BackgroundRed cell distribution width (RDW), a routine component of the complete blood count (CBC), measures variation in the size of circulating erythrocytes. It has been associated with several clinical outcomes in cardiovascular disease. We sought to strengthen the association between RDW and mortality in patients admitted for acute coronary syndrome (ACS) by pooling together data from available studies.MethodsStudies that fulfilled the following were identified for analysis: 1) observational; 2) included patients admitted for ACS; 3) reported data on all-cause or cardiovascular (CV) mortality in association with a low or high RDW; and 4) used logistic regression analysis to control for confounders. Using MEDLINE, Clinical Key, ScienceDirect, Scopus, and Cochrane Central Register of Controlled Trials databases, a search for eligible studies was conducted until January 9, 2017. The quality of each study was evaluated using the Newcastle-Ottawa Quality Assessment Scale. Our primary outcome of interest was all-cause or CV mortality. We also investigated the impact of RDW on major adverse cardiovascular events (MACEs) for the studies that reported these outcomes. Review Manager (RevMan) 5.3 was utilized to perform Mantel-Haenzel analysis of random effects and compute for relative risk.ResultsWe identified 13 trials involving 10,410 patients, showing that in ACS, a low RDW is associated with a statistically significant lower all-cause or CV mortality (RR 0.35, (95% CI 0.30 to 0.40), P < 0.00001, I2 = 53%), a finding that was consistent both in the short- and long-term.ConclusionsA low RDW is also associated with lower risk for MACEs after an ACS (RR 0.56, (95% CI 0.51 to 0.61), P < 0.00001, I2 = 91%). A low RDW during an ACS is associated with lower all-cause or CV mortality and lower risk of subsequent MACEs, providing us with a convenient and inexpensive risk stratification tool in ACS patients.

BackgroundSymptoms of mitral stenosis (MS) are worsened during tachycardia and exercise. Beta-blockers are used in controlling heart rate (HR) in MS, resulting in symptom improvement, but coming with significant side effects. Ivabradine has a selective action on the sinus node devoid of the usual side effects of beta-blockers. Small studies have recently investigated the role of ivabradine in MS in sinus rhythm. Our aim was to determine the efficacy of ivabradine, compared to beta-blockers, in terms of exercise duration, maximum HR achieved, resting HR, mean gradient, and working capacity among patients with MS in sinus rhythm.MethodsWe conducted a systematic search of studies using MEDLINE, Google Scholar, ScienceDirect, Scopus, Clinical Key, Cochrane, and clinicaltrials.gov databases in all languages and examined reference lists of studies. We included studies if they are: 1) randomized controlled trials comparing ivabradine and beta-blockers; 2) of adults ≥ 19 years old with MS in sinus rhythm; and 3) reported data on exercise duration, maximum HR achieved, resting HR, mean gradient, and working capacity. Studies identified were assessed for risk of bias using the Cochrane Collaboration Tool for Assessing Risk of Bias. We used inverse variance analysis of fixed effects to compute for mean difference, carried out using Review Manager (RevMan) 5.3.ResultsPooled analysis from five identified trials showed that among patients with MS in sinus rhythm, ivabradine was better compared to beta-blockers in total exercise duration (mean difference: 32.73 s (95% CI: 12.19, 53.27; P = 0.002; I2 = 0%)), maximum HR achieved after exercise (mean difference: -3.87 beats per minute (95% CI: -5.88, -1.860; P = 0.0002; I2 = 23%)), and work capacity (mean difference: 0.56 METS (95% CI: 0.33, 0.80; P < 0.00001; I2 = 0%)); inferior to beta-blockers in resting HR achieved (mean difference: 1.83 s (95% CI: 0.39, 3.28; P = 0.01; I2 = 91%)); and comparable to beta-blockers in terms of mean gradient (mean difference: -0.52 mm Hg (95% CI: -1.20, 0.16; P = 0.13; I2 = 6%)).ConclusionsIvabradine is better or comparable to beta-blockers in terms of the outcomes measured, and may be considered as an alternative for patients with MS in sinus rhythm who are intolerant to beta-blockers.

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Background:Chronic heart failure (HF) disease as an emerging epidemic has a high economic-psycho-social burden, hospitalization, readmission, morbidity and mortality rates despite many clinical practice guidelines’ evidenced-based and consensus driven recommendations that include trials’ initial-baseline data.Objective:To show that the survival and hospitalization-free event rates in the reviewed chronic HF clinical practice guidelines’ class I-A recommendations as initial HF drug therapy (IDT) is possibly a combination and ‘start-to-end’ synergistic effect of the add-on (‘end’) HF drug therapy (ADT) to the baseline (‘start’) HF drug therapy (BDT).Methodology:The references cited in the chronic HF clinical practice guidelines of the 2005, 2009, and 2013 American Heart Association/American College of Cardiology (AHA/ACC), the 2006 Heart Failure Society of America (HFSA), and the 2005, 2008, and 2012 European Society of Cardiology (ESC) were reviewed and compared with the respective guidelines’ and other countries’ recommendations.Results:The BDT using glycosides and diuretics is 79%-100% in the cited HF trials. The survival rates attributed to the BDT (‘start’) is 46%-89% and IDT (‘end’) 61%-92.8%, respectively. The hospitalization-free event rate of the BDT group: 47.1% to 85.3% and IDT group 61.8%-90%, respectively. Thus, the survival and hospitalization-free event rates of the ADT is 0.4%-15% and 4.6% to 14.7%, respectively. The extrapolated BDT survival is 8%-51% based on a 38% estimated natural HF survival rate for the time period109.Conclusion:The contribution of baseline HF drug therapy (BDT) is relevant in terms of survival and hospitalization-free event rates compared to the HF class 1-A guidelines initial drug therapy recommendations (IDT). Further, the proposed initial HF drug (‘end’) therapy (IDT) has possible synergistic effects with the baseline HF drug (‘start’) therapy (BDT) and is essentially the add on HF drug therapy (ADT) in our analysis. The polypharmacy HF treatment is a synergistic effect due to BDT and ADT.