Drug treatment in heart failure.
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ABSTRACT:
SUBMITTER: Lonn E
PROVIDER: S-EPMC1127584 | biostudies-literature | 2000 Apr
REPOSITORIES: biostudies-literature
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Project description:The prevalence of heart failure increases with age. Changes in the age distribution and growing life expectancy will lead to a further rise. However, data concerning drug treatment of heart failure especially in the elderly are scarce. Subgroup analyses of the heart failure trials suggest that drug therapy in older patients should follow the recommendations in the current guidelines. In doing so, several common comorbidities in these patients (e. g., impaired renal function) have to be considered and may have an influence on the therapy (e. g., drug dose, choice of active pharmaceutical ingredient, etc.). Especially in old, multimorbid patients, possible interaction of drugs might play a substantial role. In many cases the main goal of the therapy, especially in the very elderly, is to improve symptoms and quality of life.
| S-EPMC5934458 | biostudies-literature
Project description:The introduction of multiple new pharmacological agents over the past three decades in the field of heart failure with reduced ejection fraction (HFrEF) has led to reduced rates of mortality and hospitalizations, and consequently the prevalence of HFrEF has increased, and up to 10% of patients progress to more advanced stages, characterized by high rates of mortality, hospitalizations, and poor quality of life. Advanced HFrEF patients often show persistent or progressive signs of severe HF symptoms corresponding to New York Heart Association class III or IV despite being on optimal medical, surgical, and device therapies. However, a subpopulation of patients with advanced HF, those with the most advanced stages of disease, were often insufficiently represented in the major trials demonstrating efficacy and tolerability of the drugs used in HFrEF due to exclusion criteria such as low BP and kidney dysfunction. Consequently, the results of many landmark trials cannot necessarily be transferred to patients with the most advanced stages of HFrEF. Thus, the efficacy and tolerability of guideline-directed medical therapies in patients with the most advanced stages of HFrEF often remain unsettled, and this knowledge is of crucial importance in the planning and timing of consideration for referral for advanced therapies. This review discusses the evidence regarding the use of contemporary drugs in the advanced HFrEF population, covering components such as guideline HFrEF drugs, diuretics, inotropes, and the use of HFrEF drugs in LVAD recipients, and provides suggestions on how to manage guideline-directed therapy in this patient group.
| S-EPMC8820365 | biostudies-literature
Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We analyzed whether the anti-ischemic drug ranolazine could retard the progression of heart failure in an experimental model of heart failure induced by 6 months of chronic pressure overload. The study showed that 2 months of ranolazine treatment improved cardiac function of aortic constricted C57BL/6J (B6) mice with symptoms of heart failure as assessed by echocardiography. The microarray gene expression study of heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) untreated 10 month-old C57BL/6J (B6) mice with heart failure induced by 6 months of abdominal aortic constriction (AAC), (ii) 10 month-old B6 mice with 6 months of AAC and two months of treatment with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched, untreated, sham-operated B6 control mice.
2010-12-03 | E-GEOD-25766 | biostudies-arrayexpress
Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We analyzed whether the anti-ischemic drug ranolazine could retard the progression of heart failure in an experimental model of heart failure induced by 6 months of chronic pressure overload. The study showed that 2 months of ranolazine treatment improved cardiac function of aortic constricted C57BL/6J (B6) mice with symptoms of heart failure as assessed by echocardiography. The microarray gene expression study of heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine.
2010-12-03 | GSE25766 | GEO
Project description: Not available
| S-EPMC5811193 | biostudies-literature
Project description:Purpose of reviewArrhythmias are common in patients with heart failure (HF) and are associated with a significant risk of mortality and morbidity. Optimal antiarrhythmic treatment is therefore essential. Here, we review current approaches to antiarrhythmic treatment in patients with HF.Recent findingsIn atrial fibrillation, rhythm control and ventricular rate control are accepted therapeutic strategies. In recent years, clinical trials have demonstrated a prognostic benefit of early rhythm control strategies and AF catheter ablation, especially in patients with HF with reduced ejection fraction. Prevention of sudden cardiac death with ICD therapy is essential, but optimal risk stratification is challenging. For ventricular tachycardias, recent data support early consideration of catheter ablation. Antiarrhythmic drug therapy is an adjunctive therapy in symptomatic patients but has no prognostic benefit and well-recognized (proarrhythmic) adverse effects. Antiarrhythmic therapy in HF requires a systematic, multimodal approach, starting with guideline-directed medical therapy for HF and integrating pharmacological, device, and interventional therapy.
