cardiology2016 231-240
cardiology2016 151-160
Correct answer:D The drug described is representative of a class 1 antiarrhythmic medication. These drugs preferentially bind to and block activated and inactivated voltage-gated sodium channels in cardiac pacemaker cells and myocytes. Dissociation of the drug from the channel occurs during the resting state, a conformational state distinct from the inactivated state that occurs following repolarization. Class 1 antiarrhythmics exhibit use dependence, a phenomenon in which tissues undergoing frequent depolarization become more susceptible to blockage. Use dependence occurs because the sodium channels in rapidly depolarizing tissue spend more time in the activated and inactivated states, thus allowing more binding time for the drug. For class 1 antiarrhythmics. sodium-channel-binding strength is 1C > 1A > 1B. Use dependence is more pronounced in class 1C antiarrhythmics because of their slow dissociation from the sodium channel, which allows their blocking effects to accumulate over multiple cardiac cycles. This effect is enhanced with tachycardia, and the resulting increase in sodium channel blockade helps to slow conduction speed and terminate tachyarrhythmias. The prominent use dependence effects of class 1C drugs can cause a delay in conduction speed that is out of proportion to prolongation of the refractory period. This can promote arrhythmias, especially in patients with ischemic or structural heart disease. Class 1B antiarrhythmics (eg, lidocaine, mexiletine, and tocainide) bind less avidly to sodium channels than the other class 1 antiarrhythmics (Choice D). Dissociation from the channels occurs so rapidly that there is minimal cumulative effect over multiple cardiac cycles, resulting in little use dependence. These drugs are more selective for ischemic myocardium because the reduced resting membrane potential delays sodium channel transition from the inactivated to the resting state, resulting in increased drug-channel binding. Class 1B antiarrhythmics are useful for treating ischemia-induced ventricular arrhythmias, one of the most common causes of death in the short term following acute myocardial infarction. (Choice A) Amiodarone is classified primarily as a class 3 antiarrhythmic medication although it has small class 1, 2? and 4 effects as well. The class 3 antiarrhythmics act by blocking potassium channels and prolonging phase 3 repolarization. (Choice B) Disopyramide, quinidine, and procainamide are class 1A antiarrhythmic dmgs. They are represented by line 2 on the graph because of their intermediate dissociation speed. (Choice C) Propafenone and flecainide are class 1C antiarrhythmic drugs. They are represented by line 3 on the graph because of their slow dissociation speed. (Choice E) Propranolol (a nonselective (3-adrenergic blocker) is categorized as a class 2 antiarrhythmic drug. It causes decreased chronotropy and inotropy via (31 blockade. (Choice F) Verapamil as a calcium channel blocker is classified as a class IV antiarrhythmic drug; diltiazem is another drug in this class. Although nifedipine is a calcium channel blocker as well, it is selective for vascular smooth muscle and does not have a notable effect on the heart. Educational objective: Use dependence describes the phenomenon in which higher rates of depolarization lead to increased sodium channel blockade due to the channels spending less time in the resting state. For class 1 antiarrhythmics, sodium-channel-binding strength is 1C>1A>1B. Class 1C antiarrhythmics demonstrate the most use dependence, and class 1B drugs have the least
cardiology-医学英语
Diagnostic, Symptomatic, and Terms
Term Meaning
hemostasis
arrest of bleeding or circulation
hyperlipidemia
excessive amounts of lipids(cholesterol, phospolipids, and triglycerides)in the blood Condition that is present when, on several separate occasions, blood pressure registers higher than normal
Combining Forms
Combining form atri/o cardi/o hemangi/o phleb/o ven/o thromb/o sphygm/o Meaning atrium heart blood vessel vein vein blood clot pulse Example atri/o/tome cardi/o/megaly hemangi/oma phleb/o/tomy ven/ous thromb/o/lysis sphygm/o/meter
Diagnostic, Symptomatic, and Terms
Term Meaning
embolus,emboli
mass of undissolved matter(foreign object,air, gas, tissue, thrombus)circulating in a blood or lymphatic channels until it becomes lodged in a vessel outside a vessel
cardiology2016 71-80
Q2
A 35-year-old previously healthy man is brought to the emergency department after being involved in a motor vehicle accident He has significant blunt chest and head trauma. Shortly after he arrives, his blood pressure drops suddenly and he begins experiencing respiratory distress. On physical examination, the patient is tachycardic and tachypneic. His lungs are clear to auscultation with vesicular breath sounds heard bilaterally. He has jugular venous distention, and his systolic blood pressure falls 15 mm Hg with inspiration. Which of the following is the most likely cause of this patient's deterioration? A. Tension pneumothorax B. Epidural hematoma C. Hemothorax D. Aortic rupture E. Cardiac tamponade
Q1
Correct answer:G The cause of death was most likely an acute myocardial infarction. In myocardial infarction, changes on light microscopy are usually not apparent until 4 hours after the onset of severe ischemia. Although a variable waviness of myofibrils at the border of the infarct (due to myofibril relaxation) might be observed before this, more definite signs of early coagulative necrosis, such as cytoplasmic eosinophilia and nuclear pyknosis, take at least 4 hours to develop. Other potentially lethal causes of chest pain, diaphoresis, and palpitations/tachycardia include aortic dissection and/or rupture, massive pulmonary embolism, and tension pneumothorax. The chest pain of aortic dissection is typically tearing in nature and often radiates to the back. Dyspnea is typically the most prominent symptom in the event of a pulmonary embolus or tension pneumothorax. (Choices A & B) Cytoplasmic hypereosinophilia on light microscopy is one of the earliest signs of coagulative necrosis of cardiac myocytes. It begins approximately 4 hours after the onset of lethal ischemia. Light microscopy may also reveal edema and punctate hemorrhages in infarcted myocardium starting also at about 4 hours after the ischemic event. (Choice C) An interstitial infiltrate of neutrophils around a zone of myocardial infarction is not seen until 1 to 3 days after the onset of severe ischemia. (Choice D) Extensive macrophage phagocytosis of the dead cells generally does not develop until at least 5 days after myocardial infarction, and is most prominent during post-infarction days 7 to 10. (Choice E) Fibrovascular granulation tissue with neovascularization generally begins to develop 7 days after myocardial infarction, and is most prominent on post-infarction days 10 to 14. (Choice F) Increased collagen deposition and decreased cellularity in a zone of infarcted myocardium is not generally evident until 2 weeks post-infarction. Fibrosis continues during weeks 2 to 8, producing a dense collagenous scar by two months post-infarction.
