Symptomatic Chronic Heart Failure Research Articles

Predictors of short-term clinical response to cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) reduces morbidity and mortality in patients with symptomatic heart failure and QRS prolongation but there is uncertainty about which patient characteristics predict short-term clinical response. In an individual patient meta-analysis of three double-blind, randomized trials, clinical composite score (CCS) at 6 months was compared in patients assigned to CRT programmed on or off. Treatment-covariate interactions were assessed to measure likelihood of improved CCS at 6 months. MIRACLE, MIRACLE ICD, and REVERSE trials contributed data for this analysis (n = 1591). Multivariable modelling identified QRS duration and left ventricular ejection fraction (LVEF) as predictors of CRT clinical response (P < 0.05). The odds ratio for a better CCS at 6 months increased by 3.7% for every 1% decrease in LVEF for patients assigned to CRT-on compared to CRT-off, and was greatest when QRS duration was between 160 and 180 ms. In symptomatic chronic heart failure patients (NYHA class II-IV), longer QRS duration and lower LVEF independently predict early clinical response to CRT.

The relationship between natriuretic peptides and neprilysin pathways: the clinical simplification against the complexity of biological systems

A large body of evidence supports the use of natriuretic peptides (brain natriuretic peptide [BNP] and N-terminal proBNP [NT-proBNP]) for the evaluation and management of patients with heart failure over time. Elevated values reflect an enhanced counterregulatory response to hemodynamic stress and are indicative of heart failure severity, thus predicting prognosis. The clinical relevance and result interpretation of natriuretic peptides for monitoring therapy are still debated, and our understanding of their complex nature is still far from being complete. The new data about the clinical efficacy of LCZ696, a combination neprilysin inhibitor and angiotensin receptor blocker recently approved for the treatment of symptomatic chronic heart failure, showed a different susceptibility of BNP and NT-proBNP during therapy. The aim of this article is to discuss the controversial issues concerning the clinical use of cardiac natriuretic peptide measurement, the complex relationship with neprilysin pathways, and the practical implications of LCZ696 therapy for natriuretic peptide testing in clinical practice.

The relationship between serum fibrosis markers and restrictive ventricular filling in patients with heart failure with reduced ejection fraction: A technetium-99m radionuclide ventriculography study.

Myocardial fibrosis leads to a restrictive diastolic filling pattern of the left ventricle which is associated with a poor prognosis in patients with heart failure. We investigated the relationship between cardiac fibrosis and restrictive filling pattern of the left ventricle measured by Tc99m left ventriculography in patients with chronic symptomatic heart failure. Serum cardiac extracellular matrix markers including type I and III aminoterminal propeptide of procollagen (PINP and PIIINP), matrix metalloproteinase-2,9 (MMP-2,9), and tissue inhibitor of MMP-1 (TIMP-1) were analyzed. Fifty-one (39 males) patients were enrolled. Their median age was 51.8 years, and median left ventricular ejection fraction was 31.9%. Time to peak filling rate of the left ventricle was significantly correlated with serum levels of the three cardiac extracellular matrix markers (TIMP-1, PIIINP, and MMP-2). The patients with a restrictive diastolic filling pattern of the left ventricle (time to peak filling rate = 154 ms) had significantly higher levels of these extracellular matrix markers. In receiver operating characteristic curve analysis, areas under the curve of PIIINP, TIMP-1, and MMP-2 were 0.758, 0.695, and 0.751 to predict the presence of a restrictive pattern. In C-statistics, all three cardiac extracellular matrix markers significantly increased the area under the curve after adding creatinine. In net reclassification improvement and integrated discrimination improvement models, PIIINP and MMP-2 significantly improved the predictive power of age, creatinine and brain natriuretic peptide. In conclusion, serum extracellular matrix markers are significantly correlated with restrictive diastolic filling pattern of the left ventricle in patients with heart failure.

