TAFI activity and antigen plasma levels are not increased in acute coronary artery disease patients admitted to a coronary care unit

INTRODUCTION: Hypofibrinolysis, at least in part due to high levels of plasminogen activator inhibitor-1 (PAI-1), has been reported to occur frequently in patients with coronary artery disease (CAD). A recently described carboxypeptidase, thrombin-activatable fibrinolysis inhibitor (TAFI), is involved in the regulation of the balance between coagulation and fibrinolysis. High TAFI plasma levels may therefore contribute to a hypofibrinolytic state and to an increased risk for thrombotic disorders. There are contradictory results regarding TAFI levels in CAD patients, possibly because the characteristics of patients investigated and the time of blood sampling were different among different studies. MATERIALS AND METHODS: Fibrinolytic inhibitors (TAFI activity, TAFI antigen and PAI-1 activity plasma levels) were measured in 44 consecutive patients admitted to the Coronary Care Unit of the University of Florence and in a group of 44 healthy controls, matched for age and sex, to detect a possible association of their levels with acute CAD. RESULTS: No differences were found in TAFI levels, either activity or antigen, between patients and controls. PAI-1 activity was significant different between patients and controls (p=0.0001). The frequencies of TAFI activity and antigen over cut-off levels were similar in patients and controls. Instead, higher PAI-1 levels were more frequent (p=0.04) in patients respect to controls. The univariate analysis confirmed the association of increased PAI-1 levels with acute CAD [OR=3.3; p=0.04]. Among the patients, TAFI and PAI-1 levels were not different according to clinical presentation of symptoms or indication to immediate percutaneous revascularization. CONCLUSION: Our study suggests that in acute phase of CAD no increased levels of TAFI are detectable in plasma.     

Decreased fibrin network permeability and impaired fibrinolysis in the acute and convalescent phase of ischemic stroke

Introduction

We investigated fibrin network permeability and fibrinolysis in the acute and convalescent phase of ischemic stroke.

Methods

20 patients with a mean age of 74 years were studied in the acute (day 1) and convalescent phase (day 60) of ischemic stroke. 23 healthy individuals (controls) were also investigated. Fibrin formation in the samples was triggered by addition of tissue factor (1 pmol/L) and washed frozen-thawed platelets obtained from a healthy donor. The permeability constant (K_s), which reflects fibrin network permeability, was then calculated from liquid flow measurements. A global assay newly developed in our group was also employed to determine the balance between fibrin formation (“Coagulation profile”; Cp) and fibrin degradation (“Fibrinolysis profile”; Fp) in the same samples. We also measured PAI-1 antigen and fibrinogen concentrations in plasma.

Results

As compared to controls, the stroke patients had lower Ks (lower fibrin network permeability) both on day 1 and on day 60 (p < 0.01 and p < 0.05, respectively). Fibrinolysis, assessed by Fp, was reduced on both day 1 and day 60 (p < 0.001, compared to controls), and PAI-1 concentrations were increased (p < 0.01 for both, compared to controls). Fibrin formation capacity in plasma (i.e. Cp) was increased in the acute phase (p < 0.05) but not in the convalescence, as compared to controls.

Conclusion

The combination of a proneness to form a tighter fibrin network and impaired fibrinolysis is a feature of ischemic stroke that is present in both the acute and convalescent phase of the disease.     

