Risultati per: Sindromi coronariche acute

Circulation, Volume 146, Issue Suppl_1, Page A12721-A12721, November 8, 2022. Introduction:Elderly patients (age > 75) sustain larger infarcts with greater mortality from STEMI despite successful TIMI III reperfusion. Elderly age is an independent risk despite correction for clinical and angiographic variables. Mitochondria (MITO) are key mediators of injury during ischemia (ISC) and reperfusion (R) in lab studies. The acute, transient blockade of the MITO electron transport chain (ETC) at complex I during R decreases infarct size in adult heart models. Metformin (MET) inhibits ETC complex I.Hypothesis:Acute, high dose MET given at R in high-risk aged STEMI model hearts will reduce infarct size.Methods:Young (3-6 mo) and aged (22-24 mo) C57BL/6J mice, male and female (NIA), underwent in vivo ISC-R surgeryvia45 min LAD ligation. At 5 min pre-R, 2 mM MET (or vehicle) was injected via jugular vein. At 24-hr R infarction size and area at risk (AAR) were measured. Echo was performed pre-ISC and end-R.Results:MET treatment at R improved contractile function [ejection fraction (EF) and fractional shortening (FS)] following 24 hr R in both male and female aged groups as well as in the young heart (Figure A)(mean ± SD). MET at R substantially decreased infarct size in both sexes in the aged heart (Figure B) to a similar extent as in the young hearts. AAR was similar in all groups.Conclusions:Acute, high dose MET treatment directly before R decreased infarction and improved contractile function at 24 hr R in aged murine hearts. This is the initial step to move acute MET toward consideration as a cath lab treatment via intracoronary infusion immediately following R via PCI for elders suffering STEMI to reduce injury and preserve function.

Circulation, Volume 146, Issue Suppl_1, Page A15830-A15830, November 8, 2022. Introduction:Obesity is approaching epidemic status in the United States and is strongly associated with a higher risk of heart failure after myocardial infarction (MI), a major cause of morbidity and mortality in obese individuals. However, the mechanisms underlying obesity-associated heart failure are poorly understood. Lysophosphatidic acid (LPA), produced by autotaxin (ATX), is highly expressed in adipose tissue with increased levels in obesity and has been shown to mediate post-MI inflammation.Methods:3-week aged male C57BL/6J mice were randomly assigned to low-fat (LFD-10%) or high-fat (HFD-60%) diet based on the percentage of calories from fat. HFD-fed mice were randomly assigned to receive the specific ATX inhibitor, PF-8380 at 10 mg/kg twice daily. 2 months after initiating the diet, mice were randomized to undergo MI surgery (permanent ligation of the left anterior descending artery) or sham surgery.Results:MI was associated with an increased number of circulating inflammatory monocytes (CD45+/Ly6C+/CD115+), as well as cardiac total and pro-inflammatory macrophages (CD45+/F4-80+/CD11b+/CD86+), as assessed by flow cytometry (Fig. 1A). This effect was exacerbated in HFD-fed mice but significantly attenuated in HFD+PF8380 treated mice with effective ATX inhibition. Changes in circulating and cardiac immune cells were reflective of increased proliferation of bone marrow progenitors, a phenomenon that was blunted by ATX inhibition (Fig. 1B). Moreover, HFD was associated with larger scar size (Fig. 1C) and worse cardiac functional recovery (Fig. 1D) 30 days after MI. The obesity-asscoiated heart failure could be rescued by ATX inhibition.Conclusion:ATX/LPA plays an important role in modulating inflammation and could be a therapeutic target for obesity-related coronary heart diseases.