Chronic Oral Study of Myosin Activation to Increase Contractility in Heart Failure (COSMIC-HF): a phase 2, pharmacokinetic, randomised, placebo-controlled trial

Impaired contractility is a feature of heart failure with reduced ejection fraction. We assessed the pharmacokinetics and effects on cardiac function and structure of the cardiac myosin activator, omecamtiv mecarbil. In this randomised, double-blind study, done at 87 sites in 13 countries, we recruited patients with stable, symptomatic chronic heart failure and left ventricular ejection fraction 40% or lower. Patients were randomly assigned equally, via an interactive web response system, to receive 25 mg oral omecamtiv mecarbil twice daily (fixed-dose group), 25 mg twice daily titrated to 50 mg twice daily guided by pharmacokinetics (pharmacokinetic-titration group), or placebo for 20 weeks. We assessed the maximum concentration of omecamtiv mecarbil in plasma (primary endpoint) and changes in cardiac function and ventricular diameters. This trial is registered with ClinicalTrials.gov, number NCT01786512. From March 17, 2014, to March 5, 2015, we enrolled 150 patients in the fixed-dose omecamtiv mecarbil group and 149 in the pharmacokinetic-titration and placebo groups. Mean maximum concentration of omecamtiv mecarbil at 12 weeks was 200 (SD 71) ng/mL in the fixed-dose group and 318 (129) ng/mL in the pharmacokinetic-titration group. For the pharmacokinetic-titration group versus placebo group at 20 weeks, least square mean differences were as follows: systolic ejection time 25 ms (95% CI 18-32, p<0·0001), stroke volume 3·6 mL (0·5-6·7, p=0·0217), left ventricular end-systolic diameter -1·8 mm (-2·9 to -0·6, p=0·0027), left ventricular end-diastolic diameter -1·3 mm, (-2·3 to 0·3, p=0·0128), heart rate -3·0 beats per min (-5·1 to -0·8, p=0·0070), and N-terminal pro B-type natriuretic peptide concentration in plasma -970 pg/mL (-1672 to -268, p=0·0069). The frequency of adverse clinical events did not differ between groups. Omecamtiv mecarbil dosing guided by pharmacokinetics achieved plasma concentrations associated with improved cardiac function and decreased ventricular diameter. Amgen.

Clinical Benefits of Stem Cells for Chronic Symptomatic Systolic Heart Failure: A Systematic Review of the Existing Data and Ongoing Trials.

The benefits of stem cell therapy for patients with chronic symptomatic systolic heart failure due to ischemic and nonischemic cardiomyopathy (ICM and NICM, respectively) are unclear. We performed a systematic review of major published and ongoing trials of stem cell therapy for systolic heart failure and compared measured clinical outcomes for both types of cardiomyopathy. The majority of the 29 published studies demonstrated clinical benefits of autologous bone marrow-derived mesenchymal stem cells (BM-MSCs). Left ventricular ejection fraction (LVEF) was improved in the majority of trials after therapy. Cell delivery combined with coronary artery bypass grafting was associated with the greatest improvement in LVEF. Left ventricular end-systolic volume (or diameter), New York Heart Association functional classification, quality of life, and exercise capacity were also improved in most studies after cell therapy. Most ICM trials demonstrated a significant improvement in perfusion defects, infarct size, and myocardial viability. Several larger clinical trials that are in progress employ alternative delivery modes, cell types, and longer follow-up periods. Stem cells are a promising therapeutic modality for patients with heart failure due to ICM or NICM. More data are required from larger blinded trials to determine which combination of cell type and delivery mode will yield the most benefit with avoidance of harm in these patient populations.

Changing the treatment of heart failure with reduced ejection fraction: clinical use of sacubitril-valsartan combination.

Despite significant therapeutic advances, patients with chronic heart failure (HF) remain at high risk of morbidity and mortality. Sacubitril valsartan (previously known as LCZ696) is a new oral agent approved for the treatment of symptomatic chronic heart failure in adults with reduced ejection fraction. It is described as the first in class angiotensin receptor neprilysin inhibitor (ARNI) since it incorporates the neprilysin inhibitor, sacubitril and the angiotensin II receptor antagonist, valsartan. Neprilysin is an endopeptidase that breaks down several vasoactive peptides including natriuretic peptides (NPs), bradykinin, endothelin and angiotensin II (Ang-II). Therefore, a natural consequence of its inhibition is an increase of plasmatic levels of both, NPs and Ang-II (with opposite biological actions). So, a combined inhibition of these both systems (Sacubitril / valsartan) may enhance the benefits of NPs effects in HF (natriuresis, diuresis, etc) while Ang-II receptor is inhibited (reducing vasoconstriction and aldosterone release). In a large clinical trial (PARADIGM-HF with 8442 patients), this new agent was found to significantly reduce cardiovascular and all cause mortality as well as hospitalizations due to HF (compared to enalapril). This manuscript reviews clinical evidence for sacubitril valsartan, dosing and cautions, future directions and its considered place in the therapy of HF with reduced ejection fraction.