达格列净联合贝前列素钠治疗2_型糖尿病周围神经病变患者的效果及有效率评价
DOI：10.16658/ki.1672-4062.2024.04.183达格列净联合贝前列素钠治疗2型糖尿病周围神经病变患者的效果及有效率评价沈灿芳1，林莞蓉2，杨荣思1，王志伟11.石狮市总医院神经外科，福建石狮362700；2.石狮市总医院内分泌科，福建石狮362700[摘要]目的探究达格列净联合贝前列素钠治疗2型糖尿病周围神经病变患者的效果及有效率。
方法选取2021年9月—2023年10月石狮市总医院收治的2型糖尿病周围神经病变患者88例进行研究，经抽签法分组，对照组（44例）应用贝前列素钠治疗，观察组（44例）应用达格列净、贝前列素钠治疗，对比两组血糖、传导速度、临床疗效及不良反应。
结果用药4周后，观察组各项血糖水平均低于对照组，各项神经传导速度高于对照组，临床治疗有效率高于对照组，差异有统计学意义（P均<0.05）。
两组不良反应发生率比较，差异无统计学意义（P>0.05）。
结论达格列净、贝前列素钠联用可有效治疗2型糖尿病周围神经病变，血糖显著下降，神经传导速度明显加快，不良反应减少。
[关键词] 2型糖尿病周围神经病变；达格列净；贝前列素钠；血糖；有效率；不良反应[中图分类号] R4 [文献标识码] A [文章编号] 1672-4062（2024）02（b）-0183-04Evaluation of the Effectiveness and Efficacy of Dapagliflozin Combined with Beraprost Sodium in the Treatment of Patients with Peripheral Neu⁃ropathy in Type 2 Diabetes MellitusSHEN Canfang1, LIN Guanrong2, YANG Rongsi1, WANG Zhiwei11.Department of Neurosurgery, Shishi General Hospital, Shishi, Fujian Province, 362700 China;2.Department of Endo⁃crinology, Shishi General Hospital, Shishi, Fujian Province, 362700 China[Abstract] Objective To investigate the effect and efficiency of dapagliflozin combined with beraprost sodium in the treatment of patients with peripheral neuropathy in type 2 diabetes mellitus. Methods A total of 88 patients with type 2 diabetic peripheral neuropathy from Shishi General Hospital from September 2021 to October 2023 were selected for this study. They were divided by lot method. The control group (44 cases) was treated with beprost sodium, while the observation group (44 cases) was treated with dagaglizin and beprost sodium, and the blood glucose, conduction speed, clinical efficacy and adverse reactions of the two groups were compared. Results After 4 weeks of treatment, all blood glucose levels in the observation group were lower than those in the control group, all nerve conduction veloci⁃ties were higher than those in the control group, and the clinical treatment effectiveness was higher than that in the control group, the difference was statistically significant (all P<0.05). There was no statistically significant difference in the incidence of adverse reactions between the two groups (P>0.05). Conclusion Dapagliflozin and beraprost so⁃dium combination can effectively treat type 2 diabetic peripheral neuropathy, with a significant decrease in blood glu⁃cose, significantly accelerated nerve conduction velocity, with fewer adverse reactions.[Key words] Type 2 diabetes mellitus peripheral neuropathy; Dapagliflozin; Beraprost sodium; Blood glucose; Effec⁃tive rate; Adverse reaction[作者简介]沈灿芳（1988-），男，硕士，主治医师，研究方向为神经外科。
cardiology2016 61-70
A 62-year-old Caucasian female hospitalized with acute myocardial infarction dies suddenly on day four of her hospitalization. Findings at autopsy are pictured below (RV = right ventricle, LAD = left anterior descending coronary artery): Which of the following statements best describes the condition that caused this patient's death? A. It is the most common cause of death in patients hospitalized with 一 myocardial infarction B. It typically occurs 3 to 7 days after the onset of myocardial infarction C. It is a frequent complication of fibrinolytic therapy D. It is more common in patients with repetitive myocardial infarction E. Patients with left ventricular hypertrophy are especially susceptible
A2
Correct answer:E Headaches and epistaxis may be caused by hypertension in the arteries supplying the head and neck. Lower extremity muscle weakness or fatigue with exercise may be caused by inadequate lower body perfusion. In adult-type aortic coarctation, the stenosis is post-ductal (in contrast to the infantile form, where the coarctation is generally preductal and fatal soon after birth without surgical repair). Adult-type aortic coarctation can produce hypertension in the upper aortic circulation and simultaneously low perfusion in the distal aorta supplying the legs. The likelihood of an adult-type, postductal coarctation in this patient is greatly increased by the finding of enlarged, palpable intercostal vessels, which indicate the development of a collateral arterial circulation to the region of the aorta distal to the coarctation. On radiographic exam, patients with adult-type aortic coarctation often have notching of the ribs as a result of the enlarged, tortuous intercostal arteries. (Choice D) The initial left-to-right t of an isolated patent ductus arteriosus generally does not result in poor exercise tolerance until the persistent pulmonary hypertension causes pulmonary vascular sclerosis and shunt flow reversal (Eisenmenger syndrome). One would not expect to find epistaxis or enlarged intercostal arteries in these patients. (Choice F) Tetralogy of Fallot could decrease exercise tolerance via increased right-to-left shunting and hypoxemia in response to vasodilation in active skeletal muscles. However, one would not expect epistaxis or enlarged intercostal arteries in these patients. Educational Objective: The adult (postductal) type of congenital aortic coarctation can present with symptoms/signs of hypertension in the arterial tree proximal to the coarctation, and of hypoperfusion of the lower extremities, especially during ambulation. Collateral circulation to the distal aorta results in dilated intercostal arteries. The triad of upper body hypertension, diminished lower extremity pulses, and enlarged intercostal artery collaterals is typical of adult-type coarctation and is not seen in other congenital cardiovascular malformations.
