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    Early Life Sex Differences and Alterations in Mitochondrial Function in IUGR Offspring after Weaning may Contribute to Adult Sex Differences in Cerebrovascular Dysfunction and Hypertension in Rodents
    (2024-03-21) Hart, Savannah; Smith, Savanna; Smith, Jonna; Jones, Kylie; Castillo, Angie; Davis, Zandria; Springfield, Alex; Rollings, Alyssa; Narra, Sreeram; Cunningham, Mark
    Background: Preeclampsia is a hypertensive pregnancy disorder that usually occurs in the third trimester. Preeclampsia, due to placental ischemia, decreases nutrient and oxygen delivery to the fetus, causing intrauterine growth restriction (IUGR). IUGR increases the risk for chronic conditions such as cerebrovascular dysfunction (CVD) and hypertension (HTN). Human and animal studies show sex differences in CVD and HTN development in IUGR offspring, with males exhibiting a higher prevalence of both. Preliminary data from our lab showed that 17-week-old IUGR male rodents developed CVD, HTN and mitochondrial dysfunction (mtDYS), while IUGR female rodents only developed CVD. The reason for these sex differences is unknown but may be attributed to mtDYS. Although mitochondrial differences appear at 17 weeks, earlier mitochondrial function is unknown. This study investigates changes in mitochondrial function in IUGR offspring after weaning. We hypothesize that mtDYS is elevated in3-week-old IUGR rodent offspring, with greater dysfunction in IUGR males. Methods: Pregnant Sprague Dawley rats were divided into two groups: normal pregnant (NP) and preeclamptic pregnant rats, which underwent reduced uterine perfusion pressure (RUPP) surgery on gestational day 14. RUPP dams gave birth to IUGR offspring, and NP dams gave birth to control (CON) offspring. After 3 weeks of weaning, offspring were separated by sex and dam pregnancy status. Brains were collected from the following groups: IUGR males (n=6), IUGR females (n=6), CON males (n=4), and CON females (n=6) to measure mitochondrial function via respiration, electron transport chain (ETC) protein amounts, and mitochondrial dynamics of fission (DRP-1) and fusion (MFN-1) proteins. Mitochondrial respiration was assessed using the Oroboros Oxygraph O2K. Protein amounts of ETC complexes (I-V), DRP-1, and MFN-1 were quantified using Western blots. Results: 3-week-oldIUGR females had increased cerebral mitochondrial respiration suggested by State 3 (490.41 ± 49.85 vs 257.32 ± 69.76pmol O2/sec/mg; p=0.02) and increased protein amounts of ETC Complex I (135.91 ± 9.27 vs 107.77 ± 4.23IU/Protein/CON%; p=0.02) and Complex III (141.76 ± 13.99 vs 110.43 ± 7.73IU/Protein/CON%; p=0.07). MFN-1 protein amounts (133.42 ± 18.75 vs 84.67 ± 6.89IU/Protein/CON%; p=0.03) and DRP-1 protein amounts (111.31 ± 1.89 vs 95.24 ± 2.14IU/Protein/CON%; p<0.0003) were increased in IUGR compared to CON females. Conversely, 3-week-old IUGR males showed decreased cerebral mitochondrial respiration in Basal state (21.48±5.49 vs 55.79 ± 6.96pmol O2/sec/mg; p=0.03) and State 2 (146.22 ± 25.55 vs 224.70 ± 23.13pmol O2/sec/mg; p=0.13). DRP-1 protein amounts were decreased in IUGR males (85.72 ± 3.07 vs 110.18 ± 1.82IU/Protein/CON%; p=0.02), with no changes in mitochondrial ETC complexes or MFN-1 protein amounts compared to CON males. Conclusion: Early on, IUGR females show mitochondrial function, while IUGR males display mtDYS. Furthermore, the mtDYS in IUGR males at 3 weeks may contribute to HTN development observed in IUGR males and not IUGR females at 17 weeks of age. Future studies are warranted to investigate mtDYS and HTN development in IUGR males and possible protective mechanisms in IUGR females. This study highlights sex differences in cerebral mitochondrial function in prepubescent IUGR offspring, offering insight into the pathophysiology of HTN and CVD development in adulthood, along with suggestions for novel therapeutic targets to prevent HTN and CVD in adult IUGR offspring.
