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Dayuanyin (DYY) has been shown to reduce lung inflammation in both coronavirus disease 2019 (COVID-19) and lung injury. This experiment was designed to investigate the efficacy and mechanism of action of DYY against hypoxic pulmonary hypertension (HPH) and to evaluate the effect of DYY on the protection of lung function. Animal welfare and experimental procedures are approved and in accordance with the provision of the Animal Ethics Committee of the Institute of Materia Medica, Chinese Academy of Medical Science. Male C57/BL6J mice were randomly divided into 4 groups: control group, model group, DYY group (800 mg.kg-1), and positive control sildenafil group (100 mg.kg-1). The animals were given control solvents or drugs by gavage three days in advance. On day 4, the animals in the model group, DYY group and sildenafil group were kept in a hypoxic chamber containing 10% +/- 0.5% oxygen, and the animals in the control group were kept in a normal environment, and the control solvent or drugs continued to be given continuously for 14 days. The right ventricular systolic pressure, right ventricular hypertrophy index, organ indices and other metrics were measured in the experimental endpoints. Meantime, the expression levels of the inflammatory factors in mice lung tissues were measured. The potential therapeutic targets of DYY on pulmonary hypertension were predicted using network pharmacology, the expression of nuclear factor kappa B (NF- kappaB) signaling pathway-related proteins were measured by Western blot assay. It was found that DYY significantly reduced the right ventricular systolic pressure, attenuated lung injury and decreased the expression of inflammatory factors in mice. It can also inhibit hypoxia-induced activation of NF- kappaB signaling pathway. DYY has a protective effect on lung function, as demonstrated by DYY has good efficacy in HPH, and preventive administration can slow down the disease progression, and its mechanism may be related to inhibit the activation of NF-kappaB and signal transducer and activator of transcription 3 (STAT3) by DYY.Copyright © 2023, Chinese Pharmaceutical Association. All rights reserved.
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Objectives: Glycogen Storage Disease Type Ia (GSDIa) is a rare inherited disorder resulting in acute hypoglycemia due to impaired release of glucose from glycogen. Despite dietary management practices to prevent hypoglycemia in patients with GSDIa, complications still occur in children and throughout adulthood. This retrospective cohort study compared the prevalence of complications in adults and children with GSDIa. Method(s): Using ICD-10 diagnosis codes, the IQVIA Pharmetrics Plus database was searched for patients with >=2 GSDI claims (E74.01) from January 2016 through February 2020, with >=12 months continuous enrollment beginning prior to March 2019 (for one year of follow-up before COVID-19), and no inflammatory bowel disease diagnoses (indicative of GSDIb). Complication prevalence in adults and children with GSDIa was summarized descriptively. Result(s): In total, 557 patients with GSDIa were identified (adults, 67%;male, 63%), including 372 adults (median age, 41 years) and 185 children (median age, 7 years). Complications occurring only in adults were atherosclerotic heart disease (8.6%), pulmonary hypertension (3.0%), primary liver cancer (1.9%), dialysis (0.8%), and focal segmental glomerulosclerosis (0.3%). Other complications with the greatest prevalence in adults/children included gout (11.8%/0.5%), insomnia (10.0%/1.1%), osteoarthritis (22.0%/2.7%), severe chronic kidney disease (4.3%/0.5%), malignant neoplasm (10.8%/1.6%), hypertension (49.7%/8.7%), acute kidney failure (15.3%/2.7%), pancreatitis (3.0%/0.5%), gallstones (7.8%/1.6%), benign neoplasm (37.4%/8.1%), hepatocellular adenoma (7.0%/1.6%), neoplasm (41.1%/9.7%), and hyperlipidemia (45.2%/10.8%). Complications with the greatest prevalence in children/adults included poor growth (22.2%/1.9%), gastrostomy (29.7%/3.2%), kidney hypertrophy (2.7%/0.8%), seizure (1.6%/0.5%), hypoglycemia (27.0%/11.3%), hepatomegaly (28.7%/15.9%), kidney transplant (1.6%/1.1%), diarrhea (26.5%/18.6%), nausea and/or vomiting (43.8%/35.8%), acidosis (20.0%/17.2%), and anemia due to enzyme disorders (43.8%/40.6%). Conclusion(s): GSDIa is associated with numerous, potentially serious complications. Compared with children, adults with GSDIa had a greater prevalence of chronic complications, potentially indicating the progressive nature of disease. Children with GSDIa had more acute complications related to suboptimal metabolic control.Copyright © 2023
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A clinical analysis of COVID-19 cases combined with acute respiratory diseases is presented. The aim of the study was to analyze clinical and laboratory data of patients with combined COVID-19 infection. In patient A. infected with SARS-CoV-2 without X-ray confirmation of lung damage, acute tonsillitis, polyadenopathy, hepatosplenomegaly, moderate leukocytosis, lymphomonocytosis and the presence of reactive lymphocytes were detected. Serological and molecular biological studies were carried out for the purpose of differential diagnosis. A positive test result for IgM antibodies to EBV was obtained. The method of polymerase chain reaction (PCR) revealed EBV DNA in blood plasma. The result of the determination of heterogeneous IgG antibodies to the EBV caspid antigen is negative. Clinical symptoms of the patient with coronavirus infection COVID-19, confirmed by radiological and serological screening, included: fever, sore throat, hyperemia and hypertrophy of the palatine tonsils, hepatomegaly, changes of the cellular composition of the blood. At the same time, the lymph nodes in the neck, chest and abdominal cavity were not enlarged;the presence of reactive lymphocytes and plasma cells was not detected. Serological markers of EBV were also not detected. A PCR test for Epstein-Barr virus DNA was negative.Copyright © 2022 Infectious Diseases: News, Opinions, Training.
