scholarly journals Effects of Metformin in Heart Failure: From Pathophysiological Rationale to Clinical Evidence

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1834
Author(s):  
Teresa Salvatore ◽  
Raffaele Galiero ◽  
Alfredo Caturano ◽  
Erica Vetrano ◽  
Luca Rinaldi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Large Scale ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
New Drugs ◽  
Experimental Investigations ◽  
Protective Effects ◽  
Heart Metabolism ◽  
Randomized Controlled Clinical Trials ◽  
Glucose And Lipid Metabolism

Type 2 diabetes mellitus (T2DM) is a worldwide major health burden and heart failure (HF) is the most common cardiovascular (CV) complication in affected patients. Therefore, identifying the best pharmacological approach for glycemic control, which is also useful to prevent and ameliorate the prognosis of HF, represents a crucial issue. Currently, the choice is between the new drugs sodium/glucose co-transporter 2 inhibitors that have consistently shown in large CV outcome trials (CVOTs) to reduce the risk of HF-related outcomes in T2DM, and metformin, an old medicament that might end up relegated to the background while exerting interesting protective effects on multiple organs among which include heart failure. When compared with other antihyperglycemic medications, metformin has been demonstrated to be safe and to lower morbidity and mortality for HF, even if these results are difficult to interpret as they emerged mainly from observational studies. Meta-analyses of randomized controlled clinical trials have not produced positive results on the risk or clinical course of HF and sadly, large CV outcome trials are lacking. The point of force of metformin with respect to new diabetic drugs is the amount of data from experimental investigations that, for more than twenty years, still continues to provide mechanistic explanations of the several favorable actions in heart failure such as, the improvement of the myocardial energy metabolic status by modulation of glucose and lipid metabolism, the attenuation of oxidative stress and inflammation, and the inhibition of myocardial cell apoptosis, leading to reduced cardiac remodeling and preserved left ventricular function. In the hope that specific large-scale trials will be carried out to definitively establish the metformin benefit in terms of HF failure outcomes, we reviewed the literature in this field, summarizing the available evidence from experimental and clinical studies reporting on effects in heart metabolism, function, and structure, and the prominent pathophysiological mechanisms involved.

Abstract 96: Thioredoxin-1 Is Essential for Hydrogen Sulfide-Mediated Cardioprotection in the Setting of Ischemic-Induced Heart Failure

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Chad K Nicholson ◽  
Bridgette F Moody ◽  
Rebecca L Hood ◽  
Junichi Sadoshima ◽  
John W Calvert
Keyword(s):  
Heart Failure ◽  
Hydrogen Sulfide ◽  
Left Ventricular ◽  
Dominant Negative ◽  
Left Ventricular Ejection ◽  
Protective Effects ◽  
Ventricular Ejection Fraction ◽  
Left Ventricular Dimensions ◽  
Thioredoxin 1 ◽  
And Function

Background: Numerous studies have reported the cytoprotective effects of hydrogen sulfide (H2S) in various models of myocardial injury. Here we examined the role that thioredoxin-1 (Trx1) plays in mediating the protective effects of H2S in a model of heart failure. Methods and Results: Mice were subjected to 60 min of left coronary artery ischemia followed by 4 wks of reperfusion (R) at which time left ventricular dimensions and function were assessed. Mice received saline (Veh) or H2S in the form of sodium sulfide (Na2S, 100 μ g/kg) at the time of R followed by daily i.v. injections for the first 7 days of R. Mice treated with Na2S experienced less left ventricular dilatation and hypertrophy, displayed improved left ventricular ejection fraction, and displayed improved contractility and relaxation when compared to Veh-treated mice. Studies aimed at evaluating the underlying cardioprotective mechanisms found that Na2S treatment increased the expression of Trx1. Further analysis revealed that this was accompanied by an increase in phosphorylation of apoptosis signaling kinase-1 (ASK1) at serine residue 966 (inhibitory site), as well as a decrease in the phosphorylation of JNK and p38 (downstream targets of ASK1). We also found that Na2S treatment did not improve cardiac dilatation, cardiac dysfunction, or cardiac hypertrophy in cardiac specific Trx1 dominant negative transgenic (Trx1 dnTg) mice when compared to Veh-treated mice. Conclusion: These findings provide important information that the upregulation of cardiac Trx1 by H2S in the setting of ischemic-induced heart failure sets into motion events, including ASK1 inhibition, which ultimately leads to cardioprotection.