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    Upper Gastrointestinal Bleed with an Unusual Etiology: A Difficult Case with Unclear Imaging Findings.
    (2024-03-21) Wazir, Ali; Ngyuen, Michael; Takata, Theodore
    Background: Atrial fibrillation (AF) is a cardiac arrhythmia which can be managed with AF ablations, used to control aberrant electrical activity. A serious complication of ablations includes atrioesophageal fistulas (AEF), with clinical manifestations of hematemesis, fever, neurological deficits, and mental status changes. A majority of documented cases utilize computed tomography (CT) scans which demonstrate the presence of a fistula, but there remains a paucity of AEF cases with unclear imaging findings. Case Presentation: A 63-year-old Caucasian male with symptomatic persistent AF underwent radiofrequency ablation with PVs and left atrial posterior wall isolation on December 12, 2016. The patient tolerated the procedure well. On January 11, 2017, the patient returned to the emergency department with hematemesis one day prior. The patient reported chills, nausea, mild headache and a temperature of 103.2F. Patient reported taking ibuprofen with no relief. Vital signs at admission: T 98.5 F, BP 107/57, HR 62 bpm, and oxygen saturation of 100% on room air. PE: normal with no neurologic deficits. Labs: CBC indicated leukocytosis with neutrophilic shift and bandemia, thrombocytopenia, and low hemoglobin. CMP: low serum albumin and total protein. Coagulation studies: elevated aPTT and INR. Serum troponin I: minimally elevated. ECG: nonspecific T wave changes. CXR: no evidence of cardiopulmonary disease. Cranial CT scan: nonspecific bilateral subcortical frontal lobe white matter changes. Chest CTA with contrast was recommended by the EP to assess for an AEF and revealed no atrial wall defects. Gastroenterology was consulted for an upper GI bleed (UGIB) caused by NSAID usage based on imaging findings. Patient further experienced vision changes, confusion, chills, and myalgias. Blood Gram stain was positive for gram-positive cocci. Patient was started on a course of piperacillin-tazobactam and vancomycin. Magnetic Resonance Imaging illustrated bihemispheric ischemic infarctions. EGD revealed a protuberance with a small opening thirty centimeters from the incisors. Patient continued to deteriorate, and a repeat CT angiogram displayed a possible atrial wall defect but no overt fistula, pneumomediastinum, or contrast media within the esophagus. Based on high clinical suspicion of an AEF, a cardiothoracic surgery consult was requested. A cardiothoracic surgery was performed with repair of the left atrium and esophageal fistula. A 2-3 millimeter punctate defect was present between the left and right inferior pulmonary veins. Fibrinous adhesions were present on the anterior esophagus at the level of the left atrium. A punctate mucosal perforation was present in the esophageal wall measuring 2-3 millimeters in diameter. A pericardial patch was placed. The patient tolerated the procedure well and was transferred to the cardiovascular ICU. Post-operatively, the patient developed sepsis, delirium, and difficulty swallowing and was placed on tube feeding. Over the following days, mental status improved. Final culture results on postoperative day seven confirmed Streptococcus oralis, Streptococcus mitis, and Granulicatella adiacens and were treated with IV ceftriaxone outpatient. On postoperative day nine, the patient was discharged with no neurological deficits. Conclusion: This case highlights the importance of including AEFs within differential diagnoses of UGIB given recent AF ablations when imaging results are inconclusive.
