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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.
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COVID-19 , Etnicidade , Grupos Raciais , Doenças Vasculares , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , COVID-19/mortalidade , COVID-19/etnologia , COVID-19/epidemiologia , Estudos Transversais , Etnicidade/estatística & dados numéricos , Disparidades nos Níveis de Saúde , Grupos Raciais/estatística & dados numéricos , Estudos Retrospectivos , Estados Unidos/epidemiologia , Doenças Vasculares/etnologia , Doenças Vasculares/mortalidadeRESUMO
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.
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Poluição do Ar , Neoplasias , Adolescente , Humanos , Estados Unidos/epidemiologia , Estudos Transversais , Exposição Ambiental/efeitos adversos , Fatores de Risco , Neoplasias/epidemiologiaRESUMO
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.
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Aneurisma Infectado , Aneurisma Roto , Aneurisma Coronário , Humanos , Aneurisma Infectado/diagnóstico por imagem , Aneurisma Infectado/cirurgia , Aneurisma Infectado/complicações , Vasos Coronários/diagnóstico por imagem , Diagnóstico por Imagem , Aneurisma Roto/complicações , Aneurisma Coronário/diagnóstico por imagem , Aneurisma Coronário/cirurgia , Aneurisma Coronário/complicaçõesRESUMO
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.
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Infecções por HIV , Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada , Adulto , Humanos , Heroína/efeitos adversos , HIV , Tomografia por Emissão de Pósitrons/métodos , Estudos Transversais , Inflamação/complicações , Fluordesoxiglucose F18 , Infecções por HIV/complicações , Compostos RadiofarmacêuticosAssuntos
Doença da Artéria Coronariana , Intervenção Coronária Percutânea , Humanos , Cálcio , Doença da Artéria Coronariana/diagnóstico por imagem , Doença da Artéria Coronariana/cirurgia , Ponte de Artéria Coronária , Intervenção Coronária Percutânea/efeitos adversos , Resultado do Tratamento , Fatores de RiscoRESUMO
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 χ2 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.
Assuntos
COVID-19 , Doenças Cardiovasculares , Insuficiência Cardíaca , Infarto do Miocárdio , Acidente Vascular Cerebral , Humanos , Estados Unidos/epidemiologia , Pandemias , Estudos Transversais , MortalidadeRESUMO
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/m2, 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/m2, 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.
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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%, Pâ¯=â¯0.001), enasidenib (0.1%, Pâ¯=â¯0.006), ivosidenib (0.1%, Pâ¯=â¯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], Pâ¯=â¯0.008) and Fludarabine (ROR 0.65 [0.45-0.92], Pâ¯=â¯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.
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Leucemia Mieloide Aguda , Pericardite , Adolescente , Adulto , Aminopiridinas , Antraciclinas/uso terapêutico , Azacitidina/uso terapêutico , Compostos Bicíclicos Heterocíclicos com Pontes , Cladribina/uso terapêutico , Citarabina/efeitos adversos , Decitabina/uso terapêutico , Gemtuzumab , Humanos , Leucemia Mieloide Aguda/tratamento farmacológico , Farmacovigilância , Sulfonamidas , Triazinas , Estados Unidos/epidemiologia , United States Food and Drug AdministrationRESUMO
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.
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Dissecção Aórtica , Doenças Vasculares , População Negra , Feminino , Previsões , Humanos , Masculino , Estados Unidos/epidemiologiaAssuntos
Doenças Cardiovasculares , Diabetes Mellitus Tipo 2 , Inibidores do Transportador 2 de Sódio-Glicose , Doenças Cardiovasculares/complicações , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/prevenção & controle , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/tratamento farmacológico , Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas , Humanos , Hipoglicemiantes/uso terapêutico , Inibidores do Transportador 2 de Sódio-Glicose/farmacologia , Inibidores do Transportador 2 de Sódio-Glicose/uso terapêutico , Estados Unidos/epidemiologiaRESUMO
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.
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Insuficiência Cardíaca , Insuficiência Renal Crônica , Adulto , Biomarcadores , Estudos de Coortes , Fibrinogênio , Fatores de Crescimento de Fibroblastos , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/epidemiologia , Humanos , Peptídeo Natriurético Encefálico , Insuficiência Renal Crônica/complicações , Fatores de RiscoRESUMO
Vascular closure devices (VCD) are effective at achieving hemostasis. VCD failure is attributed to underlying arterial disease, leading to a hazardous situation for obtaining contralateral femoral access. Radial-to-peripheral (R2P) access has emerged as a safe option to rescue these procedural complications. Here, we present two cases of VCD failure rescue utilizing R2P and outline this approach step-by-step.
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Técnicas Hemostáticas , Dispositivos de Oclusão Vascular , Artéria Femoral/diagnóstico por imagem , Técnicas Hemostáticas/efeitos adversos , Humanos , Punções , Resultado do TratamentoRESUMO
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.