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BACKGROUND: With the widespread use of permanent pacemakers (PPM), and increased mortality associated with pacemaker endocarditis, it is essential to evaluate comorbidities that could potentially increase the risk of infective endocarditis (IE). Heart failure (HF), a common comorbidity, has not been well studied as an independent risk factor for development of IE in individuals with PPM. METHODS: The US National Inpatient Sample database was used to sample individuals with PPM. Patients with concomitant implantable cardioverter defibrillator, acute heart failure, history of endocarditis, intravenous drug use, prosthetic heart valves, or central venous catheter infection were excluded. Propensity matching was performed to match patients with and without HF. Pre- and post-match logistic regression was performed to assess HF as an independent risk factor for IE. A subgroup analysis was performed comparing IE rates between patients with HF with reduced (HFrEF) vs preserved (HFpEF) ejection fraction. RESULTS: Out of 333,571 patients with PPM included in the study, 121,862 (37â¯%) had HF. HF patients were older and had a higher prevalence of females. All comorbidities except for dental disease and cancer were more prevalent in the HF group. Patients with HF were 1.30 times more likely to develop IE [OR: 1.30 (1.16-1.47); pâ¯<â¯0.001]. The two cohorts were then matched for age, gender, and 20 comorbidities using a 1:1 propensity score matching algorithm. After matching, HF was still independently associated with increased risk of IE [OR: 1.62 (1.36-1.93); pâ¯<â¯0.001]. In our sub-group analysis, HFrEF and HFpEF patients had similar IE rates. CONCLUSION: In PPM population, HF was associated with an increased risk of IE compared to those without HF. We hypothesize that HF being a low-flow and high-inflammatory state might have contributed to this increased risk. Larger studies are required to corroborate our findings and evaluate the need for antimicrobial prophylaxis for this population.
Assuntos
Endocardite , Insuficiência Cardíaca , Marca-Passo Artificial , Humanos , Feminino , Masculino , Insuficiência Cardíaca/etiologia , Idoso , Marca-Passo Artificial/efeitos adversos , Fatores de Risco , Pessoa de Meia-Idade , Endocardite/etiologia , Endocardite/epidemiologia , Idoso de 80 Anos ou mais , Estados Unidos/epidemiologia , Comorbidade , Estudos Retrospectivos , Pontuação de Propensão , Bases de Dados FactuaisRESUMO
Background: Currently, minimal data are available to explore the composition of venous thromboembolism in patients with cancer. This case report discusses a presentation of venous thromboembolism in a patient with high-grade urothelial carcinoma and highlights the pathology findings in thrombi. Case Presentation. A 55-year-old female who was diagnosed with high-grade urothelial carcinoma with multiple metastases developed an extensive deep vein thrombosis in her left lower extremity. Endovascular revascularization was indicated due to left lower extremity pain and swelling not responsive to anticoagulation. A mechanical thrombectomy was performed, and samples were sent for pathology. Pathologic examination discovered minute fragments of metastatic carcinoma, admixed with laminated blood clots (thrombus). The morphology of metastatic carcinoma and the immunostain profile were compatible with metastatic carcinoma of bladder origin. Conclusion: Cancer is a well-known risk factor for developing VTEs, and it is estimated that approximately 4-20% of cancer patients will experience VTE at some stage, the rate being the highest in the initial period following diagnosis. Annually, 0.5% of cancer patients will experience thrombosis compared with a 0.1% incidence rate in the general population (Elyamany et al., 2014). Despite knowing the increased incidence of VTEs in cancer patients, there are few studies to date that analyze the composition of thrombi in patients with cancer.
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Granulomatosis with polyangiitis (GPA) is an autoimmune disease that affects small and medium-sized vessels. It is classically known to present with renal and respiratory tract symptoms. However, the disease can manifest in other organ systems, especially cardiovascular involvement. Though there are multiple reports of cardiac involvement in GPA, it is not commonly evaluated and is often overlooked in patients with GPA. Heart disease in GPA has a wide range of presentations ranging from subacute and silent to severe abnormalities, which can prove fatal if not identified and treated appropriately. Identifying cardiac involvement early in patients with no apparent signs can help with prevention strategies and follow-up to avoid significant complications. Pericarditis is the most common pathology noted in GPA, followed by cardiomyopathy, coronary artery disease, valvular disease, and conduction abnormality. In our report, we present a case of GPA in a young male with asymptomatic conduction abnormality of the heart. Although it was silent at the presentation, identifying the initial electrocardiogram (ECG) changes prompted us to admit him to the telemetry floor. Continuous telemetry monitoring helped us identify the progression of the conduction abnormality, which otherwise could have been missed. This led us to correlate to his symptoms which he later developed during his admission course. His symptoms subsided after prompt treatment. If not identified early, these cardiac abnormalities can delay management, leading to increased disease burden and morbidity. Hence, essential cardiac work with at least ECG and continuous telemetry monitoring is recommended.
