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Post-COVID-syndromes have a high impact on incapacity for work: a mean of over 100 days has been reported in Germany [1]. Magnesium deficiency is documented as a riskincreasing factor for fatal outcome of acute covid disease [2, 3]. A first case report of post-COVID treatment with hybrid magnesium parenteral/ oral was presented in February 2021 during the Global Magnesium COVID 19 online conference. As of yet, there is no established explanation for post-COVID or long-COVID syndrome as well as there being no established treatment. In recourse to the hypothesis that magnesiumdepletion might favour microvascular early-aging and so favour neuro- degenerative prozesses [4] now preliminary observations of these parameters in post-covid patients in our primary care office result. This is done in connection with long years documentation of pulsewave-analysis (pwv), magnesium and Mg/Caprofiles in patients who suffered covid- disease. Figure 1 shows an over 6-year series of pulse-wave-analyses in a 59-year-old female patient who suffered from post-COVID syndrome. Her augmentation index (AIX) as an indicator of the actual microvascular condition increased from favorable 8% (2020) to highly pathological 39% in the post-COVID disease period - corresponding with the mean value of an 80-year-old person [5]. Another 67-year-old female post-COVID patient recovered clinically very well and quickly with high-dosed magnesium therapy and showed coincident positive decrease of AIX to 4%. Further case reports in the context of magnesium pretests and AIX are presented. Late controlled studies concerning magnesium supplementation and PWV focus on the other parameter - the (macrovascular determined) pulse-wave-velocity (PWV) and found no association of PWV with several months of magnesium supplementation [6]. Therefore, it must be emphasized that all our observations of the last years where not based on PWV but rather focused on AIX as a volatile but more magnesium-dependent parameter. Furthermore, our patients where mostly supplemented over years and not only 24 weeks. Evident is the overall small number of clinically manifesting post-COVID cases among our COVID patients (n= 10 when writing the ) among actually 470 Corona-context treatment cases. We have two working hypotheses for this. I: Persistently high magnesium levels may contrib- ute to reducing the number of post- COVID cases - and II: In the case of post-COVID syndrome, high-dose possibly hybrid magnesium therapy might favorably influence the course of the disease. The Corona pandemic and its microvascular consequences are possibly and unfortunately a non-intended turbo-experiment for microvascular early aging in a great number of undetected magnesium- depletion patients. Facing the burden of disease for individuals - and society as a whole - this justifies not only controlled studies but also the increased attention of medical doctors to the optimal magnesium status of these patients.
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One of the key elements of Traditional Chinese Medicine (TCM) is the pulse wave diagnosis technique, and the pulse wave signal contains a variety of physiological information. A deep learning model was used in this study to train and predict 500 pieces of pulse wave data from adult males during the novel coronavirus epidemic, and it was able to do so with a prediction accuracy of over 70%. © 2022 IEEE.
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The proceedings contain 23 papers. The topics discussed include: Mg and skeletal system: a link to osteoporosis and osteoarthritis;a putative impact of IL-6 on the expression of magnesiotropic genes through the activation of the JAK/STAT3 pathway;magnesium in pain therapy - historical notes and current aspects;Alzheimer's-associated variant rs708727 might be connected to dementia in Parkinson's disease;effect of magnesium citrate supplementation on the brain tissue of patients with Miyoshi dysferlinopathy measured by 31P magnetic resonance spectroscopy;clinical status of magnesium implants;Ionized magnesium: update 2022;magnesium in the treatment of selected types of muscular dystrophy;magnesium speciation analysis in blood serum;epigenetically-induced modulation of the HPA axis might improve resilience to chronic stress;magnesium status in patients with fibromyalgia syndrome;and post-covid-syndrome and transient microvascular pathology in pulse-wave-analysis - association with Mg/Ca ratio and magnesium therapy-options.