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Introduction: SARS-CoV-2 is responsible for the current global pandemic. SARS-CoV-2 infection underlies the novel viral condition coronavirus disease 2019 (COVID-19). COVID-19 causes significant pulmonary sequelae contributing to serious morbidities. The pathogenesis of COVID-19 is complex with a multitude of factors leading to varying levels of injury numerous extrapulmonary organs. This review of 124 published articles documenting COVID- 19 autopsies included 1,142 patients. Method(s): A PubMed search was conducted for COVID-19 autopsy reports published before March 2021 utilizing the query COVID-19 Autopsy. There was no restriction regarding age, sex, or ethnicity of the patients. Duplicate cases were excluded. Findings were listed by organ system from articles that met selection criteria. Result(s): Pulmonary pathology (72% of articles;866/1142 patients): diffuse alveolar damage (563/866), alveolar edema (251/866), hyaline membrane formation (234/866), type II pneumocyte hyperplasia (165/866), alveolar hemorrhage (164/866), and lymphocytic infiltrate (87/866). Vascular pathology (41% of articles;771/1142 patients): vascular thrombi (439/771)-microvascular predominance (294/439)-and inflammatory cell infiltrates (116/771). Cardiac pathology (41% of articles;502/1142 patients): cardiac inflammation (186/502), fibrosis (131/502), cardiomegaly (100/502), hypertrophy (100/502), and dilation (35/502). Hepatic pathology (33% of articles;407/1142 patients): steatosis (106/402) and congestion (102/402). Renal pathology (30% of articles;427/1142 patients): renal arteries arteriosclerosis (111/427), sepsis-associated acute kidney injury (81/427) and acute tubular necrosis (77/427). Conclusion(s): This review revealed anticipated pulmonary pathology, along with significant extrapulmonary involvement secondary to COVID-19, indicating widespread viral tropism throughout the human body. These diverse effects require additional comprehensive longitudinal studies to characterize short-term and long-term COVID-19 sequelae and inform COVID-19 treatment.
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Case Presentation: Term male infant born to SARS-CoV-2 positive mother with infant testing negative. ECG for perinatal bradycardia revealed ventricular pre-excitation. Echocardiogram showed asymmetric LV hypertrophy with prominent trabeculations, subaortic narrowing with no pressure gradient, and normal biventricular systolic function. Rapid increase in RV pressure estimates and NT-proBNP in first week if life concerning for diastolic dysfunction. Anti-arrhythmic therapy initiated for SVT with subsequent resolution. Later, developed progressive LV dilation and systolic dysfunction. Myocardium showed regions resembling non-compaction and others concerning for infiltrative process. Cardiac MRI showed no obvious tumors, but rhabdomyomas could not be ruled out given similar appearance to myocardium. Due to worsening heart failure, everolimus therapy initiated to target potential rhabdomyomas while awaiting genetic testing for tuberous sclerosis. Subaortic narrowing and LV hypertrophy improved within days, and LV appearance became more consistent with non-compaction. Genetic testing revealed a TSC2 gene variant consistent with tuberous sclerosis. Systolic function improved, and patient discharged on afterload reduction. Echocardiogram 6 months post-discharge shows continued LV dilation and mild systolic dysfunction. Discussion(s): Although outflow obstruction and arrhythmias are common with cardiac rhabdomyomas and can cause dysfunction, our patient developed progressive dysfunction in the absence of outflow tract gradient or prolonged arrhythmia. As rhabdomyomas subsided, it became clearer that he had an underlying cardiomyopathy. We suspect that rhabdomyomas in the setting of abnormal myocardium led to abnormalities in myocardial contractility and compliance causing combined systolic and diastolic dysfunction. After complete resolution of rhabdomyomas, cardiac function has improved. However, he continues to have ventricular dilation and mild dysfunction attributable to cardiomyopathy. It is unlikely that mother's SARS-CoV-2 infection played a role as infant tested negative and clinical picture was not consistent with myocarditis.
