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1.
Curr Top Med Chem ; 19(21): 1878-1901, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31400267

RESUMEN

Chronic Heart Failure (CHF) is a complex clinical syndrome with a high incidence worldwide. Although various types of pharmacological and device therapies are available for CHF, the prognosis is not ideal, for which, the control of increased Heart Rate (HR) is critical. Recently, a bradycardic agent, ivabradine, is found to reduce HR by inhibiting the funny current (If). The underlying mechanism states that ivabradine can enter the Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) channels and bind to the intracellular side, subsequently inhibiting the If. This phenomenon can prolong the slow spontaneous phase in the diastolic depolarization, and thus, reduce HR. The clinical trials demonstrated the significant effects of the drug on reducing HR and improving the symptoms of CHF with fewer adverse effects. This review primarily introduces the chemical features and pharmacological characteristics of ivabradine and the mechanism of treating CHF. Also, some expected therapeutic effects on different diseases were also concluded. However, ivabradine, as a typical If channel inhibitor, necessitates additional research to verify its pharmacological functions.


Asunto(s)
Fármacos Cardiovasculares/uso terapéutico , Insuficiencia Cardíaca/tratamiento farmacológico , Ivabradina/uso terapéutico , Animales , Fármacos Cardiovasculares/química , Enfermedad Crónica , Humanos , Ivabradina/química , Estructura Molecular
2.
Int Heart J ; 60(4): 899-909, 2019 Jul 27.
Artículo en Inglés | MEDLINE | ID: mdl-31308326

RESUMEN

To systematically review and conduct a meta-analysis of the ivabradine-induced improvement in cardiopulmonary function, exercise capacity, and primary composite endpoints in patients with chronic heart failure (CHF).This study was a systematic review and meta-analysis.Databases, including PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), and Clinical Trials and European Union Clinical Trials, were searched for randomized placebo-controlled trials. The efficacy and safety of ivabradine treatment in patients with CHF were assessed and compared to those of the standard anti-heart failure treatment. Review Manager 5.3 software was used to analyze the relative risk (RR) for dichotomous data and the mean difference (MD) for continuous data.In total, 22 studies with 24,562 patients were included. Cardiopulmonary function analysis showed that treatment with added ivabradine reduced the heart rate (MD = -17.30, 95% confidence interval (CI): 19.52--15.08, P < 0.00001), significantly increased the left ventricular ejection fraction (LVEF) (MD = 3.90, 95% CI: 0.40-7.40, P < 0.0001), and led to a better New York Heart Association (NYHA) classification. Ivabradine significantly reduced the minute ventilation/carbon dioxide production (VE/VCO2) (MD = -2.68, 95% CI: -4.81--0.55, P = 0.01) and improved the peak VO2 (MD = 2.80, 95% CI: 1.05-4.55, P = 0.002) and the exercise capacity, including the exercise duration with a submaximal load (MD = 7.82, 95% CI: -2.57--18.21, P < 0.00001) and the 6-minute walk distance. The RR of cardiovascular death or worsening heart failure was significantly decreased (RR = 0.93, 95% CI: 0.87--0.98, P = 0.01) in the patients treated with ivabradine. Additionally, the RRs of heart failure and hospitalization also decreased (RR = 0.91, 95% CI: 0.85--0.97, P = 0.006; RR = 0.86, 95% CI: 0.79--0.93, P = 0.0002). Safety analysis showed no significant difference in the RR of severe adverse events between the ivabradine group and the standard anti-heart failure treatment group (P = 0.40). However, ivabradine significantly increased the RR of visual symptoms in CHF patients (RR = 3.82, 95% CI: 1.80--8.13, P = 0.0005).Existing evidence showed that adding ivabradine treatment significantly improved the cardiopulmonary function and increased the exercise capacity of patients with CHF. Adding ivabradine to the standard anti-heart failure treatment reduced the mortality and hospitalization risk and improved the quality of life. Finally, ivabradine significantly increased the RR of visual symptoms in CHF patients.This is the first systematic review and meta-analysis to focus on the efficacy of ivabradine, which improved the cardiac function and increased the exercise capacity in patients with chronic heart failure (CHF). Therefore, this study will help evaluate the quality of life after adding ivabradine to the treatment of patients with CHF, even though there are differences in the standard for resting heart rate, left ventricular ejection fraction (LVEF), and New York Heart Association (NYHA) class in the included studies. This hybrid effect might be smaller when analyzed separately but might have a higher heterogeneity when analyzed in multiple studies.


