Despite all the therapeutic advances in the field of cardiology, cardiovascular diseases, and in particular coronary artery disease, remain the leading cause of death and disability worldwide, thereby underlining the ...Despite all the therapeutic advances in the field of cardiology, cardiovascular diseases, and in particular coronary artery disease, remain the leading cause of death and disability worldwide, thereby underlining the importance of acquiring new therapeutic options in this field. A reduction in elevated resting heart rate (HR) has long been postulated as a therapeutic approach in the management of cardiovascular disease. An increased HR has been shown to be associated with increased progression of coronary atherosclerosis in animal models and patients. A high HR has also been associated with a greatly increased risk of plaque rupture in patients with coronary atherosclerosis. Endothelial function may be an important link between HR and atherosclerosis. An increased HR has been shown experimentally to cause endothelial dysfunction. Inflammation plays a significant role in the pathogenesis and progression of atherosclerosis. In the literature, there is data that shows an association between HR and circulating markers of vascular inflammation. In addition, HR reduction by pharmacological intervention with ivabradine (a selective HR-lowering agent that acts by inhibiting the pacemaker ionic current If in sinoatrial node cells) reduces the formation of atherosclerotic plaques in animal models of lipid-induced atherosclerosis. The aim of this editorial is to review the possible role of ivabradine on atherosclerosis.展开更多
AIM To perform a systematic-review and meta-analysis to compare outcomes of ivabradine combined with betablocker to beta-blocker alone in heart failure with reduced ejection fraction(HFr EF).METHODS We searched PubM e...AIM To perform a systematic-review and meta-analysis to compare outcomes of ivabradine combined with betablocker to beta-blocker alone in heart failure with reduced ejection fraction(HFr EF).METHODS We searched PubM ed, Cochrane, EMBASE, CINAHL and Web of Science for trials comparing ivabradine + betablocker to beta-blocker alone in HFr EF. We performed a systematic-review and meta-analysis of published literature. Primary end-point was combined end point of cardiac death and hospitalization for heart failure.RESULTS Six studies with 17671 patients were included. Mean follow-up was 8.7 ± 7.9 mo. Combined end-point of heart failure readmission and cardiovascular death was better in ivabradine + beta-blocker group compared to beta-blocker alone(RR: 0.93, 95%CI: 0.79-1.09, P = 0.354). Mean difference(MD) in heart rate was higher in the ivabradine + beta-blocker group(MD: 6.14, 95%CI: 3.80-8.48, P < 0.001). There was no difference in all cause mortality(RR: 0.98, 95%CI: 0.89-1.07, P = 0.609), cardiovascular mortality(RR: 0.99, 95%CI: 0.86-1.15, P = 0.908) or heart failure hospitalization(RR: 0.87, 95%CI: 0.68-1.11, P = 0.271). CONCLUSION From the available clinical trials, ivabradine + betablocker resulted in a significantly greater reduction in HRcoupled with improvement in combined end-point of heart failure readmission and cardiovascular death but with no improvement in all cause or cardiovascular mortality. Given the limited evidence, further randomized controlled trials are essential before widespread clinical application of ivabradine + beta-blocker is advocated for HFrEF.展开更多
Objective: To observe the effectiveness and safety of ivabradine in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and heart failure. Methods:Patients who were admitted to hospital ...Objective: To observe the effectiveness and safety of ivabradine in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and heart failure. Methods:Patients who were admitted to hospital with AECOPD during the period from August 2017 to July 2018. Then those both had heart failure with reduced ejection fraction(HFrEF) and a resting heart rate>70 beats/min were enrolled. A total of 86 cases were screened and completed, which were randomly divided into two groups for treatment. The control group(41 cases) received standard treatments, such as oxygen, anti-infection, anti-spasmodic, hormone, diuretic, ACEI/ARB, recombinant human brain natriuretic peptide (rhBNP), etc. The bisoprolol was given 2.5~5 mg orally once a day to control heart rate, and the test group(45 