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COVID-19 is a highly transmissible disease with severe course especially in patients with nephrogenic hypertensive disease and chronic kidney disease due to a higher incidence of all-type infections than in the general population. The aim of the study is to describe a clinical case of SARS-CoV-2 infection complicated by nephrogenic pulmonary edema and COVID-associated pneumonitis, alveolitis. Description of the case. Patient K.S., born in 1975, was hospitalized 24 hours after symptom onset at emergency hospital due to complaints of increased blood pressure up to 180-200/110-120 mm Hg, temperature up to 38.7degreeC, dry cough, feeling of heaviness in the chest, change in urine color. PCR smear for SARS-CoV-2 was positive. Computed tomography revealed a pattern of bilateral COVID-associated pneumonitis, alveolitis, with 75% involvement. The electrocardiogram revealed signs of left ventricular myocardial hypertrophy. Ultrasound examination showed numerous cysts in the kidneys. Urinalysis at admission: leukocytes - 499, erythrocytes - 386. Glomerular filtration rate (CKD-EPI: 29 ml/min/1.73 m2) and corresponds to stage IV of chronic kidney disease. Coagulogram: fibrinogen: 32.3 (1.6-4.0) g/l, D-dimer: 663 (0-250). Despite the treatment, the patient's condition worsened, the phenomena of cardiopulmonary and renal insufficiency increased, which led to a fatal outcome. During a virological study of sectional material: SARS-CoV-2 coronavirus RNA was found in the lung and kidneys. Signs of bilateral COVID-associated pneumonitis, alveolitis with diffuse cellular infiltrates in combination with changes in the alveolar apparatus, signs of pulmonary edema were revealed. Heart-related signs - swelling of the interstitium, fragmented muscle fibers, some of them hypertrophied, a wave-like deformation of cardiomyocytes, blurring of the transverse striation. Arteries with thickened sclerosed walls. In the kidneys - diffuse damage to the proximal tubules of the nephron with areas of cortical and proximal necronephrosis, areas of fibrinoid swelling. Conclusion. The cause of death of a 45-year-old patient was a severe course of bilateral COVID-associated pneumonitis, alveolitis, which contributed to the development of renal medullary hypoxia and type 1 cardiorenal syndrome, which led to early nephrogenic pulmonary edema.Copyright © 2023 Saint Petersburg Pasteur Institute. All rights reserved.
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Obesity is associated with several diseases, including mental health. Adipose tissue is distributed around the internal organs, acting in the regulation of metabolism by storing and releasing fatty acids and adipokine in the tissues. Excessive nutritional intake results in hypertrophy and proliferation of adipocytes, leading to local hypoxia in adipose tissue and changes in these adipokine releases. This leads to the recruitment of immune cells to adipose tissue and the release of pro-inflammatory cytokines. The presence of high levels of free fatty acids and inflammatory molecules interfere with intracellular insulin signaling, which can generate a neuroinflammatory process. In this review, we provide an up-to-date discussion of how excessive obesity can lead to possible cognitive dysfunction. We also address the idea that obesity-associated systemic inflammation leads to neuroinflammation in the brain, particularly the hypothalamus and hippocampus, and that this is partially responsible for these negative cognitive outcomes. In addition, we discuss some clinical models and animal studies for obesity and clarify the mechanism of action of anti-obesity drugs in the central nervous system.Copyright © 2023 Wolters Kluwer Medknow Publications. All rights reserved.
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Purpose of study Since mid-April 2020 in Europe and North America, clusters of pediatric cases with a newly described severe systemic inflammatory response with shock have appeared. Patients had persistent fevers >38.5 C, hypotension, features of myocardial dysfunction, coagulopathy, gastrointestinal symptoms, rash, and elevated inflammatory markers without other causes of infection. The World Health Organization, Centers for Disease Control, and Royal College of Paediatrics associated these symptoms with SARS-CoV-2 as multisystem inflammatory syndrome in children (MIS-C). Cardiac manifestations include coronary artery aneurysms, left ventricular systolic dysfunction evidenced by elevation of troponin-T (TnT) and pro-B-type naturietic peptide (proBNP), and electrocardiogram (ECG) abnormalities. We report the clinical course of three children with MIS-C while focusing on the unique atrioventricular (AV) conduction abnormalities. Case #1:19-year-old previously healthy Hispanic male presented with abdominal pain, fever, and non-bloody diarrhea for three days. He was febrile and hypotensive (80/47 mmHg) requiring fluid resuscitation. Symptoms, lab findings, and a positive COVID-19 antibody test were consistent with MIS-C. Methylprednisolone, intravenous immunoglobulin (IVIG), and enoxaparin were started. He required epinephrine for shock and high flow nasal cannula for respiratory distress. Initial echocardiogram demonstrated a left ventricular ejection fraction (LVEF) of 40% with normal appearing coronaries. Troponin and proBNP were 0.41 