Asunto(s)
Tolerancia al Ejercicio/efectos de los fármacos , Insuficiencia Cardíaca/tratamiento farmacológico , Ivabradina/uso terapéutico , Volumen Sistólico/fisiología , Función Ventricular Izquierda/fisiología , Fármacos Cardiovasculares/uso terapéutico , Insuficiencia Cardíaca/fisiopatología , Humanos , Volumen Sistólico/efectos de los fármacos , Función Ventricular Izquierda/efectos de los fármacos
3.
Medicine (Baltimore) ; 98(14): e15075, 2019 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-30946357

RESUMEN

BACKGROUND: Previous clinical trials have reported that ivabradine can effectively treat heart failure (HF). However, no systematic review has explored its efficacy and safety for HF. This systematic review will aim to evaluate the efficacy and safety of ivabradine for the treatment of patients with HF. METHODS: We will search the literature from the following electronic databases from inception to the January 31, 2019: Cochrane Central Register of Controlled Trials, EMBASE, MEDILINE, Web of Science, Cumulative Index to Nursing and Allied Health Literature, Allied and Complementary Medicine Database, Chinese Biomedical Literature Database, China National Knowledge Infrastructure, VIP Information, and Wanfang Data. All randomized controlled trials (RCTs) of ivabradine for HF will be fully considered for inclusion without any restrictions. Additionally, grey literature including clinical trial registries, dissertations, and reference lists of included studies, conference abstracts will also be searched. Two researchers will review these literatures, extract data, and assess risk of bias of included RCTs separately. Data will be pooled by either fixed-effects model or random-effects model, and meta-analysis will be conducted if it is appropriate. RESULTS: The primary outcome is all-cause mortality. The secondary outcomes comprise of change in body weight, urine output, change in serum sodium, and all adverse events. CONCLUSIONS: The results of this study will summary provide up-to-dated evidence for assessing the efficacy and safety of ivabradine for HF. ETHICS AND DISSEMINATION: It is not necessary to acquire ethical approval for this systematic review, because no individual patient data will be used in this study. The results of this systematic review will be published through peer-reviewed journals. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42019120814.


Asunto(s)
Fármacos Cardiovasculares/uso terapéutico , Insuficiencia Cardíaca/tratamiento farmacológico , Ivabradina/uso terapéutico , Revisiones Sistemáticas como Asunto , China , Insuficiencia Cardíaca/mortalidad , Humanos , Ensayos Clínicos Controlados Aleatorios como Asunto , Proyectos de Investigación
4.
BMJ Case Rep ; 12(4)2019 Apr 20.
Artículo en Inglés | MEDLINE | ID: mdl-31005863

RESUMEN

Syncope is a sudden loss and gain of consciousness. Traditionally, it is caused by the abnormalities of neurological, cardiac or vasovagal systems. We present a case of a 19-year-old woman presenting with recurrent syncopal episodes with no apparent cause. Examination and investigations were unremarkable for any aetiology except positive tilt tests for postural orthostatic tachycardia syndrome. The purpose of this report is to make physicians aware of the unique presentation of this rare aetiology with recurrent syncopal episodes and the novel management approach.


Asunto(s)
Fármacos Cardiovasculares/uso terapéutico , Ivabradina/uso terapéutico , Síndrome de Taquicardia Postural Ortostática/tratamiento farmacológico , Síncope/etiología , Electrocardiografía , Femenino , Humanos , Síndrome de Taquicardia Postural Ortostática/complicaciones , Síndrome de Taquicardia Postural Ortostática/diagnóstico , Pruebas de Mesa Inclinada , Adulto Joven
5.
J Chin Med Assoc ; 82(1): 19-24, 2019 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-30839398

RESUMEN

BACKGROUND: Ivabradine is a funny current inhibitor which is administered to patients with congestive heart failure to reduce their heart rate (HR) and attenuate oxidative stress. Chronic liver diseases are characterized by portal hypertension and hyperdynamic circulation with tachycardia. The present study aimed to investigate the effect of ivabradine on portal hypertension. METHODS: Male Sprague-Dawley rats received partial portal vein ligation (PVL) to induce portal hypertension. The PVL rats were randomly allocated to receive either vehicle or ivabradine treatment for 10 days. Then the hemodynamic data were collected. The levels of oxidative stress markers and the mRNA expression of nitric oxide synthase (NOS) were measured in the collateral vessel, the superior mesentery artery and the liver. In addition, the collateral vascular responsiveness to arginine vasopressin (AVP) was examined in the ivabradine-treated and vehicle-treated PVL rats. RESULTS: Treatment with ivabradine significantly lowered the HR (174 ± 20 vs. 374 ± 9 beats/min; p < 0.001) and the superior mesentery arterial flow (SMAf) (6.6 ± 0.3 vs. 9.1 ± 0.7 mL/min/100 g BW; p = 0.005) of the PVL rats compared with the control group. The mean arterial pressure, cardiac index, systemic vascular resistance, portal pressure and serum levels of oxidative stress markers were not significantly affected by ivabradine treatment. In addition, the NOS expression and collateral vascular responsiveness to AVP were not significantly influenced by ivabradine treatment, either. CONCLUSION: Ivabradine reduced the HR and SMAf in PVL rats, which alleviated the hyperdynamic circulatory state and splanchnic hyperemia of portal hypertension. However, whether these effects would help alleviate portal hypertension-related complications requires further clinical investigations.