Circulation, Volume 146, Issue Suppl_1, Page A10914-A10914, November 8, 2022. Introduction:Rupture of an aortic aneurysm into the right atrium (RA) is extremely rare, while rupture into the thoracic cavity or pericardial sac is a common fatal complication. We describe a case of acute heart failure due to rupture of an aortic pseudoaneurysm with aorta-right atrial fistula.Case Summary:A 73-year-old man presented to the emergency department with dyspnea and abdominal distention. He had a history of ascending aortic replacement for type A aortic dissection 18 years ago. On arrival, physical examination revealed diminished breath sounds, leg edema but no cardiac murmurs. Investigations demonstrated abnormality of hepatic and kidney function, elevated BNP (490.9 pg/ml) in blood exam, and enlargement of ascending aortic aneurysm at the proximal anastomotic site with ascites/pleural effusion on computed tomography (CT), while left ventricular function was normal on transthoracic echocardiogram. We diagnosed acute heart failure with preserved ejection fraction and started to reduce fluid using diuretics. However, the response to diuretics was not good and the progression of lactic acidosis was observed regardless of using cardiotonic agent. Since it was becoming difficult to maintain systemic circulation, we performed further investigations before introducing mechanical support. The pulmonary artery catheterization revealed elevated RA pressure with wide pulse pressure (38/12 mmHg) and Oxygen step up in RA. An aortic root angiogram, contrast-enhanced CT and transesophageal echocardiogram showed a rupture of aortic pseudoaneurysm complicated with aorta-right atrial fistula (Figure). Although emergent surgery was performed, he unfortunately died the following day.Conclusions:This is a rare case of intracardiac perforation of aortic aneurysm diagnosed by various modalities. We should consider the possibility of developing shunt disease when we meet patients with rapidly progressive circulatory failure unresponsive to drugs.

Circulation, Volume 146, Issue Suppl_1, Page A12855-A12855, November 8, 2022. Introduction:Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease worldwide. NAFLD patients have an increased risk of cardiovascular disease. Matrin-3 is a DNA- and RNA-binding protein, and its mutation causes amyotrophic lateral sclerosis in humans. Among these patients, 76% have hepatic steatosis. However, the role of matrin-3 in NAFLD has not been previously studied.Methods and Results:We found that matrin-3 expression is induced in fatty livers of humans and mice. Matrin-3 liver specific knockout mice (LKO) displayed increased levels of plasma triglycerides compared with matrin-3 floxed mice, while the body weights of the two groups of mice are similar after 16-week high-fat diet. Moreover, histological staining and triglyceride assay revealed that LKO mice had a 1.57- and 1.58-fold increase in hepatic lipid area and triglyceride levels, respectively, which associate with an increased liver/body weight ratio. Transcriptome and bioinformatics analysis identified 622 differentially expressed genes in LKO livers. Among them, 142 are target genes of constitutive androstane receptor (CAR), a transcription factor controlling the expression of many genes involved in xenobiotic and lipid metabolism. We also found that the expression of CAR and many CAR target genes was reduced in LKO livers. These data suggest that matrin-3 is important in CAR expression and matrin-3 knockout impairs CAR signaling. Interestingly, matrin-3 LKO mice had increased acute phase response and levels of phosphorylated Stat3 in the livers, indicating increased liver injury and inflammation. Mechanistically, impaired CAR signaling reversed the suppression of Plin2, Plin3, and Plin5 proteins that stabilize lipid droplet and inhibit lipolysis, and it reversed the suppression of interleukin 1 receptor type 1 that activates Stat3 signaling in LKO livers. Lastly, CAR expression positively correlates with matrin-3 expression in human livers (r=0.85,P=0.0002, n=13).Conclusion:matrin-3-CAR axis is an important mechanism to maintain lipid homeostasis and limit acute phase response in fatty livers. It can be potentially targeted to ameliorate hepatic steatosis and inflammation and reduce the risk of cardiovascular disease in NAFLD patients.

