Acute Pericarditis in Patient with Systemic Lupus Erythematosus: A Case Report

Acute pericarditis is a common disorder caused by inflammation of the pericardium and can occur as an isolated entity or as a manifestation of an underlying systemic disease. The diagnosis of acute pericarditis is established when a patient has at least two of the following symptoms or signs: chest pain consistent with pericarditis, pericardial friction rub, typical ECG changes, or a pericardial effusion of more than trivial size. Systemic Lupus Erythematosus (SLE) is a chronic autoimmune systemic disorder with unknown etio-pathogenesis. Upon the susceptible genetic, hormonal and abnormal immunologic background, the environmental factors may play role as trigger to permit disease development. Cardiovascular complications occur in more than half of the patients with SLE. Pericarditis is the most studied cardiovascular manifestation, although often not evident clinically, and it is included in the American College of Rheumatology (ACR) classification criteria for SLE. We report a clinical case of initially unremarkably findings which progressed to SLE complicated by full-blown acute pericarditis. A brief review of acute pericarditis, including etiology, clinical presentation, ECG criteria, echocardiographic manifestation, and treatment is presented.   Abstrak Perikarditis akut adalah penyakit yang disebabkan oleh inflamasi dari perikard, dapat terjadi sebagai entitas penyakit primer maupun sekunder sebagai manifestasi dari penyakit sistemik yang mendasarinya. Diagnosis perikarditis akut ditegakkan saat pasien mengalami setidaknya dua dari tanda atau gejala berikut: nyeri dada spesifik perikarditis, pericardial friction rub, perubahan EKG tipikal, atau adanya efusi perikard dengan ukuran lebih dari trivial. Lupus Eritematosus Sistemik (LES) adalah penyakit autoimun sistemik kronis dengan etiopatogenesis yang belum diketahui. Adanya kepekaan genetik, latar belakang imunologis abnormal dan hormonal, serta faktor lingkungan memegang peran sebagai pemicu perkembangan penyakit. Komplikasi kardiovaskular terjadi pada lebih dari setengah pasien dengan SLE. Perikarditis merupakan manifestasi kardiovaskular yang paling sering dijumpai, meskipun jarang ditemukan patognomonis secara klinis, dan termasuk dalam kriteria klasifikasi LES menurut American College of Rheumatology (ACR). Berikut kami laporkan kasus dengan presentasi klinis febris dan takikardia yang kemudian mengarah pada LES dengan komplikasi perikarditis akut. Kami sertakan juga ulasan tentang perikarditis akut, termasuk etiologi, presentasi klinis, kriteria EKG, manifestasi ekokardiografis, dan terapi

Detection of multi-class arrhythmia using heuristic and deep neural network on edge device

Heart disease is a heart condition that sometimes causes a person to die suddenly. One indication is a rhythm disorder known as arrhythmia. Multi-class Arrhythmia Detection has followed: QRS complex detection procedure and arrhythmia classification based on the QRS complex morphology. We proposed an edge device that detects QRS complexes based on variance analysis (QVAT) and the arrhythmia classification based on the QRS complex spectrogram. The classifier uses two-dimensional convolutional neural network (2D CNN) deep learning. We use a single board computer and neural network compute stick to implement the edge device. The outcomes are a prototype device cardiologists use as a supporting tool for analysing ECG signals, and patients can also use it for self-tests to figure out their heart health. To evaluate the performance of our edge device, we tested using the MIT-BIH database because other methods also use the data. The QVAT sensitivity and predictive positive are 99.81% and 99.90%, respectively. Our classifier's accuracy, sensitivity, predictive positive, specificity, and F1-score are 99.82%, 99.55%, 99.55%, 99.89%, and 99.55%, respectively. The experiment result of arrhythmia classification shows that our method outperforms the others. Still, for r-peak detection, the QVAT implemented in an edge device is comparable to the other methods. In future work, we can improve the performance of r-peak detection using the double-check algorithm in QVAT and cross-check the QRS complex detection by adding 1 class to the classifier, namely the non-QRS class

The Effect of Angiotensin Converting Enzyme (ACE) I/D Polymorphism on Atherosclerotic Cardiovascular Disease and Cardiovascular Mortality Risk in Non-Hemodialyzed Chronic Kidney Disease:The Mediating Role of Plasma ACE Level

The association between angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphisms and plasma ACE levels may allow for the optimization of a preventive intervention to reduce cardiovascular morbidity and mortality in the chronic kidney disease (CKD) population. In this study, we aimed to analyze the association between ACE I/D polymorphism and cardiovascular mortality risk among non-hemodialyzed chronic kidney disease patients. This cross-sectional study examined 70 patients of Javanese ethnic origin with stable CKD who did not receive hemodialysis. ACE I/D polymorphisms, plasma ACE levels, atherosclerotic cardiovascular disease (ASCVD) risk, and cardiovascular mortality risk were investigated. As per our findings, the I allele was found to be more frequent (78.6) than the D allele (21.4), and the DD genotype was less frequent than the II genotype (4.3 vs. 61.4). The ACE I/D polymorphism had a significant direct positive effect on plasma ACE levels (path coefficient = 0.302, p = 0.021). Similarly, plasma ACE levels had a direct and significant positive effect on the risk of atherosclerotic cardiovascular disease (path coefficient = 0.410, p = 0.000). Moreover, atherosclerotic cardiovascular disease risk had a significant positive effect on cardiovascular mortality risk (path coefficient = 0.918, p = 0.000). The ACE I/D polymorphism had no direct effect on ASCVD and cardiovascular mortality risk. However, our findings show that the indirect effects of high plasma ACE levels may be a factor in the increased risk of ASCVD and cardiovascular mortality in Javanese CKD patients