Asunto(s)
Hipertensión Portal/tratamiento farmacológico , Ivabradina/uso terapéutico , Animales , Hemodinámica/efectos de los fármacos , Hipertensión Portal/fisiopatología , Ivabradina/farmacología , Masculino , Arteria Mesentérica Superior/efectos de los fármacos , Arteria Mesentérica Superior/fisiología , Óxido Nítrico Sintasa de Tipo II/genética , Óxido Nítrico Sintasa de Tipo III/genética , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas Sprague-Dawley
8.
Int J Clin Pharm ; 41(1): 22-29, 2019 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-30659493

RESUMEN

Background Patients with mitral valve stenosis have increased heart rate. HR reduction is known as an important treatment and therapy strategy for patients with mitral valve stenosis. Aim of the review The aim of this systematic review and meta-analysis was to compare the efficacy of ivabradine versus beta-blockers in patients with mitral stenosis in sinus rhythm. Methods Randomized controlled trials were searched in Cochrane Library, PubMed, Web of Science, CRD, Scopus, and Google Scholar with no start time limitation and ending June 2018. Risk of bias across was assessed by the Cochrane Risk of Bias Assessment tool. Fixed effects models were used to combine the results and the mean difference with a 95% confidence interval. This meta-analysis was performed using Meta Package in R software. Results Five studies entered meta-analysis. The total number of patients treated with ivabradine and beta-blockers was 178 and 178 respectively. The results showed that the mean of maximum HR and HR at rest was lower at about 5.03 units and upper 4.32 units respectively with use of ivabradine compared with the use of beta-blockers. These values were statistically significant. Conclusion It seems that the efficacy of ivabradine is good in comparison with betablockers, but it still requires more clinical trials.


Asunto(s)
Antagonistas Adrenérgicos beta/uso terapéutico , Arritmias Cardíacas/tratamiento farmacológico , Fármacos Cardiovasculares/uso terapéutico , Ivabradina/uso terapéutico , Estenosis de la Válvula Mitral/tratamiento farmacológico , Antagonistas Adrenérgicos beta/farmacología , Arritmias Cardíacas/diagnóstico , Arritmias Cardíacas/epidemiología , Fármacos Cardiovasculares/farmacología , Frecuencia Cardíaca/efectos de los fármacos , Frecuencia Cardíaca/fisiología , Humanos , Ivabradina/farmacología , Estenosis de la Válvula Mitral/diagnóstico , Estenosis de la Válvula Mitral/epidemiología , Ensayos Clínicos Controlados Aleatorios como Asunto/métodos , Resultado del Tratamiento
9.
Biomed Pharmacother ; 109: 2499-2512, 2019 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-30551511

RESUMEN

We analyzed whether ivabradine (IVA), a hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker, clinically used for angina and arrhythmia, had anticonvulsant, antioxidant and neuroprotective properties against classical seizure models. Potential molecular targets to IVA anticonvulsant effects were evaluated by molecular docking. Mice were treated with IVA (1, 10 or 20 mg/kg, IP) for 3 days, and 30 min after the last administration were injected with pentylenetetrazole (PTZ - 85 mg/kg, IP), pilocarpine (PILO 400 mg/kg, SC), picrotoxin (PICRO 10 mg/kg, IP). The following measures were performed: presence of seizures, latency for the first seizure, latency for death, percentage of survival. Antioxidant activity was investigated by determination of lipid peroxidation (MDA), reduced glutathione (GSH) and nitrite levels in the prefrontal cortex (PFC), hippocampus and striatum (ST). Immunohistochemistry analysis for cleaved caspase-3, a pro-apoptotic and degenerative marker, in hippocampal subregions namely cornu ammonis (CA)1, CA3 and dentate gyrus (DG), were also performed. IVA attenuated PTZ- and PICRO-induced seizures while presented an antioxidant effect in all brain areas studied. IVA markedly reduced cleaved caspase-3 expression in the CA1 and DG region of PICRO- and PTZ-treated mice, respectively. Molecular docking demonstrated that IVA has high energetic affinity and binding compatibility for GABAA receptor without causing channel obstruction. However, no reproducibility in the binding of IVA to N-methyl-d-aspartate (NMDA) receptor was detected. In conclusion, IVA has anticonvulsant, antioxidant and neuroprotective effects against PTZ- and PICRO-induced seizures. Also, a high affinity of IVA to GABAA receptor was predicted, representing a potential underlying mechanism to these observable effects.