Abstract P410: A Novel Curcumin Formulation, ASD-cur Suppressed Heart Failure After Myocardial Infarction In Rats

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Hidemichi Takai ◽  
Tatsuya Morimoto
Keyword(s):  
Heart Failure ◽  
Plasma Concentration ◽  
Cardiac Fibrosis ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Cell Diameter ◽  
Maximum Plasma ◽  
Mrna Levels ◽  
Time Curve ◽  
Sd Rats

Introduction: Curcumin prevents the development of heart failure and is a potential treatment for heart failure. Although curcumin is known to be safe, its therapeutic efficiency is limited due to its low bioavailability. To overcome this problem, we developed ASD-Cur, an amorphous formulation of curcumin. In this study, we investigated the effect of ASD-Cur and compared it with Theracurmin ® , a colloidal submicron dispersion of curcumin. Methods: Male SD rats were orally administrated with ASD-Cur or Theracurmin ® (10 mg/kg curcumin). The plasma levels of curcumin were measured at 0.25, 0.5, 1, 2, 4 and 6 hours after administration. Twelve healthy volunteers, who had provided written informed consent, were administrated with ASD-Cur and Theracurmin ® containing 30 mg curcumin, and plasma curcumin concentrations were determined at 0.5, 1, 2, 4, and 8 hours. Next, male SD rats were subjected to MI or sham surgery. One week after surgery, the MI rats were randomly assigned to 4 groups: vehicle, ASD-Cur (0.2 mg/kg curcumin) or Theracurmin ® (0.2 or 0.5 mg/kg curcumin). Oral administration of these compounds was repeated for 6 weeks. After echocardiographic examinations, myocardial cell diameter, perivascular fibrosis, mRNA levels, and the acetylation of histone H3K9 were measured. Results: After administration in rats, the area under the plasma concentration-time curve ( AUC 0-6h ) and the maximum plasma concentration ( C max ) of ASD-Cur were 3.7-fold and 9.6-fold higher than those of Theracurmin ® , respectively. The AUC 0-8h and C max of ASD-Cur in humans were 3.4-fold and 5.4-fold higher than those of Theracurmin ® , respectively. Echocardiographic analysis showed that 0.2 mg/kg ASD-Cur and 0.5 mg/kg Theracurmin ® significantly improved the MI-induced deterioration of FS and left ventricular hypertrophy to the same extent. Both treatments significantly suppressed MI-induced increases in myocardial cell diameter, perivascular fibrosis, mRNA levels of hypertrophic markers and cardiac fibrosis, and acetylation of histone H3K9 to the same extent. Conclusion: These findings indicated that ASD-Cur has greater bioavailability than Theracurmin ® , and could exhibit greater therapeutic potency towards for MI-induced heart failure at a lower dose.

scholarly journals Qiliqiangxin Attenuates Cardiac Remodeling via Inhibition of TGF-β1/Smad3 and NF-κB Signaling Pathways in a Rat Model of Myocardial Infarction

2018 ◽  
Vol 45 (5) ◽  
pp. 1797-1806 ◽  
Author(s):  
Anbang Han ◽  
Yingdong Lu ◽  
Qi Zheng ◽  
Jian Zhang ◽  
YiZhou Zhao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiac Function ◽  
Signaling Pathways ◽  
Rat Model ◽  
Cardiac Remodeling ◽  
Left Ventricular ◽  
Protective Effects ◽  
Tnf Α ◽  
Tgf Β1