血浆纤溶酶原激活物抑制剂-1基因启动子区4G/5G多态性与脑血管疾病的关系

目的 探讨血浆纤溶酶原激活物抑制剂-1基因启动子区4G/5G多态性与脑血管疾病之间的关系.方法 应用PCR技术和琼脂糖电泳对30例脑出血患者、90例脑梗死患者(其中腔隙性脑梗死30例,小面积脑梗死30例,大面积脑梗死30例)进行了API-1基因启动子4G/5G多态性的检测和分析,并与30例非脑血管疾病者对照比较.结果 对照组、脑出血组、脑梗死组基因型频率及等位基因频率分布比较均有统计学差异(P＜0.05).对照组与脑出血组间基因型频率及等位基因频率比较均无统计学差异(P＞0.05).对照组与脑梗死组间基因型频率及等位基因频率比较均有统计学差异(P＜0.05),脑梗死组4G/4G基因型频率(44.4%)较对照组(20%)高;脑梗死组4G等位基因频率(63.3%)较对照组(38.8%)高,比较均有统计学差异(P＜0.05).脑梗死组各亚型基因型频率及等位基因频率比较均无统计学差异(P＞0.05).性别在各组不同基因型中分布:对照组及脑出血组性别在不同基因型分布比较无统计学差异(P＞0.05).脑梗死组性别在不同基因型分布比较有统计学差异(P＜0.05),4G/4G基因型中男性占25%;女性占65%,比较有统计学差异(P＜0.05).腔隙性脑梗死组及小面积脑梗死组性别在不同基因型中分布比较均无统计学差异(P＞0.05).大面积脑梗死组性别在不同基因型中分布比较有统计学差异(P＜0.05),4G/4G基因型男性占21.4%;女性占78.6%,比较有统计学差异(P＜0.05).结论 PAI-1基因启动子区4G/5G多态性在怀化市正常人群中大致分布为:4G/4G占20%;4G/5G占63.3%;5G/5G占16.7%.PAI-1基因启动子区4G/5G多态性与脑出血无关.PAI-1基因启动子区4G/5G多态性与缺血性脑卒中有关,4G/4G基因型可能是缺血性脑卒中的一个独立危险因素,尤其可能与女性大面积脑梗死密切相关.PAI-1基因启动子区4G/5G多态性与缺血性脑卒中的梗死面积无关.     

Antiplatelet therapies and the role of antiplatelet resistance in acute coronary syndrome

Acute coronary syndrome is the number one killer in the industrialized world and, as such, continues to be one of the most well-studied disease states in all of medicine. Advancements in antiplatelet therapies for use in patients undergoing percutaneous coronary intervention have improved outcomes dramatically. However, a proportion of patients on long-term antiplatelet therapy continue to have cardiovascular events. Resistance to antiplatelet drugs may explain some of these events and this topic has become one of major interest and rapid evolution. This review describes the pathogenesis of acute coronary syndromes, outlines the evidence behind the use of the available antiplatelet agents, and examines the current data surrounding antiplatelet resistance.     

The puzzle of depression and acute coronary syndrome: Reviewing the role of acute inflammation

The relationship between depression and coronary heart disease is well-established, but causal mechanisms are poorly understood. The aim of this review is to stimulate different ways of viewing the relationship between depression and adverse outcomes following acute coronary syndrome (ACS) and coronary artery bypass graft (CABG) surgery patients. We present an argument for depression in ACS and CABG patients being a qualitatively distinct form from that observed in psychiatric populations. This is based on three features: (1) depression developing after cardiac events has been linked in many studies to poorer outcomes than recurrent depression; (2) somatic symptoms of depression following cardiac events are particularly cardiotoxic; (3) depression following an ACS does not respond well to antidepressant treatments. We propose that inflammation is a common causal process responsible in part both for the development of depressive symptoms and for adverse cardiac outcomes, and we draw parallels with inflammation-induced sickness behaviour. Clinical implications of our observations are discussed along with suggestions for further work to advance the field.     

Genetic variation in the human thrombomodulin promoter locus and prognosis after acute coronary syndrome

INTRODUCTION: Endothelial thrombomodulin (TM) plays a critical role in both anticoagulation and anti-inflammation. An impaired TM cofactor function or reduced TM gene expression could constitute a prethrombotic abnormality leading to acute coronary events. Mutations in the TM gene occur, but their functional consequences on the expression and activity of the gene are not yet fully understood. MATERIALS AND METHODS: We performed a prospective study investigating the prevalence of TM mutations in the promoter region in 182 patients with acute coronary syndrome as well as in a control group. The patients were followed-up after 30 days and after 2 years for acute myocardial infarction (MI) and mortality. RESULTS AND CONCLUSIONS: We identified 10 point mutations and 2 small deletions: -1861 C/A, -1852 C/G, -1803 G/C, -1752 G/C, -1213/1212 delTT, -1089 C/G, -1088 C/T, -1083/1082 delCC, -1066 A/C, -801 C/G, -651 A/C and -52 G/A. Two of the mutations, -1752 G/C and -1213/1212 delTT, were frequent in the patients as well as in the controls, while all the others were rare. The only significant finding was that both -1752 G/C and -1213/1212 delTT were associated with a lower than normal risk of suffering a clinical event among smokers at 30 days and 2 years. We did not gain any support for the hypothesis that TM mutations confer an increased risk of MI or mortality.     

