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1.
Int J Cardiol ; 293: 39-44, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31178223

RESUMO

Abnormalities of myocardial energy metabolism appear as a common background of the two major cardiac disorders: ischemic heart disease (IHD) and heart failure (HF). Myocardial ischemia has been recently conceived as a multifaceted syndrome that can be precipitated by a number of mechanisms including metabolic abnormalities. HF is a progressive disorder characterised by a complex interaction of haemodynamic, neurohormonal and metabolic disturbances. HF may further promote metabolic changes, generating a vicious cycle. Thus, targeting cardiac metabolism in IHD patients may prevent the deterioration of left ventricular function, stopping the progression to HF. For these reasons, several studies have explored the potential benefits of trimetazidine (TMZ), an inhibitor of free fatty acids oxidation that shifts cardiac and muscle metabolism to glucose utilization. Because of its mechanism of action, TMZ has been found to provide a cardioprotective effect in patients with angina, diabetes mellitus, and left ventricular (LV) dysfunction, and those undergoing revascularization procedures, without relevant side effects. In addition, the lack of interference with heart rate, arterial pressure, and most of frequent comorbidities, makes TMZ an attractive option for patients and clinicians as well. The impact of TMZ on long term mortality and morbidity in ischemic syndromes and in heart failure need to be conclusively confirmed in properly designed RCT.

2.
Eur J Heart Fail ; 21(5): 553-576, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30989768

RESUMO

Cardiomyopathies are a heterogeneous group of heart muscle diseases and an important cause of heart failure (HF). Current knowledge on incidence, pathophysiology and natural history of HF in cardiomyopathies is limited, and distinct features of their therapeutic responses have not been systematically addressed. Therefore, this position paper focuses on epidemiology, pathophysiology, natural history and latest developments in treatment of HF in patients with dilated (DCM), hypertrophic (HCM) and restrictive (RCM) cardiomyopathies. In DCM, HF with reduced ejection fraction (HFrEF) has high incidence and prevalence and represents the most frequent cause of death, despite improvements in treatment. In addition, advanced HF in DCM is one of the leading indications for heart transplantation. In HCM, HF with preserved ejection (HFpEF) affects most patients with obstructive, and ∼10% of patients with non-obstructive HCM. A timely treatment is important, since development of advanced HF, although rare in HCM, portends a poor prognosis. In RCM, HFpEF is common, while HFrEF occurs later and more frequently in amyloidosis or iron overload/haemochromatosis. Irrespective of RCM aetiology, HF is a harbinger of a poor outcome. Recent advances in our understanding of the mechanisms underlying the development of HF in cardiomyopathies have significant implications for therapeutic decision-making. In addition, new aetiology-specific treatment options (e.g. enzyme replacement therapy, transthyretin stabilizers, immunoadsorption, immunotherapy, etc.) have shown a potential to improve outcomes. Still, causative therapies of many cardiomyopathies are lacking, highlighting the need for the development of effective strategies to prevent and treat HF in cardiomyopathies.

3.
Card Fail Rev ; 4(1): 9-13, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29892469

RESUMO

The introduction of heart failure (HF) with mid-range ejection fraction (HFmrEF) as a distinct phenotype has achieved its aim of stimulating research into the underlying characteristics, pathophysiology and treatment of HF patients with left ventricular ejection fraction of 40-49 %. Comparison of clinical characteristics, comorbidities, outcomes and prognosis among patients with HF with preserved ejection fraction, HFmrEF and HF with reduced ejection fraction allowed consideration of HFmrEF as an intermediate phenotype, which often resembles HF with reduced ejection fraction more than HF with preserved ejection fraction. The latest findings suggest that patients with HFmrEF seem to benefit from therapies that have been shown to improve outcomes in HF with reduced ejection fraction.