Efficacy Profile of Ivabradine in Patients with Heart Failure plus Angina Pectoris

Objectives: In the Systolic Heart Failure Treatment with the I_f Inhibitor Ivabradine Trial (SHIFT), slowing of the heart rate with ivabradine reduced cardiovascular death or heart failure hospitalizations among patients with systolic chronic heart failure (CHF). Subsequently, in the Study Assessing the Morbidity-Mortality Benefits of the I_f Inhibitor Ivabradine in Patients with Coronary Artery Disease (SIGNIFY) slowing of the heart rate in patients without CHF provided no benefit for cardiovascular death or nonfatal myocardial infarction (primary composite end point), with secondary analyses suggesting possible harm in the angina subgroup. Therefore, we examined the impact of ivabradine in the patients with CHF plus angina in SHIFT. Methods: SHIFT enrolled adults with stable, symptomatic CHF, a left ventricular ejection fraction ≤35% and a sinus rhythm with a resting heart rate ≥70 bpm. Outcomes were the SHIFT and SIGNIFY primary composite end points and their components. Results: Of 6,505 patients in SHIFT, 2,220 (34%) reported angina at randomization. Ivabradine numerically, but not significantly, reduced the SIGNIFY primary composite end point by 8, 11 and 11% in the SHIFT angina subgroup, nonangina subgroup and overall population, respectively. Ivabradine also reduced the SHIFT primary composite end point in all 3 subgroups. Conclusions: In SHIFT, ivabradine showed consistent reduction of cardiovascular outcomes in patients with CHF; similar results were seen in the subgroup of SHIFT patients with angina.

‘Cutting-edge’ medicines vs. affordable quality health care?

British Journal of Cardiac NursingVol. 11, No. 8 Guest Editorial‘Cutting-edge’ medicines vs. affordable quality health care?Nazish KhanNazish KhanSearch for more papers by this authorNazish KhanPublished Online:5 Aug 2016https://doi.org/10.12968/bjca.2016.11.8.370AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References British Heart Foundation (2016) Managing Heart Failure in the Community. http://tinyurl.com/gupbpkk (accessed 21 July 2016) Google ScholarHeart UK (2016) What is Familial Hypercholesterolaemia (FH)? http://tinyurl.com/gp7athb (accessed 21 July 2016) Google ScholarMcMurray JJ, Packer M, Desai AS et al.; PARADIGM-HF Investigators and Committees (2014) Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med 371(11): 993–1004. doi: https://doi.org/10.1056/NEJMoa1409077 Crossref, Google ScholarNHS Improvement (2011) A guide for review and improvement of hospital based heart failure services. http://tinyurl.com/h6yq45o (accessed 21 July 2016) Google ScholarNational Institute for Health and Care Excellence (2010) Chronic heart failure in adults: management. [CG108]. NICE, London. https://www.nice.org.uk/guidance/CG108 (accessed 21 July 2016) Google ScholarNational Institute for Health and Care Excellence (2016a) Sacubitril valsartan for treating symptomatic chronic heart failure with reduced ejection fraction. [TA388]. NICE, London. https://www.nice.org.uk/Guidance/TA388 (accessed 21 July 2016) Google ScholarNational Institute for Health and Care Excellence (2016b) Alirocumab for treating primary hypercholesterolaemia and mixed dyslipidaemia. [TA393]. NICE, London. https://www.nice.org.uk/guidance/ta393 (accessed 21 July 2016) Google ScholarNational Institute for Health and Care Excellence (2016c) Evolocumab for treating primary hypercholesterolaemia and mixed dyslipidaemia. [TA394]. NICE, London. https://www.nice.org.uk/guidance/ta394 (accessed 21 July 2016) Google Scholar FiguresReferencesRelatedDetails 2 August 2016Volume 11Issue 8ISSN (online): 2052-2207 Metrics History Published online 5 August 2016 Published in print 2 August 2016 Information© MA Healthcare LimitedPDF download

▼ Sacubitril valsartan for heart failure

▼ Sacubitril valsartan (Entresto—Novartis) is a new oral drug licensed for the treatment of symptomatic chronic heart failure in adults with reduced ejection fraction.1 It is described as an angiotensin...