cases) was further treated with ivabradine 2.5~5 mg orally twice a day on the basis of the control group. The average heart rate, cardiac function, lung function, and 6-minute walking test were compared between the two groups. Results: After treatment, the average heart rate of the test group was lower than the control group, and the heart rate control rate(<70 beats/min%) of the test group was superior to the control group. The level of N-terminal B-type natriuretic peptide(NT-proBNP) in test group was significantly lower than that in control group. The distance of the 6-minute walking test in e test group was significantly longer than that in control group. Conclusion: Ivabradine combined with bisoprolol could help patients with AECOPD and heart failure to further reduce the heart rates, improve heart function and exercise tolerance. Moreover, the therapeutic safety was acceptable during the short term.展开更多
Objective:To investigate the effects of ivabradine on Notch and NF-kappa B signaling pathway in myocardial cells of rats with myocardial infarction.Methods: The model of myocardial infarction was established by ligati...Objective:To investigate the effects of ivabradine on Notch and NF-kappa B signaling pathway in myocardial cells of rats with myocardial infarction.Methods: The model of myocardial infarction was established by ligating the left anterior descending coronary artery. The surviving rats were randomly divided into model group (MI group,n=8) and treatment group (IVA group,n=8). Rats with the same location but without ligation of the left anterior descending coronary artery were used as control group (CON group,n = 8). IVA was administered for 28 d. Hemodynamic and cardiac function indexes of all rats were measured: heart rate (HR), systolic pressure (SBP), diastolic pressure (DBP), mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and maximum rate of increase and decrease of left ventricular internal pressure (+dp/dt);left ventricular mass index, left ventricular cross-sectional diameter and infarct area;The expression of Notch signaling pathway components mRNA (Notch-1, Dll-4, Hes-1) in rat cardiomyocytes was detected by PT-PCR, and the expression of DICD-1 and P65 protein was detected by western-blot. One-way ANOVA was used for comparison between groups, and SNK was used for comparison between groups.Results: SBP, DBP, MAP, LASP, LVEDP and (+dp/dt) in MI group were lower than those in control group (P<0.05), while IVA was higher than those in MI group (P<0.05). Left ventricular mass index and left ventricular sectional diameter in MI group were significantly higher than those in control group (P<0.05), but lower than those in IVA group (P<0.05). The expression of Notch-1 in MI group was significantly higher than that in control group (P<0.05), but lower than that in IVA group (P<0.05). There was no significant difference in the expression of Dll-4 and Hes-1 mRNA between the three groups (P>0.05). The expression levels of NICD-1 and P 65 in MI group were significantly higher than those in CON group (P<0.05), but lower than those in IVA group (P<0.05). Conclusion: IVA may improve cardiac function and inhibit ventricular remodeling in rats with myocardial infarction through Notch and NF-kappa B signaling pathways.展开更多
The Systolic Heart failure treatment with the I( inhibitor ivabradine Trial (SHIFT, n = 6505) evaluated patients with symptomatic chronic heart failure (CHF), in sinus rhythm with resting heart rate ≥70 beats/min and...The Systolic Heart failure treatment with the I( inhibitor ivabradine Trial (SHIFT, n = 6505) evaluated patients with symptomatic chronic heart failure (CHF), in sinus rhythm with resting heart rate ≥70 beats/min and left ventricular ejection fraction (LVEF)≤ 35%, average age 60 ± 11 years[1].展开更多
