Impact of Ivabradine on Inflammatory Markers in Chronic Heart Failure

Rohm, Ilonka; Kretzschmar, Daniel; Pistulli, Rudin; Franz, Marcus; Schulze, P. Christian; Stumpf, Christian; Yılmaz, Atilla

doi:10.1155/2016/6949320

Cited by 16 publications

(16 citation statements)

References 33 publications

(49 reference statements)

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“…21 In HF patients, ivabradine increased LV ejection fraction and led to a significant reduction of tumour necrosis factor alpha serum levels and a reconstitution of circulating dendritic cells. 22 Furthermore, ivabradine reduced microvascular derangements in experimental sepsis and improved endothelial function in patients undergoing percutaneous coronary intervention, 23,24 The mortality observed in our study (60%) in ChD HF is much higher in comparison with that of the SHIFT overall population (~17.5%) and of the recent PARADIGM-HF trial (~15%) at 750 day follow-up. 11,25 This finding is in agreement with previous publication.…”

Section: Discussionmentioning

confidence: 60%

Safety profile and efficacy of ivabradine in heart failure due to Chagas heart disease: a post hoc analysis of the SHIFT trial

et al. 2017

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AimsThe SHIFT trial showed that ivabradine reduced heart rate (HR) and the risk of cardiovascular outcomes. Concerns remain over the efficacy and safety of ivabradine on heart failure (HF) due to Chagas disease (ChD). We therefore conducted a post hoc analysis of the SHIFT trial to investigate the effect of ivabradine in these patients.Methods and resultsSHIFT was a randomized, double‐blind, placebo‐controlled trial in symptomatic systolic stable HF, HR ≥ 70 b.p.m., and in sinus rhythm. The ChD HF subgroup included 38 patients, 20 on ivabradine, and 18 on placebo. The ChD HF subgroup showed high prevalence of bundle branch right block and, compared with the overall SHIFT population, lower systolic blood pressure; higher use of diuretics, cardiac glycosides, and antialdosterone agents; and lower use of angiotensin‐converting enzyme inhibitor/angiotensin II receptor blocker or target daily dose of beta‐blocker. ChD HF presented a poor prognosis (all‐cause mortality at 2 years was ~60%). The mean twice‐daily dose of ivabradine was 6.26 ± 1.15 mg and placebo 6.43 ± 1.55 mg. Ivabradine reduced HR from 77.9 ± 3.8 to 62.3 ± 10.1 b.p.m. (P = 0.005) and improved functional class (P = 0.02). A trend towards reduction in all‐cause death was observed in ivabradine arm vs. placebo (P = 0.07). Ivabradine was not associated with serious bradycardia, atrioventricular block, hypotension, or syncope.ConclusionsChD HF is an advanced form of HF with poor prognosis. Ivabradine was effective in reducing HR in these patients and improving functional class. Although our results are based on a very limited sample and should be interpreted with caution, they suggest that ivabradine may have a favourable benefit–risk profile in ChD HF patients.

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Section: Discussionmentioning

confidence: 60%

Safety profile and efficacy of ivabradine in heart failure due to Chagas heart disease: a post hoc analysis of the SHIFT trial

et al. 2017

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“…Accelerated resting heart rhythm is, in turn, associated with a higher cardiovascular risk and the risk of hospitalisation due to HF [93]. The mechanism of this relationship is partly explained by inflammation and partly by other mechanisms associated with endothelial dysfunction or neurohormonal activation [93,94]. The importance of resting heart rate as a prognostic factor and, at the same time, a therapeutic goal is welldocumented particularly in a group of patients with HFrEF with LVEF less than or equal to 35% [1,94].…”

Section: Ageing As a Factor In Inflammation And As A Promoter Of The mentioning

confidence: 99%

“…The mechanism of this relationship is partly explained by inflammation and partly by other mechanisms associated with endothelial dysfunction or neurohormonal activation [93,94]. The importance of resting heart rate as a prognostic factor and, at the same time, a therapeutic goal is welldocumented particularly in a group of patients with HFrEF with LVEF less than or equal to 35% [1,94]. In this group of patients, where the sinus rhythm is present and symptoms remain, despite the classic HF treatment, the benefits of treatment with ivabradine, a specific factor inhibiting the formation of the If current in the sinus node, were demonstrated [1,94].…”

Section: Ageing As a Factor In Inflammation And As A Promoter Of The mentioning

confidence: 99%

“…The importance of resting heart rate as a prognostic factor and, at the same time, a therapeutic goal is welldocumented particularly in a group of patients with HFrEF with LVEF less than or equal to 35% [1,94]. In this group of patients, where the sinus rhythm is present and symptoms remain, despite the classic HF treatment, the benefits of treatment with ivabradine, a specific factor inhibiting the formation of the If current in the sinus node, were demonstrated [1,94]. It is now proposed that this beneficial effect of ivabradine may result not only from the effects on heart rate, but also from changes induced by ivabradine in the immune system.…”

Section: Ageing As a Factor In Inflammation And As A Promoter Of The mentioning

confidence: 99%

“…It is now proposed that this beneficial effect of ivabradine may result not only from the effects on heart rate, but also from changes induced by ivabradine in the immune system. It has been demonstrated that in patients treated with ivabradine, contemporaneous with the reduction in heart rate, there is a significant reduction in plasma TNF-alpha concentration and the restoration of the correct level of circulating dendritic cells [94]. In a study in which these ivabradine-induced changes in the immune system were confirmed, these were significant in dilated cardiomyopathy (DCM) and ischaemic cardiomyopathy (ICM), but not in hypertensive cardiomyopathy (HCM).…”

Section: Ageing As a Factor In Inflammation And As A Promoter Of The mentioning

confidence: 99%

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Various aspects of inflammation in heart failure

et al. 2019

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Despite significant advances in the prevention and treatment of heart failure (HF), the prognosis in patients who have been hospitalised on at least one occasion due to exacerbation of HF is still poor. Therefore, a better understanding of the underlying pathophysiological mechanisms of HF is crucial in order to achieve better results in the treatment of this clinical syndrome. One of the areas that, for years, has aroused the interest of researchers is the activation of the immune system and the elevated levels of biomarkers of inflammation in patients with both ischaemic and non-ischaemic HF. Additionally, it is intriguing that the level of circulating pro-inflammatory biomarkers correlates with the severity of the disease and prognosis in this group of patients. Unfortunately, clinical trials aimed at assessing interventions to modulate the inflammatory response in HF have been disappointing, and the modulation of the inflammatory response has had either no effect or even a negative effect on the HF prognosis. The article presents a summary of current knowledge on the role of immune system activation and inflammation in the pathogenesis of HF. Understanding the immunological mechanisms pathogenetically associated with left ventricular remodelling and progression of HF may open up new therapeutic possibilities for HF.

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