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Effect of stem cell transplantation on patients with ischemic heart failure: a systematic review and meta-analysis of randomized controlled trials.

ABSTRACT: Stem cell transplantation (SCT) has become a promising way to treat ischemic heart failure (IHF). We performed a large-scale meta-analysis of randomized clinical trials to investigate the efficacy and safety of SCT in IHF patients. Randomized controlled trials (RCTs) involving stem cell transplantation for the treatment of IHF were identified by searching the PubMed, EMBASE, SpringerLink, Web of Science, and Cochrane Systematic Review databases as well as from reviews and the reference lists of relevant articles. Fourteen eligible randomized controlled trials were included in this study, for a total of 669 IHF patients, of which 380 patients were treated with SCT. The weighted mean difference (WMD) was calculated for changes in the New York Heart Association (NYHA) class, left ventricular ejection fraction (LVEF), left ventricular end-diastolic and end-systolic volumes (LVEDV and LVESV), and Canadian Cardiovascular Society (CCS) angina grade using a fixed effects model, while relative risk (RR) was used for mortality. Compared with the control group, SCT significantly lowered the NYHA class (MD = - 0.73, 95% CI - 1.32 to - 0.14, P < 0.05), LVESV (MD = - 14.80, 95% CI - 20.88 to - 8.73, P < 0.05), and CCS grade (MD = - 0.81, 95% CI - 1.45 to - 0.17, P < 0.05). Additionally, SCT increased LVEF (MD = 6.55, 95% CI 5.93 to 7.16, P < 0.05). However, LVEDV (MD = - 0.33, 95% CI - 1.09 to 0.44, P > 0.05) and mortality (RR = 0.86, 95% CI 0.45 to 1.66, P > 0.05) did not differ between the two groups. This meta-analysis suggests that SCT may contribute to the improvement of LVEF, as well as the reduction of the NYHA class, CCS grade, and LVESV. In addition, SCT does not affect mortality.

SUBMITTER: Wang Y

PROVIDER: S-EPMC6472092 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundHeart failure is the end stage of all cardiovascular diseases, which brings a heavy burden to the global health network. Arotinolol, as a new type of β Receptor blocker, has a good antihypertensive effect. Many clinical trials have observed the clinical efficacy of arotinolol in the treatment of essential hypertension. However, so far, there has been no systematic evaluation on the efficacy and safety of arotinolol in the treatment of chronic heart failure.ObjectiveThe purpose of this review was to systematically evaluate the clinical efficacy of arotinolol in patients with chronic heart failure.MethodsRandomized controlled trials (RCTs) of arotinolol in the treatment of chronic heart failure were retrieved from seven databases according to the Cochrane manual, including CNKI (China National Knowledge Infrastructure), Wan fang database, VIP database, PubMed, Sinomed, EMBASE, and the Cochrane Library databases. The main outcomes were the effective rate, left ventricular ejection fraction (LVEF), blood pressure, heart rate, cardiac index, stroke volume (SV), brain natriuretic peptide (BNP), hypersensitive C-reactive protein (Hs-CRP), left ventricular end diastolic volume (LVEDV), left ventricular end diastolic diameter (LVEDD), and adverse events (AEs).ResultsA total of 17 trials met the qualification criteria, which included 1,717 patients with heart failure. Most trials had uncertain risks in terms of random sequence generation, allocation hiding, patient loss, and result evaluation. Meta analysis showed that arotinolol significantly improved the treatment efficiency of patients with heart failure (standardized mean difference (SMD) = 4.07, 95% confidence interval (CI) [2.89, 5.72], p = 0.00, I 2 = 0), LVEF (SMD = 1.59, 95% CI [0.99, 2.19], p = 0.000 0, I 2 = 95.8%), cardiac index (SMD = 0.32, 95% CI [0.11, 0.53], p = 0.03), I 2 = 0), SV (SMD = 2.00, 95% CI [1.57, 2.34], p = 0.000, I 2 = 64.2%), lower BNP (SMD = -0.804, 95% CI [-0.97, -0.64], p = 0.000, I 2 = 94.4%), and LVEDV (SMD = -0.25, 95% CI [-0.45, -0.05], p = 0.015, I 2 = 0). There was no statistical significance for blood pressure (SMDsystolic pressure = -0.09, 95% CI [-0.69, 0.51], p = 0.775, I 2 systolic pressure = 90.2%; SMDdiastolic pressure = -0.16, 95% CI [-0.79, 0.48], P = 0.632, I 2 diastolic pressure = 91.2%), heart rate (SMD = -0.12, 95% CI [-1.00, 0.75], P = 0.787, I 2 = 96.1%), Hs-CRP (SMD = -1.52, 95% CI [-3.43, 0.40], P = 0.121, I 2 = 98.3%), and LVEDD (SMD = -0.07, 95% CI [-0.90, 0.76], P = 0.870, I 2 = 96.5%).ConclusionArotinolol can safely and effectively improve the effective rate of patients with chronic heart failure, increase LVEF, increase CI and SV, and reduce BNP and LVEDV. However, because of the low overall quality of the included randomized controlled trials, these findings need to be considered carefully. More high-quality randomized controlled trials are needed for further verification, to provide a more scientific basis for the safety and effectiveness of arotinolol in the clinical treatment of heart failure.Systematic review registration[https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=371214], identifier [CRD:420223371214].