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    Perioperative Complications in Swan Neck Deformity Repair Case Report
    (2024-03-21) Patterson, Tyler; Carpenter, Brayden; Boody, Taylor; Heidenrich, Taylor; Tamayo, Jesse; Hyatt, Brooke
    Background Excessive vagal stimulation in the intraoperative and perioperative periods can lead to bradycardia, asystole, and death. Painful stimulus or excessive pressure on the vagus nerve can lead to bradycardia. Increased stretch from a mechanical standpoint can also lead to more vagal nerve firing and input. Case Summary This case investigates the disease process of a 69-year-old female who presented to the surgical team following multiple failed conservative treatments for cervical chin on chest spinal deformity, requiring three months of hospitalization. Given the expected airway edema and swallowing dysfunction, surgical risks were high, and the patient was informed of potential complications. She consented for surgery and was educated on risks and benefits, including the possibility of requiring a tracheostomy and a Percutaneous Endoscopic Gastrostomy placement. The patient underwent a closed reduction of cervicothoracic spinal deformity, anterior cervical C4-5 osteotomy, C4-C7 corpectomies, C3-T1 anterior cervical fusion, posterior cervical C5-6 osteotomy, C2-T6 laminectomies, posterior cervical instrumented fusion C2-T8, and left L4 hemilaminectomy for placement of drains. On post op day 6, the patient requested PEG and tracheotomy placement. On post op day 10, the patient compounded a necrotizing soft tissue infection of the anterior neck that required emergent washout. The wound displayed profuse black fluid upon incision which along with imaging and crepitus on physical exam led to the diagnosis of acute necrotizing fasciitis. The patient also acquired persistent cervical esophageal perforation with a non-healed fistula and was taken to the OR two days later for tracheotomy revision and esophageal perforation repair. On post op day 20, the patient developed a neck hematoma requiring OR incision and drainage. On post op day 30, the patient was being turned by nursing to clean cervical wounds and became unresponsive. The patients became bradycardic, then developed asystole with no palpable pulses. After a few seconds, telemetry showed sinus rhythm and vitals became stable. Cardiology was consulted and attributed the patient’s episodes of asystole to pressure on the carotid sinus causing stimulation of the vagus nerve. The care team was instructed to minimize turning the patient to avoid further asystole. Local anesthesia was advised for future procedures. With an arrhythmia lasting longer than 90 seconds, pacemaker placement was indicated and performed. Discussion The interprofessional team effort allowed us to quickly identify the cause and treatment, which were vagal nerve compression and pacemaker placement, respectively. There are several explanations as to what contributed to the vagal stimulation. These include anatomical reconstruction, postoperative infection, neck hematoma, esophageal perforation, or mechanical ventilation stimulation. These may have caused vagal nerve stretching, causing increased vagal sensitivity. Above all, the increased vagal stimulation mostly occurred due to the drastic change in the patient’s anatomy, going from an extreme hyper flexed cervical position to hyperextension. This causes stretching and pulling on the structures in that region, which includes the vagus nerve. As anesthesia providers, it is crucial to recognize these possible complications and be able to adapt to care for these patients inside and outside of the operating room.