ng/mL and proBNP 15,301 pg/mL respectively. ECG showed an incomplete right bundle branch block. He eventually became bradycardic to the 30s-50s and cardiac tracing revealed a complete AV block (figure 1a). Isoproterenol, a B1 receptor agonist, supported the severe bradycardia until the patient progressed to a type 2 second degree AV block (figure 1b). A second dose of IVIG was administered improving the rhythm to a type 1 second degree AV block. An IL-6 inhibitor, tocilizumab was given as the rhythm would not improve, and the patient soon converted to a first-degree AV block. Cardiac magnetic resonance imaging showed septal predominant left ventricular hypertrophy and subepicardial enhancement along the basal inferior/anteroseptal walls typical for myocarditis. Case #2: 9-year-old previously healthy Hispanic male presented after three days of daily fevers, headaches, myalgias, diffuse abdominal pain, and ageusia. He was febrile, tachycardic, and hypotensive (68/39 mmHg). Hypotension of 50s/20s mmHg required 3 normal saline boluses of 20 ml/kg and initiation of an epinephrine drip. Severe hypoxia required endotracheal intubation. After the MIS-C diagnosis was made, he was treated with IVIG, mehtylprednisolone, enoxaparin, aspirin, and ceftriaxone. Due to elevated inflammatory markers by day 4 and patient's illness severity, a 7-day course of anakinra was initiated. Initial echocardiogram showed mild tricuspid and mitral regurgitation with a LVEF of 35-40%. Despite anti-inflammatory therapy, troponin and proBNP were 0.33 ng/mL and BNP of 25,335 pg/mL. A second echocardiogram confirmed poor function so milrinone was started. Only, after two doses of anakinra, LVEF soon normalized. Despite that, he progressively became bradycardic to the 50's. QTc was prolonged to 545 ms and worsened to a max of 592 ms. The aforementioned therapies were continued, and the bradycardia and QTc improved to 405 ms. Patient #3: 9-year-old African American male presented with four days of right sided abdominal pain, constipation, and non-bilious non-bloody emesis. He had a negative COVID test and unremarkable ultrasound of the appendix days prior. His history, elevated inflammatory markers, and positive COVID- 19 antibody were indicative of MIS-C. He was started on the appropriate medication regimen. Initial ECG showed sinus rhythm with normal intervals and echocardiogram was unremarkable. Repeat imaging by day three showed a decreased LVEF of 50%. ECG had since changed to a right bundle branch block. Anakinra as started and steroid dosing was increased. By day 5, he became bradycardic to the 50s and progressed to a junctional cardiac rhythm. Cardiac function normalized by day 7, and anakinra was subsequently stopped. Thereafter, heart rates ranged from 38-48 bpm requiring transfer to the pediatric cardiac intensive care unit for better monitoring and potential isoproterenol infusion. He remained well perfused, with continued medical management, heart rates improved. Methods used Retrospective Chart Review. Summary of results Non-specific T-wave, ST segment changes, and premature atrial or ventricular beats are the most often noted ECG anomalies. All patients initially had normal ECGs but developed bradycardia followed by either PR prolongation or QTc elongation. Two had mild LVEF dysfunction prior to developing third degree heart block and/or a junctional escape rhythm;one had moderate LVEF dysfunction that normalized before developing a prolonged QTc. Inflammatory and cardiac markers along with coagulation factors were the highest early in disease course, peak BNP occurred at approximately hospital day 3-4, and patient's typically had their lowest LVEF at day 5-6. Initial ECGs were benign with PR intervals below 200 milliseconds (ms). Collectively the length of time from initial symptom presentation till when ECG abnormalities began tended to be at day 8-9. Patients similarly developed increased QTc intervals later in the hospitalization. When comparing with the CRP and BNP trends, it appeared that the ECG changes (including PR and QTc elongation) occurred after the initial hyperinflammatory response. Conclusions Although the mechanism for COVID-19 induced heart block continues to be studied, it is suspected to be secondary to inflammation and edema of the conduction tissue. Insufficiency of the coronary arterial supply to the AV node and rest of the conduction system also seems to play a role. Although our patients had normal ECG findings, two developed bundle branch blocks prior to more complex rhythms near the peak of inflammatory marker values. Based on the premise that MIS-C is a hyperinflammatory response likely affecting conduction tissue, our group was treated with different regimens of IVIG, steroids, anakinra, and/or tocilizumab. Anakinra, being an IL-1 inhibitor, has been reported to dampen inflammation in viral myocarditis and tocilizumab has improved LVEF in rheumatoid arthritis patients. Based on our small case series, patient's with MISC can have AV nodal conduction abnormalities. The usual cocktail of IVIG and steroids helps;however, when there are more serious cases of cardiac inflammation, adjuvant immunosuppresants like anakinra and toculizumab can be beneficial. (Figure Presented).
ABSTRACT