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Objective. To study the changes in the vascular wall, vascular age and metabolic parameters in polymorbid COVID-19 conva-lescents. Material and methods. The study included 62 patients with hypertension who reached the target blood pressure (BP) with dual an-tihypertensive therapy after severe and extremely severe COVID-19. The following examinations were performed: laboratory tests of metabolic parameters, assessment of changes in the vessel elasticity indices (pulse-wave velocity (PWV), augmentation index (AI), central systolic BP (cSBP), 24-hour BP monitoring, and non-invasive markers of liver fibrosis. Results. According to office BP measurements, after the coronavirus infection, an increase in systolic BP (SBP) by 29.6% and di-astolic BP (DBP) by 23.6%, as well as heart rate (HR) by 11.8% (p<0.05) was reported during regular antihypertensive therapy. In addition, 24-hour BP monitoring data indicated an increase in the average daily SBP, DBP, and heart rate. After the coronavirus infection, an increase in PWV by 35.4% (p<0.05), AI by 24.4% (p<0.05), cSBP by 22.1% were reported. Carbohydrate and lipid metabolism parameters deteriorated. A pronounced adverse effect of coronavirus infection on liver function was observed. The vascular age (according to the modified SCORE scale) increased by 6 years (p<0.05). Conclusion. Our study showed that patients after severe and extremely severe COVID-19 have a high risk of liver fibrosis, hypertension and lipid metabolism control worsening and accelerating vascular aging.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
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Background: SARS-CoV-2 determines a framework of multi-organ dysfunction that can involve the cardiovascular system creating damages of different nature. Among these, endothelial damage could play a key role in increasing arterial stiffness and thus the cardiovascular risk of infected patients. The aim of this study is to evaluate the Pulse Wave Velocity (PWV) of a population of patients after recovery from infection and to compare them with those of a group affected by arterial hypertension. Method(s): This prospective observational monocentric study involved 143 patients with previous diagnosis of Covid-19 who undergone PWV measurement during the follow-up at a median time of 3.8 months after the infection. These patients were compared to a population of 143 patients with hypertension matched by age, sex, Systolic Blood Pressure values and Body Mass Index. Result(s): PWV values were higher in Covid-19 group comparing to hypertension group (10.5+/-3.0 m/s VS 8.9+/-2.5 m/s). Furthermore, there is a correlation between higher PWV values and lower values of SpO2% at time of admission at the Emergency Department. (R=-0.302;p<0.001). Conclusion(s): SARS-CoV-2 infection seems related to increased PWV values. Moreover, higher arterial stiffness seems correlated to a worse oxygen saturation in Emergency Department. More studies with longer follow-up time are necessary to establish whether the vascular damage is reversible and whether it correlates with an increase of long-term cardiovascular risk.
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Objective. To study the changes in the vascular wall, vascular age and metabolic parameters in polymorbid COVID-19 conva-lescents. Material and methods. The study included 62 patients with hypertension who reached the target blood pressure (BP) with dual an-tihypertensive therapy after severe and extremely severe COVID-19. The following examinations were performed: laboratory tests of metabolic parameters, assessment of changes in the vessel elasticity indices (pulse-wave velocity (PWV), augmentation index (AI), central systolic BP (cSBP), 24-hour BP monitoring, and non-invasive markers of liver fibrosis. Results. According to office BP measurements, after the coronavirus infection, an increase in systolic BP (SBP) by 29.6% and di-astolic BP (DBP) by 23.6%, as well as heart rate (HR) by 11.8% (p<0.05) was reported during regular antihypertensive therapy. In addition, 24-hour BP monitoring data indicated an increase in the average daily SBP, DBP, and heart rate. After the coronavirus infection, an increase in PWV by 35.4% (p<0.05), AI by 24.4% (p<0.05), cSBP by 22.1% were reported. Carbohydrate and lipid metabolism parameters deteriorated. A pronounced adverse effect of coronavirus infection on liver function was observed. The vascular age (according to the modified SCORE scale) increased by 6 years (p<0.05). Conclusion. Our study showed that patients after severe and extremely severe COVID-19 have a high risk of liver fibrosis, hypertension and lipid metabolism control worsening and accelerating vascular aging.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
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Objective. To study the changes in the vascular wall, vascular age and metabolic parameters in polymorbid COVID-19 conva-lescents. Material and methods. The study included 62 patients with hypertension who reached the target blood pressure (BP) with dual an-tihypertensive therapy after severe and extremely severe COVID-19. The following examinations were performed: laboratory tests of metabolic parameters, assessment of changes in the vessel elasticity indices (pulse-wave velocity (PWV), augmentation index (AI), central systolic BP (cSBP), 24-hour BP monitoring, and non-invasive markers of liver fibrosis. Results. According to office BP measurements, after the coronavirus infection, an increase in systolic BP (SBP) by 29.6% and di-astolic BP (DBP) by 23.6%, as well as heart rate (HR) by 11.8% (p<0.05) was reported during regular antihypertensive therapy. In addition, 24-hour BP monitoring data indicated an increase in the average daily SBP, DBP, and heart rate. After the coronavirus infection, an increase in PWV by 35.4% (p<0.05), AI by 24.4% (p<0.05), cSBP by 22.1% were reported. Carbohydrate and lipid metabolism parameters deteriorated. A pronounced adverse effect of coronavirus infection on liver function was observed. The vascular age (according to the modified SCORE scale) increased by 6 years (p<0.05). Conclusion. Our study showed that patients after severe and extremely severe COVID-19 have a high risk of liver fibrosis, hypertension and lipid metabolism control worsening and accelerating vascular aging.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
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In this paper, stress data collection and analysis using 'Mind Scale™' is proposed. A fingertip pulse wave sensor module is utilized along a smartphone application. Biological signals such as pulse, voice and facial expression are analyzed with questionnaire and managed in the cloud. With the post-covid world, this system helps us to detect our mental health condition for new lifestyle. © 2023 IEEE.