Circulation, Volume 146, Issue Suppl_1, Page A12001-A12001, November 8, 2022. BACKGROUND:Acute pericarditis is the most common disorder affecting the pericardium. It accounts for less than 1% of patients who are admitted to the hospital for non-ischemic chest pain and 5% who present to the emergency department with non-ischemic chest pain. The most common etiology of acute pericarditis in developed countries is idiopathic although a pre-disposing viral illness has also been recognized as a common cause. Infectious etiologies in developed countries have been seen with commonly occurring viruses such as coxsackievirus, echovirus, adenovirus and less frequently EBV.CASE:We present a 41-year-old man who came in with fevers, rigors, shortness of breath and chest pain. Transthoracic echocardiogram was (TTE) demonstrated a large pericardial effusion without evidence of tamponade. He underwent a diagnostic pericardiocentesis followed by a pericardial window during his initial hospitalization without any complications and was discharged home on NSAIDs and colchicine. Serology results demonstrated positive EBV IgG and Nuclear Antigen, concerning for active EBV pericarditis. Pathology resulted as necrotizing pericardial tissue with diffuse inflammation. The patient was readmitted within 48 hours with worsening shortness of breath and leg edema. Repeat TTE revealed a large recurrent pericardial effusion with right ventricular collapse concerning for tamponade. The patient was ultimately transferred to a tertiary care center for pericardiectomy evaluation.DISCUSSION:Ebstein-Barr virus is rarely an etiology of acute pericarditis, much less necrotizing pericarditis. When identified it should raise concern for long term complications such as recurrent pericarditis and tamponade. We believe patients who have evidence of necrotizing pericarditis are at a high risk for constrictive pericarditis and should not only have closer follow while maintaining a low clinical threshold for definitive treatment with pericardiectomy.

Circulation, Volume 146, Issue Suppl_1, Page A12188-A12188, November 8, 2022. Background:For patients with functional mitral regurgitation (MR) who remain symptomatic despite GDMT, transcatheter mitral valve repair (TMVR) is emerging as a less-invasive alternatives and can improve symptoms and longevity. We describe a rare case of cardiogenic shock following TMVR.Case:63-year-old male with PMHx of CAD with prior CABG, severe MR with EF of 40% developed progressive dyspnea and evaluated for TMVR with a Mitraclip device. TEE pre-deployment confirmed moderate to severe MR (Figure 1). Right heart catheterization revealed preserved cardiac index.Intraoperative TEE after deployment showed improved MR. Post-procedure, he developed respiratory distress and progressive hypotension requiring vasopressors and inotropes. TTE showed mild MR with severely reduced biventricular function (EF 10%). Cardiac catheterization showed a severely reduced CO/CI 3.1/1.42. Mechanical circulatory support was initiated with Impella CP due to persistent cardiogenic shock. By POD 3, he was off all inotropes and MCS was discontinued. His EF recovered to 45% during a 3- month visit.Decision Making:Causes of cardiogenic shock post mitral valve procedure include cardiac tamponade, acute mitral stenosis, intrathoracic hemorrhage and afterload mismatch. Afterload mismatch is due to reduction in left ventricular stroke volume when preload is not compensated for an acute increase in afterload. It is a known complication after mitral valve surgery; however it is rarely seen post TMVR. This patient likely experienced afterload mismatch after his mitral clipping procedure as evidenced by the acute, transient decline in LVEF (55% to 10%).Conclusion:Afterload mismatch is a rare phenomenon that can cause cardiogenic shock post percutaneous mitral repair procedures. It must be rapidly addressed with inotropic and/or mechanical support to prevent permanent end organ dysfunction and circulatory collapse. Prompt treatment allows for excellent recovery.

Circulation, Volume 146, Issue Suppl_1, Page A15157-A15157, November 8, 2022. Introduction:There are limited data on the prevalence, management and outcomes associated with concomitant aortic stenosis (AS) and acute myocardial infarction (AMI).Methods:All adult hospitalizations with a primary diagnosis of AMI were identified from the HCUP-NIS database (2000-2017). Admissions with a concomitant diagnosis of AS were compared to AMI admissions without AS. Outcomes of interest included prevalence of AS, in-hospital mortality, use of in-hospital cardiac procedures, hospitalization costs, length of stay, and discharge disposition.Results:During the study period, there were a total of 11,622,528 AMI admissions. Among these 513,688 (4.4%) were identified with concomitant AS. Adjusted temporal trends revealed an increase in prevalence of AS among STEMI (adjusted odds ratio [AOR] in 2017 vs 2000 1.15) and NSTEMI (AOR 2017 vs 2000 1.28) hospitalizations. AMI admissions with concomitant AS were on average older (78.8 ± 10.9 vs 67.1 ± 14.1), of female sex, had higher comorbidity, higher rates of NSTEMI (78.9% vs 62.1%), acute non-cardiac organ failure (13.4% vs 9.2%), and cardiogenic shock (5.1% vs 4.8%)(all p