专家共识声明：优化植入式心律转复除颤器的编程和测试
2015 HRS/EHRA/APHRS/SOLAECE Expert Consensus Statement on Optimal Implantable Cardioverter-Defibrillator Programming and TestingDeveloped in partnership with and endorsed by the European Heart Rhythm Association (EHRA), the Asia Pacific Heart Rhythm Society (APHRS), and the Sociedad Latinoamericana de Estimulacion Cardiaca y Electrofisiologia (SOLAECE)-Latin American Society of Cardiac Pacing and Electrophysiology. Endorsed by the American College of Cardiology (ACC) and American Heart Association (AHA).Bruce L. Wilkoff, MD, FHRS, CCDS (Chair)1; Laurent Fauchier, MD, PhD (co-Chair)2*; Martin K. Stiles, MBCHB, PhD (co-Chair)3‡; Carlos A. Morillo, MD, FRCPC, FHRS (co-Chair)4†; Sana M. Al-Khatib, MD, MHSc, FHRS, CCDS5; Jesús Almendral, MD, PhD, FESC6*; Luis Aguinaga, MD, PhD, FACC, FESC7†; Ronald D. Berger, MD, PhD, FHRS8; Alejandro Cuesta, MD, PhD, FESC9†; James P. Daubert, MD, FHRS5; Sergio Dubner, MD, FACC10†; Kenneth A. Ellenbogen, MD, FHRS11; N.A. Mark Estes III, MD12§;Guilherme Fenelon, MD, PhD13†; Fermin C. Garcia, MD14†; Maurizio Gasparini, MD15*; David E. Haines, MD, FHRS16; Jeff S. Healey, MD, MSc, FRCPC, FHRS4; Jodie L. Hurtwitz, MD17††; Roberto Keegan, MD18†; Christof Kolb, MD19*; Karl-Heinz Kuck, MD, FHRS20*; Germanas Marinskis, MD, FESC21*; Martino Martinelli, MD, PhD22; Mark McGuire, MBBS, PhD23‡; Luis G. Molina, MD, DSc24†; Ken Okumura, MD, PhD25‡; Alessandro Proclemer, MD26*; Andrea M. Russo, MD, FHRS27; Jagmeet P. Singh, MD, DPhil, FHRS28; Charles D. Swerdlow, MD, FHRS29; Wee Siong Teo, MBBS, FHRS30‡; William Uribe, MD, FHRS31†; Sami Viskin, MD32*; Chun-Chieh Wang, MD33‡; Shu Zhang, MD34‡Document Reviewers: Giuseppe Boriani, MD, PhD (Italy); Michele Brignole, MD, FESC (Italy); Alan Cheng, MD, FHRS (USA); Thomas C. Crawford, MD, FACC, FHRS (USA); Luigi Di Biase, MD, PhD, FACC, FHRS (USA); Kevin Donahue, MD (USA); Andrew E. Epstein, MD, FAHA, FACC, FHRS (USA); Michael E. Field, MD, FACC, FHRS (USA); Bulent Gorenek, MD, FACC, FESC (Turkey); Jin-Long Huang, MD, PhD (China); Julia H. Indik, MD, PhD, FACC, FAHA, FHRS (USA); Carsten W. Israel, MD (Germany); Mariell L. Jessup MD, FACC, FAHA, FESC (USA); Christophe Leclercq, MD, PhD (France); Robert J. MacFadyen, MD, PhD (UK); Christopher Madias, MD, FHRS (USA); Manlio F. Marquez, MD, FACC (Mexico); Brian Olshansky, MD, FACC, FAHA, FHRS (USA); Kristen K. Patton, MD (USA); Marwan M. Refaat, MD, mMBA, FACC, FAHA, FHRS, FASE, FESC, FACP, FAAMA (USA); Cynthia M. Tracy, MD, FACC, FAHA (USA); Gaurav A. Upadhyay, MD (USA); Diego Vanegas, MD, FHRS (Colombia); Paul J. Wang, MD, FHRS, CCDS (USA)Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@From 1Cleveland Clinic, Cleveland, Ohio; 2Centre Hospitalier Universitaire Trousseau, Tours, France;3Waikato Hospital, Hamilton, New Zealand; 4Department of Medicine, Cardiology Division, McMaster University-Population Health Research Institute, Hamilton, Canada; 5Duke University Medical Center, Durham, North Carolina; 6Grupo HM Hospitales, Universidad CEU San Pablo, Madrid, Spain; 7Centro Privado De Cardiologia, Tucuman, Argentina; 8Johns Hopkins University, Baltimore, Maryland; 9Servicio de Arritmias, Instituto de Cardiologia Infantil, Montevideo, Uruguay; 10Clinica y Maternidad Suizo Argentina and De Los Arcos Sanatorio, Buenos Aires, Argentina; 11Virginia Commonwealth University Medical Center, Richmond, VA; 12New England Medical Center, Boston, Massachusetts; 13Federal University of São Paulo, São Paulo, Brazil; 14Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania; 15Humanitas Research Hospital, Milan, Italy; 16William Beaumont Hospital Division of Cardiology, Royal Oak, Michigan; 17North Texas Heart Center, Dallas, Texas; 18Hospital Privado del Sur, Bahia Blanca, Argentina; 19Deutsches Herzzentrum Munchen, Munich, Germany; 20Allgemeines Krankenhaus St. Georg, Hamburg, Germany; 21Vilnius University, Clinic of Cardiac and Vascular Diseases, Lithuania; 22Instituto do Coração, Universidade de São Paulo, São Paulo, Brazil; 23Royal Prince Alfred Hospital, Sydney, Australia; 24Mexico’s National University, Mexico’s General Hospital, Mexico City, Mexico; 25Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan; 26Azienda Ospedaliero Universitaria S. Maria della Misericordia – Udine, Udine, Italy; 27Cooper University Hospital, Camden, New Jersey; 28Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; 29Cedars-Sinai Medical Center, Beverly Hills, California; 30National Heart Centre Singapore, Singapore, Singapore; 31CES Cardiología and Centros Especializados San Vicente Fundación, Medellín y Rionegro, Colombia; 32Tel Aviv Sourasky Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; 33Chang Gung Memorial Hospital, Taipei, Taiwan; 34National Center for Cardiovascular Disease and Beijing Fu Wai Hospital, Peking Union Medical College and China Academy of Medical Sciences, Beijing, China* Representative of the European Heart Rhythm Association (EHRA)§ Representative of the American Heart Association (AHA)†Representative of the Sociedad Latinoamericana de Estimulacion Cardiaca y Electrofisiologia (SOLAECE) ‡ Representative of the Asia-Pacific Heart Rhythm Society (APHRS)††Representative of the American College of Cardiology (ACC)Keywords: Implantable cardioverter-defibrillator, Bradycardia mode and rate, Tachycardia detection, Tachycardia therapy, Defibrillation Testing, Programming.Abbreviations: ICD=Implantable Cardioverter-Defibrillator, DT=Defibrillation Testing, LV=Left Ventricular, RV=Right Ventricular, LVEF=Left Ventricular Ejection Fraction, RCT=Randomized Clinical Trial, CRT=Cardiac Resynchronization Therapy, CRT-D=Cardiac Resynchronization Therapy Defibrillator, ATP= Antitachycardia Pacing, SVT=Supraventricular Tachycardia, VT=Ventricular Tachycardia, EGM= Electrogram, AF=Atrial Fibrillation, S-ICD=Subcutaneous