Effectiveness of Cardiac Rehabilitation for Prevention and Treatment of Sarcopenia in Patients with Cardiovascular Disease - A Retrospective Cross-Sectional Analysis.

Sarcopenia is a syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength, with the risk of frailty and poor quality of life. This study aimed to clarify the clinical characteristics of sarcopenia and to investigate the effects of comprehensive cardiac rehabilitation (CCR), including nutrition, physical exercise and medication, in patients with cardiovascular disease (CVD). We retrospectively studied 322 inpatients with CVD (age 72±12 years). Muscle mass, muscle strength and physical performance were assessed before and after exercise training in patients with and without sarcopenia, which was defined as either a gait speed of <0.8 m/s or reduced handgrip strength (<26 kg in males and <18 kg in females), together with lower skeletal muscle index (SMI) (<7.0 kg/m2 in males and <5.7 kg/m2 in females). The actual daily total calorie and nutrient intake was also calculated. Sarcopenia was identified in 28% of patients with CVD, these patients having a higher prevalence of symptomatic chronic heart failure and chronic kidney disease. SMI was significantly associated with protein intake and statin treatment. The ratio of peak VO2 and SMI was significantly higher in the statin treatment group. Handgrip strength, gait speed, leg weight bearing index, and nutritional intake improved after exercise training in patients both with and without sarcopenia. The present findings suggest that CCR is a promising strategy for prevention and treatment of sarcopenia in patients with CVD.

Sacubitril/valsartan for the treatment of heart failure

Sacubitril/valsartan (Entresto) is a new combined formulation licensed for the treatment of adults with symptomatic chronic heart failure with reduced ejection fraction. This articles summarises its indications, efficacy and adverse effects.

Ivabradine in Management of Heart Failure: a Critical Appraisal.

Elevated resting heart rate has been linked to poor outcomes in patients with chronic systolic heart failure. Blockade of funny current channel with ivabradine reduces heart rate without inotropic effects. Ivabradine was recently approved by US Food and Drug Administration for patients with stable, symptomatic chronic heart failure (HF) with left ventricular ejection fraction (LVEF) ≤35%, who are in sinus rhythm with resting heart rate (HR) ≥ 70bpm and either are on maximally tolerated doses of beta-blockers, or have a contraindication to beta-blockers. This article will review and evaluate the data supporting the use of ivabradine in patients with HF and explore its mechanisms and physiologic effects.

Impact of Physical Inactivity on Mortality in Patients With Heart Failure

The impact of physical inactivity on heart failure (HF) mortality is unclear. We analyzed data from the HF Adherence and Retention Trial (HART) which enrolled 902 patients with New York Heart Association class II/III HF, with preserved or reduced ejection fraction, who were followed for 36 months. On the basis of mean self-reported weekly exercise duration, patients were classified into inactive (0 min/week) and active (≥1 min/week) groups and then propensity score matched according to 34 baseline covariates in 1:2 ratio. Sedentary activity was determined according to self-reported daily television screen time (<2, 2 to 4, >4 h/day). The primary outcome was all-cause death. Secondary outcomes were cardiac death and HF hospitalization. There were 196 inactive patients, of whom 171 were propensity matched to 342 active patients. Physical inactivity was associated with greater risk of all-cause death (hazard ratio [HR] 2.01, confidence interval [CI] 1.47 to 3.00; p <0.001) and cardiac death (HR 2.01, CI 1.28 to 3.17; p = 0.002) but no significant difference in HF hospitalization (p = 0.548). Modest exercise (1 to 89 min/week) was associated with a significant reduction in the rate of death (p = 0.003) and cardiac death (p = 0.050). Independent of exercise duration and baseline covariates, television screen time (>4 vs <2 h/day) was associated with all-cause death (HR 1.65, CI 1.10 to 2.48; p = 0.016; incremental chi-square = 6.05; p = 0.049). In conclusion, in patients with symptomatic chronic HF, physical inactivity is associated with higher all-cause and cardiac mortality. Failure to exercise and television screen time are additive in their effects on mortality. Even modest exercise was associated with survival benefit.

