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Patients with continuous flow destination therapy (DT) left ventricular assist devices (LVAD) comprise a heterogeneous population. We hypothesized that phenotypic clustering of individuals with DT LVADs by their implantation characteristics will be associated with different long-term risk profiles. We analyzed 5,999 patients with continuous flow DT LVADs in Interagency Registry for Mechanically Assisted Circulatory Support using 18 continuous variable baseline characteristics. We Z-transformed the variables and applied a Gaussian finite mixture model to perform unsupervised clustering resulting in identification of 4 phenogroups. Survival analyses considered the competing risk for cumulative incidence of transplant or the composite end point of death or heart transplant where appropriate. Phenogroup 1 (n = 1,163, 19%) was older (71 years) and primarily white (81%). Phenogroups 2 (n = 648, 11%) and 3 (n = 3,671, 61%) were of intermediate age (70 and 62 years), weight (85 and 87 kg), and ventricular size. Phenogroup 4 (n = 517, 9%) was younger (40 years), heavier (108 kg), and more racially diverse. The cumulative incidence of death, heart transplant, bleeding, LVAD malfunction, and LVAD thrombosis differed among phenogroups. The highest incidence of death and the lowest rate of heart transplant was seen in phenogroup 1 (p0.001). For adverse outcomes, phenogroup 4 had the lowest incidence of bleeding, whereas LVAD device thrombosis and malfunction were lowest in phenogroup 1 (p0.001 for all). Finally, the incidence of stroke, infection, and renal dysfunction were not statistically different. In conclusion, the present unsupervised machine learning analysis identified 4 phenogroups with different rates of adverse outcomes and these findings underscore the influence of phenotypic heterogeneity on post-LVAD implantation outcomes.

Background Acute myocarditis (AM) is thought to be a rare cardiovascular complication of COVID-19, although minimal data are available beyond case reports. We aim to report the prevalence, baseline characteristics, in-hospital management, and outcomes for patients with COVID-19–associated AM on the basis of a retrospective cohort from 23 hospitals in the United States and Europe. Methods A total of 112 patients with suspected AM from 56963 hospitalized patients with COVID-19 were evaluated between February 1, 2020, and April 30, 2021. Inclusion criteria were hospitalization for COVID-19 and a diagnosis of AM on the basis of endomyocardial biopsy or increased troponin level plus typical signs of AM on cardiac magnetic resonance imaging. We identified 97 patients with possible AM, and among them, 54 patients with definite/probable AM supported by endomyocardial biopsy in 17 (31.5%) patients or magnetic resonance imaging in 50 (92.6%). We analyzed patient characteristics, treatments, and outcomes among all COVID-19–associated AM. Results AM prevalence among hospitalized patients with COVID-19 was 2.4 per 1000 hospitalizations considering definite/probable and 4.1 per 1000 considering also possible AM. The median age of definite/probable cases was 38 years, and 38.9% were female. On admission, chest pain and dyspnea were the most frequent symptoms (55.5% and 53.7%, respectively). Thirty-one cases (57.4%) occurred in the absence of COVID-19–associated pneumonia. Twenty- one (38.9%) had a fulminant presentation requiring inotropic support or temporary mechanical circulatory support. The composite of in-hospital mortality or temporary mechanical circulatory support occurred in 20.4%. At 120 days, estimated mortality was 6.6%, 15.1% in patients with associated pneumonia versus 0% in patients without pneumonia (P=0.044). During hospitalization, left ventricular ejection fraction, assessed by echocardiography, improved from a median of 40% on admission to 55% at discharge (n=47; P Conclusions AM occurrence is estimated between 2.4 and 4.1 out of 1000 patients hospitalized for COVID-19. The majority of AM occurs in the absence of pneumonia and is often complicated by hemodynamic instability. AM is a rare complication in patients hospitalized for COVID-19, with an outcome that differs on the basis of the presence of concomitant pneumonia.