Asunto(s)
Anticonvulsivantes/uso terapéutico , Encéfalo/metabolismo , Ivabradina/uso terapéutico , Fármacos Neuroprotectores/uso terapéutico , Convulsiones/metabolismo , Convulsiones/prevención & control , Animales , Anticonvulsivantes/farmacología , Encéfalo/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Ivabradina/farmacología , Masculino , Ratones , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo/efectos de los fármacos , Estrés Oxidativo/fisiología , Pentilenotetrazol/toxicidad , Pilocarpina/toxicidad , Estructura Secundaria de Proteína , Receptores de GABA-A/química , Receptores de GABA-A/metabolismo , Receptores de N-Metil-D-Aspartato/química , Receptores de N-Metil-D-Aspartato/metabolismo , Convulsiones/inducido químicamente
10.
Anatol J Cardiol ; 20(5): 266-272, 2018 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-30391964

RESUMEN

OBJECTIVE: We investigated the underlying mechanism of ivabradine (IVA) in promoting angiogenesis and reducing cardiac hypertrophy in mice with myocardial infarction (MI). METHODS: Nineteen mice were randomly assigned into three groups as follows: sham group (10 ml/kg/day phosphate buffer saline (PBS), n=6), model group (MI and 10 ml/kg/day PBS, n=6) and IVA group (MI and 10 mg/kg/day IVA, n=7). All groups received an intragastric gavage for four weeks. Heart and body mass were measured. Cardiac function and heart rate were assessed by echocardiography and electrocardiography, respectively. The collagen deposition, area of cardiomyocytes, and number of capillaries were evaluated using Masson's staining, anti-wheat germ agglutinin (WGA) staining, and platelet endothelial cell adhesion molecule-1 (CD31) staining, respectively. The protein kinase B (Akt)- endothelial nitric oxide synthase (eNOS) signaling and p-38 mitogen-activated protein kinase (MAPK) family in myocardium were determined by western blot. RESULTS: IVA treatment greatly improved cardiac dysfunction and suppressed cardiac hypertrophy at 4 weeks after MI (p<0.05). Heart rate and fibrotic area of IVA group declined notably compared to those of the model group (p<0.05). IVA administration substantially reduced cardiomyocyte size and increased capillary formation (p<0.05). Besides, IVA medication can enhance Akt-eNOS signaling and inhibit p38 MAPK phosphorylation in the heart of mice with MI (p<0.05). CONCLUSION: IVA can perform two functions, the promotion of angiogenesis and the reduction of cardiac hypertrophy, both of which were closely associated with Akt-eNOS signaling activation and p38 MAPK inhibition.


Asunto(s)
Cardiomegalia/tratamiento farmacológico , Fármacos Cardiovasculares/uso terapéutico , Ivabradina/uso terapéutico , Infarto del Miocardio/complicaciones , Administración Oral , Inductores de la Angiogénesis , Animales , Cardiomegalia/diagnóstico por imagen , Cardiomegalia/patología , Cardiomegalia/prevención & control , Fármacos Cardiovasculares/administración & dosificación , Modelos Animales de Enfermedad , Ecocardiografía , Electrocardiografía , Frecuencia Cardíaca , Ivabradina/administración & dosificación , Masculino , Ratones , Ratones Endogámicos C57BL , Miocardio/enzimología , Óxido Nítrico Sintasa de Tipo III/metabolismo , Distribución Aleatoria
11.
Kardiologiia ; 58(6): 85-89, 2018 06.
Artículo en Ruso | MEDLINE | ID: mdl-30362441

RESUMEN

Chronic heart failure with preserved ejection fraction (HFpEF) accounts for about 50% of cases of heart failure, but pharmacotherapy that improves its outcomes has not been developed. The proven principle of improving outcomes in patients with chronic heart failure with a reduced of left ventricular ejection fraction is the decrease in heart rate. The article discusses situations in which treatment with ß-blockers is not effective or negatively affects outcomes. The results of own research and the EDIFY project, in which ivabradine was used in patients with HFpEF, were compared. The importance of phenotyping patients with HFpEF is stated to increase the effectiveness of their therapy.


Asunto(s)
Insuficiencia Cardíaca/tratamiento farmacológico , Insuficiencia Cardíaca/fisiopatología , Volumen Sistólico , Antagonistas Adrenérgicos beta/uso terapéutico , Anciano , Fármacos Cardiovasculares/uso terapéutico , Enfermedad Crónica , Frecuencia Cardíaca/efectos de los fármacos , Humanos , Ivabradina/uso terapéutico , Masculino , Resultado del Tratamiento , Función Ventricular Izquierda
12.
J Int Med Res ; 46(11): 4825-4828, 2018 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-30223689

RESUMEN

Left bundle branch block increases the risk of death in patients with chronic heart failure. We herein report four clinical cases of patients with chronic heart failure caused by nonischemic cardiomyopathy with left bundle branch block that occurred when adding ivabradine to optimal medical therapy, resulting in reverse electrical and mechanical remodeling. This phenomenon might be explained by the effect of ivabradine on reverse remodeling of the left ventricle with improvement of intraventricular conduction.