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Coronavirus disease (COVID-19) is a respiratory disease, although arterial function involvement has been documented. We assess the impact of a post-acute COVID-19 rehabilitation program on endothelium-dependent vasodilation and arterial wall properties. We enrolled 60 convalescent patients from COVID-19 and one-month post-acute disease, who were randomized at a 1:1 ratio in a 3-month cardiopulmonary rehabilitation program (study group) or not (control group). Endothelium-dependent vasodilation was evaluated by flow-mediated dilation (FMD), and arterial wall properties were evaluated by carotid-femoral pulse wave velocity (cf-PWV) and augmentation index (AIx) at 1 month and at 4 months post-acute disease. FMD was significantly improved in both the study (6.2 ± 1.8% vs. 8.6 ± 2.4%, p < 0.001) and control groups (5.9 ± 2.2% vs. 6.6 ± 1.8%, p = 0.009), but the improvement was significantly higher in the study group (rehabilitation) (p < 0.001). PWV was improved in the study group (8.2 ± 1.3 m/s vs. 6.6 ± 1.0 m/s, p < 0.001) but not in the control group (8.9 ± 1.8 m/s vs. 8.8 ± 1.9 m/s, p = 0.74). Similarly, AIx was improved in the study group (25.9 ± 9.8% vs. 21.1 ± 9.3%, p < 0.001) but not in the control group (27.6 ± 9.2% vs. 26.2 ± 9.8 m/s, p = 0.15). Convalescent COVID-19 subjects of the study group (rehabilitation) with increased serum levels of circulating IL-6 had a greater reduction in FMD. Conclusively, a 3-month cardiopulmonary post-acute COVID-19 rehabilitation program improves recovery of endothelium-dependent vasodilation and arteriosclerosis.
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BACKGROUND: Pulse wave velocity (PWV) and augmentation index (AIx) are indices used to assess arterial stiffness. We aim to compare the effect of empagliflozin, liraglutide and their sequential combination on arterial stiffness indices in patients with type 2 diabetes (T2D). METHODS: This was a randomized single blind study evaluating the effect of empagliflozin vs liraglutide in adult patients with T2D. Patients were randomized to liraglutide titrated gradually to 1.8 mg or empagliflozin 25 mg in 1:1 ratio. Three months later empagliflozin was added to the liraglutide group, and liraglutide was added to the empagliflozin group. Patients were assessed with non-invasive tests for arterial stiffness (i.e., carotid-femoral PWV and AIx of aortic pressure) at baseline, 3-month and 9-month visits (final visit was extended for 3 months from the initial design due to Covid 19 pandemic). The primary outcome was the between-group difference of PWV change (ΔPWV) and ΔAIx at 3 months. Secondary outcomes included the between-group difference of ΔPWV and ΔAIx at 9 months, as well as the ΔPWV and ΔAIx between baseline and 9-month visit when total study population was assessed. RESULTS: A total of 62 patients with T2D (30 started liraglutide; 32 empagliflozin, mean age 63 years, 25 % with established cardiovascular disease) participated in the study. We failed to show any significant between-group differences of ΔPWV and ΔΑΙx at 3 and 9 months, as well as between-group difference of ΔPWV and ΔAIx for the total study population between baseline and 9-month visit. In contrast, systemic vascular resistance and lipoprotein(a) levels improved, showing better results with liraglutide than empagliflozin. Favorable effects were also observed on body weight, body mass index, body and visceral fat, blood pressure, HbA1c, and uric acid levels. CONCLUSION: No evidence of a favorable change in arterial stiffness indices was seen with empagliflozin or liraglutide or their combination in this study. Well-designed powerful studies are needed to address any potential effects on arterial stiffness in selected populations.
