ABSTRACT
BACKGROUND: Obesity is one of the most prevalent medical conditions in the Western world. There are many risk factors associated with obesity, including cardiovascular and pulmonary risk. Vascular health is not studied in obese patients, and whether obesity has an adverse effect on vascular health in these patients remains unknown. OBJECTIVE: The first objective is to find a correlation between vascular health and obesity and whether obesity can be classified as a risk factor for vascular health. The second objective is to see if weight loss leads to an improvement in vascular health in patients. METHODS: The study was conducted with pre- and post-surgical methods at Baylor Scott & White (BSWH) Medical Center, Temple, Texas, USA. Ten patients were approached, consented, and prepared to obtain baseline values through WatchPAT and EndoPAT devices prior to their bariatric surgery. Values obtained include their initial weight, respiratory disturbance index, apnea-hypopnea index, oxygen desaturation index, and degree of endothelial dysfunction via the EndoPAT device. Post-surgery, these values were obtained again and compared using Wilcoxon non-parametric analyses with a level of significance at p < 0.05. RESULTS: Our study results demonstrate a correlation between obesity and vascular health as endothelial dysfunction is widely seen. In our patients, after bariatric surgery, we saw a significant weight change (31.2% +11.2, p < 0.0001). There was a significant degree of endothelial function improvement after the weight loss (31.2% +34.7, p < 0.04). CONCLUSION: Our results indicate that there is a correlation between obesity and vascular health, which also correlates with cardiovascular risk. There is a significant reduction in endothelial dysfunction after weight loss. We believe that obesity is a risk factor for vascular health outcomes.
ABSTRACT
Sporadic inclusion body myositis (sIBM) is an autoimmune condition that is characterized by progressive weakness and muscular atrophy in the extremities. The pathophysiology is not exactly clear; however, some studies have postulated an involvement of cytotoxic T cells (CD8+), causing an autoimmune response. While the implications of COVID-19 infection are an evolving topic, myositis has been previously implicated in other viral etiologies. We discuss a case of sIBM secondary to COVID-19 in a patient with chronic myalgias bringing to light a rare implication of COVID-19 to educate the medical community.
Subject(s)
Moyamoya Disease , Female , Humans , Middle Aged , Moyamoya Disease/diagnosis , Moyamoya Disease/diagnostic imagingABSTRACT
Pembrolizumab is an immunotherapeutic agent used in various malignancies including metastatic melanoma. While immunotherapies are effective in treating several malignancies, they do come at the expense of inadvertent side effects. The numerous side effects of pembrolizumab, including, but not limited to, adrenal insufficiency, myocarditis, and pancreatitis, are well documented in clinical literature. In this case report, we describe a unique presentation of myocarditis and acute inflammatory demyelinating polyradiculoneuropathy secondary to pembrolizumab. While both side effects of pembrolizumab are well known, the delayed presentation of symptoms is of particular interest in our case report. We hope to inform the clinical community on the pharmacokinetics of pembrolizumab causing the delayed onset of symptoms.
ABSTRACT
Although Guyton's graphical analysis of cardiac output-venous return has become a ubiquitous tool for explaining how circulatory equilibrium emerges from heart-vascular interactions, this classical model relies on a formula for venous return that contains unphysiological assumptions. Furthermore, Guyton's graphical analysis does not predict pulmonary venous pressure, which is a critical variable for evaluating heart failure patients' risk of pulmonary edema. Therefore, the purpose of the present work was to use a minimal closed-loop mathematical model to develop an alternative to Guyton's analysis. Limitations inherent in Guyton's model were addressed by 1) partitioning the cardiovascular system differently to isolate left ventricular function and lump all blood volumes together, 2) linearizing end-diastolic pressure-volume relationships to obtain algebraic solutions, and 3) treating arterial pressures as constants. This approach yielded three advances. First, variables related to morbidities associated with left ventricular failure were predicted. Second, an algebraic formula predicting left ventricular function was derived in terms of ventricular properties. Third, an algebraic formula predicting flow through the portion of the system isolated from the left ventricle was derived in terms of mechanical properties without neglecting redistribution of blood between systemic and pulmonary circulations. Although complexities were neglected, approximations necessary to obtain algebraic formulas resulted in minimal error, and predicted variables were consistent with reported values.