Decreased exercise capacity portends a poor prognosis in heart failure with preserved ejection fraction (HFpEF). The hemodynamic gain index (HGI) is an integrated marker of hemodynamic reserve measured during exercise stress testing and is associated with survival. The goal of this study was to establish the association of HGI with exercise capacity, serum biomarkers, and echocardiography features in subjects with HFpEF. In 209 subjects with HFpEF enrolled in the RELAX (Phosphodiesterase-5 Inhibition to Improve Clinical Status and Exercise Capacity in Diastolic Heart Failure) trial who underwent cardiopulmonary exercise testing, we calculated the HGI ([peak heart rate [HR] × peak systolic blood pressure [SBP]-[HR at rest × SBP at rest])/(HR at rest × SBP at rest) and tested associations with outcomes of interest. The median (interquartile range) HGI was 0.94 (0.5 to 1.3) beats per min/mm Hg. In multivariable-adjusted linear regression, higher HGI was associated with greater peak oxygen consumption (VO

Background: New-onset atrial fibrillation (AF) in patients hospitalized with COVID-19 has been reported and associated with poor clinical outcomes. We aimed to understand the incidence of and outcomes associated with new-onset AF in a diverse and representative US cohort of patients hospitalized with COVID-19. Methods: We used data from the American Heart Association COVID-19 Cardiovascular Disease Registry. Patients were stratified by the presence versus absence of new-onset AF. The primary and secondary outcomes were in-hospital mortality and major adverse cardiovascular events (MACE; cardiovascular death, myocardial infarction, stroke, cardiogenic shock, and heart failure). The association of new-onset AF and the primary and secondary outcomes was evaluated using Cox proportional-hazards models for the primary time to event analyses. Results: Of the first 30 999 patients from 120 institutions across the United States hospitalized with COVID-19, 27 851 had no history of AF. One thousand five hundred seventeen (5.4%) developed new-onset AF during their index hospitalization. New-onset AF was associated with higher rates of death (45.2% versus 11.9%) and MACE (23.8% versus 6.5%). The unadjusted hazard ratio for mortality was 1.99 (95% CI, 1.81–2.18) and for MACE was 2.23 (95% CI, 1.98–2.53) for patients with versus without new-onset AF. After adjusting for demographics, clinical comorbidities, and severity of disease, the associations with death (hazard ratio, 1.10 [95% CI, 0.99–1.23]) fully attenuated and MACE (hazard ratio, 1.31 [95% CI, 1.14–1.50]) partially attenuated. Conclusions: New-onset AF was common (5.4%) among patients hospitalized with COVID-19. Almost half of patients with new-onset AF died during their index hospitalization. After multivariable adjustment for comorbidities and disease severity, new-onset AF was not statistically significantly associated with death, suggesting that new-onset AF in these patients may primarily be a marker of other adverse clinical factors rather than an independent driver of mortality. Causality between the MACE composites and AF needs to be further evaluated.

Aims Patients with obesity and ischaemic heart failure may counter‐intuitively have better outcomes compared with patients with normal body weight due to an ‘obesity paradox’. This study sought to determine if body mass index (BMI) impacts the treatment effects or safety outcomes of the treatment of ischaemic heart failure with coronary artery bypass grafting (CABG). Methods and results We obtained and reviewed the Surgical Treatment of Ischaemic Heart Failure (STICHES) data for 1212 patients. We categorized obesity by the World Health Organization (WHO) classes to define baseline characteristics and test for treatment interactions for the primary and secondary STICHES outcomes by treatment groups. While CABG decreased the risk of death, there was no evidence of treatment interaction by BMI per 5 kg/m2 (P = 0.83) or WHO obesity class. For the overall cohort, there was no interaction by WHO obesity class for the cumulative incidence of death in either the medical therapy or CABG plus medical therapy (P‐interaction = 0.90). There was a non‐significant trend for higher BMI and a lower risk of death [hazard ratio 0.92, 95% confidence interval (CI) 0.85–1.00, P = 0.051]. Increasing body size (per 5 kg/m2) was associated with return to the operating room (odds ratio 2.48, 95% CI 1.45–4.26, P

