The timing of development and subsequent clinical course of heart failure after a myocardial infarction.

AIMS: Myocardial infarction (MI) is a common cause of heart failure (HF), which may develop early and persist or resolve, or develop late. The cumulative incidence, persistence, and resolution of HF after MI are poorly described. The aim of this study is to describe the natural history and prognosis of HF after an MI. METHODS AND RESULTS: Patients with a death or discharge diagnosis of MI in 1998 were identified from records of hospitals providing services to a local community of 600 000 people. Records were scrutinized to identify the development of HF, defined as signs and symptoms consistent with that diagnosis and treated with loop diuretics. HF was considered to have resolved if diuretics could be stopped without recurrent symptoms. Totally, 896 patients were identified of whom 54% had died by December 2005. During the index admission, 199 (22.2%) patients died, many with HF, and a further 182 (20.3%) patients developed HF that persisted until discharge, of whom 121 died subsequent to discharge. Of 74 patients with transient HF that resolved before discharge, 41 had recurrent HF and 38 died during follow-up. After discharge, 145 (33%) patients developed HF for the first time, of whom 76 died during follow-up. Overall, of 281 deaths occurring after discharge, 235 (83.6%) were amongst inpatients who first developed HF. CONCLUSION: The development of HF precedes death in most patients who die in the short- or long-term following an MI. Prevention of HF, predominantly by reducing the extent of myocardial damage and recurrent MI, and subsequent management could have a substantial impact on prognosis.     

沙库巴曲缬沙坦对老年人急性心肌梗死后慢性心力衰竭发生的影响

目的评价沙库巴曲缬沙坦对老年人急性心肌梗死后慢性心力衰竭的发生的影响。方法入选2017年10月至2018年8月菏泽市立医院诊治的急性心肌梗死老年患者87例,应用随机数字法分为试验组(42例)和对照组(45例),所有患者均给予急性心肌梗死后常规药物治疗,试验组同时给予沙库巴曲缬沙坦(100 mg,2次/d),对照组给予缬沙坦(80 mg,1次/d),治疗12个月后,比较两组患者的N末端B型利钠肽原(NT-proBNP)、左心室舒张末期内径(LVDd)、左心室射血分数(LVEF)、再入院率、总死亡率。结果87例患者中,男性51例(58.6%),女性36例(41.4%),年龄(67.4±4.0)岁。治疗12个月后,实验组LVDd较对照组低[(47.86±3.86)mm比(50.73±4.39)mm,P<0.05];实验组LVEF较对照组高[(53.74±4.08)%比(44.42±7.41)%,P<0.05];实验组NT-proBNP较对照组低[(793.43±335.43)ng/L比(1068.44±344.46)ng/L,P<0.05];再住院率实验组较对照组低[5例(11.9%)比15例(33.3%),P<0.05],但两组的总死亡率差异无统计学意义[2例(4.8%)比3例(6.7%),P=0.703]。结论沙库巴曲缬沙坦较缬沙坦能减少老年人急性心肌梗死后慢性心力衰竭的发生,改善急性心肌梗死后心衰患者的左心功能,减少因心力衰竭再入院率。     

C-reactive protein and heart failure after myocardial infarction in the community

Background

There is a paucity of data on the prognostic role of C-reactive protein (CRP) measured after myocardial infarction. We prospectively examined the association of CRP with heart failure and death among patients with myocardial infarction in the community.

Methods and Results

All Olmsted County residents who had a myocardial infarction meeting standardized criteria were prospectively enrolled to measure CRP on admission and followed for heart failure and death. A total of 329 consecutive patients (mean age 69 ± 16 years, 52% men) were enrolled. At 1 year, 28% of patients experienced heart failure and 20% died. There was a strong positive graded association between CRP and the risk of developing heart failure, as well as dying over the period of follow-up (P < .001). Compared with patients in the first tertile, patients in the third tertile of the CRP distribution had a markedly increased risk of heart failure and death independently of age, sex, troponin T, Q wave, comorbidity, previous myocardial infarction, and recurrent ischemic events (adjusted hazard ratio 2.47 [95% confidence interval, 1.27-4.82] for heart failure and 3.96 [95% confidence interval, 1.78-8.83] for death).