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We reported a case of secondary hemophagocytic lymphohistiocytosis (HLH), a rare and life-threatening condition, which was suspected to have been triggered by a severe case of coronavirus disease 2019 (COVID-19). A 50-year-old man with a past medical history of ulcerative colitis with recent pancolitis status post colectomy and ileostomy two weeks before presentation presented to the emergency department with one week of subjective fevers, weakness, watery diarrhea, and decreased oral intake. A CT scan showed fluid in the rectum and post-surgical changes from his recent colectomy along with diffuse reticulonodular opacities of the lungs. His COVID-19 reverse transcriptase-polymerase chain reaction (RT-PCR) test was positive. Over the subsequent days, the patient's condition worsened as he developed worsening acute hypoxic respiratory failure with diffuse lymphadenopathy, splenomegaly, worsening cytopenias, and increased ferritin of >100,000 ng/ml on hospital day six. Hematology oncology was consulted and he was started on empiric steroid therapy followed by etoposide. However, his condition continued to worsen, and eventually, the patient passed away on hospital day eight.
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Background: Cardiovascular disease (CVD) is the leading cause of mortality in kidney transplant (KT) patients. The perceived risk of contrast-induced nephropathy (CIN) may create a reluctance to perform coronary angiography in patients presenting with non-ST segment elevation myocardial infarction (NSTEMI). Methods: National Inpatient Sample (NIS) Database was used to sample individuals presenting with NSTEMI. Patients were stratified into KT and Non-KT cohorts. Outcomes included left heart catheterization rates, mortality, arrhythmias, acute kidney injury/acute renal failure (AKI/ARF), and extended length of hospital stay (ELOS) (>72 h). Propensity matching (1:1 ratio) and regression analyses were performed. Results: Out of 336,354 patients with NSTEMI, 742 patients were in the KT group. KT patients were less likely to have LHC relative to non-KT patients (22.0 % vs 18.3 %); a difference that persisted on post-match analysis (27.1 % vs 19.4 %). On pre-match analysis, KT transplant patients that underwent LHC had lower mortality (10.3 % vs 0.7 %), AKI/ARF (44.6 % vs 27.9 %), arrhythmias (30.4 % vs 20.6 %) and lower ELOS (58.6 % vs 41.9 %). Post-match, KT cohort patient that underwent LHC had lower arrhythmias (OR:0.60[0.38-0.96]), AKI/ARF (OR = 0.51[0.34-0.77]), ELOS (OR:0.49[0.34-0.73]). Conclusion: KT patients underwent LHC much less frequently than their non-KT counterparts for NSTEMI. Coronary angiography and subsequent revascularization were associated with a significant decrease in morbidity and mortality. This theorized risk of CIN should not outweigh the benefit of LHC in KT patients.
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We present a unique case of biopsy-proven syphilitic hepatitis which presented as severe acute liver injury with significant elevation in aminotransferases and bilirubin, and improved with antibiotic therapy. However, the patient returned weeks after initial presentation with new-onset acute liver injury and had developed hypergammaglobulinemia, positive autoantibody titers, and repeat liver biopsy demonstrating interface hepatitis, supporting a diagnosis of autoimmune hepatitis. He had an otherwise unrevealing etiologic workup, and responded to glucocorticoid therapy. We believe that syphilitic hepatitis and its treatment subsequently triggered an immunogenic response, leading to autoimmune hepatitis. Autoimmune hepatitis is a chronic liver disease thought to manifest as a result of predisposing genetic factors in combination with environmental insults, especially hepatotropic pathogens. Syphilis is a sexually transmitted disease caused by Treponema pallidum that has been associated with autoimmunity and the development of autoantibodies. We propose that in the setting of syphilitic hepatitis, a molecular mimicry event resulting from structural similarities between T. pallidum and liver antigens, as well as impaired regulatory T-cell function, led to the breakdown of immune tolerance and the onset of autoimmune hepatitis. To support this hypothesis, further molecular analyses and case series are necessary to determine if syphilitic hepatitis and its treatment are risk factors for the onset of autoimmune hepatitis. Autoimmune hepatitis should be considered early as the cause of acute liver injury in susceptible patients with risk factors for the disease, as prompt recognition and appropriate treatment may prevent progression of liver injury and result in improved outcomes.
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Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome (ACS) with a high prevalence in young pregnant females. A 38-year-old female with a history of morbid obesity status post-bariatric surgery presented with chest pain. The electrocardiogram (EKG) revealed ST-segment elevation in the inferior leads as well as slightly elevated troponin. Urgent cardiac catheterization showed SCAD, and she was subsequently managed with medical therapy. We hypothesize that the history of obesity leads to a compromise in the coronary vasculature, thereby predisposing the patient to SCAD.