冠心病患者超声心动图改变与心功能及冠脉狭窄程度的相关性

目的 分析冠心病患者超声心动图指标与其心功能、冠脉狭窄之间的相关性。方法 选2020年1月至2022年12月江西省胸科医院收治的80例冠心病患者为研究组,同期体检100名健康对象为对照组。两组均行超声心动图检查[左室射血分数（LVEF）、左室舒张末期容积（LVEDV）、左室收缩末期容积（LVESV）],对不同心功能等级、不同冠脉狭窄程度冠心病患者的超声心动图检查结果行比较。结果 研究组的LVEF低于对照组,LVEDV、LVESV高于对照组,差异有统计学意义（P<0.05）;心功能等级为Ⅳ级的冠心病患者LVEF低于Ⅲ级、Ⅱ级、Ⅰ级冠心病患者,同时LVEDV、LVESV高于Ⅲ级、Ⅱ级、Ⅰ级冠心病患者,差异有统计学意义（P<0.05）;重度冠脉狭窄冠心病患者的LVEF低于中度、轻度患者,同时LVEDV、LVESV高于中度、轻度患者,差异有统计学意义（P<0.05）;冠心病患者超声心动图检测结果中LVEF与心功能等级、冠脉狭窄程度呈负相关性（P<0.05）,而LVEDV、LVESV与心功能等级、冠脉狭窄程度呈正相关性（P<0.05）。结论 冠心病患者超声心动图指标...     

血栓抽吸联合冠状动脉内注射替罗非班对ST段抬高型患者无复流和心功能的影响

目的探讨替罗非班冠状动脉给药联合血栓抽吸与替罗非班静脉给药对ST段抬高型急性心肌梗死（STEMI）患者直接冠状动脉介入术（PCI）后冠脉灌注和心功能的疗效差异。方法纳入2008年2月～2012年4月STEMI患者86例（TIMI血流≤1级）,随机分为实验组（n=43）和对照组（n=43）。对照组术前即开始静脉应用替罗非班,实验组则在PCI术中直接向梗死相关动脉（IRA）注射替罗非班并联合血栓抽吸。比较两组患者术后TIMI血流分级,检测术前、术后1周及6个月的血浆N-端脑钠肽前体（NT-proBNP）水平并采用超声心动图测定左室舒张末期容积（LVEDV）、左室收缩末期容积（LVESV）、左室射血分数（LVEF）、左室舒张末期容积指数（LVEDVI）;评价心功能并观察术后6个月内两组患者心血管事件的发生率。结果①实验组术后达到TIMI血流3级比例高于对照组（92.90%vs.66.17%,P〈0.05）;②术后1周及术后6个月实验组和对照组比较,NT-proBNP水平均显著下降（P〈0.01）,LVEF显著升高（P〈0.05）,LVESV、LVEDV、LVEDVI显著减少（P〈0.05）;③术后6个月内实验组心绞痛、心力衰竭等心血管事件发生率显著降低（P〈0.05）。结论 PCI术中IRA注射替罗非班联合血栓抽吸较静脉注射替罗非班可降低急诊PCI术中无复流的发生,改善血流再灌注,提高整体预后。     

急性心肌梗死患者心脏胶原代谢和左室重构与心功能的关系

目的观察急性心肌梗死（AMI）患者血清Ⅰ型前胶原羧基端肽（PⅠCP）和Ⅲ型前胶原（PCⅢ）水平,探讨AMI后心脏胶原代谢与左室重构及心功能的变化规律。方法应用酶联免疫法检测AMI患者发病后1周和3月的血清PⅠCP和PCⅢ含量,超声心动图同期检测左室舒张末期内径（LVEDD）、左室舒张末期容积（LVEDV）、左室射血分数（LVEF）和二尖瓣血流舒张早期流速（VE）与心房收缩期流速（VA）的比值。结果AMI后3月患者血清PⅠCP和发病后各时点血清PCⅢ均高于对照组,而AMI后3月患者PⅠCP高于AMI后1周。与正常对照组比较,AMI后各时点的LVEDD、LVEDV均增高,而LVEF和VE/VA比值降低。AMI发病后1周和3月PCⅢ分别与LVEDD和LVEDV呈正相关,与LVEF呈负相关;AMI发病后1周PⅠCP分别与LVEDD和LVEDV呈正相关,AMI发病后3月PⅠCP与LVEF呈负相关。结论AMI患者心脏胶原代谢活跃,血清PⅠCP和PCⅢ含量明显持续升高,参与左室重构,与AMI后心功能不全密切相关。     