Background/Aims: Qiliqiangxin (QL), a traditional Chinese medicine, has been demonstrated to be effective and safe for the treatment of chronic heart failure. Left ventricular (LV) remodeling causes depressed cardiac performance and is an independent determinant of morbidity and mortality after myocardial infarction (MI). Our previous studies have shown that QL exhibits cardiac protective effects against heart failure after MI. The objective of this study was to explore the effects of QL on myocardial fibrosis in rats with MI and to investigate the underlying mechanism of these effects. Methods: A rat model of acute myocardial infarction was induced by ligating the left anterior descending coronary artery. The rats were treated with QL (1.0 g/kg/day) for 4 weeks after surgery. Echocardiography and histology examination were performed to evaluate heart function and fibrosis, respectively. Protein levels of transforming growth factor-β1 (TGF-β1), phosphorylated Smad3 (p-Smad3), phosphorylated Smad7 (p-Smad7), collagen I (Col- I), alpha smooth muscle actin (a-SMA), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), nuclear factor κB (NF-κB), and phosphorylated inhibitor of kappa B alpha (p-IκBα) were measured by western blot analysis. Results: QL treatment ameliorated adverse cardiac remodeling 8 weeks after AMI, including better preservation of cardiac function, decreased inflammation, and reduced fibrosis. In addition, QL treatment reduced Col-I, a-SMA, TGF-β1, and p-Smad3 expression levels but increased p-Smad7 levels in postmyocardial infarct rat hearts. QL administration also reduced the elevated levels of cardiac inflammation mediators, such as TNF-α and IL-6, as well as NF-κB and p-IκBα expression. Conclusions: QL therapy exerted protective effects against cardiac remodeling potentially by inhibiting TGF-β1/Smad3 and NF-κB signaling pathways, thereby preserving cardiac function, as well as reducing myocardial inflammation and fibrosis.

P3476High-resolution respirometry reveals enhanced myocardial mitochondrial ketone oxidation after fasting and ventricular unloading

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
E Zweck ◽  
V Burkart ◽  
C Wessel ◽  
D Scheiber ◽  
K H M Leung ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Ex Vivo ◽  
Oxidative Capacity ◽  
Left Ventricular ◽  
University Hospital ◽  
Oxygen Flux ◽  
Protective Effects ◽  
Coa Transferase

Abstract Background Impairment of myocardial mitochondrial function is regarded as an established pathomechanism in heart failure. Enhanced oxidation of ketone bodies may potentially exert protective effects on myocardial function. High-resolution respirometry (HRR) resembles a gold-standard methodology to determine myocardial mitochondrial metabolism and oxidative function but has not been validated for ketone substrates yet. Purpose We hypothesized that (1) quantification of ketone body oxidative capacity (OC) in myocardium utilizing ex-vivo HRR is feasible and that (2) ketone-associated OC is elevated after fasting and under conditions of chronic mechanical ventricular unloading. Methods We established new HRR (Oxygraph-2k) protocols, measuring oxygen flux generated by oxidation of the ketone substrates beta-hydroxybutyrate (HBA) and acetoacetate (ACA). Ketone protocols were then applied to twelve C57BL/6 mice' (of which six were fasted for 16h) left ventricular and right liver lobe tissue, as well as to eleven terminal heart failure patients' left ventricular tissue, harvested at heart transplantation. Heart transplant recipients were subdivided into patients with left ventricular assist device prior to transplantation (LVAD group, n=6) or no unloading prior to transplantation (HTX group, n=5). Results In non-fasted rodent hearts, HBA yielded an OC of 25±4 pmol/(s*mg tissue) above basal respiration, when applied as sole substrate (21±11 pmol/(s*mg) in liver). ACA alone did not induce oxygen flux, but ACA+succinate yielded 229% higher oxygen flux than succinate alone in state III (146±32 vs 44±12 pmol/(s*mg); p=0.0003). When titrated after succinate, ACA increased OC by 93±25 pmol/(s*mg) (p=0.0003). In 16h-fasted rodent hearts, HBA-supported OC was 27% higher (41±3 vs 52±9 pmol/(s*mg); p=0.04), while OC with ACA+succinate was unchanged (p=0.60). In rodent liver, no oxygen flux was induced by ACA, reflecting absence of 3-oxoacid CoA-transferase. However, HBA-supported OC was 118% higher in fasted liver (37±13 vs 57±13 pmol/(s*mg); p=0.03). In humans, left ventricular unloading was not associated with altered myocardial OC for fatty acids and glycolytic substrates (standard protocol, p=0.13), but HBA-supported OC was 39% higher in the LVAD group compared to the HTX group (54±12 vs 39±9 pmol/(s*mg), p=0.04). Conclusion Quantification of ketone body OC with HRR is feasible in permeabilized myocardial fibers. Applying this novel method revealed increased HBA-supported myocardial mitochondrial respiration after fasting and chronic left ventricular unloading. These data support a concept of enhanced ketone oxidation following ventricular unloading in myocardial mitochondria. Our findings facilitate new studies on myocardial ketone turnover and the interaction of mitochondrial ketone metabolism with cardiac performance. Acknowledgement/Funding CRC 1116, Research commission of the University Hospital Düsseldorf