Circulation, Volume 146, Issue Suppl_1, Page A13493-A13493, November 8, 2022. Background:Microalbuminuria is associated with adverse outcome in acute coronary syndrome (ACS) patients.Methods:To evaluate the very long-term association between microalbuminuria during ACS and the overall mortality and causes of death, we prospectively studied 579 ACS patients admitted to three Italian hospitals. The baseline albumin-to-creatinine ratio (ACR) was measured on days 1, 3, and 7 in 24-h urine samples. Patients were followed for 22 years or until death.Results:Virtually all patients completed the follow-up, representing 6756 person-years. During follow-up, 449(78%) had died: 41% due to non-sudden cardiac death (non-SCD), 19% sudden cardiac death (SCD), 40% due to non-cardiac (non-CD) death. The unadjusted Cox regression analysis showed that ACR is a significant predictor of all-cause mortality (HR:1.26; 95%CI 1.22-1.31; p˂0.0001) and the 3 causes of death (HR:1.40; 95%CI 1.32-1.48; p˂0.0001), (HR:1.22; 95%CI 1.12-1.32; p˂0.0001) and (HR:1.16; 95%CI 1.09-1.23; p˂0.0001) for non-SCD, SCD and non-CD respectively. Yet the fully adjusted model showed that ACR is a significant independent predictor of all-cause mortality (HR:1.12; 95%CI 1.08-1.16; p˂0.0001) and only non-SCD (HR:1.21; 95%CI 1.14-1.29; p˂0.0001).A positive interaction between ACR and history of AMI (HR:1.15; 95%CI 1.03-1.29; p=0.01), and the presence of heart failure during admission (HR:1.11; 95%CI 1.01-1.24; p=0.04), and a negative interaction with LVEF (HR:0.89; 95%CI 0.80-0.99; p=0.03) for all-cause death was also observed at the multivariable level.Conclusion:This prospective study shows that baseline ACR during ACS seems to be a strong independent predictor of the very long-term mortality risk, chiefly associated with non-sudden cardiac death. A positive independent interaction with indicators of heart failure has been also observed.Figure 1:Relative hazard estimates for all-cause and cause-specific mortality 22 years after ACS according to baseline ACR.

Circulation, Volume 146, Issue Suppl_1, Page A13104-A13104, November 8, 2022. Introduction:Reduced serum levels of glycosylated apolipoprotein J (ApoJ-Glyc) have been proposed as a marker for the early detection of myocardial ischemia with a potential prognostic value.Objective:The EDICA clinical trial assessed the performance of ApoJ-Glyc as a biomarker for the early detection of myocardial ischemia in patients attending the A&E department with chest pain suggestive of acute coronary syndrome (ACS) and investigated -as a secondary pilot objective- its prognostic value.Methods:EDICA -a multi-centre, international, diagnostic study (NCT04119882) assessed 404 patients. Based on clinical variables and diagnostic tests, 291 patients were considered to have had a “non-ischemic” event and 113 an “ischemic” event. Blood samples were obtained for the assessment of high-sensitivity troponin and ApoJ-Glyc at admission and at 1h and 3h thereafter. GRACE Risk Score was calculated in all ischemic patients. Patients were followed up for 6 months after presentation and the occurrence of MACE (cardiac death, recovered cardiac arrest, re-infarction, cardiac failure, new admission for ACS after discharge, or unplanned revascularization for cardiac ischemia after discharge) was recorded. ApoJ-Glyc serum levels were analyzed with a novel ELISA targeting a specific glycosylated variant of ApoJ (ApoJ-GlycA2).Results:Among the patients in the ischemic group, 8.8% had MACE at 6-months and these showed a 26% mean reduction in ApoJ-GlycA2 levels 3h post-admission compared with levels at presentation. This reduction was not observed in patients without MACE. Patients in the highest GRACE Risk Score tertile ( >118 points) showed a progressive decrease in ApoJ-GlycA2 levels after presentation compared with patients in the lower risk tertiles (mean decrease: 41% at 1h, P=0.01 and 35% at 3h, P=0.02 when compared with admission levels).Conclusions:A progressive decrease in ApoJ-Glyc levels after A&E admission appears to not only identify patients with ischemic events but also those at higher risk of suffering serious recurrent cardiovascular events at 6-months’ follow-up. Further studies in larger cohorts of patients are warranted to validate the potential role of ApoJ-Glyc in risk stratification in the context of cardiac ischemic events.