肺切除术对肺癌患者左心功能的影响

目的观察肺切除术对肺癌患者左心功能的影响。方法 37例行肺切除术的肺癌患者,包括肺叶切除组23例、全肺切除组14例,术前及术后10 d采用单光子发射计算机体层扫描仪(SPECT)进行心肌灌注显像,测定患者左室射血分数(LVEF)、左室舒张末期容积(LVEDV)、左室收缩末期容积(LVESV)。结果术后10 d,两组LVEF较术前下降(P均<0.05),LVESV、LVEDV较术前升高(P均<0.05),全肺切除组术后上述指标变化较肺叶切除组明显(P均<0.05)。结论行肺叶或全肺切除术后10 d肺癌患者左心功能较术前明显下降,且全肺切除者左心功能下降较肺叶切除者更明显。     

血浆脑钠肽在心房纤颤中的应用价值

目的探讨血浆脑钠肽在心房纤颤中的应用价值。方法选取2011年2月—2013年2月我院收治的心房纤颤患者580例作为治疗组,另选择同期我院收治的无器质性心脏病窦性心律患者190例作为对照组。测定复律前两组患者血浆脑钠肽水平,以及复律成功者复律前后血浆脑钠肽水平。结果复律前治疗组血浆脑钠肽水平高于对照组(P0.05)。治疗组复律成功者复律后血浆脑钠肽水平低于复律前(P0.05)。结论心房纤颤使血浆脑钠肽水平升高,复律后水平明显降低,血浆脑钠肽是心房纤颤复律效果预测的重要指标。     

急性心肌梗死后左心室重构与室性心律失常的关系

目的 探讨急性心肌梗死（AMI）后左心室（左室）重构与室性心律失常之间的关系.方法 选取84例AMI患者,随机分为两组,A组接受ACEI治疗,B组不接受ACEI或ARB类药物治疗.随访观察梗死后左室收缩末期容积（LVESV）,左室舒张末期容积（LVEDV）、左室重量（LVM）和左室射血分数（LVEF）与室性心律失常发生率之间的关系.结果 AMI 1年后A组LVESV小于B组,LVEF大于B组.A、B两组的LVESV随病程延长而增大,LVEF随病程延长而减低.AMI 2周内发生室性心律失常组的LVM高于未发生组.AMI 6个月和一年后发生心律失常组的LVEDV、LVESV和LVM高于未发生组,未发生组的LVEF高于发生组.发生室性心律失常组的LVEDV、LVESV和LVEF在三个时间点间差异及未发生室性心律失常组的射血分数在三个时间点间差异均有显著性（P＜0.05）.室性心律失常在AMI2周内与LVM;6个月后与LVESV和LVM;1年后与LVEDV和LVESV密切相关.结论 AMI后左室重构是引起室性心律失常重要基质.     