Autonomic regulation therapy suppresses quantitative T-wave alternans and improves baroreflex sensitivity in patients with heart failure enrolled in the ANTHEM-HF study

Autonomic regulation therapy (ART) with chronic vagus nerve stimulation improves ventricular function in patients with chronic heart failure, but its effects on quantitative T-wave alternans (TWA), ventricular tachycardia (VT), baroreflex sensitivity, and autonomic tone remained unknown. Effects on TWA, a marker of risk of life-threatening arrhythmias; heart rate turbulence (HRT), an indicator of baroreflex sensitivity; heart rate variability; and VT incidence were studied in 25 patients with chronic symptomatic heart failure and reduced ejection fraction enrolled in the ANTHEM-HF study (NCT01823887). Twenty-four-hour ambulatory electrocardiographic recordings made before ART system (Cyberonics, Inc., Houston, TX) implantation involving the left or right vagus nerve and after 6 and 12 months of chronic therapy (10-Hz frequency, 250-μs pulse width, maximum tolerable current amplitude after 10 weeks of titration) at low-intensity (<2 mA; n = 10, 40%) or high-intensity (≥2 mA; n = 15, 60%) stimulation levels were analyzed. At 12 months, peak TWA levels were reduced by 29% from 71.0 ± 4.6 to 50.5 ± 1.8 μV (P < .0001). The number of patients with severely abnormal TWA (≥60 μV) was reduced by 76% from 17 to 4 (P < .0005), and the number of patients with nonsustained VT decreased by 73% from 11 to 3 (P < .025). HRT slope (P < .025), high frequency heart rate variability (HRV) (P = .05), and square root of the mean squared differences of successive normal-to-normal interval HRV (P = .013) increased. The mean heart rate derived from 24-hour Holter electrocardiograms decreased by 10% from 77 ± 2 to 69 ± 2 beats/min (P = .0002). HRT onset was unchanged. Chronic ART in patients with symptomatic heart failure improves cardiac electrical stability, as reflected by reduced TWA levels and heart rate, suppresses VT, and increases baroreceptor sensitivity. These observations deserve study in a larger population.

Abstract 16571: The Potential Impact of Expanding Cardiac Rehabilitation Coverage in Heart Failure: Insights From Get With the Guidelines Heart Failure

Background: In February 2014, coverage for cardiac rehabilitation (CR) was expanded by Centers for Medicare &amp; Medicaid to include patients with chronic symptomatic heart failure (HF) on optimal medical therapy with ejection fraction &lt;35%. Thus, we sought to characterize the patient population newly eligible for CR based on the expanded criteria and their associated outcomes. Methods: We analyzed the Get With The Guidelines-HF registry linked to Medicare claims data from 2008-2012 to assess three groups of patients age 65 or older: previously eligible (due to prior MI, CABG, stable angina, heart valve surgery, or PCI in the previous 12 months), newly eligible, and ineligible for CR. Ineligible patients met neither criteria. Incidence rate was calculated with Kaplan-Meier estimates and Cox proportional hazard models were used to determine the association of events. Results: Among 51,665 HF patients discharged alive, 27.2% (n=14,053) were newly eligible and 14.5% were previously eligible for CR (n=7477). Newly eligible patients were more likely to be black, have atrial fibrillation and EF &lt; 35%, while having fewer previous hospitalizations than patients previously eligible for CR. Newly eligible and ineligible patients had similar risk for 1-year mortality compared with those previously eligible (adjusted Hazard Ratio [HR] 0.95, 95% Confidence Interval [CI] 0.88-1.02, p-value=0.13 and [HR] 1.05, 95% [CI] 0.98-1.13, p-value=0.17, respectively). However, newly eligible and ineligible patients had lower risk for 1-year readmission compared with those previously eligible (adjusted [HR] 0.89, 95% [CI] 0.85-0.93, p-value&lt;0.001 and [HR] 0.94, 95% [CI] 0.90- 0.98, p-value&lt;0.001). Conclusions: The extension of coverage for cardiac rehabilitation has tripled the potentially eligible HF population. As these newly eligible patients are at high risk for adverse outcomes, cardiac rehabilitation should be considered.