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    Right on Target? Analysis of LDL Levels and Medication Use in a Very High-Risk ASCVD Population
    (2024-03-21) Xavier, Christy; Aguiniga, Ashlyn
    Purpose: The American College of Cardiology (ACC) released an expert consensus pathway in 2022, introducing a new low-density lipoprotein (LDL) goal < 55 for very high-risk individuals with atherosclerotic vascular disease (ASCVD) and highlighting the need for additional non-statin therapies to achieve that goal and reduce the risk of recurrent cardiovascular (CV) events, hospitalization, and death. This study seeks to investigate whether this LDL target is being achieved and the antihyperlipidemic medications used in a very high-risk ASCVD primary care population at the UNTHSC Family Medicine Clinic. Methods: This is a retrospective chart review using the NextGen electronic record to evaluate patients at the UNTHSC Family Medicine Clinic. Living adults with very high-risk ASCVD were included. Very high-risk was defined as multiple major ASCVD events (myocardial infarction [I25.2, I22] or stroke [I63, Z86.73]) or one major ASCVD event and multiple high-risk conditions (heart failure [I50], diabetes [E10-E13], hypertension [I10-16], chronic kidney disease [N18], age > 65 years old, and current tobacco use). Demographics such as gender, race/ethnicity, insurance, and medications were also collected. Very high-risk ASCVD patients were then stratified based on LDL goal achievement and analyzed using Chi-square analysis, independent sample T-test, and descriptive statistics using SPSS. Results: Of the identified very high-risk ASCVD patients (n = 199), 60 (30.2%) had achieved an LDL goal < 55 mg/dL. The average LDL achieved in this group was 44.2 + 10.8 mg/dL vs. 98.6 + 44.0 mg/dL for non-achievers. All those who achieved an LDL goal < 55 mg/dL were on at least one antihyperlipidemic medication. Of those who achieved an LDL goal < 55 mg/dL, 49 (81.7%) were on a high-intensity statin, 8 (13.33%) were on ezetimibe, 6 (10%) were on fish oil, and 3 (5%) were on a PCSK9 inhibitor. No patients were prescribed bempedoic acid or inclisirin. For non-achievers, 81 (58.2%) were on a high-intensity statin, 10 (7.2%) were on ezetimibe, 14 (10.1%) were on fish oil, and only one (0.72%) patient was on a PCSK9 inhibitor. Twenty (14.4%) of the non-achievers were not on any antihyperlipidemic agents. This subset of patients had a much higher average LDL (108.1 + 33.3 mg/dL), and 20% had a history of multiple ASCVD events. LDL goal achievers were slightly older (average age 68.2 + 9.9 years vs. 65.5 + 10.5 years), male (60% vs. 33.6%), and commercially insured compared to non-achievers. Conclusions: A majority of very high-risk ASCVD patients at the UNTHSC Family Medicine Clinic are not currently achieving the LDL goal < 55 mg/dL. Additionally, non-statin therapies are not being widely used to augment statin therapy. Further investigation is needed to determine potential barriers and limitations to achieving this lower LDL target.
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    Cardiac troponin elevation in a middle-aged female consistent with COVID myocarditis
    (2024-03-21) Segovia, Alicia; Gulley, Taylor; Bautista, Trissha
    Background: Coronavirus (SARS-CoV-2) is known to cause severe acute respiratory syndrome, but more recently, it has been linked to increased cardiac involvement. It has recently been suggested by evidence that increased troponin levels seen in patients with severe COVID-19 reliably identifies myocardial damage. However, few longitudinal observations on troponin levels in mild COVID-19 cases over time have been published. Given its recent discovery, our understanding of the long-term effects of Coronavirus infections on individuals remains incomplete. The Center for Disease Control has recently estimated an overall incidence of myocarditis secondary to COVID-19 infection to be at around 150 cases per 100000 individuals in the United States alone. Case Presentation: A 45 year-old caucasian female with past medical history of T2DM, HTN, HLD, CKD, PCOS, and past COVID-19 infection presented to the Emergency Department with recurrent chest pain associated with shortness of breath, left hand numbness, and diaphoresis while at rest. A month prior, this female was admitted for NSTEMI with cardiac catheterization showing normal coronary arteries, echo demonstrating EF of 50-55% without wall motion abnormalities, and CTA demonstrating no signs of PE. Patient had been compliant with all medications since discharge, states nitroglycerin helped with pain, and had not been taking aspirin due to scheduled hysterectomy. Initial troponin levels were 3.409 ng/mL (0.00-0.013), glucose level 107, and platelet count was 426. A focused cardiac ultrasound performed by the emergency physician demonstrated absence of pericardial effusion, normal LV function, mild LV dilation, absent RV dilation, and absence of pericardial tamponade. EKG showed no signs of acute ischemia and repeated EKG was normal. However, cardiology was consulted due to evidence of myocardial injury as indicated by elevated troponins. The patient received ASA, Plavix, and Lovenox in the ED and heparin was started as part of ACS protocol. Tylenol 650 mg Q6H PRN and Morphine 2mg Q30M PRN were added for pain. Troponin levels continued to trend upward to 7.115 over the course of 7 days. Normal studies and images led to the conclusion that this patient would benefit from a heart MRI and outpatient medical management. Conclusions: This case highlights the long-term impact of Coronavirus infections on cardiac health, as indicated by notable elevations in troponin levels. It also demonstrates the atypical presentation of elevated troponin levels in the absence of acute ischemic myocardial injury.