AMI患者血浆脑钠肽水平测定及其与左室重构的关系

测定对68例急性心肌梗死(AM I)患者发病后48 h内(早期)血浆脑钠肽(BNP)水平;于发病后28~30 d行超声心动图检查,测量左心室收缩末期容积(LVESV)、左心室舒张末期容积(LVEDV)和左心室射血分数(LVEF)。对血浆BNP水平与LVESV、LVEDV、LVEF进行相关性分析。结果LVEF≤40%者血浆BNP水平显著高于LVEF>40%者,P<0.05;血浆BNP水平与LVESV、LVEDV呈正相关,与LVEF呈负相关。认为AM I早期血浆BNP水平升高与其28~30 d左室重构程度密切相关,应积极进行干预治疗。     

冻干重组人脑钠肽对充血性心力衰竭患者心脏不良事件发生的影响

目的探讨标准治疗基础上加用重组脑钠肽对充血性心力衰竭患者疗效及心脏不良事件发生率的影响。方法将140例充血性心力衰竭患者随机分为标准治疗组74例和脑钠肽组66例。患者均采用标准治疗（洋地黄、利尿剂、β受体阻滞剂及血管紧张素转换酶抑制剂）。脑钠肽组在此基础上加用冻干重组人脑钠肽。观察治疗后症状的改变,采用彩色超声心动图检测心脏容量参数（LVEDV、LVESV）及左室射血分数（LVEF）的变化;随访10个月,统计心脏不良事件发生情况。结果脑钠肽组有效率与标准治疗组比较无统计学差异。脑钠肽组因心脏原因再次入院及室速/室颤的发生率明显高于标准治疗组（P〈0.05）。两组患者治疗后LVESV、LVEF较治疗前均有明显改善（P〈0.05）,脑钠肽组尤为明显（P〈0.01）。脑钠肽组治疗后LVESV、LVEDV、LVEF与标准治疗组比较均有统计学差异（P均〈0.05）。结论脑钠肽可显著改善充血性心力衰竭患者的症状,减少再次发生心脏不良事件的概率。     

非心源性心跳呼吸骤停患者ROSC后48h内左室功能变化分析

目的 探讨非心源性心跳呼吸骤停患者自主循环恢复（ROSC）后48h内左室功能变化情况及与存活时间的关系。方法 对64例非心源性心跳呼吸骤停患者行心肺复苏，并分别于ROSC后24h内及24～48h行心脏超声检查，测量左室射血分数（LVEF）、左心室舒张末期容积（LVEDV）、收缩末期容积（LVESV）和每搏输出量（SV）。结果39例存活〉24h者24h内LVEF、SV显著高于25例存活〈24h者、低于其48h内复测值，LVEDV、LVESV显著低于存活〈24h者、高于其48h内复测值（P均〈0．05）。结论 非心源性心跳呼吸骤停患者ROSC后48h内左室功能尚不稳定，且与患者存活时间有关。     

步长稳心颗粒联合贝那普利治疗心力衰竭合并心房纤颤的疗效

目的探索步长稳心颗粒联合贝那普利治疗心力衰竭合并心房纤颤的疗效。方法将121例心力衰竭合并心房纤颤的患者随机分为治疗组和常规组。治疗组除常规治疗并加用贝那普利基础上,再给予步长稳心颗粒1包/次,3次/d冲服。治疗前及治疗后1个月分别行常规超声心动图,临床评价心功能。结果治疗组心房纤颤转复率为91.53%,常规组心房纤颤转复率75.81%。差异有统计学意义(P0.05)。治疗组心功能分级(NYHA)及左室射血分数(LVEF)较常规有明显改善。结论步长稳心颗粒联合贝那普利不仅明显改善心力衰竭症状,而且大大减少心房纤颤复发率。     

Atrial natriuretic factor during atrial fibrillation and supraventricular tachycardia

