Background: Cardiovasculareventshavebeenreportedinthesettingofcoronavirus disease-19(COVID-19).Ithasbeenhypothesizedthatsystemicinflammationmayaggravate arrhythmias or trigger new-onset conduction abnormalities. However, the specifictypeanddistributionofelectrocardiographicdisturbancesinCOVID-19as wellastheirinfluenceonmortalityremaintobefullycharacterized. Methods: Electrocardiograms (ECGs) were obtained from 186 COVID-19-positive patientsatalargetertiarycarehospitalinNorthernNevada.Thefollowingarrhythmiaswereidentifiedbycardiologists:sinusbradycardia,sinustachycardia,atrialfibrillation (A-Fib), atrial flutter, multifocal atrial tachycardia (MAT), premature atrial contraction (PAC), premature ventricular contraction (PVC), atrioventricular block (AVB),andrightbundlebranchblock(RBBB).ThemeanPRinterval,QRSduration, andcorrectedQTintervalweredocumented.Fisher'sexacttestwasusedtocompare the ECG features of patients who died during the hospitalization with those who survived.TheinfluenceofECGfeaturesonmortalitywasassessedwithmultivariable logistic regression analysis.Results: A-Fib,atrialflutter,andST-segmentdepressionwerepredictiveofmortality.In addition,themeanventricularratewashigheramongpatientswhodiedascompared to those who survived. The use of therapeutic anticoagulation was associated with reducedoddsofdeath;however,thisassociationdidnotreachstatisticalsignificance. Conclusion:The underlying pathogenesis of COVID-19-associated arrhythmias remains to be established, but we postulate that systemic inflammation and/or hypoxiamayinducepotentiallylethalconductionabnormalitiesinaffectedindividuals.ThisisanopenaccessarticleunderthetermsoftheCreativeCommonsAttribution-NonCommercial-NoDerivsLicense,whichpermitsuseanddistributionin anymedium,providedtheoriginalworkisproperlycited,theuseisnon-commercialandnomodificationsoradaptationsaremade. ©2021TheAuthors.Annals of Noninvasive ElectrocardiologypublishedbyWileyPeriodicalsLLC.
BACKGROUND The presence of small air bubbles and foam are an impediment to a successful colonoscopy. They impair an endoscopist’s view and diminish the diagnostic accuracy of the study. This has been particularly noted to be of concern with the switch to lower volume polyethylene glycol (PEG) and bisacodyl combination preparation. AIM To evaluate the effect of oral simethicone addition to bowel preparation on intraluminal bubbles reduction during colonoscopy. METHODS Described is a prospective, randomized, multi-center, double-blinded, placebo-controlled study to evaluate the use of premixed simethicone formulation with split-regimen, low-volume PEG-bisacodyl combination bowel preparation for 168 outpatients undergoing screening, surveillance, and diagnostic colonoscopies. Primary outcome includes evaluation of bubbles during colonoscopy graded using the Intraluminal Bubbles Scale. Secondary outcomes include evaluation of the Boston Bowel Preparation Scale (BBPS), total number of polyps, polyp size differentiation, polyp laterality, adenoma detection, mass detection, cecal insertion time, withdrawal time, and patient-reported adverse events. RESULTS Higher Intraluminal Bubbles grades III and IV (less than 75% of the mucosa cleared of bubbles/foam requiring intervention with simethicone infused wash) were detected in the placebo group [Simethicone n = 4/84 vs Placebo n = 20/84 ( P = 0.007)]. BBPS total score was 7.42 [standard deviation (SD) = ± 1.51] in the simethicone group and 7.28 (SD = ± 1.44) in the placebo group ( P = 0.542) from a total of 9. Significantly higher number of adenomas were detected in the simethicone group ( P = 0.001). CONCLUSION The addition of simethicone to bowel preparation is well advised for its anti-foaming properties. The results of this study suggest that addition of oral simethicone can improve bowel wall visibility.