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    Recurrence and progression of Wolff-Parkinson-White syndrome in pediatric patient
    (2024-03-21) Bhat, Samhitha
    Background Wolff-Parkinson-White (WPW) syndrome is a rare cardiac condition characterized by ventricular pre-excitation leading to symptoms of arrhythmia and tachycardia with a risk for sudden cardiac death (SCD). WPW is uncommon in the general population and even less frequent in the pediatric population. Diagnosis of WPW is made by electrocardiogram (ECG) with the hallmark presentation of a short PR interval, widened QRS complex, and a slurred upstroke of the QRS complex known as a delta wave. Of the patients eliciting the WPW pattern, few will progress to a symptomatic state, known as WPW syndrome, and it is unknown what causes the transition from asymptomatic to symptomatic WPW. The case demonstrates WPW syndrome in a pediatric patient and identifies a potential cause for symptom development and progression in that population. Case Information A 16-year-old male presented with complaints of sudden onset episodes of palpitations and tachycardia with lightheadedness. The episodes occurred several times a month, lasting for a few seconds to an hour at a time before abruptly resolving. The symptoms appeared with actions such as bending over or getting up from a bent-over position. The patient reported having similar episodes of palpitations and tachycardia four years ago, which were less frequent, less noticeable, and subsequently self-resolved. At that time, the episodes occurred twice a month. The patient does not have a history of any other cardiac conditions. An ECG was ordered to evaluate for supraventricular tachycardia. ECG findings revealed a shortened PR interval of 102 ms (normal is 120-200 ms), a widened QRS complex of 118 ms (normal is 80-100 ms), and a delta wave indicating pre-excitation from an accessory pathway. These results confirmed the diagnosis of WPW syndrome. The patient underwent radiofrequency ablation therapy of a low-risk left lateral accessory pathway. Treatment was successful with the resolution of WPW abnormalities on ECG post-ablation therapy. The patient was allowed to return to activity one week after treatment and continues to be asymptomatic and without abnormalities on ECG four months after. Conclusions WPW syndrome is an uncommon condition symptomatically characterized by arrhythmias from ventricular preexcitation with the most dangerous associated risk of SCD. The patient underwent radiofrequency ablation therapy due to presentation with a recurrence of symptomatic episodes with increased frequency and progression. In this case, the patient fits the gender profile of WPW but developed symptoms at an unusual age. There is no clear evidence on why the patient's symptoms returned after four years with more frequency, severity, and noticeability. A probable explanation is that, in a pediatric patient, changes from puberty-related heart development and physical growth led to a progression of symptoms and a more apparent reflection of the delta wave on ECG. More research is needed to identify why symptoms reoccur or worsen and how this may impact the risk calculation for SCD in patients. If puberty is a trigger, pediatric patients must be monitored for WPW pattern on ECG and onset of symptoms for prompt delivery of treatment to avoid the risk of SCD.
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    Evaluating the efficacy of wireless near infrared spectroscopy sensors for detecting central hypovolemia during simulated hemorrhage in humans
    (2024-03-21) Muthyala, Ritika; Davis, K. Austin; Hudson, Lindsey; Dinh, Viet Q.; Roumengous, Thibault; Wallner, Josephine; Boutwell, Casey; Rickards, Caroline A.