Post-resuscitation myocardial dysfunction(PRMD)is the most severe myocardial ischemia-reperfusion injury(MIRI)and is characterized by difficult treatment and poor prognosis.Research has shown the protective effects of...Post-resuscitation myocardial dysfunction(PRMD)is the most severe myocardial ischemia-reperfusion injury(MIRI)and is characterized by difficult treatment and poor prognosis.Research has shown the protective effects of the rational use of ivabradine(IVA)against PRMD,however,the molecular mechanisms of IVA remain unknown.In this study,an ischemia-reperfusion injury(IRI)model was established using hypoxic chambers.The results demonstrated that pretreatment with IVA reduced IRI-induced cytotoxicity and apoptosis.IVA attenuated mitochondrial damage,eliminated excess reactive oxygen species(ROS),suppressed IRI-induced ATP and NAD+,and increased the AMP/ATP ratio.We further found that IVA increased the mRNA levels of sirtuin 1(SIRT1)and peroxisome proliferator-activated receptor-γcoactivator 1α(PGC-1α)and upregulated the expression levels of phosphorylated AMP-activated protein kinase(p-AMPK)/AMPK,SIRT1,and PGC-1αproteins.Interestingly,no change in AMPK mRNA levels was observed.Cardiomyocyte energy metabolism significantly changed after IRI.The aim of this study was to demonstrate the cardioprotective effect of Ivabradine via the AMPK/SIRT1/PGC-1αsignaling pathway in myocardial ischemia/reperfusion injury-induced in H9c2 cell.展开更多
Over the last 20 years, it has emerged that, while surgical revascularisation of extensive ischaemic heart disease may have prognostic advantages, the main issues considered regarding individual management are usually...Over the last 20 years, it has emerged that, while surgical revascularisation of extensive ischaemic heart disease may have prognostic advantages, the main issues considered regarding individual management are usually those of symptomatic improvement only. The major impetus towards invasive intervention is therefore failure of prophylactic anti-anginal therapy. On the other hand, many patients, especially the elderly, now present the clinical problem of ongoing angina without residual invasive options. There is an ongoing need for more effective anti-anginal therapies. Of the currently available major classes of prophylactic anti-anginal agents, neither nitrates, β-blockers nor calcium antagonists generally produce marked improvements in exercise duration. Three areas of new therapeutic development in anti-anginal therapy are worthy of note. These involve the sinus node inhibitor ivabradine, high dose allopurinol (xanthine oxidase inhibitor) and a new class of “metabolic modulators” represented by perhexiline, trimetazidine and probably ranolazine. The current review addresses the therapeutic potential of these agents. Notably, all of these “new” drugs are potentially suitable for management of angina in the setting of impaired left ventricular systolic function, and they may also be utilized in patients with angina independent of the presence of coronary disease (for example in hypertrophic cardiomyopathy). The current evidence for efficacy and potential future development in this area are reviewed.展开更多
Background: Junctional ectopic tachycardia (JET) is one troublesome supraventricular arrhythmia in postoperative pediatric cardiac surgical patients. Unless treated timely and effectively it may lead to morbidity and ...Background: Junctional ectopic tachycardia (JET) is one troublesome supraventricular arrhythmia in postoperative pediatric cardiac surgical patients. Unless treated timely and effectively it may lead to morbidity and even mortality. Aim: To understand the role of Ivabradine in the treatment of JET in postoperative pediatric cardiac surgical patients. Case: We present a postoperative case of complete repair of Tetralogy of Fallot who was in normal sinus rhythm in the preoperative period and developed JET 4 hours later in postoperative period which was persistent despite measures to optimize the internal milieu of the body and conventional antiarrhythmics, that was successfully treated with Ivabradine at a dose of 0.05 mg/kg/12 hourly. Conclusion: Ivabradine can be used to successfully treat postoperative JET in cases ofrefractory to other antiarrhythmic drugs like Digoxin and Amiodarone.展开更多
Objective:To systemically evaluate clinical efficacy and safety of traditional Chinese medicine(TCM)combined with ivabradine(IVA)in the treatment of chronic heart failure(CHF).Method:We searched China National Knowled...Objective:To systemically evaluate clinical efficacy and safety of traditional Chinese medicine(TCM)combined with ivabradine(IVA)in the treatment of chronic heart failure(CHF).Method:We searched China National Knowledge Infrastructure(CNKI)datebase,Wanfang datebase,Chinese Scientifific Journal Database(VIP)datebase,PubMed,Conchrane Library and EMbase database to enroll the random control trials(RCTs)of TCM combined with IVA treating CHF.Meta-analysis was performed by Review Manager 5.3 software.Results:A total of 10 RCTs