-1RA (P = 0.002), IL-6 (P = 0.002), IL-8 (P = 0.026), granulocyte colony-stimulating factor (P = 0.002), and monocyte chemotactic protein 1 (P = 0.007). Differences in plasma immune mediator concentrations in surviving and deceased patients were also identified. Briefly, plasma concentrations of IL-1RA, IL-6, IL-8, IL-15, eotaxin, and monocyte chemotactic protein 1 were higher in deceased patients than in survivors (P < 0.05 for all), whereas IL-4 and IL-7 were lower (P < 0.05). After adjusting for the effects of age, % TBSA burn, and inhalation injury grade, plasma IL-1RA remained significantly associated with mortality (odds ratio, 3.12; 95% confidence interval, 1.03-9.44). Plasma IL-1RA also correlated with % TBSA burn, inhalation injury grade, fluid resuscitation, Baux score, revised Baux score, Denver score, and the Sequential Organ Failure Assessment score., Conclusions: The severity of smoke inhalation injury has systemically reaching effects, which argue in favor of treating inhalation injury in a graded manner. In addition, several plasma immune mediators measured early after injury were associated with mortality. Of these, IL-1RA seemed to have the strongest correlation with injury severity and outcomes measures, which may explain the blunted pulmonary immune response we previously found in nonsurvivors.