Conclusions

These prospective data indicate that among contemporary community subjects with myocardial infarction, heart failure and death remain frequent complications. CRP is associated with a large increase in the risk of heart failure and death, independently of age, sex, myocardial infarction severity, comorbidity, previous myocardial infarction, and recurrent ischemic events. These data suggest that inflammatory processes may play a role in the development of heart failure and death after myocardial infarction independently of other conventional prognostic indicators.     

Heart rate variability in myocardial infarction and heart failure

The need to refine the identification of patients who might benefit from implantation of an implantable cardioverter defibrillator has been risen by the results of many clinical trials on ICD therapy. Traditional parameters such as left ventricular ejection fraction and the presence of non-sustained ventricular tachycardia were not strong enough to achieve this goal with reasonable cost-effectiveness. Heart rate variability (HRV) is one of the most popular parameters used to assess the autonomic tone. HRV has been reported as a strong predictor of cardiovascular mortality. Currently, three different categories of methods in HRV analysis are being used; the time domain, frequency domain, and non-linear dynamic analysis. Both time domain and frequency domain analyses of HRV have been investigated extensively regarding their use as a prognostic marker for cardiovascular mortality. The non-linear dynamic analysis is the latest tool that has shown to have an even higher predictive value than any of the traditional parameters. However, standardized and supporting evidence on this new technique is still lacking. In this article, the current role of HRV in the prediction of cardiovascular mortality in myocardial infarction and heart failure patients has been reviewed.     

Late-onset heart failure after myocardial infarction: trends in incidence and survival

BACKGROUND: Limited data are available on the epidemiology of heart failure (HF) after acute myocardial infarction (AMI). We have investigated trends in the incidence and outcome of HF developing more than 28 days after first-ever AMI. METHODS AND RESULTS: We identified all residents of Perth, Western Australia aged 25-64 years with no history of HF, who had experienced an AMI between 1984 and 1993, and followed them to 2005 (at which time survivors of the index events would have been aged up to 85 years). Of 3109 patients identified, 406 (13.1%) had at least one subsequent admission to hospital with a diagnosis of HF and 211 died. Following adjustment for age and sex, the hazard ratio for late-onset HF for the period 1989-1993 relative to 1984-1988 was 0.85 (95%CI: 0.69 to 1.04). After adjustment for age, history of diabetes and recurrent acute coronary syndrome, the hazard ratio for death in patients with late-onset HF did not change over the period of study (HR per year=1.02, 95%CI: 0.99 to 1.05). CONCLUSION: Our findings contradict recent claims that there is an epidemic of HF driven in part by improved survival after AMI.     

卡维地洛对心梗后心衰患者心功能的影响

目的观察卡维地洛对心梗后心衰的作用。方法将103例心梗后心衰的患者随机分为卡维地洛组与对照组。对照组：ACEI、利尿剂、洋地黄等基础治疗；卡维地洛组：基础治疗＋卡维地洛（达利全）。半年后行超声心动图检查，观察两组治疗后心功能改变情况。两组间均数比较采用t检验，两样本率的比较用x^2检验。结果治疗后卡维地洛组左室舒张末内径、左室收缩末期内径、因心衰再住院率、死亡率比对照组明显降低，临床心功能改善（P〈0．05），左心室射血分数明显增加，经x^2检验,x^2=4．33（P〈0．01）。结论卡维地洛能明显改善心功能，提高生活质量，降低死亡率及因心衰再住院率。     

Effects of long-term renal sympathetic denervation on heart failure after myocardial infarction in rats

