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Introduction: Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) exhibits 25-30% mortality in hospitalized patients with heart failure (HF). Cardiovascular disease is the most significant comorbidity associated with increased mortality in COVID-19 patients with data suggesting local and systemic inflammation play a critical role in cardiac functional abnormalities. SARS-CoV-2 vaccination reportedly reduces severity of infection. We sought to characterize if vaccination had any protective effect on patients with HF hospitalized for acute COVID-19. Hypothesis: Baseline cardiac biomarkers including CRP, ferritin, high sensitivity cardiac troponin I (hs-cTnI), and pro-brain natriuretic peptide (pBNP) may be lower in vaccinated COVID-19 HF patients revealing the impact of vaccination on reducing inflammation by SARS-CoV-2 infection. Method(s): Electronic health records underwent IRB exempted extraction of demographics, anthropometrics, vital signs, laboratory tests, and ICD-10-CM-based Elixhauser comorbidity categories. Continuous data summarized with median [IQR] were compared using Kruskal-Wallis test and discrete data with chi-squared test. Result(s): Among HF patients with a recorded vaccine status admitted between July 3, 2021 and March 17, 2022, 206 underwent acute COVID-19 hospitalization. Vaccinated (n=91, 44%) and unvaccinated (115, 56%) patients exhibited statistically similar distribution of males (56%), aged 78[69-86] years with comorbidities 5[4-7] distributed across Whites (88%), Blacks (8%), and other races (4%). There were no intergroup differences with most prevalent comorbidities at admission including hypertension (99%), diabetes (41%), chronic pulmonary disease (37%), obesity (36%), deficiency anemia (31%), and renal failure (25%). There were no intergroup differences in initiation of COVID-19 directed treatments. Baseline biomarkers in vaccinated versus unvaccinated were CRP 6.0[1.3-9.5] vs. 6.9[2.7-11.3] mg/dL (p=.25), ferritin 171[76-552] vs. 432[79-876] ng/mL (p=.13), LDH 245[192-317] vs. 338[260-439] U/L (p=.003), D-dimer 0.89[0.53-1.73] vs. 1.36[0.95-2.80] mg/L FEU (p=.06), hs-cTnI 27[14-67] vs. 28[16-81] ng/L (p=.39), and pro-BNP 3487[1516-7162] vs. 3278[1549 vs. 9001] pg/mL (p=.90). Clinical visit criteria respectively were hospital LOS 4.9[2.9-10.3] vs. 5.4[3.4-10.3] days (p=.27), ICU admission 10% vs. 17% (p=.15), and discharge disposition expired or Hospice 15% vs. 16% (p=.48). Rehospitalization occurred similarly between groups and was not significant. Conclusion(s): Acute and chronic inflammation are pathogenic drivers of HF. Inflammatory biomarkers lower among vaccinated patients with HF included CRP, ferritin, D-dimer, and hs-cTnI, although not significant. LDH, however, was significantly lower suggesting improved host widespread tissue perfusion as one mechanism of reduced severity in patients with HF undergoing SARS-CoV-2 vaccine breakthrough infection. One study caveat is that despite inclusion of all patients, these preliminary findings are likely not sufficiently powered to validate our hypothesis.Copyright © 2022
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Microvascular alterations were first described in critically ill patients about 20 years ago. These alterations are characterized by a decrease in vascular density and presence of non-perfused capillaries close to well-perfused vessels. In addition, heterogeneity in microvascular perfusion is a key finding in sepsis. In this narrative review, we report our actual understanding of microvascular alterations, their role in the development of organ dysfunction, and the implications for outcome. Herein, we discuss the state of the potential therapeutic interventions and the potential impact of novel therapies. We also discuss how recent technologic development may affect the evaluation of microvascular perfusion.
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Background: The aim of this study was to measure serum brain injury biomarkers in patients with COVID-19 admitted to intensive care unit (ICU), without evidence of brain impairment, and to determine potential correlations with systemic inflammatory markers, illness severity, and outcome. Methods: In patients admitted to the ICU with COVID-19, without clinical evidence of brain injury, blood S100 calcium-binding protein B (S100B), neuron-specific enolase (NSE) and interleukin-6 (IL-6) were measured on admission. Clinical, routine laboratory data and illness severity were recorded. Comparisons between 28-day survivors and non-survivors and correlations of neurological biomarkers to other laboratory data and illness severity, were analyzed. Results: We included 50 patients, median age 64 [IQR 58-78] years, 39 (78%) males, 39 (78%) mechanically ventilated and 11 (22%) under high flow nasal oxygen treatment. S100B and NSE were increased in 19 (38%) and 45 (90%) patients, respectively. S100B was significantly elevated in non-survivors compared to survivors: 0.15 [0.10-0.29] versus 0.11 [0.07-0.17] µg/L, respectively, (p = 0.03), and significantly correlated with age, IL-6, arterial lactate, noradrenaline dose, illness severity and lymphocyte count. IL-6 was significantly correlated with C-reactive protein, noradrenaline dose and organ failure severity. NSE was correlated only with lactate dehydrogenase. Conclusion: Brain injury biomarkers were frequently elevated in COVID-19 ICU patients, in the absence of clinical evidence of brain injury. S100B was significantly correlated with IL-6, low lymphocyte count, hypoperfusion indices, illness severity, and short-term outcome. These findings indicate a possible brain astrocytes and neurons involvement, also suggesting a broader role of S100B in systemic inflammatory response.