Introduction: Transthyretin amyloidosis cardiomyopathy (ATTR-CM) is a rare, progressive, life-threatening, hereditary disorder induced by a misfolded precursor protein, caused by mutations in the transthyretin gene. ATTR-CM is a challenging disease to recognize in early stages owing to its multisystem and nonspecific manifestations1-3. Case report: 65-year-old patient was hospitalized for the second time to our Clinic for Cardiovascular diseases in April 2022. Previous hospitalization happened 5 years ago and there was no ambulatory cardiology check-up between hospitalizations. He had progressive dyspnea on mild exertion and lower extremity edema. Therapy at home was furosemide occasionally. In past medical history he had left carpal tunnel surgery and Covid 19 infection in April 2022. On arrival blood pressure was 140/80 mmHg, pulse 100 beats per minute, absolutely arrhythmic. Basal weakened breath sounds, and leg edema were present. Troponin and NT pro BNP were elevated (91 ng/l and 3222 ng/l). 12-lead electrocardiogram showed peripheral micro-voltage, atrial fibrillation with ventricular rate around 110 bpm. Biatrial enlargement, increased left and right wall thickness, thickened papillary muscles, mildly reduced left ventricular ejection fraction and mono-phasic transmittal flow was found on transthoracic echocardiography. Testing for Fabry disease was negative. Cardiac magnetic resonance (CMR) found morphological changes and the pattern of contrast accumulation that suggested cardiac amyloidosis. Immunofixation electrophoresis showed no monoclonal (M) spike, gammopathy was unlikely. A biopsy of the buccal mucosa was performed, no amyloid deposits were found. Bone scintigraphy found accumulation of labelled hydroxydiphosphonate (HDP) that was visible in the myocardium, which points to ATTR-CM. Genetic testing is in progress. Conclusion: ATTR-CM requires a high index of suspicion, and it should be suspected in patients with LV hypertrophy and heart failure. The diagnosis of cardiac amyloidosis requires a combination of multi- modality imaging including echocardiography, CMR and scintigraphy. An imaging modality that can accurately diagnose ATTR-CM without the need for invasive cardiac biopsy is nuclear scintigraphy using bone-avid radio-tracers4. Timely diagnosis is important since the treatment is possible and improves prognosis in these patients. [ FROM AUTHOR] Copyright of Cardiologia Croatica is the property of Croatian Cardiac Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)
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Introduction: It is estimated that 15% of patients with AS have concomitant cardiac amyloidosis (CA). Left ventricular (LV) longitudinal strain (LS) pattern with relative apical sparing (RELAPS>1), shown as bright red in the apical segments on the polar map, has been strongly associated with CA. Its presence and its significance in AS is yet to be determined. Purpose(s): To determine the prevalence of the RELAPS>1 pattern in patients with severe AS with and without concomitant CA, and to analyze the echocardiographic phenotype associated with this strain pattern and its prognostic value. Method(s): Patients with severe symptomatic AS undergoing TAVI were prospectively and consecutively included between Jan-19 and Dec-20. Pre-procedure, a complete echocardiogram was performed that included deformation parameters using Speckle-Tracking. Strain derived Indices accepted for CA screening were calculated: RELAPS: Relative apical LS (average apical LS/average basal+mid LS);SAB: (apical-septal/basal-septal LS);EFSR: (LVEF/GLS). After TAVI, a 99Tc-PYP scintigraphy and a proteinogram were performed to screen for CA. Result(s): 324 patients were included. The mean age was 81 yo, 52% women. Strain analysis could be performed in 243 patients due to acoustic window and covid19 pandemic restrictions. Among those, 111 (46%) presented relative apical sparing (RELAPS>1). There were no differences in clinical characteristics between patients with RELAPS <1 and >1: Similar age, sex, cardiovascular risk factors and funcional class, renal function or NT-proBNP. Among patients with RELAPS>1 there was more frecuently CA with uptake grade 2 and 3 on scintigraphy (15% vs. 4.5%, P=0.006) (Figure 1). RELAPS>1 group showed greater LV hypertrophic remodeling: Thicker myocardial wall with smaller ventricular cavity, especially concentric hypertrophy;LVEF and GLS was similar, however, MAPSE and myocardial contraction fraction (MCF) were worse in RELAPS >1 group, and EFSR was significantly higher (4.2 vs 3.9, p=0.002). RELAPS >1 group had smaller aortic valve area (AVA: 0.6 vs 0.7 cm2, p=0.045), but similar transvalvular gradients due to lower stroke volume. It had larger atria and less left atrial (LA) fractional emptying, as well as higher prevalence of atrial fibrillation (AF: 41% vs 27%, p=0.03). Right ventricle (RV) size were similar, however, RV function was worse in RELAPS >1 group (TAPSE: 19 vs 21 mm, p=0.003;free Wall LS: -24 vs -27%, p=0.008). There was no difference in all-cause mortality at 1 year of follow-up between groups (6.4% vs. 6.3%, p=1). Figure 2 represents the morphological characteristics according to the LS phenotype. Conclusion(s): In severe AS, RELAPS >1 is present in almost half of the patients. It is associated with worse cardiac remodeling, as well as higher prevalence of AF. However, it wasn't associated with higher mortality at 1 year. 1 in 7 patients with AS and RELAPS >1 have concomitant ATTR CA grade 2/3.