Subject(s)
COVID-19 , Cardiovascular Diseases , Diabetes Mellitus, Type 2 , Sodium-Glucose Transporter 2 Inhibitors , Vascular Stiffness , Humans , Middle Aged , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/prevention & control , Cardiovascular Diseases/complications , COVID-19/complications , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Liraglutide/adverse effects , Prospective Studies , Pulse Wave Analysis , Single-Blind Method , Sodium-Glucose Transporter 2 Inhibitors/therapeutic use , Sodium-Glucose Transporter 2 Inhibitors/pharmacologyABSTRACT
Vascular age is determined by functional and structural changes in the arterial wall. When measured by its proxy, pulse wave velocity, it has been shown to predict cardiovascular and total mortality. Disconcordance between chronological and vascular age might represent better or worse vascular health. Cell senescence is caused by oxidative stress and sustained cell replication. Senescent cells acquire senescence-associated secretory phenotype. Oxidative stress, endothelial dysfunction, dysregulation of coagulation and leucocyte infiltration are observed in the aging endothelium. All of these mechanisms lead to increased vascular calcification and stiffness. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can involve the vascular endothelium. It enters cells using angiotensin-converting enzyme 2 (ACE-2) receptors, which are abundant in endothelial cells. The damage this virus does to the endothelium can be direct or indirect. Indirect damage is caused by hyperinflammation. Direct damage results from effects on ACE-2 receptors. The reduction of ACE-2 levels seen during coronavirus disease 2019 (COVID-19) infection might cause vasoconstriction and oxidative stress. COVID-19 and vascular aging share some pathways. Due to the novelty of the virus, there is an urgent need for studies that investigate its long-term effects on vascular health.
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Environmental noise significantly impacts human health and well-being. It is a widespread problem in Europe, where at least one in five people are exposed to harmful levels of noise. Hearing loss is the most known health effect related to noise exposure. There is, however, growing data that links noise exposure to hypertension, coronary artery disease, and stroke. According to some theories, this relationship may be explained by the indirect pathway of noise exposure, which can cause sympathetic and endocrine activation, as well as several cognitive and emotional responses, including annoyance. Noise exposure leads to stress reactions independent of cognitive involvement. There is a possibility that noise exerts its effects directly through synaptic interactions, as well as through cognitive and emotional effects. Epidemiological studies indicate that nocturnal noise exposure has more profound health consequences. Nighttime noise exposure is associated with an increase in heart rate due to sympathetic activation or parasympathetic withdrawal, and with an increase in blood pressure as well as endothelial dysfunction. Hypertension is a common condition and is an important risk indicator for other cardiovascular diseases. Previous studies showed an association between noise exposure, blood pressure and arterial hypertension. Meta-analysis of cross-sectional studies found an increase of hypertension prevalence per 10 dB increase in daytime average road traffic noise level. There is, however, some heterogeneity among these studies. Prospective studies have also found an association between aircraft noise exposure and hypertension, supporting the cross-sectional findings. The analyses, of data from the large Hypertension and Exposure to Noise near Airports (HYENA) study, showed that an increase in nocturnal aircraft noise exposure per 10 dB was associated with an increased incidence of hypertension. The meaningful effect of night-time aircraft noise on arterial hypertension was also observed in the prospective observation of the subset of individuals from that study. In a longitudinal observation of 420 participants, higher aircraft noise exposure during the night significantly associated with the incidence of hypertension. Previous cross-sectional case-control study conducted in 2015, in 2 suburban areas of Krakow, Poland, revealed an increase in blood pressure and arterial stiffness as determined by carotid - femoral pulse wave velocity in individuals exposed to increased aircraft noise levels. However, even short-term noise reduction, as experienced during the COVID-19 lockdown, may reverse those unfavorable effects. As a result of these observations, noise mitigation strategies are important for cardiovascular health.