Incidence of heparin-PF4 complex antibody formation and heparin-induced thrombocytopenia in acute coronary syndrome

A multicenter prospective study on the rate of seroconversion of antibodies to heparin-PF4 complexes (heparin-induced thrombocytopenia [HIT] antibodies) during and after heparin treatment for 4 weeks was carried out in Japanese patients with acute coronary syndrome (ACS). A total of 254 ACS patients treated with heparin were enrolled consecutively from 12 facilities of cardiology. Two patients with preexisting HIT antibodies were excluded from the analysis. The total seroconversion rate for four weeks during and after heparin treatment was 8.7% (n=22, 95% confidence interval [CI]: 5.9–13.1), including values of 3.2% (n=8) at the end of heparin infusion and 5.5% (n=14) at 4 weeks. Among 22 seroconverted patients, four developed HIT and two of the four had the complication of thrombosis. The incidence of HIT was 1.6% (n=4, 95% CI: 0.04–3.1). The risk for thromboembolic development was higher in the seroconverted patients (odds ratio, 17.4, 95% CI: 5.2–58.4, p<0.0001) than nonconverted patients. An analysis of factors affecting the seroconversion rate was carried out. The seroconversion rate for ACS patients who underwent percutaneous coronary intervention (PCI; n=163) was 12.3%, significantly higher than the 2.3% in patients who did not undergo PCI (n=89), leading to an odds ratio of 6.1 (95% CI: 1.4–26.7, p=0.009). A significant odds ratio was obtained for each factor affecting the seroconversion: 3.5 (95% CI: 1.3–9.9, p=0.014) for more than 5 days of heparin infusion, 3.0 (95% CI: 1.2–7.6, p=0.035) for a thrombotic history and 2.7 (95% CI: 1.1–6.8, p=0.039) for hyperlipidemia. No other factor, including age or diabetes mellitus, contributed to the seroconversion. Therefore, PCI, duration of heparin treatment and thrombotic history facilitated the seroconversion in ACS patients. PCI patients treated for more than 5 days with heparin showed a maximal seroconversion rate of 18.3% (95% CI: 13.8–22.2). This high rate in PCI patients did not interact with age, type of underlying disease of unstable angina or myocardial infarction or thrombotic history.

In conclusion, ACS patients demonstrating seroconversion are at risk of thromboembolic development due to the likelihood of immunomediated endothelial dysfunction. The increase in the rate of seroconversion in ACS patients would be affected by factors such as PCI with mechanical stress, longer duration of heparin treatment, thrombotic history and presence of hyperlipidemia. If PCI is undertaken with heparin anticoagulation for more than 5 days, seroconversion would easily occur, and the seroconverted patients could subsequently suffer from HIT.     

Thrombosis and acute coronary syndrome

Acute coronary syndromes (ACS) represent the main clinical manifestation of atherosclerotic progression in the coronary district. Thrombosis plays a critical role in the patho-anatomical of ACS, as disruption of an atherosclerotic plaque exposes flowing blood to subendothelial collagen, tissue factor, and other procoagulant molecules that trigger activation of platelets and formation of fibrin within the vessel lumen.Endothelial damage/dysfunction, inflammation and coagulation are closely related to the pathophysiology of ACS and may be inter-related.Platelets play key roles in both the formation of the atheromatous plaque and clinical presentation of acute atherothrombotic events following plaque rupture. In the pathogenesis of the ACS, blood clotting activation has a crucial role and thrombin generation and TF may represent useful markers for the identification of patients at high risk of vascular events. Lipoprotein-associated phospholipase A2 (Lp-PLA2) represents the crossroads between lipid metabolism and inflammatory response.     

急性冠状动脉综合征并缺血性脑卒中与血清细胞因子的关系

目的分析急性冠状动脉综合征合并缺血性脑卒中的临床治疗效果。方法选取2012-03—2013-05我院诊治的120例伴缺血性脑卒中急性冠状动脉综合征患者,均在药物治疗前12h及药物治疗2个疗程后,空腹采集静脉血检测细胞因子,观察治疗前后血清细胞因子的变化,观察临床治疗效果。结果药物治疗后,血清细胞因子IL-18、hs-CRP、干扰素-γ等细胞因子的水平产生显著变化,治疗前后的细胞因子水平有显著性差异(P0.05),总有效率94.2%。结论通过药物治疗,显著改变了伴缺血性脑卒中急性冠状动脉综合征患者的细胞因子水平,获得较好的临床效果,值得临床推广使用。     

Frequency and clinical correlates of bipolar features in acute coronary syndrome patients