4.
Int J Cardiol ; 260: 113-117, 2018 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-29622423

RESUMO

BACKGROUND: Hospitalization is an opportunity to optimize heart failure (HF) therapy. As optimal treatment for hospitalized HF patients in sinus rhythm with heart rate≥70bpm is unclear, we investigated the impact of combined beta-blocker (BB) and ivabradine versus BBs alone on short and longer term mortality and rehospitalization. METHODS AND RESULTS: A retrospective analysis was performed on 370 hospitalized HF patients with heart rate≥70bpm (150 BB+ivabradine, 220 BB alone) in the Optimize Heart Failure Care Program in Armenia, Azerbaijan, Belarus, Georgia, Kazakhstan, Russia, Ukraine, and Uzbekistan, from October 2015 to April 2016. RESULTS: At 1month, 3months, 6months and 12months, there were fewer deaths, HF hospitalizations and overall hospitalizations in patients on BB+ivabradine vs BBs alone. At 12months, all-cause mortality or HF hospitalization was significantly lower with BB+ivabradine than BBs (adjusted hazard ratio [HR] 0.45 (95% confidence interval [CI] 0.32-0.64, P<0.0001). Significantly greater improvement was seen in quality of life (QOL) from admission to 12months with BB+ivabradine vs BBs alone (P=0.0001). With BB+ivabradine, significantly more patients achieved ≥50% target doses of BBs at 12months than on admission (82.0% vs 66.6%, P=0.0001), but the effect was non-significant with BBs alone. CONCLUSIONS: Heart rate lowering therapy with BB+ivabradine started in hospitalized HF patients (heart rate≥70bpm) is associated with reduced overall mortality and re-hospitalization over the subsequent 12months. A prospective randomized trial is needed to confirm the advantages of this strategy.


Assuntos
Antagonistas Adrenérgicos beta/administração & dosagem , Benzazepinas/administração & dosagem , Fármacos Cardiovasculares/administração & dosagem , Insuficiência Cardíaca/tratamento farmacológico , Frequência Cardíaca/efeitos dos fármacos , Hospitalização/tendências , Idoso , Feminino , Seguimentos , Insuficiência Cardíaca/fisiopatologia , Frequência Cardíaca/fisiologia , Humanos , Ivabradina , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos
5.
Eur J Heart Fail ; 20(5): 853-872, 2018 05.
Artigo em Inglês | MEDLINE | ID: mdl-29520964

RESUMO

The coexistence of type 2 diabetes mellitus (T2DM) and heart failure (HF), either with reduced (HFrEF) or preserved ejection fraction (HFpEF), is frequent (30-40% of patients) and associated with a higher risk of HF hospitalization, all-cause and cardiovascular (CV) mortality. The most important causes of HF in T2DM are coronary artery disease, arterial hypertension and a direct detrimental effect of T2DM on the myocardium. T2DM is often unrecognized in HF patients, and vice versa, which emphasizes the importance of an active search for both disorders in the clinical practice. There are no specific limitations to HF treatment in T2DM. Subanalyses of trials addressing HF treatment in the general population have shown that all HF therapies are similarly effective regardless of T2DM. Concerning T2DM treatment in HF patients, most guidelines currently recommend metformin as the first-line choice. Sulphonylureas and insulin have been the traditional second- and third-line therapies although their safety in HF is equivocal. Neither glucagon-like preptide-1 (GLP-1) receptor agonists, nor dipeptidyl peptidase-4 (DPP4) inhibitors reduce the risk for HF hospitalization. Indeed, a DPP4 inhibitor, saxagliptin, has been associated with a higher risk of HF hospitalization. Thiazolidinediones (pioglitazone and rosiglitazone) are contraindicated in patients with (or at risk of) HF. In recent trials, sodium-glucose co-transporter-2 (SGLT2) inhibitors, empagliflozin and canagliflozin, have both shown a significant reduction in HF hospitalization in patients with established CV disease or at risk of CV disease. Several ongoing trials should provide an insight into the effectiveness of SGLT2 inhibitors in patients with HFrEF and HFpEF in the absence of T2DM.

6.
Int J Cardiol ; 236: 340-344, 2017 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-28214078

RESUMO

Hospitalization for heart failure (HF) places a major burden on healthcare services worldwide, and is a strong predictor of increased mortality especially in the first three months after discharge. Though undesirable, hospitalization is an opportunity to optimize HF therapy and advise clinicians and patients about the importance of continued adherence to HF medication and regular monitoring. The Optimize Heart Failure Care Program (www.optimize-hf.com), which has been implemented in 45 countries, is designed to improve outcomes following HF hospitalization through inexpensive initiatives to improve prescription of appropriate drug therapies, patient education and engagement, and post-discharge planning. It includes best practice clinical protocols for local adaptation, pre- and post-discharge checklists, and 'My HF Passport', a printed and smart phone application to improve patient understanding of HF and encourage involvement in care and treatment adherence. Early experience of the Program suggests that factors leading to successful implementation include support from HF specialists or 'local leaders', regular educational meetings for participating healthcare professionals, multidisciplinary collaboration, and full integration of pre- and post-hospital discharge checklists across care services. The Program is helping to raise awareness of HF and generate useful data on current practice. It is showing how good evidence-based care can be achieved through the use of simple clinician and patient-focused tools. Preliminary results suggest that optimization of HF pharmacological therapy is achievable through the Program, with little new investment. Further data collection will lead to a greater understanding of the impact of the Program on HF care and key indicators of success.