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Aims: To investigate the impact of coronavirus disease 2019 lockdown on trajectories of arterial pulse-wave velocity in a large population of users of connected smart scales that provide reliable measurements of pulse-wave velocity. Methods and results: Pulse-wave velocity recordings obtained by Withings Heart Health & Body Composition Wi-Fi Smart Scale users before and during lockdown were analysed. We compared two demonstrative countries: France, where strict lockdown rules were enforced (n = 26 196) and Germany, where lockdown was partial (n = 26 847). Subgroup analysis was conducted in users of activity trackers and home blood pressure monitors. Linear growth curve modelling and trajectory clustering analyses were performed. During lockdown, a significant reduction in vascular stiffness, weight, blood pressure, and physical activity was observed in the overall population. Pulse-wave velocity reduction was greater in France than in Germany, corresponding to 5.2 month reduction in vascular age. In the French population, three clusters of stiffness trajectories were identified: decreasing (21.1%), stable (60.6%), and increasing pulse-wave velocity clusters (18.2%). Decreasing and increasing clusters both had higher pulse-wave velocity and vascular age before lockdown compared with the stable cluster. Only the decreasing cluster showed a significant weight reduction (-400â g), whereas living alone was associated with increasing pulse-wave velocity cluster. No clusters were identified in the German population. Conclusions: During total lockdown in France, a reduction in pulse-wave velocity in a significant proportion of French users of connected smart bathroom scales occurred. The impact on long-term cardiovascular health remains to be established.
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Objective. Evaluation of the possibility of a fixed combination of azilsartan medoxomil + chlorthalidone in additional angioprotection in patients with arterial hypertension (HTN) and high pulse wave velocity (PWV) after confirmed severe or extremely severe COVID-19 (bilateral polysegmental viral pneumonia)treated by genetically engineered biological drugs, who had not previously received combined antihypertensive therapy. Design and methods. An open observational study lasting 12 weeks included 30 patients, 28-31 days after discharge from the hospital after a severe and extremely severe COVID-19, who received or had not previously received antihypertensive therapy. Patients underwent 24-hour blood pressure (BP) monitoring, applanation tonometry (augmentation index and central BP), measurement of PWV, laboratory tests before and after prescription of a fixed combination of azilsartan medoxomil + chlorthalidone. Results. At baseline, patients showed an increase in office blood pressure to 153,06/92,2 mmHg. After treatment with a fixed combination of azilsartan medoxomil + chlorthalidone, a decrease in systolic BP by 18,47 % and diastolic BP by 16,24 % was observed. According to ambulatory BP monitoring, the decrease in systolic BP was 19,65 % and diastolic BP - 24,68 %, PWV decreased by 34,4 %, augmentation index - by 9,42 %, central systolic BP - by 15,48 % (p < 0,05). At baseline, vascular age (VA) was increased to 44,96 years compared to the passport age of 35,03 years. After treatment, there was a significant decrease in VA to 38,74 years (p < 0,01). In addition, the levels of C-reactive protein, fibrinogen, D-dimer, glucose, blood urea nitrogen and uric acid significantly decreased. Conclusions. The fixed combination of azilsartan medoxomil + chlorthalidone provides better control of BP. It also helps to improve vascular elasticity (augmentation index, PWV, central systolic BP, decrease in VA) and to reduce post-infectious inflammation in HTN patients after a severe coronavirus infection. Copyright © 2021 All-Russian Public Organization Antihypertensive League. All rights reserved.