Asunto(s)
Remodelación Atrial/efectos de los fármacos , Bloqueo de Rama/complicaciones , Bloqueo de Rama/fisiopatología , Cardiomiopatías/complicaciones , Cardiomiopatías/fisiopatología , Frecuencia Cardíaca/efectos de los fármacos , Ivabradina/farmacología , Ivabradina/uso terapéutico , Adulto , Anciano , Bloqueo de Rama/diagnóstico por imagen , Bloqueo de Rama/tratamiento farmacológico , Cardiomiopatías/diagnóstico por imagen , Cardiomiopatías/tratamiento farmacológico , Electrocardiografía , Femenino , Humanos , Masculino , Persona de Mediana Edad
13.
Int J Clin Pract ; 72(11): e13217, 2018 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-30248211

RESUMEN

BACKGROUND: Resting heart rate (HR) reduction with ivabradine (IVA) improves outcomes of patients with heart failure and reduced ejection fraction (HFrEF). Nevertheless, the best option to slow HR in patients with HFrEF treated with beta-blockers and a HR >70 bpm is unsettled. AIMS: To evaluate whether, in patients with HFrEF, commencing therapy with digoxin (CT-DIG) is associated to a worse prognosis than commencing treatment with ivabradine (CT-IVA). METHODS: Observational study over 10 years on 2364 patients with HFrEF in sinus rhythm and a HR >70 bpm. Main outcomes were mortality, hospitalisations and visits. We analyse the independent relationship of CT-DIG or CT-IVA with the prognosis, stratifying patients for cardiovascular comorbidity, and for other potential confounders (378 patients who CT-DIG vs another 355 patients who CT-IVA vs another 1631 patients non-exposed to IVA or DIG). RESULTS: During a median follow-up of 57.5 months, 1751 patients (74.1%) died, and 2151 (91.0%) were hospitalised for HF. CT-DIG or CT-IVA was associated with a lower all-cause mortality (DIG: HR = 0.86 [95% CI, 0.82-0.90], and IVA: HR = 0.88 [0.83-0.93]), cardiovascular mortality (DIG: HR = 0.84 [0.80-0.89] and IVA: HR = 0.83 [0.78-0.89]), hospitalisation (DIG: HR = 0.86 [0.83-0.89] and IVA: HR = 0.87 [0.83-0.91]) and 30-day readmission (DIG: HR = 0.84 [0.79-0.90] and IVA: HR = 0.88 [0.79-0.95]), after adjustment for cardiovascular comorbidity, and other potential confounders. These associations with the prognosis of HFrEF did not differ between patients who CT-DIG and those who CT-IVA. CONCLUSION: Commencing therapy with digoxin or with ivabradine is associated with an improved prognosis of patients with HFrEF.


Asunto(s)
Cardiotónicos/uso terapéutico , Fármacos Cardiovasculares/uso terapéutico , Digoxina/uso terapéutico , Insuficiencia Cardíaca/tratamiento farmacológico , Ivabradina/uso terapéutico , Antagonistas Adrenérgicos beta/uso terapéutico , Anciano , Estudios de Cohortes , Comorbilidad , Femenino , Insuficiencia Cardíaca/mortalidad , Insuficiencia Cardíaca/fisiopatología , Hospitalización/estadística & datos numéricos , Humanos , Masculino , Readmisión del Paciente , Pronóstico , Volumen Sistólico , Resultado del Tratamiento
14.
Int J Clin Pharm ; 40(6): 1443-1453, 2018 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-30173307

RESUMEN

Background Ivabradine is currently indicated to lower heart rate in Heart Failure with Reduced Ejection Fraction (HFrEF) patients. However its effect apart from beta-blockers is not clear. Aim of the review To study the additional effect of ivabradine, apart from the effect of beta-blockers, on cardiovascular death, all-cause mortality, hospitalization due to HF and heart rate in HFrEF population. Method Electronic searches were conducted up to June 2016 to include randomized controlled trials where ivabradine was compared to a control group. Relative risks RRs and their 95% confidence intervals (CI 95%) were pooled and the random and fixed effect were used to summarize the results according to heterogeneity levels. Heterogeneity among studies was measured by the I-squared statistic Results Of 1790 studies, seven met the inclusion criteria for the systematic review and meta-analysis. The population consisted of 17,747 patients. Risk of bias was generally high for beta-blocker doses lower than recommended. Interventions lasted 1.5-22.9 months and pooled relative risks RR (95%) for all-cause mortality, cardiovascular death and hospitalization for HF were 0.98 (0.90-1.06); 0.99 (0.91-1.08); and 0.87 (0.68-1.12) respectively. Heart rate (CI 95%) decreased by 8.7 (6.37-11.03) beats per minute with ivabradine compared to the control group. Subgroup analysis by beta-blocker dose showed that for patients on recommended treatment (at least 50% of the beta-blocker target dose), heart rate (CI 95%) decreased by 4.70 (3.67-5.73), whereas for patients not on recommended treatment or with unreported dose, heart rate decreased by 8.60 (8.13-9.08). Conclusion Ivabradine significantly reduced heart rate and its additional effect on heart rate appears to be inversely correlated with the dose of beta-blocker. It showed no significant effect for all-cause mortality, cardiovascular death and hospitalization due to HF. Unreported beta-blocker doses and beta-blocker doses lower than recommended limited the conclusions.