Implantable Cardioverter Defibrillator, PVC= Premature Ventricular Contraction, NYHA=New York Heart Association, NCDR=National Cardiovascular Data Registry.IntroductionImplantable cardioverter-defibrillator (ICD) therapy is clearly an effective therapy for selected patients in definable populations. The benefits and risks of ICD therapy are directly impacted by programming and surgical decisions. This flexibility is both a great strength and a weakness, for which there has been no prior official discussion or guidance. It is the consensus of the 4 continental electrophysiology societies that there are 4 important clinical issues for which there are sufficient ICD clinical and trial data to provide evidence-based expert guidance. This document systematically describes the greater than 80% (83%-100%, mean: 96%) required consensus achieved for each recommendation by official balloting in regard to the programming of (1) bradycardia mode and rate, (2) tachycardia detection, (3) tachycardia therapy, and (4) the intraprocedural testing of defibrillation efficacy. Representatives nominated by the Heart Rhythm Society (HRS), European Heart Rhythm Association (EHRA), Asian Pacific Heart Rhythm Society (APHRS) and the Sociedad Latinoamericana de Estimulacion Cardiaca y Electrofisiologia (SOLAECE-Latin American Society of Cardiac Pacing and Electrophysiology) participated in the project definition, the literature review, the recommendation development, the writing of the document, and its approval. The 32 recommendations were balloted by the 35 writing committee members and were approved by an average of 96%.The classification of the recommendations and the level of evidence follow the recently updated ACC/AHA standard.1,2Class I is a strong recommendation, denoting a benefit greatly exceeding risk. Class IIa is a somewhat weaker recommendation, with a benefit probably exceeding risk, and Class IIb denotes a benefit equivalent to or possibly exceeding risk. Class III is a recommendation against aspecific treatment because there is either no net benefit or there is net harm. Level of Evidence A denotes the highest level of evidence from more than 1 high-quality randomized clinical trial (RCT), a meta-analysis of high quality RCTs, or RCTs corroborated by high-quality registry studies. Level of evidence B indicates moderate-quality evidence from either RCTs with a meta-analysis (B-R) or well-executed nonrandomized trials with a meta-analysis (B-NR). Level of evidence C indicates randomized or nonrandomized observational or registry studies with limited data (C-LD) or from expert opinions (C-EO) based on clinical experience in the absence of credible published evidence. These recommendations were also subject to a 1-month public comment period. Each society then officially reviewed, commented, edited, and endorsed the final document and recommendations. All author and peer reviewer disclosure information is provided in Appendix A.The care of individual patients must be provided in context of their specific clinical condition and the data available on that patient. Although the recommendations in this document provide guidance for a strategic approach to ICD programming, as an individual patient’s condition changes or progresses and additional clinical considerations become apparent, the programming of their ICDs must reflect those changes. Remote and in-person interrogations of the ICD and clinical monitoring must continue to inform the programming choices made for each patient. The recommendations in this document specifically target adult patients and might not be applicable to pediatric patients, particularly when programming rate criteria.Please consider that each ICD has specific programmable options that might not be specifically addressed by the 32 distinctive recommendations in this document. Appendix B, published online (/appendix-b), contains the writing committee’s translations specific to each manufacturer and is intended to best approximate the recommended behaviors for each available ICD model.Bradycardia Mode and Rate ProgrammingSingle- or Dual-Chamber Pacing ModeEvidence: Because the ICD is primarily indicated for tachycardia therapy, there might be some uncertainty regarding optimal bradycardia management for ICD patients. Data from clinical studies adequately address only the programmed mode rather than the number of leads implanted, the number of chambers stimulated, or how frequently the patients required bradycardia support. It is of note that most information on pacing modes has been collected from pacemaker patients, and these patients are clinically distinct from ICD recipients. Dual-chamber pacing (atrial and ventricular) has been compared with single-chamber pacing (atrial or ventricular) in patients with bradycardia in 5 multi-center, parallel, randomized trials, in 1 meta-analysis of randomized trials, and in 1 systematic review that also included 30 randomized crossover comparisons and 4 economic analyses.3-9Meta analyses comparing dual-chamber to single-chamber ICDs did not evaluate pacing modes.10,11Compared with single-chamber pacing, dual chamber pacing results in small but potentially significant benefits in patients with sinus node disease and/or atrioventricular block. No difference in mortality has been observed between ventricular pacing modes and dual-chamber pacing modes. Dual-chamber pacing was associated with a lower rate of atrial fibrillation (AF) and stroke.12 The benefit in terms of AF prevention was more marked in trials comprised of patients with sinus node disease. Although trends in favor of dual-chamber pacing have been observed in some trials, there was no benefit in terms of heart failure (HF). In patients without symptomatic bradycardia, however, the Dual Chamber and VVI Implantable