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Background and Aim: An infection with SARS-CoV-2 is associated with systemic inflammation, that also affects the endothelium. This may result in endothelitis, which can influence vascular regulation and morphology. Until now, the specific mechanism of vessel damage after a SARS-CoV-2 infection is still unclear, especially in children and adolescents. The LICO Study (Long term impact of COVID-19) aims to investigate the long-term effects of a SARS-CoV-2 infection on vascular structure and function in chil-dren and adolescents. Method(s): Children and adolescents with confirmed evidence of survived SARS-CoV-2 infection are screened 6 +/- 3 months post-infection. Vascular function is assessed by flow-mediated vas-odilation (FMD) and aortic pulse wave velocity (PWV). Carotid intima-media thickness (cIMT) and retinal diagnostics (arteriove-nous ratio-AVR) are used to examine vascular structure. The matched control group without prior SARS-CoV-2 infection undergoes the same examination procedure. Result(s): So far, we have been able to evaluate 24 (9 post-covid) subjects (13.5 +/- 1.9 years;9 girls). Compared to the mean refer-ence values of the control group, 5 post-covid subjects have higher cIMT (0.49 +/- 0.01 mm vs. reference value 0.46 +/- 0.03 mm). Of these, 3 post-covid subjects even deviate from the norm PWV (4.96 +/- 0.16 m/sec vs. reference value 4.63 +/- 0.29 m/sec). The same 3 post-covid subjects are also below the norm FMD (2.06 +/- 1.05 % vs. reference value 4.18 +/- 7.04 %). None of the post-covid subjects deviates from the norm AVR values (refer-ence value 0.85 +/- 0.07). Conclusion(s): It is shown that infection with SARS-CoV-2 has the potential to impair vascular regulation. These initial results provide trends for early vascular changes among children and adolescents after recovered SARS-CoV-2 infection. Due to that this is an ongoing study, the results are constantly being expanded and may still change. To determine lasting changes in morphology, the examination is repeated after 6 months and the further results of this longitudinal study must be awaited.
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SESSION TITLE: Cardiovascular Complications in Patients with COVID-19 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Pneumopericardium is the presence of air or gas in the pericardial space, usually secondary to blunt or penetrating trauma. Most pneumopericardium are non-tension. The use of positive pressure ventilation (PPV) increases the chances of developing a tension pneumopericardium. We report the case of a 22-year-old male patient admitted for COVID-19 pneumonia who developed pneumopericardium with cardiac tamponade features. CASE PRESENTATION: A 22-year-old male was admitted for acute respiratory distress syndrome due to COVID-19 pneumonia and required intubation on hospital day 10. The next day, he became febrile with new leukocytosis. A chest x-ray showed new extensive pneumomediastinum and pneumopericardium. Vasopressor support and broad-spectrum antibiotics were started for septic shock, however he continued to decompensate rapidly, requiring maximal medical support. His arterial line waveform showed pulsus paradoxus, leading to concern for underlying tension pneumopericardium. Bedside echo was unrevealing as imaging was obstructed by the air in pericardial sac. The patient was too unstable for a CT scan of the chest. After extensive discussion with his family, he was placed on palliative measures only and expired. DISCUSSION: Pneumopericardium is due to an abnormal connection between the pericardial space and a source of air or gas. Levin and Macklin describe three main mechanisms by which this connection can be made. The first: acute rises in alveolar pressure and volume or ventilator associated lung injury leading to rupture of alveoli with gas tracking along perivascular and peri bronchial sheaths to the mediastinum. The second: macro-perforation of the pericardial space leading to communication with respiratory or gastrointestinal tracts. Third: existence of a pneumothorax in the presence of traumatic pericardial tear or congenital pleuro-pericardial connection. Spontaneous pneumopericardium without any anatomic connection is rare and is due to a direct extension of infectious etiologies of the lungs or by an infection of the pericardial space with gas forming bacteria. A tension pneumopericardium causing cardiac tamponade can develop from pneumopericardium with PPV where the pericardial sac acts as a shutter valve letting air in but not out as has been reported sparingly in the literature. Cummings et al described 93 patients who developed tamponade out of 252 patients with pneumopericardium. Our patient possibly developed a pleuro-pericardial tract secondary to his pneumonia. With continued PPV his simple pneumopericardium likely developed into a tension pneumopericardium evidenced by arterial waveforms consistent with pulsus paradoxus, worsening hypotension despite maximal vasopressor support and development of ventricular tachycardia. CONCLUSIONS: Our case highlights the importance of considering pneumopericardium causing cardiac tamponade in the setting of mechanical ventilation. Reference #1: Mindaye ET, Arayia A, Tufa TH, Bekele M. Iatrogenic pneumopericardium after tube thoracostomy: A case report. Vol. 76, International journal of surgery case reports. 