Circulation, Volume 146, Issue Suppl_1, Page A12647-A12647, November 8, 2022. Introduction:Acute corticosteroid therapy has been used in the prophylaxis against atrial fibrillation following cardiac surgery or acute myocardial infarction (AMI). Glucocorticoid (GR) and mineralocorticoid (MR) receptors are highly expressed in cardiac tissue. While MR activation during AMI was linked to Na+/H+exchanger (NHE1) activation-mediated increase in infarct size and contractile dysfunction, lesser is known about GR effects. The aim of this work is to seek the functional effects of an acute dose of a low potency corticosteroid (hydrocortisone, HC) in a rat model of AMI.Methods:AMI was promoted in isolated hearts from Wistar rats by 40min of regional ischemia followed by 60min reperfusion (ischemic control “I”, n=4). 10nM HC (HC10, n=3) or HC10 plus the GR inhibitor Mifepristone (M, 10uM, n=5) was added to the perfusate during the first 10min of reperfusion. In isolated papillary muscles from non-infarcted hearts NHE1 activity was measure by analyzing the pH recovery from an acute transient acidosis (TA) in control conditions, and in the presence of HC 1nM (HC1) or HC10. Protein phosphorylation and expression were determined by western blot. Data are expressed as mean±S.E.M.Results:HC treatment reduced infarct size (% of risk area: 38±3 I; 9±3 HC10, p

Circulation, Volume 146, Issue Suppl_1, Page A15820-A15820, November 8, 2022. Background:There continues to be emerging data about the benefits of Sodium-glucose co-transporter 2 inhibitor (SGLT2i) in patients with heart failure. This has led to the addition of this medication to guideline-directed medical therapy for heart failure with reduced ejection fraction. There is a discrepancy in whether the use of SGLT2i is beneficial in patients hospitalized for decompensated heart failure.Methods:In this study, a search was completed through PubMed, Scopus, Cochrane Library, ProQuest for randomized controlled trials from 2020 to 2022 that evaluated the impact of the use of SGLT-2 inhibitors (Empagliflozin, Sotagliflozin) in patients admitted with acute HF. After screening for our preset inclusion and exclusion criteria, three randomized controlled clinical trials were eligible for inclusion. We carried out a Meta-analysis of the relative odds on the basis of the random effect model using the Mantel-Haenszel method for the major outcome of the incidence of death from any cause, the number of heart failure events, rehospitalization for heart failure, and time to first heart failure event in the acute setting. Comprehensive Meta-analysis version 3 software was used for analysis.Results:A total of 2,532 patients from the EMPULSE, SOLOIST-WHF, EMPA-RESPONSE-AHF trials were included. After analysis, it was found that the P-value was 0.000, Z-value was -4.103, and the OR 0.508 (95% CI 0.368; 0.702) for the patients on either Empagliflozin or Sotagliflozin.Conclusions:The systematic review and meta-analysis we conducted show that patients who received SGLT-2i (Empagliflozin, Sotagliflozin) during hospitalization within 24 hours or more had a statistically significant decreased odds of all-cause of death, number of heart failure events, and rehospitalization for heart failure.

Circulation, Volume 146, Issue Suppl_1, Page A10940-A10940, November 8, 2022. Introduction:The risk of myocarditis after mRNA vaccination against COVID-19 has emerged, recently. Current evidence suggests that young male patients are predominantly affected. In the majority of the cases only mild symptoms were observed. However, little is known about mRNA vaccination related myocarditis cardiac magnetic resonance (CMR) imaging patterns and their differences to classical viral myocarditis in the acute phase of inflammation.Methods:10 mRNA vaccination associated myocarditis patients were retrospectively enrolled in this study and compared to 10 patients suffering from viral myocarditis, matched with age, sex, comorbidities and laboratory markers. All patients (n = 20) were hospitalized and underwent a standardized clinical examination as well as an echocardiography and a CMR. Both, clinical and imaging findings were compared between both groups.Results:All patients described chest pain as the leading reason for their initial presentation. CMR volumetric and functional parameters did not differ significantly between both groups. In all cases the lateral left ventricular wall showed late gadolinium enhancement without significant differences in terms of the localisation or in-depth tissue characterization.Conclusions:COVID-19 mRNA vaccination associated myocarditis does not show specific CMR patterns during the very acute stage in the most affected patient group of young male patients. The observed imaging markers are closely related with regular viral myocarditis and did not yield any evidence implying adverse outcomes in the investigated patient group.