Transthyretin amyloidosis is an increasingly recognized cause of restrictive cardiomyopathy related to amyloid fibril deposition in cardiac tissues. As treatment therapies have emerged for transthyretin amyloidosis (ATTR), so has interest in using biomarkers to identify disease prior to advanced presentation. Lower levels of transthyretin and retinol binding protein-4 have been demonstrated in patients with pathogenic mutations of transthyretin either with or without clinical disease. Levels associate with the severity of mutations as well as response to treatment with transthyretin stabilizers or small interfering RNA molecules which silence transthyretin production. Transthyretin stability is the rate limiting step of amyloid fibril formation and directly measuring transthyretin kinetic stability has the potential to identify patients as risk as well as therapeutic response to treatment regardless of pathogenic or wild-type genetics. In addition, non-antibody protein-based peptide probes have been developed that directedly measure misfolded transthyretin oligomers due to transthyretin breakdown. Although promising, both TTR kinetic and protein peptide probes remain in early stages of clinical investigation. Transthyretin, retinol binding protein-4, transthyretin kinetic stability, and protein-based peptide probes have potential as biomarkers to facilitate an earlier ATTR diagnosis for patients with pathogenic transthyretin mutations.

Coronavirus disease 2019 (COVID-19) is a rapidly expanding global pandemic caused by severe acute respiratory syndrome coronavirus 2, resulting in significant morbidity and mortality. A substantial minority of patients hospitalized develop an acute COVID-19 cardiovascular syndrome, which can manifest with a variety of clinical presentations but often presents as an acute cardiac injury with cardiomyopathy, ventricular arrhythmias, and hemodynamic instability in the absence of obstructive coronary artery disease. The cause of this injury is uncertain but is suspected to be related to myocarditis, microvascular injury, systemic cytokine-mediated injury, or stress-related cardiomyopathy. Although histologically unproven, severe acute respiratory syndrome coronavirus 2 has the potential to directly replicate within cardiomyocytes and pericytes, leading to viral myocarditis. Systemically elevated cytokines are also known to be cardiotoxic and have the potential to result in profound myocardial injury. Prior experience with severe acute respiratory syndrome coronavirus 1 has helped expedite the evaluation of several promising therapies, including antiviral agents, interleukin-6 inhibitors, and convalescent serum. Management of acute COVID-19 cardiovascular syndrome should involve a multidisciplinary team including intensive care specialists, infectious disease specialists, and cardiologists. Priorities for managing acute COVID-19 cardiovascular syndrome include balancing the goals of minimizing healthcare staff exposure for testing that will not change clinical management with early recognition of the syndrome at a time point at which intervention may be most effective. This article aims to review the best available data on acute COVID-19 cardiovascular syndrome epidemiology, pathogenesis, diagnosis, and treatment. From these data, we propose a surveillance, diagnostic, and management strategy that balances potential patient risks and healthcare staff exposure with improvement in meaningful clinical outcomes.

SARS-CoV-2 infection (COVID-19) can result in myocarditis. Protocols were developed to allow competitive athletes to safely return to play (RTP) after a COVID-19 infection, but the financial impact of these protocols is unknown. Our objective was to determine the differential cost of post-COVID-19 RTP protocols for competitive collegiate athletes.This multicenter retrospective cohort study of clinical evaluation of 295 athletes after COVID-19 infection was performed at four institutions with three RTP protocols. Costs were calculated using adjusted Center for Medicare and Medicaid Services pricing. All athletes underwent electrocardiogram and clinical evaluation. A tiered approach performed cardiac imaging and biomarker analysis for major symptoms. A universal transthoracic echocardiogram (TTE) approach performed TTE and biomarkers for all athletes. A universal exercise stress echocardiogram (ESE) approach performed ESE and biomarkers for all athletes.The cost per athlete was $632.51 ± 651.80 ($44,908 total) in tiered group (n = 71), $1,072.30 ± 517.93 ($87,928 total) in the universal TTE group (n = 82), and $1357.38 ± 757.05 ($192,748 total) in the universal ESE group (n = 142) (P0.001). Extrapolated national costs for collegiate athletes would be $39 to 64 million higher for universal imaging approaches versus a tiered approach. Only seven athletes had probable/possible myocarditis with no significant difference between approaches.Cardiac screening in collegiate athletes after COVID-19 infection resulted in significant cost to the health care system. A tiered-based approach was more economical, and a universal exercise echocardiogram group detected slightly more myocardial abnormalities by cardiac magnetic resonance imaging. The clinical consequences of these approaches are unknown.