Defibrillator (DAVID) trial in ICD recipients showed that one specific choice of dual-chamber rate-responsive (DDDR) programming parameters led to poorer outcomes than VVI backup pacing, most likely secondary to unnecessary right ventricular (RV) pacing. The fact that RV stimulation was responsible was reinforced in the DAVID II trial, in which AAI pacing was demonstrated to be noninferior to VVI backup pacing.13Approximately a quarter of patients with either sinus node disease or atrioventricular block develop “pacemaker syndrome” with VVI pacing usually associated with retrograde (ventricular to atrial) conduction, which in turn is associated with a reduction in the quality of life.14In crossover trials, symptoms of pacemaker syndrome (dyspnea, dizziness, palpitations, pulsations, and chest pain) were reduced by reprogramming to a dual-chamber mode.14 Dual-chamber pacing is associated with better exercise performance compared with single-chamber VVI pacing without rate adaptation, but produces similar exercise performance when compared with rate-responsive VVIR pacing. Because of the additional lead, dual-chamber devices involve longer implantation times, have a higher risk ofcomplications, and are more expensive. However, because of the additional clinical consequences of pacemaker syndrome and AF (and its sequelae), the overall cost difference between single- and dual-pacing systems is moderated.In patients with persistent sinus bradycardia, atrial rather than ventricular dual-chamber pacing is the pacing mode of choice. There is evidence for superiority of atrial-based pacing over ventricular pacing for patients who require pacing for a significant proportion of the day. The evidence is stronger for patients with sinus node disease, in whom dual-chamber pacing confers a modest reduction in AF and stroke, but not in hospitalization for HF or death compared with ventricular pacing. In patients with acquired atrioventricular block, large randomized parallel trials were unable to demonstrate the superiority of dual-chamber pacing over ventricular pacing with regard to hard clinical endpoints of mortality and morbidity.4,6-8 The benefit of dual-chamber over ventricular pacing is primarily due to the avoidance of pacemaker syndrome and to improved exercise capacity.14 Even if it is a softer endpoint, pacemaker syndrome is associated with a reduction in quality of life that justifies the preference for dual-chamber pacing when reasonable; thus, there is strong evidence for the superiority of dual-chamber pacing over ventricular pacing that is limited to symptom improvement. Conversely, there is strong evidence of nonsuperiority with regard to survival and morbidity. The net result is that the indications for programming the dual-chamber modes are weaker and the choice regarding the pacing mode should be individualized, taking into consideration the increased complication risk and costs of dual-chamber devices. Because ICD patients usually do not require bradycardia support, with the exception of patients who require cardiac resynchronization, programming choices should avoid pacing and in particular avoid single ventricular pacing, if possible.15,16Programming of Rate ModulationThe benefit of rate response programming has been evaluated in patients with bradycardia in 5 multi-center, randomized trials and in 1 systematic review that also included 7 single-center studies.17-22 Most of these data were obtained from pacemaker studies and must be interpreted in that light.Although there is evidence of the superiority of VVIR pacing compared with VVI pacing in improving quality of life and exercise capacity, improvements in exercise capacity with DDDR compared with DDD have been inconsistent. In 2 small studies on patients with chronotropic incompetence comparing DDD and DDDR pacing, the latter had improved quality of life and exercise capacity; however, a larger, multicenter randomized trial (Advanced Elements of Pacing Randomized Controlled Trial [ADEPT]) failedto show a difference in patients with a modest blunted heart rate response to exercise.17-19 In addition, DDDR programming in CRT patients has the potential to impair AV synchrony and timing. It should be noted that trials evaluating CRT generally did not use rate responsive pacing, and many in fact avoided atrial stimulation using atrial sensed and ventricular paced pacing modes with a lower base rate. However, the Pacing Evaluation-Atrial Support Study in Cardiac Resynchronization Therapy (PEGASUS CRT) trial is the exception and did not demonstrate adverse impact on mortality and HF events.23Sinus Node DiseaseIn patients with persistent or intermittent sinus node dysfunction or chronotropic incompetence, the first choice is DDDR with algorithms responding to intermittent atrioventricular conduction. There is sufficient evidence for the superiority of VVIR compared with VVI in improving quality of life and exercise capacity. The evidence is much weaker in dual-chamber pacing (DDDR vs DDD).Although only an issue when there is some concomitant AV block, the upper rate limit should be programmed higher than the fastest spontaneous sinus rhythm to avoid upper rate limit behavior. To avoid symptomatic bradycardia, the lower rate should be programmed on an individual basis, according to the clinical characteristics and the underlying cardiac substrate of the patient.Atrial Fibrillation and Atrioventricular BlockPatients with permanent atrial fibrillation and either spontaneous or AV junctional ablation-induced high-degree atrioventricular block have little to no chronotropic response to exercise, thus VVIR pacing is associated with better exercise performance, improved daily activities, improved quality of life, and decreased symptoms of shortness of breath, chest pain, and heart