BackgroundDepression and acute coronary syndrome (ACS) are both extremely prevalent diseases. Studies aimed at evaluating whether depression is an independent risk factor for cardiac events provided no definitive results. In most of these studies, depression has been broadly defined with no differentiation between unipolar (MDD) versus bipolar forms (BD). The aim of this study was to evaluate the frequency of DSM-IV BD (bipolar I and bipolar II subtypes, cyclothymia), as well as temperamental or isolated bipolar features in a sample of 171 patients hospitalized for ACS. We also explored whether these psychopathological conditions were associated with some clinical characteristics of ACS.MethodsPatients with ACS admitted to three neighboring Cardiac Intensive Care Units (CICUs) in a 12-month continuative period of time were eligible for inclusion if they met the criteria for either acute myocardial infarct with or without ST-segment elevation or unstable angina, verified by standard ACS criteria. All patients underwent standardized cardiological and psychopathological evaluations.ResultsOf the 171 ACS patients enrolled, 37 patients (21.7%) were found to have a DSM-IV mood disorder. Of these, 20 (11.7%) had bipolar type I or type II or cyclothymia, while 17 (10%) were the cases of MDD. Rapid mood switches ranged from 11% of ACS patients with no mood disorders, to 47% of those with MDD to 55% of those with BD. Linear regression analysis showed that a diagnosis of BD (p = .023), but not that of MDD (p = .721), was associated with a significant younger age at the index episode of ACS. A history of previous coronary events was more frequent in ACS patients with BD than in those with MDD.ConclusionsOur data indicate that bipolar features and diagnosis are frequent in ACS patients. Bipolar disorder has a negative impact on cardiac symptomatology. Further research in this area is warranted.     

The role of thrombin-activatable fibrinolysis inhibitor in diabetic wound healing

Introduction

One of the major complications in patients with diabetes mellitus is impaired wound healing. The fibrinolytic system is involved in parts of the wound healing process and deficiency of thrombin-activatable fibrinolysis inhibitor (TAFI) results in delayed wound closure. Moreover, levels of TAFI are affected by diabetes mellitus. The aim of this study was to elucidate the effect of hyperglycaemia on TAFI and to determine the effect of deficiency of TAFI on wound healing under hyperglycaemic conditions.

Materials and methods

Hyperglycaemia was induced with streptozotocin (STZ) and used as a model for diabetes mellitus. TAFI plasma levels and TAFI gene expression in the liver were determined. Incisional and excisional wound healing were studied in non-treated and STZ-treated wild-type and TAFI-deficient mice. Wound closure was scored daily as open or closed.

Results

Mice treated with STZ showed hyperglycaemia, and TAFI plasma levels and TAFI gene expression were increased in diabetic mice. TAFI-deficient mice and diabetic wild-type and diabetic TAFI-deficient mice showed delayed wound healing of incisional wounds. No differences were observed between diabetic and non-diabetic TAFI-deficient mice and between diabetic wild-type and diabetic TAFI-deficient mice.

Conclusions

This study illustrated that TAFI was affected by hyperglycaemia and confirmed that TAFI is involved in wound healing. No additional effect was observed under hyperglycaemic conditions, indicating that deficiency of TAFI did not have an additive or synergistic effect in diabetic wound healing. Further research has to elucidate if TAFI and hyperglycemia affect wound healing via similar mechanisms.     

Acute depressed mood as a trigger of acute coronary syndromes.

BACKGROUND: Some cases of acute coronary syndrome (ACS) may be triggered by emotional states such as anger, but it is not known if acute depressed mood can act as a trigger. METHODS: 295 men and women with a verified ACS were studied. Depressed mood in the two hours before ACS symptom onset was compared with the same period 24 hours earlier (pair-matched analysis), and with usual levels of depressed mood, using case-crossover methods. RESULTS: 46 (18.2%) patients experienced depressed mood in the two hours before ACS onset. The odds of ACS following depressed mood were 2.50 (95% confidence intervals 1.05 to 6.56) in the pair-matched analysis, while the relative risk of ACS onset following depressed mood was 4.33 (95% confidence intervals 3.39 to 6.11) compared with usual levels of depressed mood. Depressed mood preceding ACS onset was more common in lower income patients (p = .032), and was associated with recent life stress, but was not related to psychiatric status. CONCLUSIONS: Acute depressed mood may elicit biological responses that contribute to ACS, including vascular endothelial dysfunction, inflammatory cytokine release and platelet activation. Acute depressed mood may trigger potentially life-threatening cardiac events.     