| S-EPMC10828006 | biostudies-literature
Project description:Despite recent advances in chronic heart failure management (either pharmacological or non-pharmacological), the prognosis of heart failure (HF) patients remains poor. This poor prognosis emphasizes the need for developing novel pathways for testing new HF drugs, beyond neurohumoral and hemodynamic modulation approaches. The development of new drugs for HF therapy must thus necessarily focus on novel approaches such as the direct effect on cardiomyocytes, coronary microcirculation, and myocardial interstitium. This review summarizes principal evidence on new possible pharmacological targets for the treatment of HF patients, mainly focusing on microcirculation, cardiomyocyte, and anti-inflammatory therapy.
| S-EPMC8131549 | biostudies-literature
Project description:Identifying effective pharmacological treatments for heart failure (HF) patients remains critically important. Given that the development of drugs de novo is expensive and time consuming, drug repositioning has become an increasingly important branch. In the present study, we propose a two-step drug repositioning pipeline and investigate the novel therapeutic effects of existing drugs approved by the US Food and Drug Administration to discover potential therapeutic drugs for HF. In the first step, we compared the gene expression pattern of HF patients with drug-induced gene expression profiles to obtain preliminary candidates. In the second step, we performed a systems biology approach based on the known protein-protein interaction information and targets of drugs to narrow down preliminary candidates to obtain final candidates. Drug set enrichment analysis and literature search were applied to assess the performance of our repositioning approach. We also constructed a mode of action network for each candidate and performed pathway analysis for each candidate using genes contained in their mode of action network to uncover pathways that potentially reflect the mechanisms of candidates' therapeutic efficacy to HF. We discovered numerous preliminary candidates, some of which are used in clinical practice and supported by the literature. The final candidates contained nearly all of the preliminary candidates supported by previous studies. Drug set enrichment analysis and literature search support the validity of our repositioning approach. The mode of action network for each candidate not only displayed the underlying mechanisms of drug efficacy but also uncovered potential biomarkers and therapeutic targets for HF. Our two-step drug repositioning approach is efficient to find candidates with potential therapeutic efficiency to HF supported by the literature and might be of particular use in the discovery of novel effective pharmacological therapies for HF.
| S-EPMC6773955 | biostudies-literature
Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E (apoE)- deficient mice as a model of atherosclerosis-induced heart failure to analyze whether the anti-ischemic drug ranolazine could retard the progression of heart failure. The study showed that 2 months of ranolazine treatment improved cardiac function of 18 month-old apoE-deficient mice with symptoms of heart failure as assessed by echocardiography. To identify changes in cardiac gene expression induced by treatment with ranolazine a microarray study was performed with heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts. The microarray approach identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from (i) untreated 18 month-old apoE-deficient mice with heart failure relative to (ii) 18 month-old apoE-deficient mice treated for two months with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched non-transgenic C57BL/6J (B6) control mice.
2010-12-03 | E-GEOD-25767 | biostudies-arrayexpress
Project description:Purpose of reviewHeart failure (HF) is commonly associated with iron deficiency (ID), defined as insufficient levels of iron to meet physiological demands. ID's association with anaemia is well understood but it is increasingly recognised as an important comorbidity in HF, even in the absence of anaemia. This review summarises contemporary evidence for the measurement and treatment of ID, in both HFrEF and HFpEF, and specific HF aetiologies, and highlights important gaps in the evidence-base.Recent findingsID is common among patients with HF and associated with increased morbidity and mortality. Correcting ID in patients with HF can impact upon functional status, exercise tolerance, symptoms, and overall quality of life, irrespective of anaemia status. ID is a modifiable comorbidity in HF. Therefore, recognising and treating ID has emerging therapeutic potential and is important for all clinicians who care for patients with HF to understand the rationale and approach to treatment.
| S-EPMC10307722 | biostudies-literature