17 research outputs found

    MFL-Net: An Efficient Lightweight Multi-Scale Feature Learning CNN for COVID-19 Diagnosis From CT Images.

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    Timely and accurate diagnosis of coronavirus disease 2019 (COVID-19) is crucial in curbing its spread. Slow testing results of reverse transcription-polymerase chain reaction (RT-PCR) and a shortage of test kits have led to consider chest computed tomography (CT) as an alternative screening and diagnostic tool. Many deep learning methods, especially convolutional neural networks (CNNs), have been developed to detect COVID-19 cases from chest CT scans. Most of these models demand a vast number of parameters which often suffer from overfitting in the presence of limited training data. Moreover, the linearly stacked single-branched architecture based models hamper the extraction of multi-scale features, reducing the detection performance. In this paper, to handle these issues, we propose an extremely lightweight CNN with multi-scale feature learning blocks called as MFL-Net. The MFL-Net comprises a sequence of MFL blocks that combines multiple convolutional layers with 3 ×3 filters and residual connections effectively, thereby extracting multi-scale features at different levels and preserving them throughout the block. The model has only 0.78M parameters and requires low computational cost and memory space compared to many ImageNet pretrained CNN architectures. Comprehensive experiments are carried out using two publicly available COVID-19 CT imaging datasets. The results demonstrate that the proposed model achieves higher performance than pretrained CNN models and state-of-the-art methods on both datasets with limited training data despite having an extremely lightweight architecture. The proposed method proves to be an effective aid for the healthcare system in the accurate and timely diagnosis of COVID-19

    Outcomes With Ultrafiltration Among Hospitalized Patients With Acute Heart Failure (from the National Inpatient Sample)

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    Acute heart failure (HF) management is a complex and often involves a delicate balance of both cardiac and renal systems. Although pharmacologic diuresis is a mainstay of the pharmacologic management of decompensated HF, ultrafiltration (UF) represents a nonpharmacologic approach in the setting of diuretic resistance. We conducted a cross-sectional analysis of the 2009 through 2014 hospitalization data from the National Inpatient Sample. The study population consisted of hospitalizations with a discharge Diagnosis Related Groups of HF who were older than 18 years of age, did not have end-stage kidney disease, acute kidney injury and had not undergone hemodialysis or hemofiltration. There were 6,174 hospitalizations which included UF among the 7,799,915 hospitalizations for HF. Hospitalizations which included UF were among patients significantly younger in age (68.1 ± 1.0 vs 73.8 ± 0.1 years), male (61.9% vs 47.7%), and with higher prevalence of co-morbid conditions including chronic kidney disease (58% vs 31%), diabetes mellitus (53% vs 42%), and higher rates of co-morbidity (Charlson comorbidity score ≥2, 92% vs 80%). All-cause mortality was significantly higher among hospitalizations which included an UF (4.68% vs 2.24%). Hospitalizations with UF had a longer mean length of stay (6.2 vs 4.3 days, p \u3c0.01) average total charges ($42,035 vs 24,867 USD, p \u3c0.01) as compared with those without UF. Hospitalizations with UF were associated with a greater adjusted odds of all-cause mortality (odds ratio: 3.36, [95% confidence interval 1.76,6.40]), greater than DRG-level target length of stay (odds ratio, 2.46; [95 confidence interval 1.65,3.67]), and a 72% increase in the average hospital charges. In conclusion, hospitalizations which included UF identified a subgroup of HF patients with more co-morbid conditions who are at higher risk of mortality and increased resource burden in terms of length of stay and costs. These findings also highlight that the need for UF may identify patients who are most likely to benefit from a multidisciplinary cardiorenal approach to alter the trajectory of their disease

    Utilization of Emicizumab in Acquired Factor VIII Deficiency.