A Review of Carvedilol Arrhythmia Data in Clinical Trials

2005 ◽  
Vol 10 (4_suppl) ◽  
pp. S59-S68 ◽  
Author(s):  
Peter R. Kowey
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Clinical Trials ◽  
Sudden Death ◽  
Large Scale ◽  
Left Ventricular ◽  
Antiarrhythmic Agents ◽  
Adrenergic Blockade ◽  
Variable Effect ◽  
Β Blockers

β-Blockers are currently being evaluated more intensively to define their role in clinical use as antiarrhythmic agents. β-Adrenergic blockade has been studied in relation to atrial fibrillation, ventricular arrhythmias, and sudden death; however, it is apparent from a number of studies that not all β-blockers are equally effective. Randomized clinical trial data, both in heart failure and post-myocardial infarction (MI) patients, have shown differences in mortality benefits in addition to a variable effect on arrhythmias and sudden death. Carvedilol, a third-generation β-blocker with proven clinical benefit in the management of heart failure and post-MI patients, has properties that may make it an effective antiarrhythmic agent. This paper reviews the current clinical arrhythmia data available for carvedilol from large-scale clinical trials and small studies. The trial evidence demonstrates that carvedilol therapy can be an effective adjunctive rate-control therapy in patients with atrial fibrillation, prevent mortality in patients with heart failure or post-MI with left ventricular dysfunction, with or without atrial fibrillation, and reduce its onset and the incidence of ventricular arrhythmia and sudden death.

scholarly journals P933 Peak left atrial systolic strain as a marker of left ventricular diastolic dysfunction in patients with ischemic heart failure with depressed ejection fraction after STEMI: pilot study

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
A I Scarlatescu ◽  
M Stoian ◽  
N M Popa-Fotea ◽  
G Nicula ◽  
N Oprescu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Large Scale ◽  
Roc Analysis ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Ischemic Heart Failure ◽  
Systolic Strain ◽  
Global Strain

Abstract Funding Acknowledgements This work was supported by CREDO Project - ID: 49182, financed through the SOP IEC -A2-0.2.2.1-2013-1 cofinanced by the ERDF Background Echocardiographic assessment of diastolic dysfunction and left ventricular (LV) filling pressures is a complex and challenging process, requiring a multiparameter analysis. In recent years strain imaging has been emerging as a promising method for evaluation of left atrium (LA) function, being correlated with LV systolic dysfunction. Purpose We sought to evaluate LA mechanics in a cohort of patients with ischemic heart failure (HF) at one month after ST elevation myocardial infarction (STEMI) Material and methods 40 patients were enrolled in this study: 30 consecutive patients with ischemic HF after STEMI, with LVEF < 50% and 10 healthy age- and sex-matched controls. All patients had standard echocardiographic examination; also LA strain curves were obtained using speckle tracking with measurement of peak LA systolic strain. Categorization of diastolic dysfunction severity into 3 grades was realized according to 2016 guidelines. Results 2D and 3D LVEF (33% vs 55%, p = 0.00), LV global strain (-10 vs -19, p = 0.00) and peak LA systolic strain (16 vs 33, p = 0.00) were significantly reduced in HF patients compared to controls. In both groups LA strain correlated with the following parameters: 2D EF (p = 0.024), 3D EF (p = 0.02), LV global strain (p = 0.00), E/A (p = 0.05), septal e’ (p = 0.00), lateral e’ (p = 0.00), E/septal e’ (p = 0.006), E/lateral e’ (p = 0.003), E/mean e’ (p = 0.014), LA volume (p = 0.014) and LV filling pressures (p = 0.001). Peak LA systolic strain (PALS) values progressively decreased with worsening of diastolic function showing significant differences between all diastolic dysfunction grades. Using ROC analysis we identified 3 PALS thresholds to distinguish between normal diastolic function and the 3 diastolic dysfunction grades. The optimal cut off values were as follows: between normal diastolic function and grades 1-3 with PALS cut off value of 26.5 (Sb 90%, Sp 87%), AUC 0.963, CI 95%, p = 0.00; between grades 0-1 and grades 2-3 with peak LA strain cut off value of 17.2 (Sb 75%, Sp 93%) AUC = 0.828, CI 95%, p = 0.002; between grade 0-2 and grade 3 with peak LA strain cut off value of 11 (Sb 85%, Sp 93%), AUC 0.942, CI 95%, p = 0.00. Also, PALS value differed significantly between patients with normal vs high LV filling pressures. Using ROC analysis we determined a cut off value for LA of 15.1 to differentiate between the two subgroups with excellent discrimination power AUC 0.902, CI 95%, p = 0.00, Sb 88.9%, Sp 83% thus making LA strain an accurate surrogate estimate of LV filling pressures. Conclusions Global peak LA systolic strain is significantly correlated with LV systolic and diastolic function. PALS is a feasible option for detection and categorization of diastolic dysfunction in patients with HF and depressed LVEF after STEMI. Incorporating LA strain into noninvasive assessment of LV diastolic dysfunction may improve the detection of elevated LV filling pressures. Further large scale studies are needed to validate this data.