palpitations, compared with VVI.20-22,24-26 Therefore, rate-adaptive pacing is the first choice of pacing mode; fixed-rate VVI pacing should be abandoned in patients with permanent AF and atrioventricular block. It is the experts’ opinion that the minimum rate can be programmed higher (e.g., 70 bpm) than for sinus rhythm patients, in an attempt to compensate for the loss of active atrial filling. In addition, the maximum sensor rate should be programmed restrictively (e.g., 110–120 bpm) to avoid “overpacing” (i.e. pacing with a heart rate faster than necessary), which can be symptomatic, particularly in patients with coronary artery disease. In a small study, however, it was found that rate-responsive pacing could be safe and effective in patients with angina pectoris, without an increase in subjective or objective signs of ischemia.25 The lower rateshould be programmed on an individual basis, according to the clinical characteristics and the underlying cardiac substrate of the patient. The clinical benefit of programming a lower resting rate at night based on internal clocks has not been evaluated in ICD patients. There is some concern that atrioventricular junction ablation and permanent ventricular pacing might predispose the patient to an increased risk of sudden cardiac death related to a bradycardia-dependent prolongation of the QT interval. This risk might be overcome by setting the ventricular pacing rate to a minimum of 80 or 90 bpm for the first 1–2 months following the atrioventricular junction ablation, then reducing it to a conventional 60–70 bpm.27,28Not all patients with AF and milder forms of atrioventricular block will require a high percentage of ventricular pacing or have a wide QRS. Physicians should consider the risk of increasing pre-existing left ventricular dysfunction with RV pacing versus improved chronotropic responsiveness and the potential value of cardiac resynchronization therapy.Intact Atrioventricular ConductionRight-Ventricular PacingThe results of a number of large-scale, prospective randomized trials demonstrated a significant reduction in AF in pacemaker patients with atrial-based pacing (AAI or DDD) compared with patients with ventricular-based pacing.4,8,29 In the Mode Selection Trial, which enrolled 2010 patients with sick sinus syndrome, the risk of AF increased linearly with the increasing percentage of RV pacing.30 At the same time, deleterious effects of right ventricular (RV) pacing in patients with left ventricular (LV) dysfunction (LVEF ≤40%) implanted with dual-chamber ICD systems were observed in the Dual Chamber and VVI Implantable Defibrillator (DAVID) trial, which included 506 ICD patients without indications for bradycardia pacing. Patients within the DDDR-70 group (with paced and sensed atrioventricular delays of 170 and 150 ms, respectively, in most of the DDDR group patients) showed a trend toward higher mortality and an increased incidence of HF compared with the patients programmed to ventricular backup pacing—the VVI-40 group. Within the DDDR-70 group, there were more cardiac events when the percentage of ventricular pacing exceeded 40% (P= .09) compared with patients with <40% of RV pacing, although almost all the patients had >95% RV stimulation (DDDR-70) or <5% RV stimulation (VVI-40).31,32However, a more detailed post-hoc analysis of the Inhibition of Unnecessary RV Pacing With Atrial-Ventricular Search Hysteresis in ICDs (INTRINSIC RV) trial revealed that the most favorable clinical results were not in the VVI groups with the least percentage of RV pacing, but in the subgroup that hadDDD pacing with longer atrioventricular delays and 11%–19% of ventricular pacing. This parameter selection probably helped patients to avoid exceedingly low heart rates while preserving intrinsic atrioventricular conduction most of the time.31,33In the Second Multicenter Automated Defibrillator Implantation Trial (MADIT II), a higher risk of HF was observed in patients who had a greater than 50% burden of RV pacing.34 In another large observational study of 456 ICD patients without HF at baseline, a high RV pacing burden (RV pacing more than 50% of the time) was associated with an increased risk of HF events and appropriate ICD shocks.35 Optimally, right ventricular stimulation should be avoided but the precise tradeoff between the percentage of ventricular pacing and atrioventricular timing is unclear in non-CRT patients.Non-CRT Devices: Algorithms to Reduce Right Ventricular StimulationThe importance of reducing or avoiding right ventricular pacing in ICD patients with left ventricular dysfunction was illustrated in the DAVID trial.31 The feasibility of algorithms designed to decrease the burden of unnecessary ventricular pacing has been demonstrated in patients with dual-chamber pacemakers.36-38These algorithms usually provide functional AAI pacing with monitoring of atrioventricular conduction and an automatic mode switch from AAI to DDD during episodes of atrioventricular block. Some studies directly compared various algorithms to decrease ventricular pacing, showing that a “managed ventricular pacing” (MVP) algorithm result ed in greater ventricular pacing reduction than an “atrioventricular s earch” algorithm;39,40however, no randomized studies comparing these two algorithms with respect to important cardiovascular endpoints (e.g., HF, cardiac death) have been performed. The results of the studies on these pacing algorithms are summarized in Table 1.Table 1. Influence of pacing modes and algorithms on clinical endpoints.AT=atrial tachycardia, PM=pacemaker, HF=heart failure, MVP=Managed Ventricular PacingUnnecessary RV pacing should be minimized by using specific algorithms or programming longer atrioventricular delays, and this process is more important for patients with a higher risk of AF or