Plasma immunoreactive atrial natriuretic factor was measured in 10 patients with chronic atrial fibrillation before and after cardioversion to sinus rhythm, and in 14 patients during electrophysiologic evaluation of paroxysmal supraventricular tachycardia. The mean plasma concentration of atrial natriuretic factor in atrial fibrillation was 138 +/- 48 pg/ml and decreased to 116 +/- 45 pg/ml 1 hour after cardioversion to sinus rhythm (p less than 0.005). The mean plasma concentration of atrial natriuretic factor increased from 117 +/- 53 pg/ml in sinus rhythm to 251 +/- 137 pg/ml during laboratory-induced supraventricular tachycardia (p less than 0.005). Right atrial pressures were recorded in 12 patients; the baseline atrial pressure was 4.3 +/- 1.9 mm Hg and increased to 7.4 +/- 3.6 mm Hg during supraventricular tachycardia (p less than 0.005). A modest but significant linear relation was noted between the changes in plasma atrial natriuretic factor and right atrial pressure measurements during induced supraventricular tachycardia (r = 0.60, p less than 0.05). In conclusion, changes in atrial rhythm and pressure may be an important factor modulating the release of atrial natriuretic factor in the circulation and raised levels of this hormone may be a contributing factor for the polyuria and the hypotension associated with paroxysmal supraventricular tachyarrhythmias.     

Relationship between efficacy of antiarrhythmic drug therapy and structural remodeling in patients with paroxysmal atrial fibrillation

OBJECTIVES: To evaluate whether the response to antiarrhythmic drug therapy in patients with paroxysmal atrial fibrillation affects the development of structural remodeling in the left atrium and ventricle. METHODS: This study included 230 patients (158 men and 72 women, mean age 67 +/- 11 years) in whom antiarrhythmic drug therapy was attempted for > or = 12 months to maintain sinus rhythm (mean follow-up period 45 +/- 27 months). The patients were divided into three groups according to the response to antiarrhythmic drug therapy: group A consisted of 78 patients without recurrence of atrial fibrillation, group B consisted of 87 patients with recurrence of atrial fibrillation and electrical and/or pharmacological cardioversion to restore sinus rhythm, and group C consisted of 65 patients with permanent conversion despite antiarrhythmic drug therapy. RESULTS: In group A, left atrial dimension (LAD), left ventricular end-diastolic dimension (LVDd), and left ventricular ejection fraction (LVEF) did not change after antiarrhythmic drug therapy. In group B, LAD increased significantly after antiarrhythmic drug therapy (from 32.6 +/- 6.4 to 36.0 +/- 6.5 mm, p < 0.01), Whereas either LVDd or LVEF did not change after antiarrhythmic drug therapy. In group C, LAD increased significantly after antiarrhythmic drug therapy (from 37.3 +/- 7.0 to 40.5 +/- 7.9 mm, p < 0.01) and LVEF was significantly reduced after antiarrhythmic drug therapy (from 69.4 +/- 6.2% to 66.5 +/- 8.9%, p < 0.05). LVDd did not change after antiarrhythmic drug therapy. The plasma concentration of human atrial natriuretic peptide during sinus rhythm at the initiation of antiarrhythmic drug therapy in group A (30.5 +/- 26.7 pg/ml) was significantly lower than those in group B (48.0 +/- 49.7 pg/ml) and group C (49.7 +/- 39.5 pg/ml). CONCLUSIONS: The development of structural remodeling in human myocardium can be prevented with antiarrhythmic drug therapy if sinus rhythm is maintained without recurrence of atrial fibrillation in patients with paroxysmal atrial fibrillation.     

心房颤动患者复律后心房顿抑与脑利钠肽的研究

目的:通过对心房颤动(房颤)患者复律后心房超声检查及血浆脑利钠肽(BNP)的检测,探讨心房顿抑与BNP的关系。方法:将76例房颤患者分为阵发性房颤组(40例)和持续性房颤组(36例),另入选对照组患者20例。在房颤复律后2h、1d、1周和1个月时经胸壁超声心动图(TTE)检查测定舒张晚期血流速度(A峰)和心房充盈分数(AFF),以A峰<50cm/s作为心房顿抑的标准,并测定上述时间点及复律前血浆BNP。结果:阵发性房颤组复律后2h心房顿抑的发生率为45.0%,复律后A峰和AFF至1周时恢复正常;持续性房颤组复律后2h左房顿抑的发生率为61.6%,A峰和AFF至1个月时恢复正常。2组复律后1d和1周时BNP与A峰有显著的相关性,在房颤复律后1d和1周时仍然存在心房顿抑的患者BNP显著高于无顿抑发生的患者(P<0.01),心房顿抑消失后,BNP迅速下降。结论:房颤复律后1d和1周时血浆BNP水平与跨二尖瓣A峰有相关性,较高的血浆BNP可能提示心房顿抑的持续存在,有助于了解左心房功能恢复情况。     

