ABSTRACT
BackgroundSince December 2019, a cluster of coronavirus disease 2019 (COVID-19) occurred in Wuhan, Hubei Province, China and spread rapidly from China to other countries. In-hospital mortality are high in severe cases and cardiac injury characterized by elevated cardiac troponin are common among them. The mechanism of cardiac injury and the relationship between cardiac injury and in-hospital mortality remained unclear. Studies focused on cardiac injury in COVID-19 patients are scarce. ObjectivesTo investigate the association between cardiac injury and in-hospital mortality of patients with confirmed or suspected COVID-19. MethodsDemographic, clinical, treatment, and laboratory data of consecutive confirmed or suspected COVID-19 patients admitted in Wuhan No.1 Hospital from 25th December, 2019 to 15th February, 2020 were extracted from electronic medical records and were retrospectively reviewed and analyzed. Univariate and multivariate Cox regression analysis were used to explore the risk factors associated with in-hospital death. ResultsA total of 110 patients with confirmed (n=80) or suspected (n=30) COVID-19 were screened and 48 patients (female 31.3%, mean age 70.58{+/-}13.38 year old) among them with high-sensitivity cardiac troponin I (hs-cTnI) test within 48 hours after admission were included, of whom 17 (17/48, 35.4%) died in hospital while 31 (31/48, 64.6%) were discharged or transferred to other hospital. High-sensitivity cardiac troponin I was elevated in 13 (13/48, 27.1%) patents. Multivariate Cox regression analysis showed pulse oximetry of oxygen saturation (SpO2) on admission (HR 0.704, 95% CI 0.546-0.909, per 1% decrease, p=0.007), elevated hs-cTnI (HR 10.902, 95% 1.279-92.927, p=0.029) and elevated d-dimer (HR 1.103, 95%CI 1.034-1.176, per 1mg/L increase, p=0.003) on admission were independently associated with in-hospital mortality. ConclusionsCardiac injury defined by hs-cTnI elevation and elevated d-dimer on admission were risk factors for in-hospital death, while higher SpO2 could be seen as a protective factor, which could help clinicians to identify patients with adverse outcome at the early stage of COVID-19.
ABSTRACT
Objective To identify predictors of prescription initiation and persistence of warfarin in non-valvular atrial fibrillation ( NVAF ) patients with high risk of stroke ( CHA2 DS2-VASc≥2 ) . Methods NVAF patients consulted in our hospital from Aug , 2011 to Apr, 2015 were enrolled.Patients who underwent radiofrequency catheter ablation were excluded . Patients were divided into two groups (warfarin group and non-warfarin group).Logistic regression was used to estimate the predictors of initiation warfarin prescription.Kaplan-Meier survival and Cox proportional hazards model was performed to determine rate of warfarin persistence and its associated factors .Results A total of 622 AF patients were enrolled and 490 patients with CHA2DS2-VASc≥2.Ten patients lost follow up and 480 patients were followed up with a mean follow-up period of ( 40.0 ±11.55 ) months.Of which 245 NVAF patients ( 51%) had a warfarin prescription.Patients with ischemic stroke ( OR 2.447 , 95%CI 1.435-4.171 , P=0.001 ) , heart failure ( OR 2.009 , 95%CI 1.084-3.724 , P=0.027 ) and persistent AF ( OR 2.231 , 95%CI 1.448-3.437 , P=0.0001 ) had a higher likelihood of warfarin prescription .Anemia ( OR 0.479 , 95%CI 0.238-0.964 , P=0.039), concommitant Traditional Chinese Medicine (TCM) use (OR 0.638, 95%CI 0.456-0.891, P=0.008 ) and longer distance to hospital ( OR 0.759 , 95%CI 0.610-0.945 , P=0.014 ) decreased the likelihood of warfarin prescription . One hundred and seventy-six ( 71.8%) warfarin users continued persistent therapy and the overall proportion of warfarin persistence was 78.3% for one year , 71.0% for 3 years.Seventy-six existing warfarin users continued the warfarin therapy (80%, 76/95),one hundred new users showed persistence to therapy ( 66.7%, 100/150 ) .Warfarin use before enrollment significantly increased warfarin persistence than new prescription ( P =0.008 ) .Variables associated with higher discontinuation were new prescription ( HR 1.786 , 95% CI 1.029-3.100 , P=0.039 ) , TCM use ( HR 1.687 , 95%CI 1.201-2.37 , P=0.003 ) and longer distance to hospital ( HR 1.446 , 95% CI 1.121-1.865, P=0.005).Conclusions In anticoagulation clinic, concommitant TCM use, distance to hospital and other factors were associated with warfarin initiation prescription and persistence .Identifying factors associated with warfarin treatment could help in developing adherence of patients .
ABSTRACT
Prolonged QT interval is usually seen on routine electrocardiogram (ECG), but in some patients it may only be seen immediately before the evolution of torsades de pointes (Tdp). To unmask the potential risk of Tdp in a patient with normal or borderline prolongation of QTc interval and recurrent syncope, dobutamine was given intravenously at a rate of 20 microg/kg/min. Strikingly, QTc prolongation was induced along with syncope after dobutamine infusion. Torsades de pointes occurred 5 d later when the patient received an implantable cardioverter defibrillator (ICD). Genetic testing revealed a mutation of the KNCQ(1)-gene encoding serine instead of glycine. The patient was treated with 75 mg of metoprolol twice daily, and at 12 mo follow-up he had no syncope or chest tightness. The ICD revealed no ventricular tachyarrhythmias or therapy delivered.
Subject(s)
Adrenergic beta-Agonists , Dobutamine , Electrocardiography , Long QT Syndrome/diagnosis , Torsades de Pointes/diagnosis , Adrenergic beta-Agonists/administration & dosage , Anti-Arrhythmia Agents/therapeutic use , DNA Mutational Analysis , Defibrillators, Implantable , Dobutamine/administration & dosage , Electric Countershock/instrumentation , Humans , Infusions, Intravenous , KCNQ1 Potassium Channel/genetics , Long QT Syndrome/complications , Long QT Syndrome/genetics , Long QT Syndrome/therapy , Male , Metoprolol/therapeutic use , Middle Aged , Mutation , Recurrence , Syncope , Torsades de Pointes/etiology , Torsades de Pointes/genetics , Torsades de Pointes/therapy , Treatment OutcomeABSTRACT
The treatment of vasovagal syncope has been by far unsatisfactory. Beta-blockers may prevent vasovagal syncope, but they exacerbates heart asystole. Cardiac pacing prevents syncope but notpresyncope. The frequent, serious vasovagal syncope attacks of a 63- year-old woman patient were completely prevented by administration of 100 mg metoprolol (b.i.d) for 3 months until the patient experienced a complete heart block. A DDD pacemaker implantation abolished syncope but not the presyncope, which was eventually prevented in a follow-up period of 24 months by adding 75 mg atenalol twice a day. This case suggests a different mechanism involved in vasovagal syncope.