Background: Acute myocarditis (AM) is thought to be a rare cardiovascular complication of COVID-19, although minimal data are available beyond case reports. We aim to report the prevalence, baseline characteristics, in-hospital management, and outcomes for patients with COVID-19–associated AM on the basis of a retrospective cohort from 23 hospitals in the United States and Europe. Methods: A total of 112 patients with suspected AM from 56 963 hospitalized patients with COVID-19 were evaluated between February 1, 2020, and April 30, 2021. Inclusion criteria were hospitalization for COVID-19 and a diagnosis of AM on the basis of endomyocardial biopsy or increased troponin level plus typical signs of AM on cardiac magnetic resonance imaging. We identified 97 patients with possible AM, and among them, 54 patients with definite/probable AM supported by endomyocardial biopsy in 17 (31.5%) patients or magnetic resonance imaging in 50 (92.6%). We analyzed patient characteristics, treatments, and outcomes among all COVID-19–associated AM. Results: AM prevalence among hospitalized patients with COVID-19 was 2.4 per 1000 hospitalizations considering definite/probable and 4.1 per 1000 considering also possible AM. The median age of definite/probable cases was 38 years, and 38.9% were female. On admission, chest pain and dyspnea were the most frequent symptoms (55.5% and 53.7%, respectively). Thirty-one cases (57.4%) occurred in the absence of COVID-19–associated pneumonia. Twenty-one (38.9%) had a fulminant presentation requiring inotropic support or temporary mechanical circulatory support. The composite of in-hospital mortality or temporary mechanical circulatory support occurred in 20.4%. At 120 days, estimated mortality was 6.6%, 15.1% in patients with associated pneumonia versus 0% in patients without pneumonia ( P =0.044). During hospitalization, left ventricular ejection fraction, assessed by echocardiography, improved from a median of 40% on admission to 55% at discharge (n=47; P Conclusions: AM occurrence is estimated between 2.4 and 4.1 out of 1000 patients hospitalized for COVID-19. The majority of AM occurs in the absence of pneumonia and is often complicated by hemodynamic instability. AM is a rare complication in patients hospitalized for COVID-19, with an outcome that differs on the basis of the presence of concomitant pneumonia.

Background Emerging evidence links acute kidney injury (AKI) in patients with COVID‐19 with higher mortality and respiratory morbidity, but the relationship of AKI with cardiovascular disease outcomes has not been reported in this population. We sought to evaluate associations between chronic kidney disease (CKD), AKI, and mortality and cardiovascular outcomes in patients hospitalized with COVID‐19. Methods and Results In a large multicenter registry including 8574 patients with COVID‐19 from 88 US hospitals, data were collected on baseline characteristics and serial laboratory data during index hospitalization. Primary exposure variables were CKD (categorized as no CKD, CKD, and end‐stage kidney disease) and AKI (classified into no AKI or stages 1, 2, or 3 using a modification of the Kidney Disease Improving Global Outcomes guideline definition). The primary outcome was all‐cause mortality. The key secondary outcome was major adverse cardiac events, defined as cardiovascular death, nonfatal stroke, nonfatal myocardial infarction, new‐onset nonfatal heart failure, and nonfatal cardiogenic shock. CKD and end‐stage kidney disease were not associated with mortality or major adverse cardiac events after multivariate adjustment. In contrast, AKI was significantly associated with mortality (stage 1 hazard ratio [HR], 1.72 [95% CI, 1.46–2.03]; stage 2 HR, 1.83 [95% CI, 1.52–2.20]; stage 3 HR, 1.69 [95% CI, 1.44–1.98]; versus no AKI) and major adverse cardiac events (stage 1 HR, 2.17 [95% CI, 1.74–2.71]; stage 2 HR, 2.70 [95% CI, 2.07–3.51]; stage 3 HR, 3.06 [95% CI, 2.52–3.72]; versus no AKI). Conclusions This large study demonstrates a significant association between AKI and all‐cause mortality and, for the first time, major adverse cardiovascular events in patients hospitalized with COVID‐19.