Background Hypertensive disorders of pregnancy are associated with vascular complications, including ischemic stroke and cervical artery dissection. Vertebral artery dissection (VAD), however, is rare. We describe a 31-year-old female who presented with vertigo, nausea, and vomiting and was found to have a VAD. In addition, we discuss the presentation, differential diagnosis, and pathogenesis of this uncommon but clinically significant vascular event and summarize other cases of vertebral artery dissection described in the medical literature. Case presentation A 31-year-old Hispanic woman presented 10 days postpartum with a one-day history of vertigo, nausea, vomiting, and frontal headache. The patient’s pregnancy course had been complicated by preeclampsia, chorioamnionitis, and iron-deficiency anemia, and her delivery was complicated by acute hemorrhage. Physical examination was significant for left leg ataxia. Laboratory studies showed marked thrombocytosis. Emergent computed tomography (CT) scan of the head was obtained and revealed a left cerebellar ischemic large vessel stroke. Subsequent CT angiography of the head and neck showed a left VAD. Based on correlation of the clinical history and laboratory and imaging findings, a diagnosis of vertebral artery dissection secondary to reactive (secondary) thrombocytosis from overlapping iron-deficiency anemia and acute hemorrhage was established. The patient was started on a heparin infusion and experienced significant improvement after a four-day hospitalization. Conclusion VAD is a rare but important cause of neurologic symptoms in the postpartum period and should be considered in the differential diagnosis for women who present with headache and/or vertigo. Women aged 30 years or older and those with a history of a hypertensive disorder of pregnancy are at particularly high risk. Prompt diagnosis and management of VAD is essential to ensure favorable outcomes.
BACKGROUND Timely and accurate identification of subgroup at risk for major adverse cardiovascular events among patients presenting with acute chest pain remains a challenge. Currently available risk stratification scores are suboptimal. Recently, a new scoring system called the Symptoms, history of Vascular disease, Electrocardiography, Age, and Troponin (SVEAT) score has been shown to outperform the History, Electrocardiography, Age, Risk factors and Troponin (HEART) score, one of the most used risk scores in the United States. AIM To assess the potential usefulness of the SVEAT score as a risk stratification tool by comparing its performance to HEART score in chest pain patients with low suspicion for acute coronary syndrome and admitted for overnight observation. METHODS We retrospectively reviewed medical records of 330 consecutive patients admitted to our clinical decision unit for acute chest pain between January 1 st to April 17 th , 2019. To avoid potential biases, investigators assigned to calculate the SVEAT, and HEART scores were blinded to the results of 30-d combined endpoint of death, acute myocardial infarction or confirmed coronary artery disease requiring revascularization or medical therapy [30-d major adverse cardiovascular event (MACE)]. An area under receiving-operator characteristic curve (AUC) for each score was then calculated. C-statistic and logistic model were used to compare predictive performance of the two scores. RESULTS A 30-d MACE was observed in 11 patients (3.33% of the subjects). The AUC of SVEAT score (0.8876, 95%CI: 0.82-0.96) was significantly higher than the AUC of HEART score (0.7962, 95%CI: 0.71-0.88), P = 0.03. Using logistic model, SVEAT score with cut-off of 4 or less significantly predicts 30-d MACE (odd ratio 1.52, 95%CI: 1.19-1.95, P = 0.001) but not the HEART score (odd ratio 1.29, 95%CI: 0.78-2.14, P = 0.32). CONCLUSION The SVEAT score is superior to the HEART score as a risk stratification tool for acute chest pain in low to intermediate risk patients.
Drug-induced thrombocytopenia is rarely associated with statin medications. We describe the case of a 69-year-old woman who developed refractory thrombocytopenia following atorvastatin use. To our knowledge, this is the fourth reported case of atorvastatin-induced thrombocytopenia and the first reported case of atorvastatin-induced refractory thrombocytopenia. Additionally, we summarize the cases of statin-induced thrombocytopenia reported in the medical literature.
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