The purpose of the present study was to investigate the effects of long-term renal denervation (RD) on heart failure due to myocardial infarction (MI). Wistar rats were anesthetized and the bilateral renal nerves were surgically denervated 2 days before MI was induced by coronary artery ligation. Four weeks later, left ventricular (LV) function and sodium excretion were determined. In MI rats, RD improved the reduced sodium excretion. MI + RD rats revealed lower LV end-diastolic pressure and greater maximum dP/dt as compared with those of MI+ innervation (INN) rats. LV end-diastolic and end-systolic dimensions were significantly smaller and LV fractional shortening was greater in MI + RD rats than in MI + INN rats (20.9% ± 3.2% vs 14.9% ± 3.0%). In rats without MI, RD did not affect either sodium excretion or LV function and dimensions. The present results suggest that the long-term RD reduces LV filling pressure and improves LV function after MI, probably due to a restoration of impaired natriuresis. Increased renal sympathetic nerve activity might contribute to the progression of heart failure after MI. Received: June 11, 2001 / Accepted: September 22, 2001     

Heart failure after myocardial infarction: clinical presentation and survival

OBJECTIVES: To characterize the presentation and outcome of patients with heart failure (HF) after myocardial infarction (MI) according to left ventricular ejection fraction (LVEF) and test the hypothesis that the outcome of HF did not change over time. BACKGROUND: Little is known about the presentation and outcome of HF post-MI and how these may have changed over time. METHODS: Using the Rochester Epidemiology Project, all residents of Olmsted County, Minnesota who experienced an incident MI between 1979 and 1998 were identified; MI and HF were validated using standardized criteria. Subjects were followed through their community medical record. RESULTS: Between 1979 and 1998, 1915 patients with incident MI and no prior history of HF were identified. Of these, 791(41%) experienced new onset HF as defined by Framingham criteria during 6.6+/-5.0 years of follow-up. Forty-seven percent were men, mean age was 73+/-12 years. Forty-four percent had impaired LVEF, 18% preserved LVEF and 38% had no LVEF measurement within 60 days after the HF event. Median survival after HF onset was 4 years and at 5 years after HF onset, only 45% were alive. Older age, male sex, comorbidity, hypertension and no LVEF assessment were associated with increased risk of death, however, patients with impaired LVEF had the worst outcome. Over time, survival did not improve (HR for year: 1.00; 95% CI 0.99, 1.02; P=0.919) even after adjustment for baseline characteristics. CONCLUSION: In this geographically defined cohort of patients with MI, new onset HF after the MI was frequent. When measured, LVEF was most frequently reduced, consistent with systolic heart failure. Mortality was high and did not decline over time and death was independently associated with male sex, older age, hypertension and comorbidity. It also differed according to LVEF, which was inconsistently ascertained in this setting, potentially representing practice opportunities.     

Prognostic significance of new atrial fibrillation and its relation to heart failure following acute myocardial infarction

BACKGROUND: New-onset atrial fibrillation (AF) after acute myocardial infarction (AMI) frequently occurs in association with postinfarction complications, particularly with heart failure (HF). AIMS: To evaluate whether postinfarction HF is associated with the subsequent development of AF and whether AF independently predicts poorer prognosis. METHODS AND RESULTS: We examined 650 patients with AMI and compared patients with AF (n=320) to those without (n=330). AF patients were classified as either early AF (n=208)-patients who developed AF within 24 h of symptom onset or late AF (n=112)-patients who had AF thereafter. We compared outcomes between these groups, adjusting for differences in baseline characteristics and postinfarction HF. Heart failure was the most important predictor of AF. In most patients, AF occurred secondary to HF. AF patients had poorer outcomes, including higher in-hospital and 7-year mortality. After multivariate adjustment, overall, AF was not an independent predictor of in-hospital [odds ratio (OR)=0.70) and 7-year [relative risk (RR)=1.14] mortality, but late AF remained an independent predictor of 7-year (RR=2.48, 95% confidence interval, 1.26-4.87) mortality. CONCLUSIONS: Heart failure mostly preceded the occurrence of new-onset atrial fibrillation after acute myocardial infarction, but only late atrial fibrillation was independently related to long-term mortality.     