Abstract 17891: Impact of Physical Activity and Sedentary Time on Heart Failure Outcomes

Introduction: The impact of physical inactivity and sedentary time on heart failure (HF) outcomes in patients not participating in exercise program is unclear. Hypothesis: Physical inactivity and sedentary time are associated with worse HF outcomes. Methods: We analyzed data from the multicenter, HF Adherence and Retention Trial (HART) which enrolled 902 NYHA - II/III HF patients with preserved or reduced ejection fraction, followed for 36 months. Based on the mean weekly purposeful physical activity duration, patients were classified into inactive (0 min/wk), partially active (1-90 min/wk), and active (&gt;90min/wk) groups. Patients were also classified according to average daily sedentary television (TV) time into &lt;2 hrs/d, 2-4 hrs/d, and &gt;4 hrs/d groups. Study groups were propensity score matched according to 33 baseline covariates in 1:1:1 ratio. The primary outcome was all-cause death. Secondary outcomes were cardiac death and HF hospitalization. Results: There were 196 inactive, 341 partially active and 365 active patients, of whom 492 (164 in each group) were successfully propensity matched. Physical inactivity was associated with higher risk of death and cardiac death than any level of physical activity, Fig 1. There was no significant difference in HF hospitalization. Furthermore, 465 subjects were propensity matched into three sedentary TV time groups (155 in each group). Sedentary TV time &gt;4 hrs/d was independently and incrementally associated with all-cause death (Δ χ 2 = 6.05; P=0.049), beyond physical activity time, Fig 1. There was no significant difference in mortality between &lt;2 and 2-4 hrs/d sedentary TV time groups, after adjusting to physical activity time, Fig 2. Conclusions: In symptomatic chronic HF patients, physical inactivity is associated with higher all-cause and cardiac mortality. Modest purposeful physical activity was associated with survival benefit. Extended sedentary time was associated incremental increased mortality.

Shenfu decoction as adjuvant therapy for improving quality of life and hepatic dysfunction in patients with symptomatic chronic heart failure

Ethnopharmacological relevanceShenfu decoction (SFD) is a water extract of the dried root or root stalk of Panax ginseng C. A. Mey (Asian ginseng) and the lateral root of Aconitum carmichaeli Debx (prepared by Fuzi, Heishunpian in Chinese). It has been used to treat heart failure for over a thousand years. The main active components of SFD, ginsenosides and higenamine, enhance heart contractility, increase the coronary blood supply, improve ischemic myocardial metabolism, scavenge free radicals and protect myocardial ultrastructure. Aim of the studyTo investigate the effect of SFD on quality of life (QOL) and hepatic function in symptomatic chronic heart failure (CHF) patients. Materials and methodsForty patients enrolled in the study were randomized into two groups: an SFD group (18 cases) and a control group (22 cases). All the patients received standard heart failure therapy, and the SFD group patients were also treated with Shenfu granules for 14 days as an adjunctive therapy. The effects of SFD on QOL, plasma alanine aminotransferase (ALT) level, cardiac function, left ventricular ejection fraction (LVEF) and tumor necrosis factor-α (TNF-α) level were studied. ALT threshold in hepatic injury are 21U/L for men and 17U/L for women. ResultsMinnesota Living with Heart Failure Questionnaire (MLHFQ) scores were improved by 35.27±10.72 vs. 23.87±11.96 in the SFD and control groups respectively (p<0.01). Subgroup analysis of the MLHFQ results demonstrated that both physical and emotional scores were significantly higher in the SFD group (21.00±5.66 vs. 16.75±6.25, p<0.05; 4.64±4.84 vs. 1.13±2.85, p<0.05). Circulating ALT was significantly decreased by SFD (13.3IU/L vs. 0.6IU/L, p<0.01). The grading of cardiac function and LVEF were increased by 1.6±0.5 vs. 1.1±0.3 and 18%±13% vs. 8%±8% in the SFD and control groups respectively (p<0.05 and p<0.05). The level of TNF-α declined more in SFD than control group (64.8±5.0 to 57.6±4.1, p<0.05; vs. 61.6±5.9 vs. 57.7±3.2. p>0.05). ConclusionCompared with standard heart failure treatment, oral SFD as an adjuvant therapy significantly improved QOL and hepatic injury in CHF patients.

