Atraumatic acute compartment syndrome in anticoagulated patient: A case report

Abstract Introduction and importance Compartment syndrome is a well-known surgical emergency caused by increasing pressure inside the fascial or osteo-fascial compartment, resulting in vascular compromise, ischemia, and necrosis. This condition usually occurs following a traumatic incident. Here we present a report of nontraumatic acute compartment syndrome caused by systemic anticoagulation in patients presenting with the acute coronary syndrome. Case presentation We report a case of a 51-year-old male with acute coronary syndrome receiving systemic anticoagulation, which later developed significant swelling and tensing on his right arm. He also complained of pallor and paresthesia with decreased peripheral oxygen saturation on his right arm. Clinical discussion The patient was diagnosed with atraumatic acute compartment syndrome and underwent fasciotomy promptly. His symptoms improved after undergoing fasciotomy. Conclusions Atraumatic acute compartment syndrome is a rare case. Identifying this condition without a typical history of underlying predisposition is important to avoid delaying emergent surgery as the key therapy

Peran Hiperhomosisteinemia dalam Atherosklerosis

Hiperhomosistenemia adalah peningkatan kadar homosistein dalam darah di atas 15 μmol/L. Di dalam siklus daur homosistein terdapat beberapa enzim yang memerlukan vitamin B12 dan asam folat sebagai kofaktor. Hiperhomosisteinemia dapat disebabkan defek genetik bawaan seperti defisiensi enzim Metilentetrahidrofolat reduktase, Metionin sintase, dan Sistationin β sintase, atau oleh faktor didapat seperti gagal ginjal, kanker, psoriasis, diabetes, paparan asap rokok, alkohol, kopi, usia tua, menopause, serta obat-obatan. Berbagai studi menunjukkan hiperhomosisteinemia berhubungan dengan disfungsi endotel, aktivasi platelet, dan pembentukan thrombus yang dapat berujung pada aterosklerosis dan penyakit jantung koroner.Hyperhomocysteinemia is defined as plasma homocystein level above 15 μmol/L. Several enzymes involved in homocysteine metabolism require vitamin B and folic acid as cofactor. Hyperhomocysteinemia could be caused by inherited genetic disease such as deficiency of Methylentetrahydrofolate reductase and Methionin synthase, or by acquired factors such as kidney failure, cancer, psoriasis, diabetes, smoking, alcohol, caffeine, elderly, menopause, and drugs. Prospective studies has shown that hyperhomocysteinaemia is associated with endothelial injury and dysfunction, promoting platelet activation and thrombus formation, which could result in atherosclerosis and coronary artery disease

PENGEMBANGAN KNOWLEDGE MANAGEMENT PADA SEKOLAH PELANGI KASIH

PENGEMBANGAN KNOWLEDGE MANAGEMENT PADA SEKOLAH PELANGI KASIH - Knowledge Management, Knowledge Management System, Budaya Sharing

Case Report: Complete heart block as a manifestation of cardiac metastasis of oral cancer [version 2; peer review: 2 approved]

Metastatic tumors of the heart presenting with complete heart block (CHB) is an extremely uncommon case. There are no available guidelines in managing CHB in terminal cancer. Permanent pacemaker implantation in such cases is a challenge in terms of clinical utility and palliative care. We report a case of a 24-year-old man suffering from tongue cancer presenting with CHB. An intracardiac mass and moderate pericardial effusion were present, presumed as the metastatic tumor of tongue cancer. We implanted a temporary pacemaker for his symptomatic heart block and cardiogenic shock, and pericardiocentesis for his massive pericardial effusion. We decided that a permanent pacemaker would not be implanted based on the low survival rate and significant comorbidities. Multiple studies report a variable number of cardiac metastasis incidence ranging from 2.3% to 18.3%. It is rare for such malignancies to present with CHB. The decision to implant a permanent pacemaker is highly specific based on the risks and benefits of each patient. It needs to be tailored to the patient’s functional status, comorbid diseases, prognosis, and response to conservative management