左西孟坦治疗急性心肌梗死合并心力衰竭患者的疗效研究

目的：评价左西孟坦治疗急性心肌梗死（AMI）合并充血性心力衰竭（CHF）的临床疗效。方法：选择58例确诊AMI后一周内并发CHF患者,采用随机数字法分为左西孟旦组（30例,予以左西孟坦治疗）和多巴胺对照组（28例,给予多巴胺治疗）。观察两组治疗前后临床指标及N末端B型利钠肽前体（NT—proBNP）等指标的变化。结果：治疗前两组各指标均无显著差异（P〉0．05）;与治疗前及多巴胺组治疗后比较,左西孟坦组治疗后心率[（120．91±11．78）次／min、（122．67±9．01）次／min比（114．93±10．76）次／min]、呼吸频率[（26．00±3．13）次／min、（23．18±2．38）次／min比（21．47±2．67）次／min]、呼吸困难程度评分[（2．50±0．90）分、（2．07±0．77）分比（1．70±0．59）分]、肺毛细血管楔压[（22．50±2．57）mmHg、（19．57±2．87）mmHg比（16．80±2．39）mmHg]、NT-proBNP水平[（1207．5±95．6）pg／ml、（1097．85±87．6）pg／ml比（729．60±62．9）pg／ml]均显著下降（P〈0．05或〈0．01）,LVEF[（38．40±3．09）％、（41．57±3．10）％比（44．10±3．94）％]、心脏指数[（2．09±0．27）L·min^-1·m^-2、（2．24±0．27）L·min^-1·m^-2比（2．40±0．29）L·min^-1·m^-2]显著提高（P〈0．05或P〈0．01）。结论：左西孟坦可以短期内明显改善急性心肌梗死患者心力衰竭病情。     

Changes in haemoglobin levels during hospital course and long-term outcome after acute myocardial infarction.

AIMS: To study the prevalence and long-term prognostic significance of changes in haemoglobin levels during hospital course in survivors of acute myocardial infarction (AMI). METHODS AND RESULTS: A prospective study involving 1390 patients who were admitted with AMI. Median follow-up was 24 months. Multivariable Cox models were used to evaluate the relationship between nadir and discharge haemoglobin and mortality after hospital discharge. Anaemia was present in 248 patients on admission (17.8%) and in 502 patients at discharge (36.1%). Nadir haemoglobin during hospital course was 1.3 g/dL lower (IQR 0.6-2.2) when compared with baseline haemoglobin (P < 0.0001). Low nadir haemoglobin and discharge haemoglobin were strongly associated with increased mortality. After adjusting for clinical variables and ejection fraction, the hazard ratios for a 1 g/dL decrease in nadir haemoglobin and discharge haemoglobin were 1.36 (95% CI 1.19-1.55; P < 0.0001) and 1.27 (95% CI 1.16-1.40; P < 0.0001), respectively. CONCLUSION: The development of anaemia during hospitalization for AMI is frequent and is associated with an increased long-term mortality.     

Reduction in oxidative stress and modulation of heart failure subsequent to myocardial infarction in rats

BACKGROUND:

Patients surviving myocardial infarction (MI) are at a heightened risk for the development of congestive heart failure. This clinical syndrome has been associated with an antioxidant deficit and elevated oxidative stress in the myocardium. Effects of dietary vitamin E, a lipid-soluble antioxidant, on myocardial anti-oxidant enzyme activities, oxidative stress and hemodynamic function, were examined separately in the viable left ventricle (LV) and right ventricle (RV) of rats at 16 weeks post-MI.