who already have poorer LV function.49Patients with longer baseline PR intervals have a higher risk of AF regardless of the percentage of ventricular pacing or the length of the programmed atrioventricular interval.50 Use of the AAIR pacing mode with exceedingly long atrioventricular conduction times can lead t o “AAIR pacemaker syndrome” and actually increases the risk of AF compared with the DDDR mode, as was shown in the Danish Multicenter Randomized Trial on Single Lead Atrial versus Dual-Chamber Pacing in Sick Sinus Syndrome (DANPACE).3,51Therefore, excessively long atrioventricular delays resulting in non-physiologic atrioventricular contraction patterns should be avoided. The potential harm of atrial pacing with a prolonged atrioventricular delay was also demonstrated in the MVP trial. In the MVP trial, dual-chamber pacing with the MVP algorithm was not superior to ventricular backup pacing (VVI 40 bpm) with respect to HF events. After a follow-up of 2.4 years, there was an apparent increase in HF events that was limited primarily to patients with a baseline PR interval of >230 ms (mean PR of 255 to 260 ms).42Long atrioventricular intervals also predispose the patient to repetitive atrioventricular reentrant rhythms, “repetitive nonreentrant VA synchrony,” or “atrioventricular desynchronization arrhythmia,” which manifest as mode switching but which also cause sustained episodes with poor hemodynamics.52 Thus, based on the available data, it appears that atrial pacing with excessively long atrioventricular delays should be avoided.Algorithms that minimize ventricular pacing sometimes lead to inadvertent bradycardia or spontaneous premature, beat-related short-long-short RR interval sequences with proarrhythmic potential.53-55 However, in a study retrospectively analyzing the onset of ventricular tachycardia (VT) in ICD patients, the MVP mode was less frequently associated with the onset of VT compared with the DDD and VVI modes.54 Atrioventricular decoupling (greater than 40% of atrioventricular intervals exceeding 300 ms) was observed in 14% of the ICD patients in the Marquis ICD MVP study, which might have a negative effect on ventricular filling.56In ICD patients with structural heart disease, spontaneous atrioventricular conduction can become prolonged instead of shortening, with increased atrial paced heart rates.33This outcome frequently leads to a higher percentage of ventricular paced complexes. In view of the results of the ADEPT trial, which failed to demonstrate the clinical superiority of combined rate modulation and DDD pacing, the need for and aggressiveness of sensor-driven rate responses should be individualized or eliminated.19Rate-dependent shortening of atrioventricular delay could have the same effect and should usually be avoided.Patients with hypertrophic cardiomyopathy represent a small but intricate subset of the ICD population for whom pacing has not been demonstrated to be a consistently effective treatment for outflow tract obstruction. However, according to the 2011 ACCF/AHA Hypertrophic Cardiomyopathy Guideline, dual-chamber ICDs are reasonable for patients with resting LV outflow tract gradients more than 50 mm Hg, and who have indications for ICD implantation to reduce mortality.57 In these patients, atrioventricular delays should be individually programmed to be short enough to achieve RV pre-excitation and decrease LV outflow tract gradient, but not too short, which would impair LV filling; usually in the ranges of 60–150 ms.58,59There are few studies of pacing modes in these patients, and they are limited by small numbers and the failure to quantify important cardiac outcomes.In conclusion, atrioventricular interval programming and choosing between DDDR and MVP or other atrioventricular interval management modes should be performed on an individual basis. The goal is to minimize the percentage of RV pacing and to avoid atrial-based pacing with atrioventricular intervals exceeding 250–300 ms leading to atrioventricular uncoupling. In patients with prolonged PR intervals and impaired LV function, biventricular pacing can be considered.Cardiac Resynchronization Therapy: Consistent Delivery of Ventricular PacingCardiac resynchronization therapy in combination with a defibrillator device (CRT-D) improves survival and cardiac function in patients with LV systolic dysfunction, prolonged QRS duration, and mild-to-severe HF.60-62 The beneficial effect of CRT-D compared with ICD is likely to be derived from biventricular pacing, with a decrease in dyssynchrony and an improvement in cardiac function. The percentage of biventricular pacing capture in the ventricles can be negatively influenced by a number of factors, including atrial tachyarrhythmias, premature ventricular complexes, and programming of the atrioventricular delay, giving way to the intrinsic conduction of the patient and a reduced percentage of biventricular pacing. Some large observational studies have investigated the optimal level of biventricular pacing percentage and found a higher percentage to be associated with more pronounced CRT benefits. An optimal CRT benefit was observed with a biventricular pacing percentage as close to 100% as possible.63-66In the analysis of the LBBB population in the MADIT-CRT trial, those patients with less than 90% biventricular pacing had similar rates of HF and death compared with the patients randomized to no。
维生素D缺乏与女性生殖关系的研究进展
维生素D缺乏与女性生殖关系的研究进展楚琪;郑连文;马亚兰;李丹;徐影【摘要】维生素D在体内不止作为维生素,也可以作为激素发挥作用.它是一种可以调节钙磷代谢的固醇类衍生物,在心血管疾病、免疫调节、抗炎、癌症、生殖等各方面都能发挥一定的生物学作用.该生物学作用通常通过可溶性蛋白维生素D受体(VDR)来实现.VDR是一种位于靶细胞核内的转录因子,分布在人类各种系统组织中,包括女性生殖系统.近年有关维生素D与女性生殖系统的关系引起人们关注.维生素D一定程度上影响卵巢生理功能及女性生育力,同时与一些女性生殖系统疾病有关,如多囊卵巢综合征、子痫前期、子宫内膜异位症、妊娠期糖尿病等.现就维生素D缺乏与女性生殖系统关系的相关研究进行综述.【期刊名称】《国际生殖健康/计划生育杂志》【年(卷),期】2019(038)003【总页数】4页(P240-243)【关键词】维生素D;维生素D缺乏;生育力;女(雌)性泌尿生殖系统疾病和妊娠并发症;维生素D受体【作者】楚琪;郑连文;马亚兰;李丹;徐影【作者单位】130000长春,吉林大学第二医院生殖医学中心;130000长春,吉林大学第二医院生殖医学中心;130000长春,吉林大学第二医院生殖医学中心;130000长春,吉林大学第二医院生殖医学中心;130000长春,吉林大学第二医院生殖医学中心【正文语种】中文脂溶性维生素D是类固醇激素家族中的一员，主要有两种形式——D2和D3。
