Predictors of left atrial appendage thrombus in atrial fibrillation patients undergoing cardioversion.

BACKGROUND: Atrial fibrillation and atrial flutter represent the most prevalent clinically significant cardiac arrhythmias. While the CHA2DS2-VASc score is commonly used to inform anticoagulation therapy decisions for patients with these conditions, its predictive power is limited. Therefore, we sought to improve risk prediction for left atrial appendage thrombus (LAAT), a known risk factor for stroke in these patients. METHODS: We developed and validated an explainable machine learning model using the eXtreme Gradient Boosting algorithm with 5 × 5 nested cross-validation. The primary outcome was to predict the probability of LAAT in patients with atrial fibrillation and atrial flutter who underwent transesophageal echocardiogram prior to cardioversion. Our algorithm used 37 demographic, comorbid, and transthoracic echocardiographic variables. RESULTS: A total of 795 patients were included in our analysis. LAAT was present in 11.3% of the patients. The average age of patients was 63.3 years and 34.7% were women. Patients with LAAT had significantly lower left ventricular ejection fraction (29.9% vs 43.5%; p < 0.001), lower E' lateral velocity (5.7 cm vs. 7.9 cm; p < 0.001) and higher E/A ratio (2.6 vs 1.8; p = 0.002). Our machine learning model achieved a high AUC of 0.79, with a high specificity of 0.82, and modest sensitivity of 0.57. Left ventricular ejection fraction was the most important variable in predicting LAAT. Patients were split into 10 buckets based on the percentile of their predicted probability of having thrombus. The lower the percentile (e.g., 10%), the lower the probability of having thrombus. Using a cutoff point of 0.16 which includes 10.0% of the patients, we can rule out thrombus with 100% confidence. CONCLUSION: Using machine learning, we refined the predictive power of predicting LAAT and explained the model. These results show promise in providing better guidance for anticoagulation therapy and cardioversion in AF and AFL patients.

A Rare Presentation of Lyme Disease in an Immunocompromised Patient.

Lyme disease is a progressive infectious disease caused by the Borrelia species that affects multiple organ systems, including the brain, heart, skin, and musculoskeletal systems. The cardiac manifestations of Lyme disease typically present with atrioventricular nodal conduction abnormalities and, more rarely, myocarditis. We report a case of an immunocompromised 57-year-old woman who presented with acute onset shortness of breath, hypervolemia, injective conjunctiva, and global vision loss of the left eye in the setting of a recent tick bite. Serologic testing confirmed borreliosis, and cardiac testing demonstrated acute isolated systolic heart failure without any cardiac conduction system abnormalities on the electrocardiogram. The diagnosis of Lyme carditis was made, and the patient was started on doxycycline with complete recovery of cardiac systolic function. This case demonstrates atypical cardiac manifestations of Lyme disease and highlights the difficulty in workup and understanding of Lyme carditis particularly in immunocompromised patients.

Fixed right ventricular collapse: A loculated pericardial effusion due to metastatic pulmonary adenocarcinoma.

Pericardial effusions can occur as either circumferential or loculated when referencing their anatomic distribution in the pericardium. These effusions can result from multiple different etiologies, including malignancy, infection, trauma, connective tissue disease, acute pericarditis drug induced, or idiopathic. Loculated pericardial effusions can be difficult to manage. Even small loculated effusions can result in hemodynamic compromise. Oftentimes in the acute setting, point of care ultrasound can be used to evaluate pericardial effusions directly at the bedside. We present a case of a malignant loculated pericardial effusion and offer insight into management and clinical evaluation using point of care ultrasound.

A Woman With Progressive Dyspnea and Seronegative Rheumatoid Arthritis.

CASE PRESENTATION: A 66-year-old woman with a medical history of seronegative rheumatoid arthritis on long-standing methotrexate and adalimumab therapy was referred to the pulmonary clinic for abnormal chest imaging. The patient was also under evaluation by rheumatology physicians for increased fatigue, nonproductive cough, and recurrent sinus infections. At the time of the initial pulmonary visit, the patient complained of acute onset of bilateral blurry vision and subsequently was diagnosed with anterior uveitis and received ophthalmic steroids with significant improvement. The patient's biologic therapy was discontinued because of a concern for possible drug toxicity. Over the course of 4 months, the patient experienced worsening dyspnea with exertion. She was a lifelong nonsmoker and had no history of recent travel. However, on review of possible environmental exposures, patient stated using feather pillows and bedding for several decades.

Assessment of Cardiovascular Risk for Noncardiac and Nonsurgical Activities.