METHODS AND RESULTS:

Animals were fed either a basal diet or a diet enriched with 1500 U of vitamin E/kg beginning two weeks before MI-inducing surgery and continued 16 weeks post-MI. In the MI animals on the basal diet, LV systolic pressure (LVSP) and RVSP were significantly depressed and LV end-diastolic pressure (LVEDP) and RVEDP were significantly elevated. These hemodynamic alterations were accompanied by clinical signs of heart failure including dyspnea, lethargy and cyanotic limbs. Supplementation of MI animals with dietary vitamin E resulted in complete normalization of RVSP and RVEDP. An increase in LVSP and a decrease in LVEDP was observed in the vitamin E-supplemented MI animals, although mild residual LV dysfunction remained. The myocardial enzymatic antioxidants catalase and glutathione peroxidase declined substantially in each of the ventricles of unsupplemented MI animals. Myocardial levels of vitamin E were reduced by 33% in the LV and no change was observed in the RV of the MI animals. Vitamin E-supplemented control animals and MI animals showed a significant increase in vitamin E levels in both ventricles. Myocardial oxidative stress, as assessed by lipid peroxidation and the ratio of reduced to oxidized glutathione, was significantly increased in each of the respective ventricles of untreated MI animals. Supplementation with dietary vitamin E resulted in a substantial increase in the myocardial activities of catalase and glutathione peroxidase in both the LV and RV. Furthermore, an increase in the ratio of reduced to oxidized glutathione concomitant with significantly less lipid peroxidation was also observed in each of the respective ventricles of MI animals supplemented with vitamin E. No overt clinical signs of heart failure were evident in these vitamin E-supplemented animals.

CONCLUSIONS:

An improved myocardial redox state and endogenous antioxidant reserve with vitamin E therapy, coupled with the modulation of the development of heart failure, lend strong support in favour of a pathophysiological role for increased oxidative stress in the pathogenesis of heart failure, at least in experimental animals. Association between an increase in oxidative stress and cardiac events in patients requires further examination.     

Acute heart failure in patients with acute myocardial infarction treated with primary percutaneous coronary intervention

BACKGROUND: Scanty data exist about the relation between acute heart failure (HF) and acute myocardial infarction (AMI). AIM: To assess the impact of HF on outcome in AMI patients treated with primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: Out of 2,089 AMI patients, 82% did not present HF, 17% presented HF on admission and 1% developed HF after hospitalisation. Predictors of HF on admission were age, diabetes, prior MI, time delay to admission, anterior location, and TIMI grade 0-1 in the culprit vessel. Predictors of HF during hospitalisation were age and peak creatine kinase. The 1- and 6-month mortalities were 1.1% and 2.2%, 8% and 12%, 26% and 33% in patients without HF, with HF on admission and after hospitalisation, respectively. The risk of death was higher in patients with HF than in patients without HF (HR 3.47), as well as in patients with HF after admission (HR 5.19) than in patients with HF on admission (HR 2.44). CONCLUSIONS: In a primary PCI setting, the incidence of HF on hospital admission remains high, but mortality is lower when compared with historical patient series. Primary PCI may prevent the development of HF during hospitalisation; however, when HF develops, the prognosis remains severe.     

ST2与心肌梗死和心力衰竭的关系

<正>白介素1(interleukin-1,IL-1)受体家族包括IL-1R、IL-18R及其辅助蛋白IL-1RAcP、IL-18RAcP等[1]。1989年,ST2作为IL-1受体家族的新成员被发现,之后证实其参与多种病理生理过程,在炎症和变态反应性疾病中发挥重要作用,     

IL-6 levels in acute and post myocardial infarction: their relation to CRP levels, infarction size, left ventricular systolic function, and heart failure