N末端脑钠肽前体及高敏C反应蛋白在阵发陛心房纤颤患者中的应用

目的研究测量血清N末端脑纳肽前体（N-terminalpro-brainnatriureticpeptide,NT-pro-BNP）及高敏C反应蛋白（high-sensitivityc-reactiveprotein,hs-CRP）浓度在阵发性心房纤颤的应用价值。方法选择中山市人民医院2007年1月至2010年1月明确诊断为阵发性心房纤颤的患者60例为研究对象（心房纤颤组）。予以胺碘酮注射液（5ITIg／kg,静脉注射;600mg／24h,静脉注射）治疗后,分为复律组（38例）、未复律组（22例）。另外,选取同期住院非瓣膜性心脏病窦性心律患者60例为窦律组。分别测量各组血清NT-pro-BNP及hs-CRP浓度,并进行比较。结果治疗前心房纤颤组血清NT-pro-BNP及hs-CRP浓度显著高于窦律组,差异有统计学意义[NT．pro-BNP：（619．3±275．0）ng／LVS．（235．2±80．4）ng／L,P〈0．05;hs-CRP：（4．5±O．7）ng／L、（6．9±1．2）ng／L7）8．（1．1±0．6）ng／L,P〈0．05]。复律组血清Nt-pro-BNP及hs．CRP浓度明显低于复律前,差异有统计学意义[（460．6±162．7）ng／Lus（699．6±310．0）ng／L,P〈0．05;（1．3±0．6）ng／Lus．（4．5±0．7）ng／L,P〈0．05]。复律组复律后血清NT-pro-BNP及hs-CRP浓度与窦律组比较,差异无统计学意义（P〉0．05）。复律前复律组血清NT-pro-BNP及hs-CRP浓度与未复律组比较,差异无统计学意义（P〉0．05）。结论NT．pro-BNP及hs-CRP可能参与心房纤颤的发生、发展,测量NT．pro-BNP及hs-CRP浓度在心房纤颤的治疗及预后判断方面有一定的应用价值。     

氯沙坦联合胺碘酮对阵发性心房颤动复律及复律后窦性心律维持的影响

目的 了解氯沙坦联合胺碘酮对阵发性心房颤动的复律效果及复律后窦性心律维持的影响.方法 2003年1月至2005年10月将解放军421医院心内科86例非瓣膜病阵发性心房颤动患者分为胺碘酮治疗组和氯沙坦 胺碘酮治疗组,观察治疗24 h,3 d和7 d时心房颤动的转复情况.在心房颤动复律后,继续药物治疗并随访观察1年,评价两组窦性心律的维持效果.结果 胺碘酮组44例心房颤动患者治疗24 h,3 d和7 d心房颤动的转复率分别为65.90%,75.00%和86.36%,氯沙坦 胺碘酮治疗组的转复率为66.66%,80.95%和95.23%.两组在7 d时心房颤动的转复率差异有显著性意义(P＜0.05).随访1年时两组窦性心律的维持率分别为71.05%和87.50%(P＜0.05),两组左房内径分别为(37.45±1.44)mm和(35.83±1.38)mm(P＜0.05).结论 氯沙坦联合胺碘酮对阵发性心房颤动的复律及复律后窦性心律维持均优于单用胺碘酮治疗,可能与氯沙坦抑制肾素-血管紧张素系统,降低心脏负荷,抑制心房电及结构重构有关.     

Atrial natriuretic peptide response to cardioversion of atrial flutter and fibrillation and role of associated heart failure.