Cardiovascular risk stratification is a frequent evaluation performed by health professionals. Not uncommonly, requests for risk stratification involve activities or procedures that fall outside of the scope of current evidence-based guidelines. Estimating risk and providing guidance for these requests can be challenging due to limited available evidence. This review focuses on some of these unique requests, each of which are real examples encountered in our practice. We offer guidance by synthesizing the available medical literature and formulating recommendations on topics such as the initiation of testosterone and erectile dysfunction therapy, SCUBA and skydiving, polygraphy, and electroconvulsive therapy.

A review of cardio-pulmonary microvascular dysfunction in pulmonary hypertension.

Microvascular dysfunction progressing to pulmonary hypertension can be a primary cause of right ventricular failure or a secondary cause because of an underlying systemic illness. Little is known regarding the etiology and epidemiology of coronary microvascular dysfunction in pulmonary hypertension. Despite this limitation, its presence has been described in patients with pulmonary hypertension. This review focuses on the pathogenesis of cardiac and pulmonary microvascular dysfunction in pulmonary hypertension. Additionally, this review provides a contemporary assessment on the diagnosis and treatment of microvascular dysfunction in patients in pulmonary hypertension. This topic is important to raise awareness of microvascular dysfunction in the coronary and pulmonary circulation, so that future studies will investigate its impact on the pulmonary hypertension patient cohort.

Epithelial-Derived Reactive Oxygen Species Enable AppBCX-Mediated Aerobic Respiration of Escherichia coli during Intestinal Inflammation.

The intestinal epithelium separates host tissue and gut-associated microbial communities. During inflammation, the host releases reactive oxygen and nitrogen species as an antimicrobial response. The impact of these radicals on gut microbes is incompletely understood. We discovered that the cryptic appBCX genes, predicted to encode a cytochrome bd-II oxidase, conferred a fitness advantage for E. coli in chemical and genetic models of non-infectious colitis. This fitness advantage was absent in mice that lacked epithelial NADPH oxidase 1 (NOX1) activity. In laboratory growth experiments, supplementation with exogenous hydrogen peroxide enhanced E. coli growth through AppBCX-mediated respiration in a catalase-dependent manner. We conclude that epithelial-derived reactive oxygen species are degraded in the gut lumen, which gives rise to molecular oxygen that supports the aerobic respiration of E. coli. This work illustrates how epithelial host responses intersect with gut microbial metabolism in the context of gut inflammation.

Hiatal hernia repair and magnetic sphincter augmentation to treat laryngopharyngeal reflux aiding the prevention of recurrent laryngeal cancer.

Laryngopharyngeal reflux (LPR) is a difficult disease to treat and can result in mucosal injury in the pharynx and larynx. This typically results in symptoms such as cough, hoarseness, and globus sensation, but the manifestation of cancer is a possibility. We present a patient with a squamous cell cancer of the larynx who was diagnosed with gastroesophageal reflux disease (GERD) and found to have LPR. The cancer was treated locally and GERD was eradicated with magnetic sphincter augmentation. After 15 months of follow-up, there was no residual cancer. This case highlights the role that untreated LPR may play in patients' risk of developing laryngeal cancer.

Intrapartum leprosy.

Leprosy is caused by an infection with Mycobacterium leprae, an acid-fast, slow-growing, obligate intracellular rod-shaped bacillus. Intrapartum leprosy most commonly occurs in the third trimester of pregnancy. This is likely due to pregnancy decreasing cellular immunity, thus allowing the organism to proliferate unchecked. This case report reviews the current understanding of intrapartum leprosy and details the hospital course of a patient who presented with active intrapartum leprosy at 32 weeks gestation.

Microbial Respiration and Formate Oxidation as Metabolic Signatures of Inflammation-Associated Dysbiosis.

Intestinal inflammation is frequently associated with an alteration of the gut microbiota, termed dysbiosis, which is characterized by a reduced abundance of obligate anaerobic bacteria and an expansion of facultative Proteobacteria such as commensal E. coli. The mechanisms enabling the outgrowth of Proteobacteria during inflammation are incompletely understood. Metagenomic sequencing revealed bacterial formate oxidation and aerobic respiration to be overrepresented metabolic pathways in a chemically induced murine model of colitis. Dysbiosis was accompanied by increased formate levels in the gut lumen. Formate was of microbial origin since no formate was detected in germ-free mice. Complementary studies using commensal E. coli strains as model organisms indicated that formate dehydrogenase and terminal oxidase genes provided a fitness advantage in murine models of colitis. In vivo, formate served as electron donor in conjunction with oxygen as the terminal electron acceptor. This work identifies bacterial formate oxidation and oxygen respiration as metabolic signatures for inflammation-associated dysbiosis.