Asunto(s)
Cardiotónicos/uso terapéutico , Insuficiencia Cardíaca/tratamiento farmacológico , Insuficiencia Cardíaca/fisiopatología , Ivabradina/uso terapéutico , Volumen Sistólico , Antagonistas Adrenérgicos beta/efectos adversos , Antagonistas Adrenérgicos beta/uso terapéutico , Cardiotónicos/efectos adversos , Insuficiencia Cardíaca/mortalidad , Humanos , Ivabradina/efectos adversos , Resultado del Tratamiento
15.
Crit Care ; 22(1): 193, 2018 08 17.
Artículo en Inglés | MEDLINE | ID: mdl-30115103

RESUMEN

BACKGROUND: Low cardiac output syndrome (LCOS) is a severe condition which can occur after cardiac surgery, especially among patients with pre-existing left ventricular dysfunction. Dobutamine, its first-line treatment, is associated with sinus tachycardia. This study aims to assess the ability of intravenous ivabradine to decrease sinus tachycardia associated with dobutamine infused for LCOS after coronary artery bypass graft (CABG) surgery. METHODS: In a phase 2, multi-center, single-blind, randomized controlled trial, patients with left ventricular ejection fraction below 40% presenting sinus tachycardia of at least 100 beats per minute (bpm) following dobutamine infusion for LCOS after CABG surgery received either intravenous ivabradine or placebo (three ivabradine for one placebo). Treatment lasted until dobutamine weaning or up to 48 h. The primary endpoint was the proportion of patients achieving a heart rate (HR) in the 80- to 90-bpm range. Secondary endpoints were invasive and non-invasive hemodynamic parameters and arrhythmia events. RESULTS: Nineteen patients were included. More patients reached the primary endpoint in the ivabradine than in the placebo group (13 (93%) versus 2 (40%); P = 0.04). Median times to reach target HR were 1.0 h in the ivabradine group and 5.7 h in the placebo group. Ivabradine decreased HR (112 to 86 bpm, P <0.001) while increasing cardiac index (P = 0.02), stroke volume (P <0.001), and systolic blood pressure (P = 0.03). In the placebo group, these parameters remained unchanged from baseline. In the ivabradine group, five patients (36%) developed atrial fibrillation (AF) and one (7%) was discontinued for sustained AF; two (14%) were discontinued for bradycardia. CONCLUSION: Intravenous ivabradine achieved effective and rapid correction of sinus tachycardia in patients who received dobutamine for LCOS after CABG surgery. Simultaneously, stroke volume and systolic blood pressure increased, suggesting a beneficial effect of this treatment on tissue perfusion. TRIAL REGISTRATION: European Clinical Trials Database: EudraCT 2009-018175-14 . Registered February 2, 2010.


Asunto(s)
Gasto Cardíaco Bajo/etiología , Puente de Arteria Coronaria/efectos adversos , Ivabradina/uso terapéutico , Administración Intravenosa , Anciano , Cardiotónicos/uso terapéutico , Fármacos Cardiovasculares/uso terapéutico , Puente de Arteria Coronaria/métodos , Dobutamina/uso terapéutico , Procedimientos Quirúrgicos Electivos/efectos adversos , Procedimientos Quirúrgicos Electivos/métodos , Femenino , Humanos , Masculino , Persona de Mediana Edad , Placebos/uso terapéutico , Método Simple Ciego
16.
Pacing Clin Electrophysiol ; 41(10): 1378-1380, 2018 10.
Artículo en Inglés | MEDLINE | ID: mdl-29989676

RESUMEN

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a potentially lethal hereditary disease characterized by complex ventricular arrhythmias provoked by exercise or emotional stress and by a high mortality rate in young individuals. Nadolol alone or in combination with flecainide is the most effective therapy. However, compliance to treatment is often low due to side effects. We report two patients with CPVT in whom side effects of treatment prompted discontinuation of flecainide or nadolol and in whom ivabradine was successfully added to therapy. In these two patients, ivabradine in combination with nadolol or flecainide was well tolerated and successfully suppressed nonsustained polymorphic ventricular tachycardia and couplets. Thus, ivabradine could limit the use of implantable cardioverter-defibrillators or left cardiac sympathetic denervation in CPVT patients with uncontrollable ventricular arrhythmias.