Cardio-protective effects of sodium-glucose co-transporter 2 inhibitors: focus on heart failure

2020 ◽  
Vol 26 ◽  
Author(s):  
Dimos Karangelis ◽  
C. David Mazer ◽  
Dimitrios Stakos ◽  
Aphrodite Tzifa ◽  
Spiros Loggos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Large Scale ◽  
Mechanisms Of Action ◽  
Sglt2 Inhibitors ◽  
Protective Effects ◽  
Reduced Ejection Fraction ◽  
Risk Of Death ◽  
Sodium Glucose Cotransporter ◽  
Myocardial Energetics

Background: Type 2 diabetes mellitus (DM) is associated with a considerable risk of cardiovascular and renal disease, including heart failure. Sodium–glucose cotransporter 2 (SGLT2) inhibitors have demonstrated unprecedented cardiorenal protective effects in large scale clinical trials of patients with or without diabetes and either established cardiovascular disease (CV) or multiple CV risk factors. Objective: Herein we aim to focus on the role of SGLT2 inhibitors regarding the improvement in heart failure outcomes and the proposed mechanisms of action by which these drugs confer their beneficial effect. Methods: PubMed, Embase and Google Scholar databases were searched to identify eligible articles which are comprehensively summarized and discussed. Results: The most commonly discussed mechanisms of action are diuresis and natriuresis, reduction in preload, afterload, and ventricular mass, as well as stimulation of erythropoietin production and improved myocardial energetics. SGLT2 inhibitors improve outcomes in patients with established heart failure (HF) and reduce the risk of death and HF admissions in patients with established chronic HF with reduced ejection fraction (HFrEF), either with or without diabetes. Conclusion: Potential key mechanisms that may explain the notable cardioprotective benefits of SGLT2 inhibitors have been outlined. These agents have recently received class Ia recommendation in specific groups of people with DM to lower the risk of hospitalization for HF and risk of death, while these benefits may also extend to people without diabetes. It remains to be seen whether they will also emerge as treatment approaches in the acute phase of CV episodes.

Abstract 85: A Novel Mitochondrial Targeted Fusion Protein Containing Endonuclease III Protects the Heart Against Myocardial Infarction and Pressure Overload Heart Failure

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Jessica M Bradley ◽  
Hiroyuki Otsuka ◽  
Chelsea L Organ ◽  
Shashi Bhushan ◽  
David J Polhemus ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Fusion Protein ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Myocardial Infarct Size ◽  
Ventricular Ejection Fraction ◽  
Endonuclease Iii ◽  
Mtdna Repair