    Background: Early identification of blood loss is essential to decrease mortality from hemorrhage, a major cause of death in the military and civilian trauma settings. An industry partner has created noninvasive and wireless near infrared spectroscopy (NIRS) sensors to measure somatic tissue oxygenation (StO₂) for early detection of blood loss. In this study, we investigated the efficacy of these sensors for tracking the reduction in central blood volume (indexed by stroke volume) in humans undergoing simulated hemorrhage. We hypothesized that each NIRS sensor will progressively track the reduction in central blood volume during simulated hemorrhage in humans. Methods: Eight healthy humans (3 F, 5M; 25.3 ± 2.0 y) participated in a simulated hemorrhage protocol induced via application of lower body negative pressure (LBNP) to presyncope. Following baseline, the LBNP chamber pressure was decreased every 5-min to -15, -30, -45, -60, -70, -80, -90 and -100 mmHg, or until the onset of presyncopal symptoms (defined as a systolic arterial pressure <80 mmHg or subjective symptoms). Heart rate (via lead II ECG) and arterial pressure (via finger photoplethysmography) were monitored continuously. Stroke volume was estimated from pulse contour analysis of the finger photoplethysmography waveform. A total of five NIRS sensors measured StO2 at different anatomical locations including the sternum, forearm, deltoid, thigh, and calf. Data were analyzed over the final 3-min of each LBNP stage and the 1-min immediately prior to the onset of presyncope. Correlations between the relative changes in StO₂ of each sensor and stroke volume were assessed. Results: Stroke volume decreased by 46.9± 16.3 % at presyncope. StO₂ decreased by 1.5 ± 7.8 % at the sternum, 9.6 ± 7.4 % at the forearm, 1.5 ± 3.6 % at the deltoid, 21.3 ± 15.8 % at the thigh, and 30.4 ± 27.5 % at the calf. Of all the sites, the strongest relationship between decreases in StO₂ and stroke volume was at the calf (R-value range: 0.70-0.99, R-value mean: 0.89 ± 0.11). The sensors located at each of the other sites tracked stroke volume with high inter-participant variability (sternum, R-value range: -0.71-0.99, R-value mean: 0.24 ± 0.79; forearm, R-value range: -0.09-0.99, R-value mean: 0.61 ± 0.40; deltoid, R-value range: -0.97-0.96, R-value mean: 0.26 ± 0.83; thigh, R-value range: -0.75-0.99; R-value mean: 0.68 ± 0.64). Conclusion: Unexpectedly, the NIRS sensor on the calf, which was inside the LBNP chamber, performed the best out of the five sites in tracking the progressive reduction in central blood volume in healthy human participants. This may be due to the pooling of blood volume in the lower limbs with the LBNP stimulus, which increased deoxygenated hemoglobin, resulting in an overall lower measurement of tissue oxygen saturation. This finding is interesting, and further modifications and testing of these sensors are required to reliably track blood volume loss in patient populations.
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    Understanding the Pressure Recovery Phenomenon: A Case Study on the Discrepancies Between Echocardiography and Cardiac Catheterization in Aortic Stenosis Assessment
    (2024-03-21) Jafferji, Fatema; Patel, Kavita; Kline, Geoffrey
    This detailed case study addresses the significant clinical implications of the pressure recovery phenomenon in the assessment of aortic stenosis (AS), emphasizing the discrepancies that can arise between echocardiography (ECHO) and cardiac catheterization measurements. The focal point of this study is an 80-year-old male patient with a complex medical history of coronary artery disease, hypertension, diabetes, and dyslipidemia, who underwent evaluation for AS. Our patient presented with a grade 3/6 systolic murmur loudest at the right upper sternal border consistent with AS but was asymptomatic for common cardiac-related symptoms such as angina, dyspnea, extremity edema, and syncope. The echocardiographic assessment indicated severe AS, with the aortic valve area measured at0.79 cm² and pressure gradients at 50 mmHg (mean) and86 mmHg (peak). However, a significant divergence was observed during cardiac catheterization, which showed a considerably lower gradient of30 mmHg, indicative of moderate AS. This discrepancy is analyzed through understanding the pressure recovery phenomenon. This phenomenon occurs when blood, having flowed through a narrowed valve at high velocity (and hence low pressure), enters a larger vessel like the ascending aorta, leading to a reconversion of kinetic energy into potential energy, and thus, a recovery of pressure. This results in an overestimation of pressure gradients when using ECHO, as opposed to the direct measurements obtained via cardiac catheterization. The study delves into the broader clinical implications of this phenomenon, particularly its influence on the categorization of AS severity and the subsequent impact on clinical management decisions. The case demonstrates how a diagnosis of severe AS based on ECHO findings might lead to considerations for surgical or percutaneous interventions, which could be unnecessary or even risky for the patient, as highlighted by the more moderate classification derived from catheterization results. In conclusion, this study emphasizes the necessity for clinicians to be aware of the pressure recovery phenomenon and its potential to skew AS assessments. It advocates for a comprehensive, multimodal diagnostic approach, integrating both echocardiography and catheterization findings along with a thorough clinical evaluation. This approach would ensure a more accurate assessment of AS severity, leading to safer and more effective patient management strategies. The study also suggests the need for enhanced educational efforts to increase awareness and understanding of this phenomenon among healthcare providers.