Background: Obesity may contribute to adverse outcomes in coronavirus disease 2019 (COVID-19). However, studies of large, broadly generalizable patient populations are lacking, and the effect of body mass index (BMI) on COVID-19 outcomes— particularly in younger adults—remains uncertain. Methods: We analyzed data from patients hospitalized with COVID-19 at 88 US hospitals enrolled in the American Heart Association’s COVID-19 Cardiovascular Disease Registry with data collection through July 22, 2020. BMI was stratified by World Health Organization obesity class, with normal weight prespecified as the reference group. Results: Obesity, and, in particular, class III obesity, was overrepresented in the registry in comparison with the US population, with the largest differences among adults ≤50 years. Among 7606 patients, in-hospital death or mechanical ventilation occurred in 2109 (27.7%), in-hospital death in 1302 (17.1%), and mechanical ventilation in 1602 (21.1%). After multivariable adjustment, classes I to III obesity were associated with higher risks of in-hospital death or mechanical ventilation (odds ratio, 1.28 [95% CI, 1.09–1.51], 1.57 [1.29–1.91], 1.80 [1.47–2.20], respectively), and class III obesity was associated with a higher risk of in-hospital death (hazard ratio, 1.26 [95% CI, 1.00–1.58]). Overweight and class I to III obese individuals were at higher risk for mechanical ventilation (odds ratio, 1.28 [95% CI, 1.09–1.51], 1.54 [1.29–1.84], 1.88 [1.52–2.32], and 2.08 [1.68–2.58], respectively). Significant BMI by age interactions were seen for all primary end points ( P -interaction70 years. Severe obesity (BMI ≥40 kg/m 2 ) was associated with an increased risk of in-hospital death only in those ≤50 years (hazard ratio, 1.36 [1.01–1.84]). In adjusted analyses, higher BMI was associated with dialysis initiation and with venous thromboembolism but not with major adverse cardiac events. Conclusions: Obese patients are more likely to be hospitalized with COVID-19, and are at higher risk of in-hospital death or mechanical ventilation, in particular, if young (age ≤50 years). Obese patients are also at higher risk for venous thromboembolism and dialysis. These observations support clear public health messaging and rigorous adherence to COVID-19 prevention strategies in all obese individuals regardless of age.

Two months prior to presenting to our facility, a 63-year-old man was diagnosed with acute pericarditis and treated with colchicine. His chest pain resolved, but he was readmitted a few weeks later with tamponade due to a large exudative pericardial effusion requiring percutaneous drainage. He was discharged on colchicine and furosemide; however, he presented to our institution two weeks later with persisting dyspnea and edema. His blood pressure was 114/84 mmHg without a pulsus paradoxus. Jugular venous pressure was 13 cm H 2 O with a prominent Kussmaul’s sign and 3+ bilateral leg edema. Further evaluation with a transthoracic echocardiogram, cardiac MRI and cardiac catheterization were all consistent with effusive-constrictive pericarditis (Fig A-F). 8-months prior to admission a mediastinal lymph node biopsy noted histoplasma. During admission, chronic histoplasmosis was suspected and a serum histoplasma antigen was reactive (1:256). He was initiated on 12 weeks of itraconazole; however, despite anti-inflammatory therapies, he had refractory congestion. Cardiothoracic surgery was consulted and he underwent pericardial stripping (Fig. G). Pericardial fungal cultures were negative and histopathology noted acute and chronic fibrinous pericarditis without fungal organisms (Fig. H-I). He had an uncomplicated recovery with symptom resolution. Histoplasma capsulatum is endemic to the United States and despite >80% of individuals in endemic areas demonstrating exposure, cases of pericarditis, tamponade or pericardial constriction are rare. Pericardial inflammation likely reflects an autoimmune reaction to H. capsulatum rather than direct pericardial infection and may respond to anti-inflammatories. In sum, we describe a rare diagnosis of effusive-constrictive pericarditis secondary to chronic histoplasmosis. Our case highlights the salient findings of pericardial constriction and the continued importance of a detailed clinical history.