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SESSION TITLE: Challenges in Asthma SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Asthma is a chronic illness affecting 334 million people worldwide[1]. Asthma affects the respiratory gas exchange, which plays a significant role in acid-base balance. Acid-base disorders in asthma involve respiratory alkalosis, respiratory acidosis, and AG acidosis[2]. CASE PRESENTATION: A 37 years old Hispanic male with a PMH of intermittent asthma presents with progressive dyspnea for three days, worse with activity and decreases with rest. He reported no [cough, fever, rhinorrhea, chest pain]. No orthopnea. He is vaccinated for COVID ( 2 Pfizer doses), has no sickness exposure, and works as a driver. The patient is not a smoker. Physical Exam: Blood pressure 124/72 mmHg. Heart Rate 100 PPM. Temperature 97.1 F.Respiratory Rate 21BPM.SPO2 90% General appearance: acute distress with nasal flaring. Heart: Normal S1, S2. RRR. Lung: Poor air entry with diffuse wheeze bilaterally. He was placed on a 6 LPM NC. CBC and differential were unremarkable. He was started on methylprednisone, Ceftriaxone, and azithromycin. The patient was started on inhaled Salbutamol and Budesonide. Chest X-ray was unremarkable, Chemistry was unremarkable except for elevated Lactic acid 4.7, There was no concern for reduced tissue perfusion or hypoxia, with no evidence of an infectious process because both viral and bacterial causes for pneumonia were excluded, and antibiotics were stopped. A serial lactic acid level trend was 4.5/4.3/ 4.1/ 4 on the first day, while on the next day, it was 3.1/ 2.9/ 2.7/ 2.5/ 3.5, we stopped trending his lactic acid level. He improved and was discharged on an oral taper steroid and inhaled steroids with a B2 agonist. DISCUSSION: There are two types of Lactic acidosis in patients with asthma: 1- Type-A results from impaired oxygen delivery to tissues and reduced tissue perfusion in severe acute asthma may be accompanied by reduced cardiac output. 2- Type B where oxygen delivery is normal, but the cellular function is impaired due to increased norepinephrine in plasma, increasing metabolic rate and lactate production, drugs like beta-agonists increase glycogenolysis leading to an increased pyruvate concentration;pyruvate is converted to lactic acid. B2 agonist increases lipolysis and increases Acetyl CoA, this increase in Acetyl CoA inhibits the conversion of pyruvate to Acetyl CoA, increasing pyruvate which will be converted to lactic acid[2], Theophylline is a non-selective 5'-phosphodiesterase inhibitor and potentiates the activity of ß-adrenergic agents by increasing the intracellular concentration of cAMP, Glucocorticoids are also known to increase the ß-receptor's sensitivity to ß-adrenergic agonists. CONCLUSIONS: Providers are increasingly challenged by hyperlactatemia,it is not harmful but elevated Lactic acid levels and clearance rate is used for prognostication,hyperlactatemia might be misleading,and all possible causes of elevated lactic acid levels must be explored. Reference #1: 10.5334/aogh.2412 Reference #2: https://doi.org/10.3390/jcm8040563 Reference #3: Edwin B. Liem, Stephen C. Mnookin, Michael E. Mahla;Albuterol-induced Lactic Acidosis. Anesthesiology 2003;99:505–506 doi: https://doi.org/10.1097/00000542-200308000-00036 DISCLOSURES: No relevant relationships by Vasudev Malik Daliparty No relevant relationships by Abdallah Khashan No relevant relationships by Samer Talib No relevant relationships by MATTHEW YOTSUYA
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BACKGROUND: Some clinical and histological studies have reported that SARS-CoV-2 infection may damage the endothelium. However, the impact of this virus on endothelial function in vivo remains poorly characterized. In this single-center pilot observational study, we performed iontophoresis of acetylcholine coupled with Laser doppler to investigate microvascular endothelial reactivity in COVID-19 patients compared to patients with non-COVID-19 bacterial pneumonia (NCBP) patients. RESULTS: During three consecutive months, 32 COVID-19 patients and 11 control NCBP patients with acute respiratory failure were included. The median age was 59 [50-68] and 69 [57-75] years in COVID-19 and NCBP groups, respectively (P = 0.11). There was no significant difference in comorbidities or medications between the two groups, except for body mass index, which was higher in COVID-19 patients. NCBP patients had a higher SAPS II score compared to COVID-19 patients (P < 0.0001), but SOFA score was not different between groups (P = 0.51). Global hemodynamic and peripheral tissue perfusion parameters were not different between groups. COVID-19 patients had significantly lower skin microvascular basal blood flow than NCBP patients (P = 0.02). In addition, endothelium-dependent microvascular reactivity was threefold lower in COVID-19 patients than NCBP patients (P = 0.008). CONCLUSIONS: Both baseline skin microvascular blood flow and skin endothelial-dependent microvascular reactivity were impaired in critically ill COVID-19 patients compared to NCBP patients, despite a lower disease severity score supporting a specific pathogenic role of SARS-CoV-2 on the endothelium.