BACKGROUND: Inflammatory mechanisms in heart disease are of great interest. The proinflammatory cytokine interleukin (IL) 6 has been linked to increased morbidity in unstable angina pectoris and depressed myocardial function in heart failure (HF). METHODS: We studied the relation of IL-6 levels to C-reactive protein (CRP), infarction size, left ventricular function, and HF in acute myocardial infarction (MI) and after hospital discharge in 31 consecutive patients (19 males, mean age 69+/-13 years). Blood sampling for IL-6 was performed on admittance, four times on day 1, twice on day 2, and once daily on days 3-5, and 6 and 12 weeks later. Clinical signs of HF were evaluated daily during hospitalization and after 6 and 12 weeks. Echocardiography was performed on day 3 and at 6 weeks. RESULTS: IL-6 showed a curved time course with elevated levels already on admittance (mean+/-S.D. 19.3+/-26.9 ng/l), thereafter increasing to a peak on days 1 and 2 (maximum 68.5+/-152.9 ng/l), and then declining rapidly to lower, although not normalized, levels during hospitalization and at 6 and 12 weeks. CRP showed a similar time pattern, but with a later peak and a seemingly less rapid decline in levels. Mean levels of IL-6 and CRP on days 1-5 correlated highly (r=0.794, p<0.0001). IL-6 and infarction size did not correlate. HF during hospitalization and at 6 weeks was not related to IL-6; however, patients with HF at 12 weeks had higher IL-6 levels, both at 6 and 12 weeks. Patients on ACE inhibitors or diuretics at discharge had higher IL-6 levels at 6 weeks. IL-6 during hospitalization was not related to LVF; yet, patients with depressed LVF in the hospital and at 6 weeks had higher IL-6 levels at 6 and 12 weeks. CONCLUSIONS: IL-6 in acute MI shows a curved time course and is highly correlated to CRP. It peaks on days 1 and 2 and remains elevated even after 12 weeks. Increased IL-6 levels after hospital discharge are associated with HF and depressed LVF. Whether anti-inflammatory agents will influence left ventricular dysfunction and outcome postacute MI has yet to be determined.     

主动脉内球囊反搏在急性心肌梗死并右心衰竭中的应用

目的：探讨主动脉内球囊反搏（IABP）在急性心肌梗死并右心衰竭中应用的价值。方法：69例急性心肌梗死并心源性休克行IABP辅助循环治疗患者中急性右心衰竭12例（17.4%）,回顾性分析此12例患者临床资料,病人年龄（64.1±9.7）岁,IABP辅助循环治疗时间15～288h,（95±76）h,9例（75%）行经皮冠状动脉介入术（PCI）。结果：12例患者住院期间主要并发症包括：出血3例（25%）,肢体缺血1例（8.3%）,急性肾功能衰竭2例（16.7%）,多器官功能衰竭1例（8.3%）。1例死于多器官功能衰竭,其余11例（91.7%）成功撤除IABP辅助循环,病情好转出院。结论：急性心肌梗死并严重右心衰竭死亡率高,在常规治疗疗效不佳时,主动脉内球囊反搏辅助循环治疗可能有益。     

Translational overview of cytokine inhibition in acute myocardial infarction and chronic heart failure

Many cytokines are currently under investigation as potential target to improve cardiac function and outcome in the setting of acute myocardial infarction (MI) or chronic heart failure (HF). Here we aim to provide a translational overview of cytokine inhibiting therapies tested in experimental models and clinical studies. In various experimental studies, inhibition of interleukin-1 (IL-1), -6 (IL-6), -8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), CC- and CXC chemokines, and tumor necrosis factor-α (TNF-α) had beneficial effects on cardiac function and outcome. On the other hand, neutral or even detrimental results have been reported for some (IL-1, IL-6, IL-8, and MCP-1). Ambivalence of cytokine function, differences in study designs, treatment regimens and chosen endpoints hamper the translation of experimental research into clinical practice. Human studies are currently limited to IL-1β inhibition, IL-1 receptor antagonists (IL-1RA), IL-6 receptor antagonists (IL-6RA) or TNF inhibition. Despite favorable effects on cardiovascular events observed in retrospective cohort studies of rheumatoid arthritis patients treated with TNF inhibition or IL-1RA, most prospective studies reported disappointing and inconsistent results. Smaller studies (n < 100) generally reported favorable results of anticytokine therapy on cardiac function, but only one of the larger studies (n > 100) evaluating IL-1β inhibition presented positive results on outcome. In conclusion, of the 10 anticytokine therapies tested in animals models beneficial effects have been reported in at least one setting. In larger clinical studies, findings were unsatisfactory in all but one. Many anticytokine therapies with promising animal experimental data continue to require further evaluation in humans.     