involving 960 patients were included.The results of Meta-analysis showed that compared with control group,the experimental group could improve the efficiency of cardiac function improvement[RR=1.19,95%CI(1.12,1.27),P<0.00001],increase left ventricular ejection fraction[MD=4.36,95%CI(2.88,5.83),P<0.0001]and reduce heart rate[MD=-8.21,95%CI(-12.08,-4.34),P<0.00001],the incidence of adverse reactions was similar between two groups[RR=1.00,95%CI(0.62,1.61),P=1.00].Conclusion:Traditional Chinese medicine combined with ivabradine has significant efficacy and good safety in improving cardiac function,improving left ventricular ejection fraction and reducing heart rate in the treatment of chronic heart failure.展开更多
A sensitive and specific liquid-chromatography tandem mass spectrometry(LC-MS/MS)assay has been developed and validated for the simultaneous quantification of ivabradine and its active metabolite N-desmethylivabradine...A sensitive and specific liquid-chromatography tandem mass spectrometry(LC-MS/MS)assay has been developed and validated for the simultaneous quantification of ivabradine and its active metabolite N-desmethylivabradine in human plasma and urine.The assay employed a single liquid–liquid extraction of the analytes from plasma and urine samples,and diazepam was used as internal standard(IS).The chromatographic separation was achieved on a Diamonsil C18 column(150 mm4.6 mm,5 mm,Dikma)using a mixture of methanol and aqueous 5 mM ammonium acetate buffer containing 0.2%formic acid(80:20,v/v)as mobile phase.The assay for ivabradine and N-desmethylivabradine in plasma showed good linearity(r≥0.99)over the ranges 0.1013–101.3 ng/mL and 0.085–25.5 ng/mL,respectively.The assay for ivabradine and N-desmethylivabradine in urine showed good linearity(r≥0.99)over the ranges 10.13–6078 ng/mL and 8.5–850 ng/mL,respectively.The intra-and inter-day accuracy and precision values were found to be within the assay variability limits(RSD<15%)in accordance with FDA guidelines.The methods were successfully used for evaluating the pharmacokinetic properties of ivabradine and N-desmethylivabradine in human plasma and urine in Chinese healthy volunteers.展开更多
目的评价伊伐布雷定对冠心病患者血管内皮功能的影响。方法检索PubMed、Embase、Cochrane图书馆、Web of Science、中国知网、万方数据、维普网、中国生物医学文献数据库,收集伊伐布雷定(干预组)对比安慰剂或β受体阻滞剂(对照组)的随...目的评价伊伐布雷定对冠心病患者血管内皮功能的影响。方法检索PubMed、Embase、Cochrane图书馆、Web of Science、中国知网、万方数据、维普网、中国生物医学文献数据库,收集伊伐布雷定(干预组)对比安慰剂或β受体阻滞剂(对照组)的随机对照试验(RCT),检索时限为各数据库建库起至2023年3月20日。筛选文献、提取数据和评价质量后,采用RevMan5.4软件进行Meta分析。结果共纳入12项RCT,共计1206例患者。Meta分析结果显示,干预组患者的内皮依赖性血管舒张功能(FMD)[MD=1.71,95%CI(0.96,2.46),P<0.00001]、一氧化氮(NO)[MD=5.80,95%CI(5.02,6.59),P<0.00001]水平均显著高于对照组,内皮素1(ET-1)水平显著低于对照组[MD=-7.45,95%CI(-8.42,-6.47),P<0.00001]。两组患者的非内皮依赖性血管舒张功能(NMD)比较,差异无统计学意义[MD=0.13,95%CI(-0.74,1.00),P=0.77]。按照对照组用药和干预时间的不同进行的亚组分析结果显示,与安慰剂比较,使用伊伐布雷定患者的FMD水平显著升高(P<0.05);与安慰剂、β受体阻滞剂比较,使用伊伐布雷定患者的NO水平均显著升高(P<0.05)、ET-1水平均显著降低(P<0.05)。无论干预时间长短,干预组患者的FMD、NO、ET-1水平均较对照组显著改善(P<0.01),NMD比较差异无统计学意义(P>0.05)。结论伊伐布雷定能显著改善冠心病患者的血管内皮功能。展开更多
文摘Despite all the therapeutic advances in the field of cardiology, cardiovascular diseases, and in particular coronary artery disease, remain the leading cause of death and disability worldwide, thereby underlining the importance of acquiring new therapeutic options in this field. A reduction in elevated resting heart rate (HR) has long been postulated as a therapeutic approach in the management of cardiovascular disease. An increased HR has been shown to be associated with increased progression of coronary atherosclerosis in animal models and patients. A high HR has also been associated with a greatly increased risk of plaque rupture in patients with coronary atherosclerosis. Endothelial function may be an important link between HR and atherosclerosis. An increased HR has been shown experimentally to cause endothelial dysfunction. Inflammation plays a significant role in the pathogenesis and progression of atherosclerosis. In the literature, there is data that shows an association between HR and circulating markers of vascular inflammation. In addition, HR reduction by pharmacological intervention with ivabradine (a selective HR-lowering agent that acts by inhibiting the pacemaker ionic current If in sinoatrial node cells) reduces the formation of atherosclerotic plaques in animal models of lipid-induced atherosclerosis. The aim of this editorial is to review the possible role of ivabradine on atherosclerosis.