维生素D2主要通过紫外线照射在植物、酵母和真菌中产生，只有通过食物才进入人体。
而维生素D3主要在阳光照射的皮肤中合成。
人体内大约95%的维生素D3产生于阳光照射下的皮肤，只有少量的维生素D3通过膳食补充剂获得。
维生素D 的生物学功能由维生素D受体（VDR）实现。
VDR是配体依赖性的转录因子，主要位于靶细胞的细胞核中，可以介导维生素D的活性形式1，25二羟基维生素D3[1，25（OH）2D3]的生物学效应[1]。
湖南省职称论文认可期刊
16
Journal of Genetics and Genomics遗传学报（英文版）
11-5450/R
17
Journal of Integrative Medicine结合医学学报（英文）（曾用刊名中西医结合学报）
31-2083/R
18
Journal of Otology中华耳科学杂志（英文版）
13-1214/R
168
河南大学学报（医学版）
41-1361/R
169
河南科技大学学报（医学版）
41-1363/R
170
河南外科学杂志
41-1235/R
171
河南医学研究
41-1180/R
172
河南预防医学杂志
41-1220/R
173
河南职工医学院学报
41-1292/R
174
河南中医
41-1114/R
44-1550/R
197
华西口腔医学杂志
51-1169/R
198
华西药学杂志
51-1218/R
199
华西医学
51-1356/R
200
华夏医学
45-1236/R
201
华中科技大学学报（医学版）
42-1678/R
202
华中科技大学学报（医学英德文版）
42-1679/R
203
化工与医药工程（曾用刊名医药工程设计）
附件
湖南省卫生计生系列高级职称评审论文发表
认可期刊目录
序号
期刊名称
期刊号
1
Asian Journal of Andrology亚洲男性学杂志（英文版）
31-1795/R
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A1
Correct answer:E The anthracyclines (daunorubicin, doxorubicin, epirubicin and idarubicin) are chemotherapeutic agents associated with severe cardiotoxicity. The generation of free radicals is implicated in the unique ability of these agents to cause cardiotoxicity. Dilated cardiomyopathy is cumulative dose-dependent and may present many months after discontinuation of the drug. Swelling of the sarcoplasmic reticulum is the morphologic sign of an early stage of doxorubicin-associated cardiomyopathy. It is followed by loss of cardiomyocytes ("myofibrillar dropout"). Its symptoms are those of biventricular CHF including dyspnea on exertion, orthopnea, and peripheral edema. The most effective method of preventing doxorubicin cardiomyopathy is dexrazoxane. It is an iron-chelating agent that decreases formation of oxygen free radicals by doxorubicin and other anthracyclines. (Choice A) Right ventricular overload (cor pulmonale) presents with fatigue, dyspnea on exertion, and peripheral edema Physical examination reveals accentuation and splitting of the pulmonary component of S2, distended neck veins and hepatomegaly with hepatojugular reflux. Right ventricular failure is commonly a consequence of pulmonary hypertension or left heart failure. (Choice C) Restrictive cardiomyopathy is associated with hemochromatosis, amyloidosis, sarcoidosis and radiation therapy. (Choice D) Hypertrophic cardiomyopathy is an autosomal dominant disorder caused by mutation of the p-myosin heavy chain. (Choice B) Focal myocardial scarring commonly results following a myocardial infarction. (Choice F) Pericardial fibrosis usually follows cardiac surgery, radiation therapy or viral infections of the pericardium. Educational Objective:
Correct answer:D Right-sided endocarditis involving the tricuspid valve commonly occurs in intravenous drug users and is most often due to Staphylococcus aureus. Daptomycin is a lipopeptide antibiotic with activity against gram-positive organisms It can be used for treating skin and skin structure infections and bacteremia (with or without endocarditis) due to S aureus, including methicillin-resistant S aureus (MRSA). Daptomycin disrupts the bacterial membrane by creating transmembrane channels that cause intracellular ion leakage. The resulting cellular membrane depolarization and macromolecular (eg, DNA, RNA, protein) synthesis inhibition ultimately lead to cell death. Daptomycin cannot permeate the outer membrane of gram-negative bacteria, so it is ineffective in the treatment of gram-negative infections. It also binds to and is inactivated by pulmonary surfactant, so it is ineffective in the treatment of pneumonia. Daptomycin is associated with increased creatine phosphokinase (CPK) levels and an increased incidence of myopathy (possibly due to muscle fiber membrane disruption), particularly in patients using other drugs associated with myopathy (eg, statins). CPK level monitoring with assessment for muscle pain and weakness should be performed regularly in patients taking daptomycin. (Choice A) DNA winding-unwinding is affected by fluoroquinolones. Fluoroquinolones are not effective for MRSA infections. (Choice B) Folic acid metabolism is affected by trimethoprim/sulfamethoxazole which is used to treat skin and soft-tissue infections caused by community-acquired MRSA, but not bacteremic infections. Side effects include hyperkalemia; neutropenia; and uncommon, severe dermatologic reactions (eg, Stevens-Johnson syndrome). (Choice C) Vancomycin binds tightly to the D-alanyl-D-alanine portion of cell wall precursors, thereby blocking glycopeptide polymerization and inhibiting bacterial cell wall synthesis. Vancomycin is a first-line agent for MRSA bacteremia, including that associated with infective endocarditis, but it does not typically cause myopathy or CPK elevation. This patient is allergic to vancomycin. (Choice E) Linezolid inhibits bacterial protein synthesis by binding to the bacterial 23S ribosomal RNA of the 50S subunit. This prevents the formation of a functional 70S initiation complex required for bacterial protein translation. Linezolid is also used for MRSA infections, but its important side effects are thrombocytopenia optic neuritis, and increased risk of serotonin syndrome, especially if used concomitantly with proserotonergic drugs (eg. citalopram). Educational objective: Daptomycin is a lipopeptide antibiotic with activity limited to gram-positive organisms, including methicillin-resistant Staphylococcus aureus. It causes depolarization of bacterial cellular membrane and inhibition of DNA, RNA. and protein synthesis.Daptomycin is associated with increased creatine phosphokinase levels and an increased incidence of myopathy.