Asunto(s)
Fármacos Cardiovasculares/uso terapéutico , Ivabradina/uso terapéutico , Taquicardia Ventricular/tratamiento farmacológico , Adolescente , Antiarrítmicos/uso terapéutico , Electrocardiografía , Prueba de Esfuerzo , Femenino , Flecainida/uso terapéutico , Humanos , Masculino , Nadolol/uso terapéutico , Taquicardia Ventricular/fisiopatología , Adulto Joven
17.
Georgian Med News ; (278): 87-93, 2018 May.
Artículo en Ruso | MEDLINE | ID: mdl-29905551

RESUMEN

This review is devoted to the urgent problem of cardiology and oncology - the cardiotoxicity of chemotherapy drugs - anthracyclines, which are considered to be one of the most cardiotoxic and cause a variety of cardiotoxic effects. The review also examines the diagnosis, treatment or preventive treatment of this pathology. The urgency of the problem is associated with the possibility of early or late manifestations of cardiotoxicity, manifestations of cardiotoxicity against the background of cross treatment, manifestations of cardiotoxicity against the background of various concomitant diseases. The review identified 9 main categories of cardiovascular complications during chemotherapeutic treatment and presents the types of cardiotoxicity caused by the use of anthracyclines. The issue of heart failure as a manifestation of anthracycline cardiotoxicity and the approaches to early diagnosis of cardiac insufficiency were examined in detail. The recommendations of the European Society of Medical Oncology (ESMO) (2012), the recommendations the European Society of Cardiology (ESC) in 2016 regarding the diagnosis and treatment of these patients are reviewed. An overview of the literature on the treatment and diagnosis of this category of patients is presented, especially with concomitant diseases. Examination of the patients, the timing of the initiation of therapy, preventive treatment, medication correction of heart failure, the doses, the combinations of chemotherapeutic drugs are issues that are recommended for the multidisciplinary team to successfully manage these patients.


Asunto(s)
Antraciclinas/efectos adversos , Antineoplásicos/efectos adversos , Cardiomiopatías/tratamiento farmacológico , Cardiotónicos/uso terapéutico , Cardiotoxicidad/tratamiento farmacológico , Insuficiencia Cardíaca/prevención & control , Biomarcadores/sangre , Cardiomiopatías/sangre , Cardiomiopatías/inducido químicamente , Cardiomiopatías/diagnóstico , Cardiotoxicidad/sangre , Cardiotoxicidad/diagnóstico , Cardiotoxicidad/etiología , Ecocardiografía , Venenos Elapídicos/sangre , Corazón/efectos de los fármacos , Corazón/fisiopatología , Insuficiencia Cardíaca/sangre , Insuficiencia Cardíaca/inducido químicamente , Insuficiencia Cardíaca/diagnóstico , Humanos , Ivabradina/uso terapéutico , Péptido Natriurético Tipo-C/sangre , Neoplasias/sangre , Neoplasias/tratamiento farmacológico , Neoplasias/patología , Análisis de Supervivencia , Trastuzumab/efectos adversos , Trimetazidina/uso terapéutico , Troponina I/sangre
18.
Ann Intern Med ; 168(11): ITC81-ITC96, 2018 06 05.
Artículo en Inglés | MEDLINE | ID: mdl-29868816

RESUMEN

Heart failure affects more than 6 million people in the United States and incurs a heavy toll in morbidity, mortality, and health care costs. It frequently coexists with other important disorders, including hypertension, coronary artery disease, diabetes, and obesity. Decades of clinical trials have shown that several medications and interventions are effective for improving outcomes; however, mortality and hospitalization rates remain high. More recently, additional medications and devices have shown promise in reducing the health burden of heart failure.


Asunto(s)
Insuficiencia Cardíaca/diagnóstico , Insuficiencia Cardíaca/terapia , Antagonistas Adrenérgicos beta/uso terapéutico , Antagonistas de Receptores de Angiotensina/uso terapéutico , Inhibidores de la Enzima Convertidora de Angiotensina/uso terapéutico , Anticoagulantes/uso terapéutico , Rehabilitación Cardiaca , Fármacos Cardiovasculares/uso terapéutico , Enfermedad de la Arteria Coronaria/complicaciones , Desfibriladores Implantables , Complicaciones de la Diabetes , Técnicas de Diagnóstico Cardiovascular , Digoxina/uso terapéutico , Diuréticos/uso terapéutico , Insuficiencia Cardíaca/etiología , Hospitalización , Humanos , Hidralazina/uso terapéutico , Hipertensión/complicaciones , Dinitrato de Isosorbide/uso terapéutico , Ivabradina/uso terapéutico , Estilo de Vida , Antagonistas de Receptores de Mineralocorticoides/uso terapéutico , Cuidados Paliativos , Prevención Primaria , Derivación y Consulta , Factores de Riesgo
19.
Pacing Clin Electrophysiol ; 41(10): 1372-1377, 2018 10.
Artículo en Inglés | MEDLINE | ID: mdl-29856078