Olmesartan inhibits transdifferentiation of rabbit’s valvular interstitial cells into myofibroblast based on α – smooth muscle actin expression

Recent studies revealed that differentiation of valvular interstitial cell (VIC) into myofibroblasts played an important role in valvular remodeling and fibrosis. Study was performed on in vitro cultured of VIC from New Zealand rabbit (Oryctolagus cuniculus). Isolated VIC was pretreated using 5 ng/mL of TGF-β1 and divided into groups of olmesartan (100 nanomol/L) as short 30 minutes exposure duration and as continuous 72 hours exposure duration. Inhibition of myofibroblast differentiation was quantified by the expression of α-SMA levels detected by immunofluorescence staining. Olmesartan administration either, as short 30 minutes exposure duration or as continuous 72 hours exposure duration, were significantly reduced TGF-β1-induced VIC differentiation into myofibroblast expressed by α-SMA levels compared to control (short 30 minutes exposure duration: 9.18 ±2.25, as continuous 72 hours exposure duration: 10.13 ±0.69, and control 22.29 ±2.78; p < 0.001), but without significant difference between the two treatment groups (p 0.403). Olmesartan both on short and continuous exposure can inhibit the differentiation of valve interstitial cells into myofibroblasts based on the expression of αSMA, but without a significant difference in the inhibitory effect

Moderate cardiovascular risk factor among Indonesian: do carotid intima-media thickness (CIMT) predict further?

Abstract. Background. Determining management strategies in an individual with intermediate cardiovascular risk represent a great challenge. The impact of increased CIMT to improve estimated cardiovascular disease (CVD) risk score in individual at intermediate cardiovascular risk has not yet been fully elucidated. Aims. For this reason, we sought to determine the association between CIMT increment and incident of CVD. Methods. We conducted a longitudinal retrospective cohort study involving 28 patients with intermediate cardiovascular risk (Framingham risk score 10% - 20%). Subjects with criteria fulfillment had their data collected through history taking, physical examination, and CIMT re-measurement using echocardiography. Results. Bivariate analysis with regression logistic showed significant correlation between increased CIMT with CVD event (p= 0.016). CIMT measurement is a plausible noninvasive method to predict subclinical cardiovascular disease to further promote more aggressive management

Dexamethasone and olmesartan as potential antiremodelling agents of valvular interstitial cell into myofibroblast

Rheumatic heart disease is a late complication of valvular inflammation caused by rheumatic fever. Studies have shown that the differentiation of valvular interstitial cells (VIC) into fibroblasts plays an important role in valvular remodeling and fibrosis. Various strategies to minimize valvular fibrosis has increased recently. This study aims to analyze the effect of dexamethasone, olmesartan, and its combination in inhibiting TGF-β1-induced VIC differentiation into myofibroblast. In vitro laboratory experimental-posttest only control group design was conducted. Isolated VIC of Oryctolagus cuniculus was pretreated using 2,5 ng/mL of TGF-β1 and divided into groups of dexamethasone (0.1 uM/L), olmesartan (100 nmol/L), and its combination. Inhibition of myofibroblast differentiation was quantified by the expression of α-SMA levels detected by immunofluorescence. Dexamethasone, olmesartan, and its combination administration were significantly reduced TGF-β1-induced VIC differentiation into myofibroblast expressed by α-SMA levels (dexamethasone 6823 ± 1735.3, olmesartan 6683.7 ± 2795.05). Combination of dexamethasone and olmesartan exhibit the most potent inhibition compared to control (5051.87 ± 1612.210 vs 22286.73 ± 2780.2; p < 0.000). In conclusion, dexamethasone, olmesartan, and the combination can significantly reduce the differentiation of VIC into myofibroblasts. The greatest potential is the combined effect of dexamethasone and olmesartan, while dexamethasone and olmesartan have the same potential