Hypothesis Because there may be signals of sex-based differences in response to HFpEF therapy according to left ventricular ejection fraction, we hypothesize that there will be a prognostic difference in clinical outcomes by sex according to global longitudinal strain (GLS) in HFpEF and this may be associated with treatment heterogeneity with spironolactone. Methods Participants from the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist trial with core lab strain echo data (N=477) were stratified into 4 categories based on sex and GLS relative to the median. Cox-proportional hazards models adjusted for age, race, atrial fibrillation, NYHA class, stroke, and creatinine determined the association of sex/GLS categories with the composite primary endpoint (cardiovascular death, heart failure hospitalization, or aborted cardiac arrest), heart failure hospitalization, cardiovascular death, and all-cause mortality. Results In this cohort (age 70±20 y, 46% male, LVEF 60±16%) the median GLS was -15.6%. Kaplan-Meier estimates for the primary composite outcome stratified by the four sex/GLS groups are shown below (Figure). In adjusted Cox-proportional hazards models, both sex groupings with above-median (e.g. impaired) GLS were associated with a higher risk for the composite primary endpoint, cardiovascular death, and heart failure hospitalizations, but not all cause mortality in comparison with men with below-median GLS (e.g. preserved). However, there was no significant difference in the risk of any of the endpoints between men and women with below-median GLS. Lastly, sex/GLS groupings did not impact the treatment effect of spironolactone vs placebo for any of the endpoints (P-interaction>0.05 for all). ConclusionS The prognostic importance of systolic dysfunction as measured by GLS in HFpEF did not appear to be impacted by sex, and grouping by sex and GLS did not modify the effect of spironolactone on long-term outcomes.

Symptomatic improvement through decongestive therapy is a cornerstone for treatment of acute decompensated heart failure (ADHF). Visual analog scales (VAS) are instruments that can capture patients' perceptions of dyspnea (DVAS) or global well-being (GVAS). However, the clinical implications of these instruments and their changes over time during treatment for ADHF need further clarification. DVAS and GVAS were collected in 657 patients randomized in the DOSE-AHF and ROSE-AHF trials. To determine factors associated with symptom change, multivariable predictors of changes in DVAS and GVAS over 72 hours were determined. In addition, time-to-event analyses determined the association between these assessments and post-discharge clinical outcomes. The median baseline DVAS and GVAS scores were 54 (interquartile range 35 to 76) and 50 (30 to 66), respectively. These scores increased from baseline to 72 hours (ΔDVAS 16 [0 to 35] and ΔGVAS 19 [2 to 37]). Although changes in both scales were associated with their baseline values, 72-hour change in NT-proBNP was associated with each scale in multivariable analysis. However, there were additional variables associated with 72-hour change in GVAS including 72-hour change in creatinine, implantable cardioverter-defibrillator presence, baseline loop diuretic dose, and 72-hour total loop diuretic dose. There were no consistent associations between DVAS or GVAS and clinical composite outcomes at 60 days. In conclusion, DVAS and GVAS may be related to different clinical factors during treatment for ADHF and VAS scores were not consistently associated with clinical outcomes in ADHF. These findings inform the utility of the DVAS and GVAS instruments as measurements of symptom change for future ADHF clinical trials and registries.