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    Maternal Risk Factors Do Not Correlate With AKI in Patients With Congenital Heart Disease (CHD)
    (2024-03-21) Carl, Christopher; Najjar, Sam; Ogunyankin, Fadeke; Modem, Vinai; Lanier, Lane
    Purpose: Acute kidney injury (AKI) is a common complication in children who undergo cardiopulmonary bypass (CPB) and is correlated with longer hospital courses and worse outcomes. Several risk factors exist which increase the risk of AKI in pediatric populations, including premature birth, congenital heart disease (CHD), and prolonged CPB time. Maternal risk factors can impair nephrogenesis in utero, thereby increasing the likelihood for developing AKI. However, it is yet to be shown if maternal risk factors lead to an increased incidence in AKI in pediatric patients with CHD who undergo CPB. We examine the incidence of four maternal risk factors—pre-eclampsia, maternal hypertension, gestational diabetes mellitus, and maternal smoking—in 252 pediatric CHD patients who underwent CPB surgery. The purpose of this project was to examine the incidence and predictors of AKI in pediatric patients who underwent cardiopulmonary bypass (CPB) surgery at our institution. We hypothesize an association between maternal risk factors and AKI incidence in pediatric patients with CHD who underwent CPB surgery. Methods: We performed a retrospective study on 252 patients who underwent CPB for repair of a CHD between March1, 2020, and March 1, 2022. Patients were between ages 0-12 months at time of surgery and received care in the cardiac intensive care unit (CICU). P-value of 0.05 was used to determine statistical significance. NGAL levels and Cystatin C levels were also obtained. Results: Forty-four patients (17.5%) developed AKI by KDIGO criteria, with only 2.4% of those meeting stage 2 or 3 AKI. Fifty-one (24%) patients demonstrated elevated urine NGAL levels after bypass (>125). Eighteen patients (8.4%) had elevated levels of Cystatin C. Pre-eclampsia was not protective in regards to AKI in our population. Maternal smoking, maternal gestational diabetes and maternal hypertension did not correlate with development of AKI in children with CHD undergoing CPB. Conclusion: We found no association between maternal risk factors and AKI incidence in CHD patients undergoing CPB surgery in this cohort. Elevated NGAL levels and Cystatin C levels following CPB did not individually correlate with increased odds of developing AKI.