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Background: The role of genetic conditions in the development of cardiomyopathy is well established;however, recognition and referral for genetic testing remains underutilized. Systematic review of complex cases can increase general awareness in this area of practice. Here we describe the case of a patient with resolved severe stress induced cardiomyopathy (SIC), who was ultimately found to have heterozygous transthyretin-mediated amyloidosis (TTRA). Case: A 27-year-old man (family history positive for a brother status post heart transplant) presented with ataxia and cough due to legionella pneumonia. TTE showed left ventricular (LV) diastolic diameter of 6.2cm, LV ejection fraction 20-25%. He suffered rapid decompensation with mixed cardiogenic/septic shock requiring peripheral VA ECMO and Impella-CP placement. Course notable for brief cardiac arrest on hospital day (HD) 2, incidental diagnosis of COVID 19 on HD 14, conversion to VV ECMO on HD 15, and ECMO decannulation on HD 23. Repeat TTE prior to discharge showed normalization of biventricular function. Discussion(s): Despite resolution of refractory shock and normalization of biventricular function prior to discharge, the TTE finding of mild LV dilation and strong family history prompted outpatient pursuit of genetic testing which revealed a heterozygous TTRA mutation (val142ile). Work-up to assess cardiac involvement included: a 99m-technetium pyrophosphate scintigraphy found to be indeterminate, an aborted endomyocardial biopsy due to inability to smoothly advance a bioptome (presumably related to ECMO cannulation), and a cardiac MRI (pending at the time of this submission). If a cardiac phenotype is discovered, the patient will be started on targeted treatment of cardiac amyloid. Screening of first-degree family members has been initiated. Conclusion(s): Given the current state of under-diagnosis of genetic cardiomyopathies and its association with significant morbidity and mortality, it is prudent to consider genetic testing in young patients based on clinical history. Examples of clinical scenarios to prompt further testing include: anatomical findings (i.e. cardiac chamber enlargement, left ventricular hypertrophy), family history of cardiomyopathy, or clinical markers suggestive of alternative diagnoses (i.e. neuropathy, renal insufficiency, mediastinal lymphadenopathy). This thoughtful and algorithmic use of genetic testing may help improve long-term patient outcomes given improvements in both detection, family screening, and treatment for disease-specific cardiomyopathies.Copyright © 2022
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Background Graft versus host disease (GVHD) most often occurs 100-365 days after hematopoietic stem cell transplant (HSCT). Manifestations most often are dermatologic, hepatic or pulmonic, and are rarely cardiac. We present a unique case of GVHD inducing cardiogenic shock necessitating advanced heart failure therapies. Case This is a 34 year-old male with a history of acute lymphoblastic leukemia who completed chemoradiation and HSCT from an HLA perfect sibling in 1992. In May 2020, he presented with dyspnea for 6 weeks. An echocardiogram at that time showed an EF of 10% and severe biventricular dilatation. He was originally hospitalized at an outside institution for hypoxia where a left heart catheterization showed normal coronaries and goal directed therapy was initiated. After 2 negative COVID tests, he was discharged with a LifeVest. One month later, despite medication compliance, he returned in cardiogenic shock after his LifeVest was activated for ventricular tachycardia (VT). Decision-making He was started on inotropic therapy and an intra-aortic balloon pump (IABP) was placed 1:1 prior to transfer to our tertiary center. After support was started, a right heart catheterization showed a right atrial pressure of 13 mmHg, a wedge of 17, and a cardiac index of 2.6. His course was complicated by VT storm. Differentials for his non-ischemic cardiomyopathy (NICMO) included myocarditis (viral vs. giant cell) with a possible component of chemotherapy/radiation induced NICMO. Immediate AHFT work-up was started. He was unable to be weaned off his IABP or inotropic support. The decision was made to pursue emergent left ventricular assist device placement (LVAD) and achieve a definitive diagnosis with a core biopsy. Pathology resulted with myocyte hypertrophy, chronic inflammation with eosinophils concerning for chronic GVHD. Conclusion There have only been a handful of case reports describing cardiac manifestations of GVHD, and none with NICMO and cardiogenic shock requiring an LVAD. Despite this, suspicion should remain present for GVHD in HSCT patients regardless of time frame from oncologic therapies or specificity of HLA match when presenting in cardiogenic shock.Copyright © 2023 American College of Cardiology Foundation
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Background and Aims: In the Covid era, Continuous blood glucose monitoring(CGM) was used more frequently and it proved to be quite a helpful and accurate tool for glycemic regulation. Method(s): 75 yrs old Saudi gentleman, had Type 2 diabetes >30yrs, Hypertension, Primary Hypothyroidism, dyslipidemia, mixed polyneuropathy, Iron deficiency anemia, and benign prostatic hypertrophy. In March,2020 his BP and blood glucose readings were high at home. He had a past history of subdural hematoma with hydrocephalus(staus post-shunting). He was on Glargine, oral hypoglycemic agents, anti-hypertensives, Levothyroxine, Atorvastatin, Aspirin, iron fumarate, calcium carbonate and cholecalciferol. Fully conscious, and co-operative, of average built and height.BP 170/70 mmHg, pulse 93/m, RR 18/ m,O2sat 100%, afebrile, BMI 24.96 kg/m2. Fundoscopy normal. He had dry feet and impaired monofilament and vibration testing. Result(s): Hb% 13.1g/dl(12.6 before),MCV 93.8fl,S.Ferritin 10.5ug/l(30-400),Vit.B12 270 pmol/l(145-637),HbA1c 8%(6.4 in Feb.2020).The renal, liver and thyroid functions-intact. Albumin creatinine ratio 12.23mg/g(0-30). Nerve conduction study-mixed polyneuropathy. He continued to follow-up physically even during the Covid crisis due to the elevated SMBG and BP values. Gliclazide & antihypertensive doses were optimized and Glargine was started.On patient's follow-up in August, 2020, time in range had improved to 80%(33% in June,2020),average glucose was 147 mg/dl(200 before), glucose variability was 27.8%(28.9), hypoglycemia (54-79mg/dl) was 1%(0). On last follow-up on 27.06.2022 his HbA1c had climbed up to 8.3%(7.3 in September, 2021). He was compliant to the diabetes regime, but had stopped using the Libre sensor. Conclusion(s): The case signifies the advantage of a meticulous CGM usage during the Covid pandemic, that resulted in a reasonable glycemic control.