Obesity is a well-established risk factor for hypertension and cardiovascular disease [(1)][1]. Given the rising obesity prevalence, it is unclear whether previously established hypertension treatment targets are generalizable to a more contemporary obese population [(2)][2]. Whether or not obesity

Targeting systolic blood pressure (SBP)

A previously healthy 44-year-old woman presented with 3 days of worsening petechial rash, epistaxis and fatigue. Admission labs revealed pancytopenia, low reticulocyte index and elevated liver enzymes. Bone marrow biopsy demonstrated a profoundly hypocellular bone marrow without dysplasia and additional testing demonstrated an acute hepatitis B infection. In the context of an acute hepatitis B infection, elevated liver enzymes and aplastic anaemia, our patient was diagnosed with severe hepatitis-associated aplastic anaemia due to an acute hepatitis B infection. She was initiated on antiviral therapy with tenofovir and briefly received immunosuppressive therapy with a robust sustained improvement in her blood counts. Acute hepatitis B-associated aplastic anaemia is an exceptionally rare presentation of aplastic anaemia. We present acute hepatitis B-associated aplastic anaemia that resolved with antiviral therapy, which to our knowledge is the second such case reported in the literature and the first using tenofovir.

A 61-year-old female with a history of advanced HIV disease and chronic hepatitis B was presented with an 8-week history of painful oral ulcers. She appeared systemically well but examination revealed multiple well-demarcated clean-based ulcers on the tongue and hard palate. Biopsy of one of the lesions showed numerous histiocytes containing intracellular yeast forms consistent with Histoplasma capsulatum var. capsulatum. Fungal blood cultures subsequently grew H. capsulatum var. capsulatum, confirming a diagnosis of disseminated histoplasmosis. She was treated with intravenous amphotericin B for 2 weeks followed by a prolonged course of oral itraconazole, with which her ulcers resolved completely and have not recurred. This case exemplifies how oral ulcers may be a manifestation of an underlying systemic disease and demonstrates the utility of biopsy in establishing a diagnosis.

A 57-year-old male Mexican immigrant living in Dallas presented with altered mental status, progressive confusion, mild headache and fevers. He was diagnosed with embryonal liver sarcoma one year prior to admission and had recently started dexamethasone therapy for metastatic spinal lesions. Blood and cerebrospinal fluid cultures from a lumbar puncture were both positive for Escherichia coli. He was diagnosed with spontaneous gram negative rod (GNR) meningitis. Given his travel history, immunosuppression and GNR meningitis, a stool ova and parasite sample was obtained to screen for Strongyloides stercoralis. His stool was markedly positive for Strongyloides stercoralis larvae and he was further diagnosed with Strongyloides hyperinfection syndrome. Strongyloides is capable of chronically re-infecting human hosts without an external life cycle via autoinfection. In chronic infections, hyperinfection can be triggered with immunosuppressive medications, especially steroids. Disseminated Strongyloides should be considered as the source for unexplained GNR bacteremia or meningitis especially in immunosuppressed patients. Our patient likely had a chronic asymptomatic Strongyloides infection acquired in Mexico that became a hyperinfection resulting in GNR meningitis after starting high doses of dexamethasone.

A 28-year-old visiting from Central America presented with twenty-four hours of lower extremity swelling, dyspnea and orthopnea. Clinically, she was diagnosed with acute heart failure requiring inotropes with a transthoracic echocardiogram revealing severe mitral regurgitation with a normal ejection fraction. Subsequent transesophageal echocardiogram confirmed severe mitral regurgitation with aortic root dilatation (Z-score: 3.9). She was also found to have arachnodactyly, scoliosis on X-ray and severe mitral valve prolapse. Given her clinical features she was assessed for Marfan syndrome with the modified Ghent nosology systemic score and met diagnostic criteria. A FBN1 genetic test confirmed the diagnosis of Marfan syndrome discovering a frameshift mutation resulting in an inappropriate stop codon and peptide truncation. For patients presenting with heart failure at an atypical age without typical risk factors, rare conditions such as Marfan syndrome should be considered. Marfan syndrome can accurately and quickly be screened for and diagnosed using the systemic score from the modified Ghent nosology.