Plasma atrial natriuretic peptide (ANP) concentrations were measured before and 1 hour after cardioversion in 40 patients (27 with atrial flutter and 13 with atrial fibrillation) admitted for elective cardioversion. Fourteen (11 with atrial flutter and 3 with atrial fibrillation) had clinical evidence of congestive heart failure (CHF). Conversion to sinus rhythm was successful in 39 patients. The mean ANP concentration in the entire group decreased after cardioversion from 38 +/- 4 to 17 +/- 2 pmol/liter (p less than 0.001). In the subgroup with CHF, the ANP level, which was not significantly higher than that in the group without CHF, decreased from 47 +/- 8 to 19 +/- 3 pmol/liter (p less than 0.01). Neither mode of cardioversion (spontaneous 1, pharmacologic 2 and direct-current countershock 36) nor associated CHF influenced ANP response to cardioversion. One patient with atrial flutter and "failed cardioversion" had unchanged ANP level. The decrease after cardioversion in ANP concentration correlated with its control level (r = 0.88, p less than 0.001) but not with the decrease in heart rate. The ANP level in patients with atrial fibrillation was 45 +/- 9 vs 38 +/- 5 pmol/liter in those with atrial flutter (difference not significant). Arrhythmia duration, left atrial size, and ventricular rate or arterial blood pressure did not correlate with ANP concentration in any subgroup. It is concluded that (1) the ANP level is elevated comparably in patients with both atrial flutter and fibrillation regardless of the presence or absence of CHF; and (2) the level decreases, independent of the mode of cardioversion or presence of CHF, promptly after successful cardioversion.     

Favorable effects of flecainide in transvenous internal cardioversion of atrial fibrillation

ObjectivesThe aim of the study was to evaluate the effects of intravenous (IV) flecainide on defibrillation energy requirements in patients treated with low-energy internal atrial cardioversion.BackgroundInternal cardioversion of atrial fibrillation is becoming a more widely accepted therapy for acute episode termination and for implantable atrial defibrillators.MethodsTwenty-four patients with atrial fibrillation (19 persistent, 5 paroxysmal) underwent elective transvenous cardioversion according to a step-up protocol. After successful conversion in a drug-free state, atrial fibrillation was induced by atrial pacing; IV flecainide (2 mg/kg) was administered and a second threshold was determined. In patients in whom cardioversion in a drug-free state failed notwithstanding a 400- to 550-V shock, a threshold determination was attempted after flecainide.ResultsChronic persistent atrial fibrillation was converted in 13/19 (68%) patients at baseline and in 16/19 (84%) patients after flecainide. Paroxysmal atrial fibrillation was successfully cardioverted in all the patients. A favorable effect of flecainide was observed either in chronic persistent atrial fibrillation (13 patients) or in paroxysmal atrial fibrillation (5 patients) with significant reductions in energy requirements for effective defibrillation (persistent atrial fibrillation: 4.42 ± 1.37 to 3.50 ± 1.51 J, p < 0.005; paroxysmal atrial fibrillation: 1.68 ± 0.29 to 0.84 ± 0.26 J, p < 0.01). In 14 patients not requiring sedation, the favorable effects of flecainide on defibrillation threshold resulted in a significant reduction in the scores of shock-induced discomfort (3.71 ± 0.83 vs. 4.29 ± 0.61, p < 0.005). No ventricular proarrhythmia was observed for any shock.ConclusionsIntravenous flecainide reduces atrial defibrillation threshold in patients treated with low-energy internal atrial cardioversion. This reduction in threshold results in lower shock-induced discomfort. Additionally, flecainide may increase the procedure success rate in patients with chronic persistent atrial fibrillation.     