RESUMEN

Junctional ectopic tachycardia (JET) is a rare form of arrhythmia that is most commonly seen during infancy. JET is continuous and incessant, characterized by persistently high heart rates that may result in impaired cardiac function and tachycardia-induced cardiomyopathy. Despite the availability of multiple antiarrhythmic treatments, including flecainide and amiodarone, management of JET is generally very difficult. Catheter ablation has a high risk of atrioventricular block and it may require the placement of a pacemaker. Ivabradine, also known as a cardiac pacemaker cell inhibitor, is a new-generation antiarrhythmic used to treat sinus tachycardia and angina pectoris in adult patients. In this article, we present three cases of subjects with infantile congenital JET who were admitted to our clinic with a tachycardia-induced cardiomyopathy. The age of the subjects ranged from 52 days to 10 months. Although the cases of tachycardia could not be controlled by multiple antiarrhythmics, including a combination of amiodarone and flecainide combined with either propranolol or digoxin, they were rapidly converted into sinus rhythm with an ivabradine treatment of 0.1-0.2 mg/kg/day. No cardiac or other side effects were observed during ivabradine treatment, and left ventricular functions and rhythms improved within 24 hours. These three cases therefore provide hope that ivabradine may be a suitable standard initial treatment for congenital JET. However, additional research is needed to confirm the validity of these results in other circumstances.


Asunto(s)
Cardiomiopatías/tratamiento farmacológico , Fármacos Cardiovasculares/uso terapéutico , Ivabradina/uso terapéutico , Taquicardia Ectópica de Unión/tratamiento farmacológico , Cardiomiopatías/etiología , Cardiomiopatías/fisiopatología , Electrocardiografía , Femenino , Humanos , Lactante , Masculino , Taquicardia Ectópica de Unión/complicaciones , Taquicardia Ectópica de Unión/congénito , Taquicardia Ectópica de Unión/fisiopatología
20.
J Cardiovasc Med (Hagerstown) ; 19(7): 351-356, 2018 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-29762337

RESUMEN

: Ivabradine is a selective and specific inhibitor of If current. With its pure negative chronotropic action, it is recommended by European Society of Cardiology and American College of Cardiology/American Heart Association guidelines in symptomatic heart failure patients (NYHA ≥ 2) with ejection fraction 35% or less, sinus rhythm and heart rate (HR) at least 70 bpm, despite maximally titrated ß-blocker therapy. Data supporting this indication mainly derive from the SHIFT study, in which ivabradine reduced the combined endpoint of mortality and hospitalization, despite the fact that only 26% of patients enrolled were on optimal ß-blocker doses. The aim of the present analysis is to establish the real-life eligibility for ivabradine in a population of patients with systolic heart failure, regularly attending a single heart failure clinic and treated according to guideline-directed medical therapy (GDMT). The clinical cards of 308 patients with heart failure with reduced ejection fraction (HFrEF) through a 68-month period of observation were retrospectively analyzed. GDMT, including ß-blocker up-titration to maximal tolerated dose, was implemented during consecutive visits at variable intervals. Demographic, clinical and echocardiographic data were collected at each visit, together with 12-leads ECG and N-terminal pro-B-type natriuretic peptide levels. Out of 308 analyzed HFrEF patients, 220 (71%) were on effective ß-blocker therapy, up-titrated to effective/maximal tolerated dose (55 ±â€Š28% of maximal dose) (HR 67 ±â€Š10 bpm). Among the remaining 88 patients, 10 (3.2%) were on maximally tolerated ß blocker and ivabradine; 21 patients (6.8%), despite being on maximal tolerated ß-blocker dose, had still HR ≥70 bpm, ejection fraction 35% or less and were symptomatic NYHA ≥2, being therefore eligible for ivabradine treatment. The remaining 57 (18%) patients were not on ß blocker due to either intolerance or major contraindications. Among them, 13 (4%) were taking ivabradine alone. Of the final 44 (14%) patients, 27 (9%) showed an inadequate HR control (74 ±â€Š6 bpm). Of these, only eight (3%) patients resulted to be eligible for ivabradine introduction according to HR and ejection fraction parameters. Overall ivabradine was indicated in 52 patients (16.8%) out of 308 enrolled.In conclusion, in a carefully managed population of patients with moderate and stable HFrEF, in which optimal GDMT is properly attained, indication to ivabradine treatment is around 17%.


Asunto(s)
Antagonistas Adrenérgicos beta/uso terapéutico , Fármacos Cardiovasculares/uso terapéutico , Insuficiencia Cardíaca Sistólica/tratamiento farmacológico , Insuficiencia Cardíaca Sistólica/mortalidad , Ivabradina/uso terapéutico , Anciano , Anciano de 80 o más Años , Enfermedad Crónica , Ecocardiografía , Femenino , Frecuencia Cardíaca/efectos de los fármacos , Hospitalización/estadística & datos numéricos , Humanos , Masculino , Persona de Mediana Edad , Péptido Natriurético Encefálico/sangre , Fragmentos de Péptidos/sangre , Estudios Retrospectivos , Volumen Sistólico/efectos de los fármacos , Función Ventricular Izquierda/efectos de los fármacos
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