Background: Oxidative stress is a primary cause of mitochondrial DNA (mtDNA) damage and plays a role in myocardial cell death. mtDNA repair enzymes are crucial for mtDNA repair and cell survival. We tested the efficacy of a novel, mitochondrial targeted fusion protein that traffics Endonuclease III (Exscien1-III) in murine models of myocardial ischemia/reperfusion (MI/R) injury and transverse aortic constriction (TAC) heart failure (HF). We previously demonstrated that Exscien1-III administered at R reduced myocardial infarct size and preserved left ventricular ejection fraction (LVEF) following MI/R. We hypothesized that delayed administration of Exscien1-III would promote mtDNA repair and protect the myocardium against MI/R and TAC heart failure. Methods: Male C57/BL6J (10-12 wks) were subjected to 45 min of MI and 24 hrs of R. Exscien1-III (4 mg/kg, i.p., n=13) or vehicle (VEH, n=13) was administered 30 min after R. Male C57/BL6J were subjected to TAC (27 g needle) and Exscien1-III (4 mg/kg/d, i.p., n=10) or VEH (n=6) were administered starting at 3 wks post TAC. Echocardiography was performed at baseline and following TAC to assess LVEF. Results: Exscien1-III reduced myocardial INF/AAR by 24% (p < 0.05 vs. VEH). Exscien1-III preserved LVEF (49.1 ± 4.0% vs. 32.9 ± 3.2%, p < 0.01) and reduced LV dilation (LVEDD/LVESD; 3.8/2.8 vs. 4.4/3.4, p < 0.05) at 8 wks compared to vehicle. Conclusion: These results demonstrate that delayed administration of Exscien1-III significantly attenuates myocardial cell death and preserves LV function in acute MI and HF. Studies are currently underway to define the molecular mechanisms involved in Exscien1-III induced cardioprotection.

Ventricular-arterial coupling as a potential therapeutic target in diabetes

2021 ◽  
Author(s):  
Sahrai Saeed ◽  
Hannes Holm ◽  
Peter Nilsson
Keyword(s):  
Heart Failure ◽  
Therapeutic Target ◽  
Cardiovascular Complications ◽  
Left Ventricular ◽  
Arterial System ◽  
Protective Effects ◽  
Potential Therapeutic Target ◽  
Lower Plasma Glucose ◽  
Glucagon Like Peptide 1 ◽  
Long Term Prognosis

Patients with type 2 diabetes (T2D) are at high risk of cardiovascular complications. Novel anti-diabetic medications such as sodium-glucose cotransporter-2 inhibitors (SGLT-2i) and Glucagon-like peptide-1 receptor agonists (GLP-1RA) have been shown to possess cardiac and renal protective effects beyond their ability to lower plasma glucose. Use of SGLT-2i and GLP-1RA in patients with T2D and heart failure reduce cardiovascular risk and heart failure related hospitalizations. SGLT-2i treatment has shown to improve the long-term prognosis of patients with heart failure. Both drugs also have the potential to normalize ventricular-arterial coupling (VAC). VAC is the crosstalk between the left ventricular function and the arterial system, and is an indicator of the global cardiovascular performance. In this overview, we will describe the concept of VAC and the features of diabetic cardiomyopathy, as well as VAC as a potential therapeutic target in diabetes by use of novel anti-diabetic drugs, primarily SGLT-2i and GLP-1RA. Continuous...

scholarly journals The Significance of Shocks in Implantable Cardioverter Defibrillator Recipients

2016 ◽  
Vol 5 (2) ◽  
pp. 110 ◽  
Author(s):  
Anthony Li ◽  
Amit Kaura ◽  
Nicholas Sunderland ◽  
Paramdeep S Dhillon ◽  
Paul A Scott ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Implantable Cardioverter Defibrillator ◽  
Large Scale ◽  
Strong Association ◽  
Shock Therapy ◽  
Left Ventricular ◽  
Cardioverter Defibrillator ◽  
Patients With Heart Failure ◽  
The Relationship

Large-scale implantable cardioverter defibrillator (ICD) trials have unequivocally shown a reduction in mortality in appropriately selected patients with heart failure and depressed left ventricular function. However, there is a strong association between shocks and increased mortality in ICD recipients. It is unclear if shocks are merely a marker of a more severe cardiovascular disease or directly contribute to the increase in mortality. The aim of this review is to examine the relationship between ICD shocks and mortality, and explore possible mechanisms. Data examining the effect of shocks in the absence of spontaneous arrhythmias as well as studies of non-shock therapy and strategies to reduce shocks are analysed to try and disentangle the shocks versus substrate debate.

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