Circulating thrombospondine-2 in patients with moderate-to-severe chronic heart failure due to coronary artery disease.

Chronic heart failure (CHF) remains a leading cause of morbidity and mortality. In the current study, we aimed to evaluate the predictive value of circulating thrombospondin-2 (TSP-2) for cumulative survival in patients with ischemic CHF due to coronary artery disease (CAD). The results showed that during a median follow-up of 2.18 years, 21 participants died and 106 subjects were hospitalized repeatedly. The median circulating levels of TSP-2 in patients who survived and those who died were 0.63 ng/mL (95%CI=0.55-0.64 ng/mL) and 1.03 ng/mL (95% CI=0.97-1.07 ng/mL) (P<0.001). Circulating TSP-2 independently predicted all-cause mortality (OR=1.27; 95%CI=1.08-1.59; P=0.002), CHF-related death (OR=1.16; 95%CI=1.02-1.50; P<0.001), and also CHF-related rehospitalization (OR=1.12; 95%CI=1.07-1.25; P<0.001). In conclusion, among CAD patients with symptomatic CHF, increased circulating TSP-2 is correlated with increased 3-year CHF-related death, all-cause mortality, and risk for recurrent hospitalization.

Circulating thrombospondin-2 in patients with moderate-to-severe chronic heart failure due to coronary artery disease

Chronic heart failure (CHF) remains a leading cause of morbidity and mortality. In the current study, we aimed to evaluate the predictive value of circulating thrombospondin-2 (TSP-2) for cumulative survival in patients with ischemic CHF due to coronary artery disease (CAD). The results showed that during a median follow-up of 2.18 years, 21 participants died and 106 subjects were hospitalized repeatedly. The median circulating levels of TSP-2 in patients who survived and those who died were 0.63 ng/mL (95%CI = 0.55-0.64 ng/mL) and 1.03 ng/mL (95% CI = 0.97-1.07 ng/mL) (P<0.001). Circulating TSP-2 independently predicted all-cause mortality (OR = 1.27; 95%CI = 1.08–1.59; P = 0.002), CHF-related death (OR = 1.16; 95%CI = 1.02–1.50; P<0.001), and also CHF-related rehospitalization (OR = 1.12; 95%CI = 1.07–1.25; P<0.001). In conclusion, among CAD patients with symptomatic CHF, increased circulating TSP-2 is correlated with increased 3-year CHF-related death, all-cause mortality, and risk for recurrent hospitalization.

EFFICACY PROFILE OF IVABRADINE IN PATIENTS WITH HEART FAILURE PLUS ANGINA PECTORIS

Objectives: In the Systolic Heart Failure Treatment with the If Inhibitor Ivabradine Trial (SHIFT), slowing of the heart rate with ivabradine reduced cardiovascular death or heart failure hospitalizations among patients with systolic chronic heart failure (CHF). Subsequently, in the Study Assessing the Morbidity-Mortality Benefits of the If Inhibitor Ivabradine in Patients with Coronary Artery Disease (SIGNIFY) slowing of the heart rate in patients without CHF provided no benefit for cardiovascular death or nonfatal myocardial infarction (primary composite end point), with secondary analyses suggesting possible harm in the angina subgroup. Therefore, we examined the impact of ivabradine in the patients with CHF plus angina in SHIFT. Methods: SHIFT enrolled adults with stable, symptomatic CHF, a left ventricular ejection fraction ≤35% and a sinus rhythm with a resting heart rate ≥70 bpm. Outcomes were the SHIFT and SIGNIFY primary composite end points and their components. Results: Of 6,505 patients in SHIFT, 2,220 (34%) reported angina at randomization. Ivabradine numerically, but not significantly, reduced the SIGNIFY primary composite end point by 8, 11 and 11% in the SHIFT angina subgroup, nonangina subgroup and overall population, respectively. Ivabradine also reduced the SHIFT primary composite end point in all 3 subgroups. Conclusions: In SHIFT, ivabradine showed consistent reduction of cardiovascular outcomes in patients with CHF; similar results were seen in the subgroup of SHIFT patients with angina.