Project description:Acute heart failure (AHF) is a major public health concern, affecting 26 million worldwide. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a class of glucose-lowering drugs, comprising canagliflozin, dapagliflozin, and empagliflozin that are being explored for AHF. We aim to meta-analyze the effectiveness of SGLT2 inhibitors compared to placebo for primary outcomes including all-cause and cardiovascular mortality, heart failure events, symptomatic improvement, and readmissions. Our secondary outcome is the risk of serious adverse events. This meta-analysis has been designed in accordance with the PRISMA Statement 2020. A systematic search across PubMed, Scopus, and Cochrane Library was conducted through August 13, 2022. The following keywords were utilized: sglt2, sodium-glucose transporter 2 inhibitors, sglt2 inhibitors, decompensated heart failure, de-novo heart failure, and/or acute heart failure. Only randomized controlled trials (RCTs) with adult patients (>18 years), hospitalized with de-novo AHF, acutely decompensated chronic heart failure with reduced, borderline, or preserved ejection, and receiving SGLT2 inhibitors were included. A quantitative analytical methodology was applied where the standardized mean difference (SMD) applying 95% confidence intervals (CI) for continuous outcomes and risk ratio (RR) with 95% CI was yielded. All tests were carried out on Review Manager 5.4 (Cochrane). In total, three RCTs were included pooling in a total of 1831 patients where 49.9% received SGLT2 inhibitors. The mean age was 72.9 years in the interventional group compared to 70.6 years in the placebo. Only 33.7% of the sample was female. The follow-up spanned 2−9 months. Heart failure events were reduced by 62% in the interventional group (RR = 0.66, p < 0.0001). readmissions had a reduced risk of 24% with SGLT2 inhibitors (RR = 0.76, p = 0.03). We assessed the efficacy and safety of SGLT2 inhibitors in preventing complications post-AHF. The odds of all-cause mortality, cardiovascular mortality, heart failure events, and re-admissions rates were substantially reduced within the first 1−9 months of hospitalization.

Project description:Background: The effect of testosterone supplementation in patients with chronic heart failure (CHF) remains uncertain. Methods: A meta-analysis of randomized controlled trials (RCTs) was performed. RCTs that evaluate the chronic effect of testosterone supplementation on exercise capacity and cardiac function in CHF were identified via searching of PubMed, Embase, and the Cochrane's Library databases. Heterogeneity was evaluated by the Cochrane's Q test and I 2 statistics. A fixed-effect model was used if the heterogeneity was not significant (I 2 < 50%); otherwise, a random-effect model was applied. Results: Eight studies including 170 patients in the testosterone supplementation group and 162 in the control group were included. Overall, testosterone supplementation was not associated with an improved exercise capacity (walking test: standardized mean difference [SMD] = 0.36, p = 0.07). Sensitivity analyses limited to male patients showed similar results (SMD = 0.21, p = 0.15), and subgroup analyses also showed similar results in male HF patients with baseline total testosterone (TT) ? or < 10 nmol/L. However, patients with TT at endpoint ? 25 nmol/L was associated with improved exercise capacity (SMD = 1.12, p = 0.02), but not for those with TT at endpoint < 25 nmol/L (SMD = 0.24, p = 0.12). In addition, VO2max (weight mean difference [WMD] = 0.85, p = 0.43), the functional classification (the New York Heart Association classification: WMD = -0.08, p = 0.16) and quality of life (Minnesota Living with Heart Failure [MLHF] questionnaire: WMD = -6.03, p = 0.12) were not significantly affected. Moreover, testosterone supplementation did not significantly affect left ventricular ejection fraction (WMD: -1.52%, p = 0.37), serum B-type natriuretic peptide (SMD: -0.19, p = 0.23), or a composite outcome of death or HF hospitalization (risk ratio [RR]: 1.02, p = 0.96). Although testosterone supplementation increased systolic blood pressure (BP) in CHF patients (WMD: 5.68 mmHg, p < 0.001), diastolic BP or heart rate was not significantly changed as compared to control. Conclusions: Testosterone supplementation within a physiological range is not associated with significantly improved exercise capacity, cardiac function, quality of life, or clinical outcome in CHF patients.

Project description:Sacubitril-valsartan has been shown to have superior effects over angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in patients with heart failure (HF) and hypertension. The efficacy and safety of sacubitril-valsartan in patients with HF are controversial. We performed a meta-analysis of randomized controlled trials to assess and compare the effect and adverse events of sacubitril-valsartan, valsartan, and enalapril in patients with HF. We conducted a systematic search using PubMed, Embase, the Cochrane Library, and ClinicalTrials.gov. Randomized controlled trials involving the use of sacubitril-valsartan in patients with HF were included. We assessed the pooled odds ratio (OR) of all-cause mortality, cardiovascular mortality, and hospitalization for HF in fixed-effects models and the pooled risk ratio (RR) of symptomatic hypotension, worsening renal function, and hyperkalaemia in fixed-effects models. Of the 315 identified records, six studies involving 14 959 patients were eligible for inclusion. Sacubitril-valsartan reduced the endpoints of all-cause mortality and cardiovascular mortality in patients with HF with reduced ejection fraction (HFrEF) in three trials with pooled ORs of 0.83 (P = 0.0006) and 0.78 (P < 0.0001), respectively. Regarding the composite outcome of hospitalization for HF in five trials, the pooled OR was 0.79 (P < 0.00001). Compared with enalapril or valsartan, sacubitril-valsartan was associated with a high risk of symptomatic hypotension (RR 1.47, P < 0.00001), low risk of worsening renal function (RR 0.81, P = 0.005), and low rate of serious hyperkalaemia (≥6.0 mmol/L) (RR 0.76, P = 0.0007) in all six trials. Compared with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, sacubitril-valsartan significantly decreased the risk of death from all causes or cardiovascular causes in HFrEF and hospitalization for HF in both patients with HFrEF and HF with preserved ejection fraction. Sacubitril-valsartan reduced the risk of renal dysfunction and serious hyperkalaemia but was associated with more symptomatic hypotension.

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Effect of stem cell transplantation on patients with ischemic heart failure: a systematic review and meta-analysis of randomized controlled trials.

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