The Role of Klotho G395A Gene Polymorphism in Atherosclerotic Cardiovascular Disease and Mortality Risk Scores in Non-dialysis Chronic Kidney Disease

BACKGROUND: Cardiovascular disease (CVD) is the leading cause of death in patients with chronic kidney disease (CKD). Klotho expression was reduced in patients with CKD, leading to vascular calcification, endothelial dysfunction, and atherosclerosis. We investigated the role of the klotho G395A gene polymorphism and plasma klotho level in the ten-year risk of atherosclerotic cardiovascular disease (ASCVD) and CVD mortality in CKD patients.METHODS: We used the PCR-CTPP assay method to genotype klotho G395A single nucleotide polymorphism (SNP) in 72 non-dialysis CKD patients. The klotho level was determined using the enzyme-linked immunoassay (ELISA) method. Path analysis was used to determine the relationship between the klotho G395A SNP, plasma klotho level, ASCVD risk score, and CVD mortality risk score.RESULTS: Our results showed that the GA genotype had lower plasma klotho levels than the GG genotype (path coefficient=-0.185, p=0.000). There was a significant negative correlation between plasma klotho level and the ASCVD risk score (r=-0.243, p=0.040), but no significant correlation was found between plasma klotho level and the CVD mortality risk score (r=-0.145, p=0.225). Path analysis showed that plasma klotho level had a significant negative direct effect on ASCVD risk score (path coefficient=-0.272, p=0.000) and an indirect effect on CVD mortality risk score (path coefficient=0.187, p=0.005).CONCLUSION: Klotho G395A SNP might reduce lower plasma klotho levels, which increased ASCVD and CVD mortality risk scores in non-dialysis CKD patients. However, other risk factors such as age, CKD stages, hypertension, and smoking should be taken into consideration. Therefore, large-scale genetic association studies with adjusted variables could be conducted in various ethnic groups for a more robust result.KEYWORDS: klotho, single nucleotide polymorphism, cardiovascular disease, chronic kidney diseas

The Role of Plasma Interleukin-6 Levels on Atherosclerotic Cardiovascular Disease and Cardiovascular Mortality Risk Scores in Javanese Patients with Chronic Kidney Disease

Interleukin-6 (IL-6) has been identified as an important pro-inflammatory factor involved in mediating the severity of chronic kidney disease (CKD). This study sought to determine the effect of plasma IL-6 levels on atherosclerotic cardiovascular disease (ASCVD) and cardiovascular mortality risk scores in Javanese CKD patients. We also analyzed the frequency of IL-6 G174C single nucleotide polymorphism (SNP) in the population. This study was a cross-sectional study involving seventy-three patients of Javanese ethnic origin with stable chronic kidney disease. We assessed the ASCVD risk score, cardiovascular mortality score, genotyping of IL-6 G174C SNP, and plasma IL-6 levels in these patients. The genotype distribution and allele frequencies of the IL-6 G174C SNP were predominated by the G genotype/allele (GG: 97.26%, GC: 1.37%, CC: 1.37%, G-allele: 97.95%, and C-allele: 2.05%). Despite the fact that plasma IL-6 levels did not directly affect cardiovascular mortality risk, further analysis revealed its direct effect on the ASCVD risk score (path coefficient = 0.184, p = 0.043, 95% CI = 0.018–0.380), which in turn affected cardiovascular mortality risk (path coefficient = 0.851, p = <0.01, 95% CI = 0.714–0.925). In conclusion, plasma IL-6 levels play important roles on ASCVD risk and cardiovascular mortality risk in Javanese patients with CKD

Clinical outcomes of opioid administration in acute and chronic heart failure: A meta-analysis

BACKGROUND AND AIMS: Opioid use in heart failure (HF) management is controversial, and whether rapid symptomatic relief outweighs the risks of opioid use in HF remains unknown. This study aimed to explore the clinical outcomes of opioid administration in patients with acute or chronic HF. METHODS: A systematic search for eligible studies was conducted in databases (MEDLINE, Scopus, Web of Science, EBSCO) and registries (ClinicalTrials.gov, WHO Clinical Trial Registry) until June 8, 2022. Odds ratios (ORs) or adjusted OR (aORs) and mean difference (MD) or standardized MD were quantified for binary and continuous outcomes, respectively. Meta-regression was performed using the restricted maximum likelihood method. RESULTS: A total of 20 studies (154,736 participants) were included. In acute HF, opioid use presented a high risk for in-hospital mortality (OR = 2.35; 95% confidence interval (CI): 1.03-5.38; I2 = 97%), invasive (OR = 2.78; 95%CI: 1.17-6.61; I2 = 93%) and noninvasive (OR = 2.97; 95%CI: 1.06-8.28; I2 = 95%) ventilations, intensive care unit admission (OR = 3.62; 95%CI: 3.11-4.21; I2 = 6%), and inotrope use (OR = 2.54; 95%CI: 1.94-3.32; I2 = 63%). In chronic HF New York Heart Association (NYHA) Class II/III, opioid use improved ventilatory efficiency (MD = -3.16; 95%CI: (-4.78)-(-1.54); I2 = 0%), and exercise test duration (MD = 69.24; 95%CI: 10.11-128.37; I2 = 89%). CONCLUSIONS: Opioids are not recommended for acute HF management; however, they showed an advantage in exercise testing by improving ventilatory efficiency, chemosensitivity, and exercise test duration in stable patients with chronic HF NYHA Class II/III. Nonetheless, larger randomized controlled trials and individual patient-level data meta-analyses are warranted