Effect of lanthanum carbonate on the progression of coronary artery calcification in hemodialysis patients: A meta-analysis of randomized controlled trials.

INTRODUCTION: Coronary artery calcification and cardiac abnormalities are common in hemodialysis patients. The value of lanthanum carbonate over calcium-based phosphate binders in managing the progression of coronary artery calcification is debated. We reviewed all randomized controlled trials (RCTs) comparing the two strategies in these patients. METHODS: RCTs comparing lanthanum carbonate with calcium-based phosphate binders used in adult hemodialysis patients were identified in the PubMed, EMBASE, Cochrane Library, China National Knowledge Infrastructure, China Science and Technology Journal, and Wanfang databases. FINDINGS: Ten RCTs involving 687 patients were suitable for inclusion. Compared with calcium-based phosphate binders, lanthanum carbonate yielded lower coronary artery calcium scores (weighted mean difference, WMD: -74.28, 95% CI: -149.89, 1.33), change in coronary artery calcium scores (WMD: -105.18, 95% CI: -113.83, -96.53), and left ventricular mass index (WMD: -29.95, 95% CI: -54.25, -7.45). Lanthanum carbonate was significantly associated with lower levels of serum phosphate (WMD: -0.18, 95% CI: -0.26, -0.10), calcium (WMD: -0.22, 95% CI: -0.25, -0.20), and fibroblast growth factor 23 (FGF23) (standard mean difference: -3.78, 95% CI: -5.60, -1.96) but not intact parathyroid hormone (WMD: -4.23, 95% CI: -64.12, 55.65). Moreover, a reduced risk of nonfatal cardiovascular events (OR: 0.31, 95% CI: 0.10-0.97) but not all-cause mortality (OR: 1.08, 95% CI: 0.39-3.01) in lanthanum carbonate therapy was observed. DISCUSSION: In hemodialysis patients, lanthanum carbonate therapy may impede the progression of coronary artery calcification and left ventricular mass index and lead to reduced serum phosphate, calcium, FGF23, and nonfatal cardiovascular events compared with calcium-based phosphate binders. However, more well-designed RCTs are required for confirmation.

Trimethylamine-N-oxide has prognostic value in coronary heart disease: a meta-analysis and dose-response analysis.

BACKGROUND: Previous clinical studies have suggested that trimethylamine-N-oxide (TMAO) could contribute to the development of atherosclerosis cardiovascular disease. However, the synthetic analysis in coronary heart disease (CHD) was not yet performed. We aimed to clarify the relationship between elevated plasma concentrations of TMAO and the incidence of major adverse cardiovascular events (MACE) in CHD patients. METHODS: Meta-analysis and dose-response analysis of hazard ratio data from prospective observational studies reporting on the association between TMAO plasma concentrations and the incidence of MACE in patients with CHD were conducted. RESULTS: Of the 2369 published articles identified in the search, seven papers, with data from nine cohort studies (10,301 patients), were included in the meta-analysis. Combined data showed that elevated plasma TMAO concentrations could increase 58% higher risk of MACE in patients with CHD (hazard ratios [HR]: 1.58; 95% confidence interval [CI] = 1.35-1.84, P = 0.000). For follow-up ≥ 1 year, it was associated with 62% higher risk of MACE in patients with longer-term than shorter-term (HR for follow-up ≥ 4 years: 1.96; 95% CI = 1.52-2.52 vs one to 3 years: 1.34; 95% CI = 1.26-1.43, P = 0.004). The dose-response analysis revealed a 'J' shaped association between TMAO concentration and the incidence of MACE (P = 0.033), with the concentration above 5.1 µmol/L being associated with HR of > 1. CONCLUSIONS: Elevated levels of TMAO are associated with an increased incidence of MACE in patients with CHD. TMAO concentration of 5.1 µmol/L may be a cut-off value for prognosis.

Clinical Practice Guideline of Integrative Chinese and Western Medicine for Acute Myocardial Infarction.