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The COVID-19 pandemic is a worldwide problem. The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic or paucity-symptomatic forms to conditions such as pneumonia, acute respiratory distress syndrome and multiple organ failure. Objective was to describe a clinical case of SARS-CoV-2 infection in the patient with sarcoidosis and cardiovascular pathology developing acute respiratory syndrome and lung edema. Material and methods. There were analyzed accompanying medical documentation (outpatient chart, medical history), clinical and morphological histology data (description of macro- and micro-preparations) using hematoxylin and eosin staining. Results. Lung histological examination revealed signs of diffuse alveolar damage such as hyaline membranes lining and following the contours of the alveolar walls. Areas of necrosis and desquamation of the alveolar epithelium in the form of scattered cells or layers, areas of hemorrhages and hemosiderophages are detected in the alveolar walls. In the lumen of the alveoli, a sloughed epithelium with a hemorrhagic component, few multinucleated cells, macrophages, protein masses, and accumulated edematous fluid were determined. Pulmonary vessels are moderately full-blooded, surrounded by perivascular infiltrates. Signs of lung sarcoidosis were revealed. Histological examination found epithelioid cell granulomas consisting of mononuclear phagocytes and lymphocytes, without signs of necrosis. Granulomas with a proliferative component and hemorrhage sites were determined. Giant cells with cytoplasmic inclusions were detected — asteroid corpuscles and Schauman corpuscles. Non-caseous granulomas consisting of clusters of epithelioid histiocytes and giant Langhans cells surrounded by lymphocytes were detected in the lymph nodes of the lung roots. Hamazaki–Wesenberg corpuscles inside giant cells were found in the zones of peripheral sinuses of lymph nodes. In the lumen of the bronchi, there was found fully exfoliated epithelium, mucus. Granulomas are mainly observed subendothelially on the mucous membrane, without caseous necrosis. Histological examination of the cardiovascular system revealed fragmentation of some cardiomyocytes, cardiomyocyte focal hypertrophy along with moderate interstitial edema, erythrocyte sludge. Zones of small focal sclerosis were determined. The vessels of the microcirculatory bed are anemic, with hypertrophy of the walls in small arteries and arterioles. Virological examination of the sectional material in the lungs revealed SARS-CoV-2 RNA. Conclusion. Based on the data of medical documentation and the results of a post-mortem examination, it follows that the cause of death of the patient R.A., 50 years old, was a new coronavirus infection COVID-19 that resulted in bilateral total viral pneumonia. Сo-morbidity with competing diseases such as lung sarcoidosis and cardiovascular diseases aggravated the disease course, led to the development of early ARDS and affected the lethal outcome. © 2022 Saint Petersburg Pasteur Institute. All rights reserved.
ABSTRACT
Objectives: The study aims to determine the association between electrocardiographic abnormalities and in-hospital mortality of patients with Coronavirus Disease 2019 (COVID-19) infection admitted in a tertiary hospital in the Philippines. Material(s) and Method(s): We conducted a retrospective study of confirmed COVID-19-infected patients. Demographic, clinical characteristics, and clinical outcomes were extracted from the medical records. Electrocardiographic analysis was derived from the 12-lead electrocardiogram (ECG) recorded upon admission. The frequencies and distributions of various clinical characteristics were described, and the ECG abnormalities associated with in-hospital mortality were investigated. Result(s): A total of 163 patients were included in the study, most were female (52.7%) with a median age of 55 years old. Sinus rhythm (40%), nonspecific ST and T wave changes (35%), and sinus tachycardia (22%) were the frequently reported ECG findings. The presence of any ECG abnormality was detected in 78.5% of patients and it was significantly associated with in-hospital mortality (p = 0.038). The analysis revealed a statistically significant association between in-hospital mortality and having atrial fibrillation or flutter (p = 0.002), supraventricular tachycardia (SVT) (p = 0.011), ventricular tachycardia (p = 0.011), third-degree atrioventricular block (AVB) (p = 0.011), T wave inversion (p = 0.005) and right ventricular hypertrophy (RVH) (p = 0.011). Conclusion(s): The presence of any ECG abnormality in patients with COVID-19 infection was associated with in-hospital mortality. ECG abnormalities that were associated with mortality were atrial fibrillation or flutter, SVT, ventricular tachycardia, third-degree AVB, T wave inversion, and RVH. Supporting Documents Association of electrocardiographic abnormalities with in-hospital mortality in adult patients with COVID-19 infection TARRANZA, Jannah Lee [1];RAMIREZ, Marcellus Francis [1,2];YAMAMOTO, Milagros [1] 1 Section of Adult Cardiology, Department of Internal Medicine, University of Santo Tomas Hospital, Manila, Philippines 2 Division of Electrophysiology, Section of Adult Cardiology, Department of Internal Medicine, University of Santo Tomas Hospital, Manila, Philippines.
ABSTRACT
Introduction: COVID-19 causes morbid pathological changes in different organs including lungs, kidney, liver,etc especially in those who succumb. Though clinical outcomes in those with comorbidities are known to be different from those without - not much is known about the differences at histopathological level. Aim(s): It was to compare the morbid histopathological changes in COVID-19 patients between those who were immunocompromised(Gr 1), malignancy(Gr 2) or had cardiometabolic conditions (hypertension, diabetes or coronary artery disease)(Gr 3). Method(s): Post-mortem tissue sampling (MITS) was done from the lungs, kidney, heart, and liver using biopsy gun within two hours of death. Routine (H & E stain) and special stains (AFB, SM, PAS) were done besides immunohistochemistry. Result(s): A total of 100 patients underwent MITS and data of 92 were included (immunocompromised: 27, maligancy:18, cardiometabolic conditions:71). Within lung histopathology, capillary congestion was more in those with malignancy while others like diffuse alveolar damage, microthrombi, pneumocyte hyperplasia etc was equally distributed. Within liver, architecture distortion was significantly different in immunocompromised while steatosis, portal inflammation, Kupffer cell hypertrophy, confluent necrosis were equally distributed. There was a trend towards higher acute tubular injury in those with cardiometabolic conditions as compared to the other groups. No significant histopathological differences in heart was discerned. Conclusion(s): Certain histopathological features are markedly different in different groups (Gr 1,2 and3)of COVID-19 patients with fatal outcome.