2020. p. 259–62. Reference #2: Cummings RG, Wesly RL, Adams DH, Lowe JE. Pneumopericardium resulting in cardiac tamponade. Ann Thorac Surg. 1984 Jun;37(6):511–8. Reference #3: Levin AI, Visser F, Mattheyse F, Coetzee A. Tension pneumopericardium during positive-pressure ventilation leading to cardiac arrest. J Cardiothorac Vasc Anesth. 2008 Dec;22(6):879–82. MACKLIN CC. TRANSPORT OF AIR ALONG SHEATHS OF PULMONIC BLOOD VESSELS FROM ALVEOLI TO MEDIASTINUM: CLINICAL IMPLICATIONS. Arch Intern Med [Internet]. 1939 Nov 1;64(5):913–26. Available from: https://doi.org/10.1001/archinte.1939.00190050019003 DISCLOSURES: No relevant relationships by Aarti Mittal No relevant relationships by Beenish Naqvi
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Objectives: Paraplegia is known to complicate extensive iliocaval and lower extremity deep vein thrombosis (DVT) in rare instances. The most common pathophysiology is ischemia from severe venous hypertension in phlegmasia cerulea dolens. Less understood, however, is paresis or paraplegia in the absence of ischemia. We present a case of paraplegia in extensive iliocaval and lower extremity DVT without ischemia, which was successfully treated by percutaneous pharmacomechanical therapy. Methods: A 46-year-old African American woman with a history of hypertension, insulin-dependent diabetes mellitus, indwelling inferior vena cava filter since 2005, and recent coronavirus disease 2019 diagnosis, presented with acute abdominal pain with severe bilateral lower extremity edema, pain, and paresis. She was found to have bilateral iliocaval to tibial DVT (Fig 1). The patient was noted to have multiphasic arterial waveforms on ankle-brachial index and duplex ultrasound examination. Paresis quickly progressed to flaccid bilateral lower extremity paralysis. Neurologic workup was unrevealing. Despite her symptoms, thrombolytic therapy was delayed due to severe menstrual bleeding requiring a blood transfusion. Therapeutic anticoagulation was initiated. Results: On hospital day 10, the patient underwent 24-hour catheter-directed thrombolysis via bilateral popliteal vein access. Bilateral mechanical thrombectomy was then performed, achieving recanalization of the bilateral lower extremities, iliac veins, and inferior vena cava with minimal residual thrombus (Fig 2). The patient's edema and sensorimotor function immediately improved and never incurred lower extremity tissue ischemia. She was discharged on lifelong rivaroxaban. With physical therapy, the patient ambulated independently at 1 month postoperatively. Venous duplex ultrasound examination revealed continued iliocaval and lower extremity patency at 6 months postoperatively. Conclusions: We postulate that this patient suffered lower extremity paralysis secondary to cauda equina syndrome. Pharmacomechanical thrombectomy is a pragmatic means that reestablishes venous patency and relieves venous hypertension. This pathophysiology and its treatment should be considered in extensive iliocaval DVT and lower extremity neurologic compromise despite duration of paralysis. [Formula presented] [Formula presented]
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Background and Objectives: Individuals with type 2 diabetes mellitus (T2DM) have an increased risk of cardiovascular disease. Arterial stiffness is an independent prognostic marker for cardiovascular disease development. We aimed at determining the effect of two different sodium-glucose co-transporter-2 (SGLT-2) inhibitors on ambulatory arterial stiffness in individuals with T2DM. Materials and Methods: In this single-center, single-arm, prospective study performed from January 2020 to August 2021, we planned to enroll adult subjects with T2DM and stable antidiabetic and antihypertensive treatment, assigned either to empagliflozin or dapagliflozin for 6 months. All eligible subjects underwent ambulatory blood pressure monitoring. We set as the primary efficacy outcome the change in ambulatory pulse wave velocity (PWV) from baseline to week 24. Results: We finally enrolled 46 diabetic subjects, with a mean age of 62.89 (8.53) years and mean T2DM duration of 9.72 (6.37) years. Thirty patients received dapagliflozin, while sixteen patients received empagliflozin. Due to COVID-19 pandemic restrictive measures during the study, the mean follow-up period extended from 6 months to 9.98 (3.27) months. Regarding the prespecified primary efficacy outcome, we found that the SGLT-2 inhibitor treatment did not have a significant effect on PWV (p = 0.65). Prior history of cardiovascular disease did not significantly affect the observed effects. Other indices of arterial stiffness, such as augmentation index and central pulse pressure, were not significantly affected, neither by empagliflozin nor by dapagliflozin. Conclusions: SGLT-2 inhibitor treatment with empagliflozin or dapagliflozin in subjects with T2DM failed to improve ambulatory PWV over a mean follow-up of 10 months. Registration number: ISRCTN88851713.