厄贝沙坦联合胺碘酮对阵发性房颤复律后维持窦性心律的效果

目的：观察厄贝沙坦联合胺碘酮对阵发性心房颤动复律后维持窦性心律的临床效果及其对左心房内径的影响。方法：选择阵发性心房颤动患者89例,分为胺碘酮治疗组（44例,单纯服用胺碘酮）,联合治疗组（45例,服用胺碘酮及厄贝沙坦）,随访12个月,观察两组患者治疗前后窦性心律维持率,左房内径的变化,并进行比较分析。结果：治疗12个月后,与胺碘酮组比较,联合治疗组窦性心律维持率明显提高（64.3%比81.4%）,左房内径明显减小[（40.12±10.6）mm比（34.10±10.11）mm],P均〈0.05。结论：厄贝沙坦联合胺碘酮对阵发性心房颤动复律后维持窦性心律的作用明显优于单用胺碘酮,且明显抑制左房扩大,无明显不良反应。     

Atrial fibrillation

The prevalence and incidence of atrial fibrillation increase with age. Atrial fibrillation is associated with a higher incidence of coronary events, stroke, and mortality than sinus rhythm. A fast ventricular rate associated with atrial fibrillation may cause tachycardia-related cardiomyopathy. Management of atrial fibrillation includes treatment of underlying causes and precipitating factors. Immediate direct-current cardioversion should be performed in persons with atrial fibrillation associated with acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta-blockers, verapamil, or diltiazem may be used to immediately slow a fast ventricular rate associated with atrial fibrillation. An oral beta-blocker, verapamil, or diltiazem should be given to persons with atrial fibrillation if a rapid ventricular rate occurs a rest or during exercise despite digoxin. Amiodarone may be used in selected persons with symptomatic life-threatening atrial fibrillation refractory to other drug therapy. Nondrug therapies should be performed in persons with symptomatic atrial fibrillation in whom a rapid ventricular rate cannot be slowed by drug therapy. Paroxysmal atrial fibrillation associated with the tachycardia-bradycardia syndrome should be managed with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in persons with atrial fibrillation in whom symptoms such as dizziness or syncope associated with non-drug-induced ventricular pauses longer than 3 seconds develop. Elective direct-current cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than medical cardioversion in converting atrial fibrillation to sinus rhythm. Unless transesophageal echocardiography shows no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective direct-current or drug cardioversion of atrial fibrillation and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer the treatment strategy of ventricular rate control plus warfarin rather than to maintain sinus rhythm with antiarrhythmic drugs, especially in older patients. Digoxin should not be used in persons with paroxysmal atrial fibrillation. Patients with chronic or paroxysmal atrial fibrillation who are at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio (INR) of 2.0 to 3.0. Persons with atrial fibrillation who are at low risk for stroke or who have contraindications to warfarin should receive 325 mg aspirin daily.     

Effect of verapamil on immediate recurrence of atrial fibrillation

INTRODUCTION: The purpose of this study was to assess the effect of verapamil on immediate recurrences of atrial fibrillation occurring after successful electrical cardioversion. METHODS AND RESULTS: The effect of verapamil on the recurrence of atrial fibrillation within 5 minutes after successful transthoracic cardioversion was assessed in 19 (5%) of 364 patients undergoing electrical cardioversion. The mean duration of atrial fibrillation was 4.44+/-3.0 months. In the 19 patients, cardioversion was successful after each of three consecutive cardioversion attempts per patient; however, atrial fibrillation recurred 0.4+/-0.3 minutes after cardioversion. Verapamil 10 mg was administered intravenously and a fourth cardioversion was performed. Cardioversion after verapamil was successful in each patient, and atrial fibrillation did not recur in 9 (47%) of 19 patients (P < 0.001 vs before verapamil). In the remaining 10 patients in whom atrial fibrillation recurred, the duration of sinus rhythm was significantly longer compared with before verapamil (3.6+/-2.4 min, P < 0.001). The density of atrial ectopy occurring after cardioversion was significantly less after verapamil (21+/-14 ectopic beats per min) compared with before verapamil (123+/-52 ectopic beats per min, P < 0.001). CONCLUSION: Among patients with immediate recurrence of atrial fibrillation after electrical cardioversion, acute calcium channel blockade by verapamil reduces recurrence of atrial fibrillation and extends the duration of sinus rhythm.