文摘AIM To perform a systematic-review and meta-analysis to compare outcomes of ivabradine combined with betablocker to beta-blocker alone in heart failure with reduced ejection fraction(HFr EF).METHODS We searched PubM ed, Cochrane, EMBASE, CINAHL and Web of Science for trials comparing ivabradine + betablocker to beta-blocker alone in HFr EF. We performed a systematic-review and meta-analysis of published literature. Primary end-point was combined end point of cardiac death and hospitalization for heart failure.RESULTS Six studies with 17671 patients were included. Mean follow-up was 8.7 ± 7.9 mo. Combined end-point of heart failure readmission and cardiovascular death was better in ivabradine + beta-blocker group compared to beta-blocker alone(RR: 0.93, 95%CI: 0.79-1.09, P = 0.354). Mean difference(MD) in heart rate was higher in the ivabradine + beta-blocker group(MD: 6.14, 95%CI: 3.80-8.48, P < 0.001). There was no difference in all cause mortality(RR: 0.98, 95%CI: 0.89-1.07, P = 0.609), cardiovascular mortality(RR: 0.99, 95%CI: 0.86-1.15, P = 0.908) or heart failure hospitalization(RR: 0.87, 95%CI: 0.68-1.11, P = 0.271). CONCLUSION From the available clinical trials, ivabradine + betablocker resulted in a significantly greater reduction in HRcoupled with improvement in combined end-point of heart failure readmission and cardiovascular death but with no improvement in all cause or cardiovascular mortality. Given the limited evidence, further randomized controlled trials are essential before widespread clinical application of ivabradine + beta-blocker is advocated for HFrEF.
文摘Objective: To observe the effectiveness and safety of ivabradine in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and heart failure. Methods:Patients who were admitted to hospital with AECOPD during the period from August 2017 to July 2018. Then those both had heart failure with reduced ejection fraction(HFrEF) and a resting heart rate>70 beats/min were enrolled. A total of 86 cases were screened and completed, which were randomly divided into two groups for treatment. The control group(41 cases) received standard treatments, such as oxygen, anti-infection, anti-spasmodic, hormone, diuretic, ACEI/ARB, recombinant human brain natriuretic peptide (rhBNP), etc. The bisoprolol was given 2.5~5 mg orally once a day to control heart rate, and the test group(45 cases) was further treated with ivabradine 2.5~5 mg orally twice a day on the basis of the control group. The average heart rate, cardiac function, lung function, and 6-minute walking test were compared between the two groups. Results: After treatment, the average heart rate of the test group was lower than the control group, and the heart rate control rate(<70 beats/min%) of the test group was superior to the control group. The level of N-terminal B-type natriuretic peptide(NT-proBNP) in test group was significantly lower than that in control group. The distance of the 6-minute walking test in e test group was significantly longer than that in control group. Conclusion: Ivabradine combined with bisoprolol could help patients with AECOPD and heart failure to further reduce the heart rates, improve heart function and exercise tolerance. Moreover, the therapeutic safety was acceptable during the short term.
文摘Objective:To investigate the effects of ivabradine on Notch and NF-kappa B signaling pathway in myocardial cells of rats with myocardial infarction.Methods: The model of myocardial infarction was established by ligating the left anterior descending coronary artery. The surviving rats were randomly divided into model group (MI group,n=8) and treatment group (IVA group,n=8). Rats with the same location but without ligation of the left anterior descending coronary artery were used as control group (CON group,n = 8). IVA was administered for 28 d. Hemodynamic and cardiac function indexes of all rats were measured: heart rate (HR), systolic pressure (SBP), diastolic pressure (DBP), mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and maximum rate of increase and decrease of left ventricular internal pressure (+dp/dt);left ventricular mass index, left ventricular cross-sectional diameter and infarct area;The expression of Notch signaling pathway components mRNA (Notch-1, Dll-4, Hes-1) in rat cardiomyocytes was detected by PT-PCR, and the expression of DICD-1 and P65 protein was detected by western-blot. One-way ANOVA was used for comparison between groups, and SNK was used for comparison between groups.Results: SBP, DBP, MAP, LASP, LVEDP and (+dp/dt) in MI group were lower than those in control group (P<0.05), while IVA was higher than those in MI group (P<0.05). Left ventricular mass index and left ventricular sectional diameter in MI group were significantly higher than those in control group (P<0.05), but lower than those in IVA group (P<0.05). The expression of Notch-1 in MI group was significantly higher than that in control group (P<0.05), but lower than that in IVA group (P<0.05). There was no significant difference in the expression of Dll-4 and Hes-1 mRNA between the three groups (P>0.05). The expression levels of NICD-1 and P 65 in MI group were significantly higher than those in CON group (P<0.05), but lower than those in IVA group (P<0.05). Conclusion: IVA may improve cardiac function and inhibit ventricular remodeling in rats with myocardial infarction through Notch and NF-kappa B signaling pathways.