Assuntos
Lista de Checagem/tendências , Saúde Global/tendências , Insuficiência Cardíaca/epidemiologia , Insuficiência Cardíaca/terapia , Hospitalização/tendências , Lista de Checagem/normas , Saúde Global/normas , Insuficiência Cardíaca/diagnóstico , Humanos , Alta do Paciente/normas , Alta do Paciente/tendências
7.
Int J Cardiol ; 224: 145-148, 2016 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-27657463

RESUMO

Treatment of hypertensive patients with beta-blockers decreases central blood pressure (CBP) less than other antihypertensive drugs, which is believed to account for their lesser cardiovascular protection in this setting. Some authors have suggested that decreasing heart rate (HR) with beta-blockers would increase CBP. In contrast to beta-blockers, the anti-anginal agent ivabradine reduces HR without other hemodynamic effects, and represents an attractive tool for exploring the direct relationship between HR and CBP. Here, we review the available clinical data assessing the effect of selective HR reduction with ivabradine on CBP in patients with stable coronary artery disease (CAD). We collected data from five studies which report either increase, decrease, or neutral effects of ivabradine on CBP. Further studies are needed to clarify the exact role of ivabradine on CBP. However, as supported by its pharmacodynamic effect in patients with stable CAD, available evidence to date suggests that ivabradine does not negatively impact CBP when associated with beta-blocker. HR reduction with both beta-blockers and ivabradine remains well-established treatments for the symptomatic treatment of angina patients.


Assuntos
Pressão Arterial/efeitos dos fármacos , Benzazepinas/farmacologia , Doença da Artéria Coronariana , Fármacos Cardiovasculares/farmacologia , Doença da Artéria Coronariana/tratamento farmacológico , Doença da Artéria Coronariana/fisiopatologia , Humanos , Ivabradina , Resultado do Tratamento
8.
Card Fail Rev ; 2(2): 123-129, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-28785466

RESUMO

The prevalence of heart failure (HF) is increasing, representing a major cause of death and disability, and a growing financial burden on healthcare systems. Despite the use of effective treatments with both drugs and devices, mortality remains high. There is therefore a need for new and effective therapeutic agents. Ivabradine is a specific sinus node inhibiting agent that was approved in 2005 by the European Medicines Agency, alone or in combination with a beta-blocker. Trimetazidine is a cytoprotective, anti-ischaemic agent established in the treatment of angina pectoris. In the 2012 European Society of Cardiology (ESC) guidelines for diagnosis and treatment of HF, ivabradine was recommended in symptomatic HF patients who are in sinus rhythm with left ventricular ejection fraction ≤35 % and heart rate higher than 70 beats per minute, despite optimal medical therapy, including maximally tolerated dose of beta-blocker. The role of trimetazidine in this setting was not mentioned. In the 2016 ESC guidelines, recommendations for ivabradine are unchanged but trimetazidine is included for the treatment of angina pectoris with HF. This article discusses the need for new therapeutic options in HF and reviews clinical evidence in support of these two therapeutic options.

9.
Int J Cardiol ; 203: 909-15, 2016 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-26618252

RESUMO

Heart failure is a systemic and multiorgan syndrome with metabolic failure as a fundamental mechanism. As a consequence of its impaired metabolism, other processes are activated in the failing heart, further exacerbating the progression of heart failure. Recent evidence suggests that modulating cardiac energy metabolism by reducing fatty acid oxidation and/or increasing glucose oxidation represents a promising approach to the treatment of patients with heart failure. Clinical trials have demonstrated that the adjunct of trimetazidine to the conventional medical therapy improves symptoms, cardiac function and prognosis in patients with heart failure without exerting negative hemodynamic effects. This review focuses on the rationale and clinical benefits of trimetazidine by acting on cardiac metabolism in heart failure, and aims to draw attention to the readiness of this agent to be included in all the major guidelines dealing with heart failure.


Assuntos
Metabolismo Energético , Insuficiência Cardíaca/tratamento farmacológico , Miocárdio/metabolismo , Trimetazidina/farmacocinética , Insuficiência Cardíaca/metabolismo , Humanos , Prognóstico , Resultado do Tratamento , Vasodilatadores/farmacocinética
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