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    Patients Present With Recurrent Takotsubo Cardiomyopathy
    (2024-03-21) Sumsion, Jarom; Holper, Elizabeth
    Takotsubo Cardiomyopathy (TTC) was first characterized by Sato and his research group in Japan 1990. It is characterized by hypokinesis of various sections of the heart wall in the left ventricle and most commonly ballooning of the apical section of the heart. These findings are generally resolved within 21 days of the onset without major intervention. Since its discovery many articles have focused on classifying the effects of TTC and case studies have illustrated interesting cases of TTC; however, few publications exist highlighting recurring cases of TTC. This publication focuses on two patients who presented with a recurring case of TTC. Case Presentation: Patient 1 first presented with a two-day history or worsening pain. Upon admission into the emergency department labs reported elevated troponin and low ejection fraction (EF) of 47%. Heart catheterization showed no signs of coronary artery obstruction but confirmed systolic compression at be decreased to 40%. Three years later the same patient presented with severe chest pain, shortness of breath, elevated troponin, and ST segment depression. Heart catheterization again showed no signs of coronary artery obstruction and reduced EF. Patient 2 first presented with pneumonia and sepsis. There were no indications for coronary issues however labs showed elevated troponin. Catheterization showed no signs coronary artery disease, but cardiac echogram demonstrated an EF of 20%. Seven years later the patient was brought to the hospital by emergency services with nausea, vomiting, diarrhea, loss of consciousness, and seizures. Labs revealed elevated troponin and acute ischemia. Follow up with an echo cardiogram showed severe hypokinesis and reduced EF of 25%. Conclusions: Due to how rare recurring cases of TCC are, there is little research regarding outcomes of patients with recurrent TCC. More case presentations and long-term statistics on these patients is required to build a more accurate picture of this cardiomyopathy and educate patients on their condition.
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    The effects of esmolol on the control of coronary blood flow and myocardial oxygen supply-demand balance in sepsis
    (2024-03-21) Digilio, Michaela; Warne, Cooper; Heard, Michael; Tucker, Selina; Essajee, Sal; Bradford, Ni' Ja D.; Hodge, Lisa; Tune, Johnathan; Dick, Gregory
    Purpose: Sepsis is an acute organ dysfunction secondary to infection that results in tachycardia, tachypnea, fever, decreased blood pressure, and lactic acidosis. This results in an overall myocardial oxygen supply-demand imbalance leading to cardiac dysfunction and ultimately death. The current treatment for sepsis is antibiotic therapy, vasopressors, and fluid therapy. However, this regimen does not address the tachycardia that leads to cardiovascular decompensation. Beta-blocker therapy addresses this myocardial oxygen supply-demand imbalance and is expected to promote survival in sepsis. We hypothesize that treatment with beta-blocker therapy during acute sepsis will address the myocardial oxygen supply-demand imbalance to maintain coronary perfusion pressure, improve myocardial oxygen delivery, and promote survival. Methods: Female and male Yorkshire pigs were used as the animal model for this project. Pigs were anesthetized, intubated, and a rectal thermometer and oximeter were placed. Catheters placed in ear vein, great cardiac vein, femoral artery, and bilateral femoral veins. Pressure transducer placed in the femoral artery. A transonic flow transducer placed around the left anterior descending artery. After instrumentation, baseline values were collected. Then, infusion with Escherichia coli lipopolysaccharide (LPS) at 10 µg/kg over the course of 2 hours was used to induce sepsis. LPS was infused via the femoral vein at a rate of 0.5mL/min. After 2 hours, intervention began depending on the treatment group. Intervention lasted 4 hours. Experiment groups included Sham (without LPS, fluids, norepinephrine (NE), or esmolol), Control (with LPS, no fluids, NE, or esmolol), Standard (with LPS, fluids, and NE), and Experimental (with LPS, fluids, NE and esmolol). Doses: LPS 10 µg/kg, esmolol escalating from 100mg/hr, and NE escalating from 0.4 µg/kg/min. Goals during the intervention included keeping the mean arterial pressure (MAP) above 65mmHg and heart rate below 100. Results: All control pigs died during the 4-hour follow-up. 1 out of 3 standard treatment pigs survived. All esmolol-treated pigs survived. The esmolol group had better MAP, coronary blood flow, myocardial oxygen delivery, and oxygen extraction than the standard treatment group. Conclusion: Esmolol improves survival, coronary perfusion pressure, and myocardial oxygen delivery. This data provides support for our hypothesis and the clinical use of esmolol in sepsis.