文摘The Systolic Heart failure treatment with the I( inhibitor ivabradine Trial (SHIFT, n = 6505) evaluated patients with symptomatic chronic heart failure (CHF), in sinus rhythm with resting heart rate ≥70 beats/min and left ventricular ejection fraction (LVEF)≤ 35%, average age 60 ± 11 years[1].
基金the National Natural Science Foundation Youth Science Foundation(No.81601661)the Science Foundation for Post-doctoral researchers in Anhui Province of China(No.2016B140).
文摘Post-resuscitation myocardial dysfunction(PRMD)is the most severe myocardial ischemia-reperfusion injury(MIRI)and is characterized by difficult treatment and poor prognosis.Research has shown the protective effects of the rational use of ivabradine(IVA)against PRMD,however,the molecular mechanisms of IVA remain unknown.In this study,an ischemia-reperfusion injury(IRI)model was established using hypoxic chambers.The results demonstrated that pretreatment with IVA reduced IRI-induced cytotoxicity and apoptosis.IVA attenuated mitochondrial damage,eliminated excess reactive oxygen species(ROS),suppressed IRI-induced ATP and NAD+,and increased the AMP/ATP ratio.We further found that IVA increased the mRNA levels of sirtuin 1(SIRT1)and peroxisome proliferator-activated receptor-γcoactivator 1α(PGC-1α)and upregulated the expression levels of phosphorylated AMP-activated protein kinase(p-AMPK)/AMPK,SIRT1,and PGC-1αproteins.Interestingly,no change in AMPK mRNA levels was observed.Cardiomyocyte energy metabolism significantly changed after IRI.The aim of this study was to demonstrate the cardioprotective effect of Ivabradine via the AMPK/SIRT1/PGC-1αsignaling pathway in myocardial ischemia/reperfusion injury-induced in H9c2 cell.
文摘Over the last 20 years, it has emerged that, while surgical revascularisation of extensive ischaemic heart disease may have prognostic advantages, the main issues considered regarding individual management are usually those of symptomatic improvement only. The major impetus towards invasive intervention is therefore failure of prophylactic anti-anginal therapy. On the other hand, many patients, especially the elderly, now present the clinical problem of ongoing angina without residual invasive options. There is an ongoing need for more effective anti-anginal therapies. Of the currently available major classes of prophylactic anti-anginal agents, neither nitrates, β-blockers nor calcium antagonists generally produce marked improvements in exercise duration. Three areas of new therapeutic development in anti-anginal therapy are worthy of note. These involve the sinus node inhibitor ivabradine, high dose allopurinol (xanthine oxidase inhibitor) and a new class of “metabolic modulators” represented by perhexiline, trimetazidine and probably ranolazine. The current review addresses the therapeutic potential of these agents. Notably, all of these “new” drugs are potentially suitable for management of angina in the setting of impaired left ventricular systolic function, and they may also be utilized in patients with angina independent of the presence of coronary disease (for example in hypertrophic cardiomyopathy). The current evidence for efficacy and potential future development in this area are reviewed.
文摘Background: Junctional ectopic tachycardia (JET) is one troublesome supraventricular arrhythmia in postoperative pediatric cardiac surgical patients. Unless treated timely and effectively it may lead to morbidity and even mortality. Aim: To understand the role of Ivabradine in the treatment of JET in postoperative pediatric cardiac surgical patients. Case: We present a postoperative case of complete repair of Tetralogy of Fallot who was in normal sinus rhythm in the preoperative period and developed JET 4 hours later in postoperative period which was persistent despite measures to optimize the internal milieu of the body and conventional antiarrhythmics, that was successfully treated with Ivabradine at a dose of 0.05 mg/kg/12 hourly. Conclusion: Ivabradine can be used to successfully treat postoperative JET in cases ofrefractory to other antiarrhythmic drugs like Digoxin and Amiodarone.