瑞舒伐他汀对急性冠脉综合征患者血清IMA及hs-CRP的影响

目的探讨不同剂量的瑞舒伐他汀对急性冠脉综合征（ACS）患者血清缺血修饰清蛋白（IMA）和超敏C反应蛋白（hs-CRP）水平的影响。方法将诊断为急性冠脉综合征患者96例随机分为瑞舒伐他汀常规治疗组（10mg/d）和强化治疗组（20mg/d）,同时给予常规治疗,观察治疗前后2组血清IMA、hs-CRP水平的变化。结果治疗2周后2组ACS患者血清IMA、hs-CRP、血脂水平明显下降;与常规治疗组相比,强化治疗组效果更为明显,差异均有统计学意义（P〈0.01）。结论强化瑞舒伐他汀治疗能显著降低ACS患者血清缺血修饰清蛋白、超敏C反应蛋白水平,抑制斑块内炎症反应,在ACS的早期诊断中有重要价值,可作为诊断早期ACS的敏感指标。     

An examination of the psychometric properties of the Hospital Anxiety and Depression Scale in Chinese patients with acute coronary syndrome

The psychometric properties of the Hospital Anxiety and Depression Scale (HADS) as a screening instrument for patients with acute coronary syndrome (ACS) were investigated in a translated Chinese version of the instrument. A confirmatory factor analysis (CFA) was conducted on the HADS to establish its psychometric properties in 138 ACS patients over two observation points (within 1 week and 6 months post-admission for ACS). Internal and test–retest reliability values for the HADS total and HADS anxiety sub-scales were found to be acceptable. The HADS depression sub-scale lacked acceptable internal reliability. The underlying factor structure of the HADS comprised three distinct factors, though inconsistency between the best three-factor model fit was observed between observation points. The HADS was confirmed to be a useful screening instrument to assess symptoms of psychological distress in ACS patients. Further research is required to determine the most appropriate use of HADS sub-scale structures in clinical populations.     

Metabolic syndrome as a risk factor for deep vein thrombosis after acute cardiac conditions

The metabolic syndrome (MS), a cluster of cardiovascular risk factors known to be associated with type II diabetes and arterial disease, has been recently reported to be associated with venous thromboembolism (VTE). In this case-control study MS was tested as a potential risk factor for deep vein thrombosis (DVT) after acute coronary syndromes (ACS) and acute heart failure (AHF).Globally, 86 patients with objectively diagnosed DVT during cardiac rehabilitation after ACS and AHF were compared with a sex and age-matched population of cardiac patients without objectively confirmed DVT. MS was significantly associated to the presence of DVT (OR 2.38; 95% CI 1.64, 3.12), independent from type of cardiac event, prolonged hospitalization, and obesity. Among single determinants of MS, only hypertriglyceridemia was significantly associated with VTE.The presence of MS could increase the risk of VTE after acute cardiac events, thus affecting morbidity and mortality in this patient population.     

Physical health status assessed during hospitalization for acute coronary syndrome predicts mortality 12 months later

Objective

Self-report measures of health status predict mortality in several groups of patients with cardiovascular disease, although overlap with symptoms of depression may reduce or eliminate this relationship. The association between self-reported health status and mortality has not been examined in patients hospitalized for acute coronary syndrome (ACS). The objective was to investigate whether the Physical Component Summary (PCS) and Mental Component Summary (MCS) scores of the SF-12 predicted 12-month all-cause mortality after controlling for cardiac risk factors and symptoms of depression.

Methods

The SF-12 and Beck Depression Inventory were administered 2-5 days after admission to 800 ACS patients from 12 coronary care units. Logistic regression was used to assess the relationship of the PCS and MCS with mortality 12 months later, controlling for age, sex, cardiac diagnosis (acute myocardial infarction vs. unstable angina), Killip class, history of myocardial infarction, and in-hospital depressive symptoms.

Results

Lower scores on the SF-12 PCS (worse health) were associated with a significantly higher risk of mortality [odds ratio (OR)=0.94, 95% confidence interval (CI)=0.92-0.97, P<.001]. MCS scores failed to reach significance (OR=0.98, CI=0.95-1.00, P=.053). The PCS significantly predicted mortality even after controlling for other cardiac risk factors and depressive symptoms (OR=0.96, CI=0.93-0.99, P=.008), equivalent to a 34% increase in risk per 10-point (1 SD) decrement in PCS scores.