ABSTRACT
Inferior turbinate reduction procedures have been performed for decades. After significant evolution, turbinoplasty and other mucosal-sparing techniques have become the main method to successfully reduce turbinate hypertrophy. The debate of which technique produces the most effective and durable outcomes is ongoing. During this critical era of widespread communicable diseases, including but not limited to COVID-19, HIV, and hepatitis, additional attention is necessary to balance outcomes with a degree of generation of airborne particles when selecting a technique. This review article aims to identify the optimal method for inferior turbinate reduction that weighs both outcomes and aerosol production. The MEDLINE database was searched to discover relevant publications through August 2022. Key search terms included inferior turbinate hypertrophy, turbinate reduction surgery, turbinoplasty methods, surgical management of turbinate hypertrophy, surgical aerosol generation, COVID-19 surgery, surgery smoke plume, SARS-CoV-2 transmission during surgery, and nasal procedures COVID-19 aerosols. Surgical management of the inferior turbinates includes radiofrequency ablation (RFA), microdebrider-assisted turbinoplasty (MAIT), electrocautery, laser, and ultrasound. Piezo-assisted turbinoplasty and a turbinate-specific coblation wand are new additions to the literature. All techniques appear to improve patient symptoms of nasal obstruction. MAIT and RFA are comparable, although MAIT demonstrated better long-term outcomes in some studies and appears to generate fewer airborne particles. Studies evaluating the production of aerosols due to RFA are lacking. Ultrasound outcomes are also excellent and generate no aerosols, but the technique has not been compared against the microdebrider. Electrocautery can result in increased pain and crusting for patients and causes the highest amount of aerosols. Deficiencies of current studies, including a lack of comparison of aerosol generation, duration of follow-up, omission of outfracture, and inadequate randomized controlled trials among existing and new techniques, have limited the identification of the best inferior turbinate reduction method. Given the durability of MAIT and its minimal aerosol production, it can be reinforced as the most sensible technique until further evidence is available.
ABSTRACT
The COVID-19 pandemic is a worldwide problem. The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic or paucity-symptomatic forms to conditions such as pneumonia, acute respiratory distress syndrome and multiple organ failure. Objective was to describe a clinical case of SARS-CoV-2 infection in the patient with sarcoidosis and cardiovascular pathology developing acute respiratory syndrome and lung edema. Material and methods. There were analyzed accompanying medical documentation (outpatient chart, medical history), clinical and morphological histology data (description of macro- and micro-preparations) using hematoxylin and eosin staining. Results. Lung histological examination revealed signs of diffuse alveolar damage such as hyaline membranes lining and following the contours of the alveolar walls. Areas of necrosis and desquamation of the alveolar epithelium in the form of scattered cells or layers, areas of hemorrhages and hemosiderophages are detected in the alveolar walls. In the lumen of the alveoli, a sloughed epithelium with a hemorrhagic component, few multinucleated cells, macrophages, protein masses, and accumulated edematous fluid were determined. Pulmonary vessels are moderately full-blooded, surrounded by perivascular infiltrates. Signs of lung sarcoidosis were revealed. Histological examination found epithelioid cell granulomas consisting of mononuclear phagocytes and lymphocytes, without signs of necrosis. Granulomas with a proliferative component and hemorrhage sites were determined. Giant cells with cytoplasmic inclusions were detected — asteroid corpuscles and Schauman corpuscles. Non-caseous granulomas consisting of clusters of epithelioid histiocytes and giant Langhans cells surrounded by lymphocytes were detected in the lymph nodes of the lung roots. Hamazaki–Wesenberg corpuscles inside giant cells were found in the zones of peripheral sinuses of lymph nodes. In the lumen of the bronchi, there was found fully exfoliated epithelium, mucus. Granulomas are mainly observed subendothelially on the mucous membrane, without caseous necrosis. Histological examination of the cardiovascular system revealed fragmentation of some cardiomyocytes, cardiomyocyte focal hypertrophy along with moderate interstitial edema, erythrocyte sludge. Zones of small focal sclerosis were determined. The vessels of the microcirculatory bed are anemic, with hypertrophy of the walls in small arteries and arterioles. Virological examination of the sectional material in the lungs revealed SARS-CoV-2 RNA. Conclusion. Based on the data of medical documentation and the results of a post-mortem examination, it follows that the cause of death of the patient R.A., 50 years old, was a new coronavirus infection COVID-19 that resulted in bilateral total viral pneumonia. Сo-morbidity with competing diseases such as lung sarcoidosis and cardiovascular diseases aggravated the disease course, led to the development of early ARDS and affected the lethal outcome.