With increasing morbidity and mortality, acute myocardial infarction (AMI) has become one of the major causes of human death, leading to heavy burdens to individuals, families and society. Previous researches have found that though large amount of resources and great effort were devoted, no significant improvements were achieved in reducing the in-hospital mortality of AMI patients. Meanwhile, extensive studies about Chinese medicine (CM) have found that CM has special advantages in treating AMI patients. However, there is no standardized and unified clinical practice guideline (CPG) of CM for AMI. Therefore, a CPG with strict standard and generally acknowledgement is urgent to be established. This guideline was developed following the methodological process established by the World Health Organization Handbook for Guideline Development. Extensive search on clinical evidences including systematic review (SR), randomized controlled trial (RCT), observational study and case reports was launched, covering evidence of CM for AMI on several aspects, such as diagnosis, CM patterns, CM interventions on AMI and complications, cardiac rehabilitation and clinical pathway management. Besides, the application of Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach enabled the evaluation of evidence and formulation of grade of recommendation (GOR) and level of evidence (LOE). With the help of GOR and LOE, this CPG recommends the integrative CM and WM treatment method in AMI patients and provides useful information on medical decision for clinical physicians.

Left ventricular ejection fraction and left atrium diameter related to new-onset atrial fibrillation following acute myocardial infarction: a systematic review and meta-analysis.

BACKGROUND: New-onset atrial fibrillation (NOAF) occurs frequently in patients with acute myocardial infarction (AMI), and is associated with increased subsequent cardiovascular mortality. However, only a few studies directly evaluated the relationship of left ventricular ejection fraction (LVEF) or left atrium diameter (LAD) and NOAF following AMI. MATERIALS AND METHODS: MEDLINE®, EMBASE® and the Cochrane Library were carried out to find studies until January 2017. Pooled mean difference (MD) and 95% confidence interval (CI) were calculated to evaluate the value of LVEF and LAD in the prediction of NOAF after AMI. We performed sensitivity analyses to explore the potential sources of heterogeneity. Statistical analyses were carried out using the Revman 5.3. RESULT: We included 10 qualifying studies comprising a total of 708 patients with NOAF and 6785 controls. Overall, decreased LVEF and increased LAD levels had a significant positive association with NOAF in patients with AMI. The MD in the LVEF levels between the patients with and those without NOAF was -4.91 units (95% Cl: -5.70 to -4.12), test for overall effect z-score = 12.18 (p < 0.00001, I2 = 35%). Moreover, in a subgroup analysis, the MD for LAD and NOAF was 2.55 units (95% Cl: 1.91 to 3.19), test for overall effect z-score = 7.80 (p < 0.00001, I2 = 57%). CONCLUSIONS: Our meta-analysis demonstrated that both decreased LVEF and increased LAD levels were associated with greater risk of NOAF following AMI.

Relationship of non-cardiac biomarkers with periprocedural myocardial injury in patients undergoing percutaneous coronary intervention.

percutaneous coronary intervention (PCI) is one of the dominant methods for revascularization in patient with coronary artery disease (CAD), which accompanied with high incidence of periprocedural myocardial injury (PMI) evaluated by postprocedural cardiac biomarker elevation. For the convenience of risk stratification of PMI following PCI, the aim of present review provides a unique opportunity to summarize the relationship of non-cardiac biomarkers with PMI by extensively searching in the MEDLINE to identify all the relevant studies. In conclusion, we found that PCI related PMI might be correlated positively to those non-cardiac biomarkers such as low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol, total cholesterol, triglyceride, the ratios of LDL-C to high-density lipoprotein cholesterol (HDL-C), the ratios of HDL-C to apolipoprotein A-I, the ratio of eicosapentaenoic acid to arachidonic acid, lectin-like oxidized low-density lipoprotein receptor-1, C-reactive protein, high on-treatment platelet reactivity, platelet-monocyte aggregates, N-term pro-B-type natriuretic peptide, hemoglobin and albuminuria. Inversely, no relationships of PMI with those non-cardiac biomarkers such as mean platelet volume, platelet distribution width, platelet-larger cell ratio, uric acid, eosinophils count and the genetic variant of methylenetetrahydrofolate reductase (MTHFR) 677 C>T polymorphism. Moreover, there were controversial associations between PMI and those non-cardiac biomarkers such as high-density lipoprotein cholesterol, glycosylated hemoglobin, homocysteine and the polymorphism Leu33Pro of platelet glycoprotein IIbIIIa. However, almost all studies failed to provide definite mechanism of its findings, and further reaches are needed to focus on the potential mechanisms of association between non-cardiac biomarkers and PMI related to PCI.