Conclusion

The brief SF-12 PCS presents an attractive option for improving risk stratification among hospitalized ACS patients.     

Specificity of depression following an acute coronary syndrome to an adverse outcome extends over five years

Many studies have demonstrated that depression is associated with a worse cardiovascular outcome and increased risk of death in those experiencing an acute coronary syndrome (ACS). Recent studies have suggested, however, that any association is strongly influenced by the timing of the depression, with post-ACS depression providing the greatest risk. Establishing any timing impact should assist etiological clarification. We initially recruited 489 subjects hospitalized for an ACS, assessed lifetime and current depression, and then - at 1 and 12 months - assessed subsequent depression. Subjects were followed for up to 5 years to assess cardiovascular outcome and the impact of depression at differing time points, with three defined poor outcome categories (i.e. cardiac admission and/or cardiac rehospitalization). While outcome was associated with a number of non-depression variables, a poor outcome was most clearly associated with depressive episodes emerging at the time of the ACS but with some risk affected by episodes that commenced prior to the ACS and being persistent. Neither lifetime depressive episodes nor transient depressive episodes occurring around the baseline ACS event appeared to provide any risk. Study findings indicate that any differential deleterious impact of post-ACS depression has both short-term and longer-term outcomes, and, by implicating the centrality of post-ACS depression, should assist studies seeking to identify causal explanations.     

Central sleep apnea after acute coronary syndrome and association with ticagrelor use

Study objectivesBy modifying the apneic threshold, the antiplatelet agent ticagrelor could promote central sleep apnea hypopnea syndrome (CSAHS). We aimed to assess the association between CSAHS and ticagrelor administration.MethodsPatients were prospectively included within 1 year after acute coronary syndrome (ACS), if they had no heart failure (and left ventricular ejection fraction ≥ 45%) and no history of sleep apnea. After an overnight sleep study, patients were classified as “normal” with apnea hypopnea index (AHI) < 15, “CSAHS patients” with AHI ≥ 15 mostly with central sleep apneas, and “obstructive sleep apnea hypopnea syndrome (OSAHS) patients” with AHI ≥ 15 mostly with obstructive sleep apneas.ResultsWe included 121 consecutive patients (mean age 56.8 ± 10.8, 88% men, mean body mass index 28.3 ± 4.4 kg/m², left ventricular ejection fraction 56 ± 5%, at a mean of 67 ± 60 days (median 40 days, interquartile range: 30–80 days) after ACS. In total, 49 (45.3%) patients had AHI ≥ 15 (27 [22.3%] CSAHS %, 22 [18.2%] OSAHS).For 80 patients receiving ticagrelor, 24 (30%) had CSAHS with AHI ≥ 15, and for 41 patients not taking ticagrelor, only 3 (7.3%) had CSAHS with AHI ≥ 15 (chi-square = 8, p = 0.004). On multivariable analysis only age and ticagrelor administration were associated with the occurrence of CSAHS, (p = 0.0007 and p = 0.0006).ConclusionCSA prevalence after ACS is high and seems promoted by ticagrelor administration. Results from monocentric study suggest a preliminary signal of safety.Clinical trials.gov idNCT03540459.     

Prophylactic antidepressant treatment following acute coronary syndrome: A systematic review of randomized controlled trials

Major depressive disorder is significantly increased in patients following acute coronary syndrome resulting in twofold increased mortality compared with patients without depression. The depression diagnosis is often missed leading to considerable undertreatment. This systematic review assesses the current evidence of primary prophylactic treatment of depression in patients after acute coronary syndrome. The study protocol was prospectively registered at PROSPERO (registration number CRD42015025587). A systematic review were conducted and reported according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. PubMed, Embase, PsychINFO, CINAHL, and Cochran Library was searched. Two independent reviewers screened the records. The inclusion criteria were randomized controlled trials on adult patients with acute coronary syndrome treated prophylactically with an antidepressant intervention of any kind. A validated assessment tool should measure depression and depressive symptoms. Languages were limited to articles written in English. Six articles were included. Four studies utilized different components of case and disease management, health coaching, or relaxational audiotapes as intervention compared with usual care or with no formal program of rehabilitation. None of the studies showed any significant prophylactic effect against depression. One study with a program of health education and counselling and another study with a pharmacological antidepressant showed significant prophylactic effect on depression and depressive symptoms. All six included studies were associated with high risk of bias. There is not strong evidence of the effects of any type of routine antidepressant prophylaxis in patients following acute coronary syndrome. Further high quality studies are warranted.