Circulation, Volume 146, Issue Suppl_1, Page A13194-A13194, November 8, 2022. SARS-CoV2 (CoV2) infection causes both acute and long-term health effects via damaging multiple organs including lung. The endothelial dysfunction associated with the infection may contribute to pathogenesis of acute COVID-19 and long COVID. However, the mechanisms underlying the endothelial dysfunction remain elusive. Development of mouse models for these diseases will help us better dissect these mechanisms and facilitate the development of therapeutics for treatment of the disease. Previously, we developed an acute COVID model by infecting human ACE2 transgenic (K18) mice with a lethal CoV2 dose. K18 mice developed severe COVID-19, including progressive body weight loss and fatality at days 7 post infection (DPI), severe lung interstitial inflammation, edema, hemorrhage, perivascular inflammation, systemic lymphocytopenia, and eosinopenia. We detected CoV2 in capillary endothelial cells, activation and adhesion of platelets and immune cells to the vascular wall of the alveolar septa, and increased complement deposition in the lungs in this model. These results indicate that CoV2 infection and infection-mediated immune activation caused endothelial dysfunction, which contributes to the pathogenesis of severe COVID-19. To further develop a model for long COVID, we infected K18 mice with sub lethal CoV2 dose, monitored the body weight and survival rate and characterized the lung and brain histological changes at 21 and 45 DPI. The infected mice progressively lost body weights from 5 to 7 DPI and started to rebound from 8 DPI and then returned to baseline at 13 DPI. Mice had extensive patchy inflammation in the lungs associated with collagen deposition and smooth muscle action expression. We also found moderate levels of total viral RNA in the lung but not brain while viral subgenomic RNA (a correlate of viral replication) was undetectable in lung or brain by qRT-PCR assay. Fluorescence staining showed co-localization of CoV2 spike protein and CD206 in lungs, suggesting macrophage engulfment CoV2 at late time points. Together, we have successfully established long-term COVID mouse models, which will be useful tools for further defining the role of endothelial dysfunction in pathogeneses of CoV2-related acute and long COVID.

Circulation, Volume 146, Issue Suppl_1, Page A11699-A11699, November 8, 2022. Introduction:Coronary artery dissection is an emergency condition due to a tear in the coronary arterial wall, and it’s an uncommon cause of acute coronary syndrome. The Effect of Obesity on the outcome of acute coronary artery dissection is poorly documented. Hence, our study sought to estimate the impact of Obesity on clinical outcomes of hospitalizations of patients with acute Coronary artery dissection using the national database.Methods:We queried the National Inpatient Sample (NIS) database from 2016 to 2019. The NIS is the largest inpatient hospitalization database in the United States. The NIS was searched for hospitalization of adult patients with acute Coronary artery dissection as a principal diagnosis with and without Obesity as a secondary diagnosis using ICD-10 codes. The primary outcome was inpatient mortality. The secondary results were Acute kidney injury (AKI), Cardiogenic shock (CS), Cardiac arrest (CA), Total hospital charge (THC), and length of stay (LOS). Multivariate logistic and linear regression analyses were used accordingly to adjust for confounders.Results:About 2440 patients were admitted for acute Coronary artery dissection; 17.4% (425) had underlying obesity. Cohorts with obesity vs No obesity had a mean age of 52.9 years [CI 50.4 – 55.5] vs 55.9 years [CI 54.5 – 57.4]; male (20% vs 25.8%), female (80% vs 74.2%); white (71.3% vs 73.3%), black (21.3% vs 12.0%), and Hispanic (6.3% vs 7.8%). Compared to patients without obesity, patients admitted with coexisting obesity had similar inpatient mortality (7.1% vs 3.2%, AOR 3.22, 95% CI 0.74 – 13.88, P=0.118), AKI (15.3% vs 9.9%, P 0.357), CS (9.4% vs 11.2% P=0.098), CA (5.9% vs 5.0% P=0.530), THC (IRR 0.94, 95% CI 0.64 – 1.37, P=0.738), and LOS (IRR 0.79, 95% CI 0.59 – 1.05, P=0.107).Conclusions:Patients admitted primarily for acute Coronary artery dissection with co-existing Obesity had similar inpatient mortality, AKI, CS, CA, THC, and LOS compared to patients without Obesity.