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    BACKGROUND Acquired hemophilia A (AHA) is a rare autoimmune disease caused by immunoglobulins that bind and inactive factor VIII, thereby predisposing to life-threatening bleeding. Bleeding is typically stabilized by utilizing bypassing agents, such as recombinant factor VIIa (rVIIa). Select case reports have demonstrated the success of alternative prophylaxis for clearance of factor VIII inhibitors through the use of emicizumab, a current FDA approved medication for treatment of congenital hemophilia A. In this case report we present the efficacy of utilizing emicizumab as a prophylactic agent in a patient that was unable to tolerate first-line therapy for prophylaxis. CASE REPORT A 91-year-old male presented for ongoing hematuria for 5 weeks with prior workup unrevealing. He was given a day\u27s course of recombinant factor VIIa to stabilize his bleeding and was started on cyclophosphamide and prednisone after a revealing hematological workup including activated partial thromboplastin time (aPTT) \u3e100 seconds and factor VIII inhibitor level of 44 BU/mL. He continued to require VIIa infusions to control his bleeding and was started on emicizumab once stabilized. His bleeding remained controlled and his inhibitor decreased after 6 months of therapy with repeat factor VIII inhibitor level of 1.9 BU/mL. CONCLUSIONS The success of utilizing emicizumab for bleeding prophylaxis in AHA is demonstrated by this patient\u27s resolution of bleeding. The high frequency of dosing and higher risk for thrombosis with factor VIIa, in conjunction with our patient\u27s medical history and ease of administration, make emicizumab an ideal agent for bleeding prophylaxis while awaiting clearance of factor VIII inhibitors

    Concomitant Presentation With Cardioembolic Ischemic Stroke and Non ST Elevation Myocardial Infarction in a Patient With New Onset Atrial Fibrillation

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    Introduction: Although Atrial Fibrillation (AF) is a common cause of ischemic stroke, it rarely causes acute coronary syndromes (ACS). Cardioembolic events from AF cause considerable morbidity and mortality. Concomitant ischemic stroke and ACS remains an exceedingly rare event. We describe the case of a patient presenting with cardioembolic ischemic stroke and acute coronary syndrome. Case Presentation: An 83 year old male with a prior history of heart failure with preserved ejection fraction, permanent pacemaker for complete heart block, and chronic kidney disease on hemodialysis presented with acute left sided facial and extremity weakness, gait ataxia and profound dysarthria. Physical examination and stroke work up demonstrated right M1 territory ischemic stroke (A). EKG demonstrated AF with ventricular pacing (B). The patient subsequently underwent emergent right middle cerebral artery thrombectomy. Device interrogation confirmed new onset AF for ten days. Hemodynamic instability and up trending troponin post-procedurally prompted an echocardiogram which demonstrated new LAD wall motion abnormality with an ejection fraction of 15%. The patient underwent cardiac catheterization with coronary thrombectomy for a 100% mid-LAD occlusion with good angiographic result (C, D). He was initiated on intravenous anticoagulation in the setting of AF. Unfortunately, given his significant comorbidities and need for multiple pressors, the patient succumbed to his profound cardiogenic shock. Discussion: This case highlights that clinicians should maintain a high degree of suspicion for coronary embolic phenomena in patients presenting with clinical or biochemical signs of acute MI in the setting of AF and its sequela. Though the most common cause of MI is atherosclerotic plaque rupture, coronary embolism is the underlying etiology in 3% of cases. Expeditious identification of at risk patients is critical to appropriate and timely intervention

    Vascular Inflammation, Cancer, and Cardiovascular Diseases.

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    PURPOSE OF REVIEW: Cancer and cardiovascular disease are among the leading causes of morbidity and mortality in the USA. Cancer and cardiovascular disease have inflammatory underpinnings that have been associated with both the development and progression of these disease states. RECENT FINDINGS: Inflammatory signaling has been found to be a critical event in both cardiovascular disease and cancer formation and progression. Further, many chemotherapeutic agents potentiate inflammation exacerbating existing cardiovascular disease or leading to its presence. The exact mechanisms of these interactions remain poorly understood. The proinflammatory milieu observed in both cancer and cardiovascular disease likely plays an important role in the development and potentiation of both conditions. Further evaluation of this relationship will be critical in the development of new diagnostic and therapeutic modalities

    Microtubule Inhibitors and Cardiotoxicity.

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    PURPOSE OF REVIEW: Cancer and heart disease are the leading causes of mortality in the USA. Advances in cancer therapies, namely, the development and use of chemotherapeutic agents alone or in combination, are becoming increasingly prevalent. RECENT FINDINGS: Many chemotherapeutic agents have been associated with adverse cardiovascular manifestations. The mechanisms of these sequelae remain incompletely understood. In particular, microtubule inhibitor (MTI) agents have been related to the development of heart failure, myocardial ischemia, and conduction abnormalities. At present, there are no guidelines for patients undergoing MTI therapy as it pertains to both preventative and mitigatory strategies for cardiovascular complications. We conducted a literature review focusing on content related to the use of MTIs and their effect on the cardiovascular system. MTIs have been associated with various forms of cardiotoxicity, and fatal cardiotoxicities are rare. The most well-described cardiotoxicities are brady- and tachyarrhythmias. The co-administration of anthracycline-based agents with MTIs can increase the risk of cardiotoxicity
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