Interleukin-10 improves left ventricular function in rats with heart failure subsequent to myocardial infarction

Evidence has shown that pro-inflammatory cytokines, especially TNF-alpha, are involved in the inflammatory response in the remodelling process after myocardial infarction (MI). Although IL-10, an anti-inflammatory cytokine, has been shown to antagonize some of the deleterious effects of TNF-alpha, little is known about its role in post-MI left ventricular (LV) dysfunction. The aim of the present study was to investigate whether a therapy with rhIL-10 could be beneficial in an animal model of post-MI heart failure (HF). Rats with experimental MI were treated with rhIL-10 (75 microg/kg/d sc) starting directly after MI induction, and continuing for 4 weeks. Controls were untreated MI and sham-operated rats. Cardiac function was assessed by echocardiography and cardiac catheterization 4 weeks after MI induction. Membrane-bound and soluble fractions of TNF-alpha, IL-6 and IL-10, the ratio of TNF-alpha to IL-10, serum levels of MCP-1 as well as myocardial macrophage infiltration, were analyzed. Treatment with rhIL-10 significantly improved post-MI LV function (FS +127%;, dP/dt(max) +131%; LVEDP -36%). This effect was associated with a significant decrease in pro-inflammatory cytokine and chemokine levels (TNF-alpha, IL-6, MCP-1) and furthermore resulted in a reduced myocardial infiltration of macrophages.     

Digoxin: A systematic review in atrial fibrillation,congestive heart failure and post myocardial infarction

AIM: To review digoxin use in systolic congestive heart failure, atrial fibrillation, and after myocardial infarction.METHODS: A comprehensive PubMed search was performed using the key words “digoxin and congestive heart failure”, “digoxin and atrial fibrillation”, “digoxin, atrial fibrillation and systolic congestive heart failure”, and “digoxin and myocardial infarction”. Only articles written in English were included in this study. We retained studies originating from randomized controlled trials, registries and included at least 500 patients. The studies included patients with atrial fibrillation or heart failure or myocardial infarction and had a significant proportion of patients (at least 5%) on digoxin. A table reviewing the different hazard ratios was developed based on the articles selected. Our primary endpoint was the overall mortality in the patients on digoxin vs those without digoxin, among patients with atrial fibrillation and also among patients with atrial fibrillation and systolic heart failure. We reviewed the most recent international guidelines to discuss current recommendations.RESULTS: A total of 18 studies were found that evaluated digoxin and overall mortality in different clinical settings including systolic congestive heart failure and normal sinus rhythm (n = 5), atrial fibrillation with and without systolic congestive heart failure (n = 9), and myocardial infarction (n = 4). Overall, patients with systolic congestive heart failure with normal sinus rhythm, digoxin appears to have a neutral effect on mortality especially if close digoxin level monitoring is employed. However, most of the observational studies evaluating digoxin use in atrial fibrillation without systolic congestive heart failure showed an increase in overall mortality when taking digoxin. In the studies evaluated in this systematic review, the data among patients with atrial fibrillation and systolic congestive heart failure, as well as post myocardial infarction were more controversial. The extent to which discrepancies among studies are based on statistical methods is currently unclear, as these studies’ findings are generated by retrospective analyses that employed different techniques to address confounding.CONCLUSION: Based on the potential risks and benefits, as well as the presence of alternative drugs, there is a limited role for digoxin in the management of patients with normal sinus rhythm and congestive heart failure. Based on the retrospective studies reviewed there is a growing volume of data showing increased mortality in those with only atrial fibrillation. The proper role of digoxin is, however, less certain in other subgroups of patients, such as those with both atrial fibrillation and systolic congestive heart failure or after a myocardial infarction. Further studies may provide helpful information for such subgroups of patients.