Circulation, Volume 146, Issue Suppl_1, Page A13191-A13191, November 8, 2022. Case Presentation:Infective endocarditis (IE) can sometimes be a diagnostic challenge because its presentation in its early stages may coincide with that of several other disease processes. It has an incidence of ~7 per 100,000 annually yet has an in-hospital mortality of about 20-25%. We present a case of a 56-year-old immunocompetent male with a recent diagnosis of leukocytoclastic vasculitis (LCV) who was admitted for acute renal failure (ARF). With his history of LCV (Figure 1), renal vasculitis was thought to be contributing to his ARF. On admission, he was afebrile and had a creatinine of 5.25 (baseline of 0.8), hyponatremia, anemia, mild leukocytosis, and mildly elevated lactate. No other infectious sequelae were noted. Nephrology was consulted for workup of renal failure, and a renal biopsy was recommended. Before the biopsy was able to be performed, blood cultures returned positive for Enterococcus faecalis. Transesophageal echocardiogram revealed a large, mobile 1.3-centimeter vegetation attached to the left ventricular outflow tract side of the non-coronary cusp of the aortic valve. Parenteral antibiotics were initiated, and cardiothoracic surgery was consulted for surgical correction. The patient ultimately underwent aortic valve replacement successfully with renal recovery to baseline and resolution of his leukocytoclastic vasculitis soon thereafter.Discussion:LCV has been established as a rare, but well-reported sign of IE. Similarly, only a few cases of IE presenting as ARF have been reported. In patients presenting with both LCV and ARF, it is important to maintain a high index of suspicion for IE. Going down the pathway to work up renal vasculitis may unnecessarily expose patients to invasive procedures, incorrect treatment modalities, and other complications.

Circulation, Volume 146, Issue Suppl_1, Page A10194-A10194, November 8, 2022. Introduction:Acute pericarditis has not been linked to long-term heart-specific morbidity in breast cancer patients. Carcinomatous pericardial involvement has been detected at autopsy in 10-20% of breast cancer patients. In clinical practice, when it comes to primarily echocardiographically-diagnosed pericardial diseases: pericardial effusion, cardiac tamponade, and pericardial constriction have all been reported in breast cancer patients. Acute pericarditis is primarily a clinical non-imaging bedside diagnosis derived from the combination of chest pain, pericardial rub, and typical electrocardiographic changes, irrespective of the presence or absence of pericardial fluid on imaging. It can be the initial clinical manifestation of a malignancy.Methods:The Myocardial Infarction Data Acquisition System (MIDAS) database is an ongoing, longitudinal, and validated database that comprises discharge data, along with demographics, comorbidities, and length of hospital stay; for all patients with cardiovascular diseases admitted to every non-federal acute care hospital in the state of New Jersey. We searched for the diagnosis of acute pericarditis (ICD-9 codes 420.0, 420.90, 420.91, and 420.99), in first hospital admissions of female patients with breast cancer (ICD-9 codes 174.0-174.9) between January 1995 to December 2015. Controls were female breast cancer patients without the diagnosis of acute pericarditis.Results:There were 60,435 female patients with breast cancer. Of those, 253 (0.4%) were also diagnosed with acute pericarditis on the same admission as the first breast cancer diagnosis, or later. Analysis for comorbidities showed that 116 (45.8%) of the 253 patients with acute pericarditis had admissions for heart failure, as opposed to 26.4% (15,895 out of 60,182) of breast cancer patients without acute pericarditis (p < 0.00001).Conclusions:Since New Jersey has a diverse population that resembles the profile of the United States in age, gender, and race/ethnicity; our findings could also be generalized to other geographic areas, and may help with future clinical guidelines. Although it is rare, acute pericarditis in breast cancer patients can indicate long-term cardiovascular morbidity.