基金National 12th Five-Year Science and Technology Support Plan(No.2013BAI02B01)National Key Science and Technology Project of"Major New Drug Creation"(No.2019ZX09201005-002-006)+1 种基金Beijing TCM Science and Technology Development Fund Project(No.JJ-2020-79)Science and Technology Innovation Project of China Academy of Chinese Medical Sciences(No.CI2021A00920)。
文摘Objective:To systemically evaluate clinical efficacy and safety of traditional Chinese medicine(TCM)combined with ivabradine(IVA)in the treatment of chronic heart failure(CHF).Method:We searched China National Knowledge Infrastructure(CNKI)datebase,Wanfang datebase,Chinese Scientifific Journal Database(VIP)datebase,PubMed,Conchrane Library and EMbase database to enroll the random control trials(RCTs)of TCM combined with IVA treating CHF.Meta-analysis was performed by Review Manager 5.3 software.Results:A total of 10 RCTs involving 960 patients were included.The results of Meta-analysis showed that compared with control group,the experimental group could improve the efficiency of cardiac function improvement[RR=1.19,95%CI(1.12,1.27),P<0.00001],increase left ventricular ejection fraction[MD=4.36,95%CI(2.88,5.83),P<0.0001]and reduce heart rate[MD=-8.21,95%CI(-12.08,-4.34),P<0.00001],the incidence of adverse reactions was similar between two groups[RR=1.00,95%CI(0.62,1.61),P=1.00].Conclusion:Traditional Chinese medicine combined with ivabradine has significant efficacy and good safety in improving cardiac function,improving left ventricular ejection fraction and reducing heart rate in the treatment of chronic heart failure.
文摘A sensitive and specific liquid-chromatography tandem mass spectrometry(LC-MS/MS)assay has been developed and validated for the simultaneous quantification of ivabradine and its active metabolite N-desmethylivabradine in human plasma and urine.The assay employed a single liquid–liquid extraction of the analytes from plasma and urine samples,and diazepam was used as internal standard(IS).The chromatographic separation was achieved on a Diamonsil C18 column(150 mm4.6 mm,5 mm,Dikma)using a mixture of methanol and aqueous 5 mM ammonium acetate buffer containing 0.2%formic acid(80:20,v/v)as mobile phase.The assay for ivabradine and N-desmethylivabradine in plasma showed good linearity(r≥0.99)over the ranges 0.1013–101.3 ng/mL and 0.085–25.5 ng/mL,respectively.The assay for ivabradine and N-desmethylivabradine in urine showed good linearity(r≥0.99)over the ranges 10.13–6078 ng/mL and 8.5–850 ng/mL,respectively.The intra-and inter-day accuracy and precision values were found to be within the assay variability limits(RSD<15%)in accordance with FDA guidelines.The methods were successfully used for evaluating the pharmacokinetic properties of ivabradine and N-desmethylivabradine in human plasma and urine in Chinese healthy volunteers.
文摘目的评价伊伐布雷定对冠心病患者血管内皮功能的影响。方法检索PubMed、Embase、Cochrane图书馆、Web of Science、中国知网、万方数据、维普网、中国生物医学文献数据库,收集伊伐布雷定(干预组)对比安慰剂或β受体阻滞剂(对照组)的随机对照试验(RCT),检索时限为各数据库建库起至2023年3月20日。筛选文献、提取数据和评价质量后,采用RevMan5.4软件进行Meta分析。结果共纳入12项RCT,共计1206例患者。Meta分析结果显示,干预组患者的内皮依赖性血管舒张功能(FMD)[MD=1.71,95%CI(0.96,2.46),P<0.00001]、一氧化氮(NO)[MD=5.80,95%CI(5.02,6.59),P<0.00001]水平均显著高于对照组,内皮素1(ET-1)水平显著低于对照组[MD=-7.45,95%CI(-8.42,-6.47),P<0.00001]。两组患者的非内皮依赖性血管舒张功能(NMD)比较,差异无统计学意义[MD=0.13,95%CI(-0.74,1.00),P=0.77]。按照对照组用药和干预时间的不同进行的亚组分析结果显示,与安慰剂比较,使用伊伐布雷定患者的FMD水平显著升高(P<0.05);与安慰剂、β受体阻滞剂比较,使用伊伐布雷定患者的NO水平均显著升高(P<0.05)、ET-1水平均显著降低(P<0.05)。无论干预时间长短,干预组患者的FMD、NO、ET-1水平均较对照组显著改善(P<0.01),NMD比较差异无统计学意义(P>0.05)。结论伊伐布雷定能显著改善冠心病患者的血管内皮功能。
