Admission troponin T, advanced age and male gender identify patients with improved myocardial tissue perfusion after abciximab administration for ST-segment elevation myocardial infarction

The aim was to investigate the effect of abciximab on microvascular perfusion in different subgroups of patients undergoing direct PCI for acute STEMI. We enrolled 145 consecutive patients with TIMI grade 3 flow after direct PCI for acute STEMI. The GPIIb/IIIa inhibitor abciximab was administered in 57 patients (39.3%). Myocardial perfusion was the primary outcome measure and was assessed by analysis of cardiac troponin T wash-out. Treatment effects on myocardial perfusion and clinical outcome were tested for predefined subgroups including patients with an admission cTnT > or = 0.1 microg/L, diabetes mellitus, male gender, age > 70 years, and time from symptom onset to reperfusion > 6 hours. A significant improvement of cTnT wash-out was seen in patients with an admission cTnT > or = 0.1 microg/L, in males and in older patients. Improved tissue level reperfusion did not translate into a significant reduction of cardiac mortality or the incidence of the combined endpoint consisting of cardiac death, nonfatal reinfarction and need for target vessel revascularisation during 30 day- and long-term follow-up (mean 274 days). In conclusion, adjunctive administration of abciximab improves myocardial perfusion in patients with normal epicardial flow after direct PCI, particularly in patients with an cTnT > or = 0.1 microg/L on admission, age over 70 years and male gender.     

Mean platelet volume predicts patency of the infarct-related artery before mechanical reperfusion and short-term mortality in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

Background and aims

Patency of infarct-related artery (IRA) before mechanical reperfusion with primary percutaneous coronary intervention (PPCI) has been associated with better prognosis in patients with ST-Elevation myocardial infarction (STEMI). Mean platelet volume (MPV) increases in STEMI patients and may be associated with increased thrombotic potential. In STEMI patients scheduled for PPCI we sought to assess whether mean platelet volume (MPV), as measured at admission, correlates with “spontaneous” reperfusion of the IRA and short-term clinical outcome.

Methods

Blood samples were obtained on hospital admission in 617 consecutive patients (82% men; age 64 ± 12 years) with STEMI, before PPCI. 372 (61%) patients were treated with the GP IIb/IIIa blocker abciximab. The main study endpoint was mortality at 30 days.

Results

MPV was significantly lower in patients with basal TIMI flow grade 2 -3 compared to patients with TIMI grade 0-1 (median, 9 vs. 8.5 fL, p < 0.0001). After adjustment, MPV remained an independent predictor of the patency of the IRA (OR 0.63, CI 95% 0.51 - 0.78). A cut off value of 8.95 fL had a predictive negative value of 82% to identify patients with patent IRA. Using this cut point, and after adjusting for confounders, MPV was an independent predictor of 30-day mortality (HR 2.92, CI 95% 1.36 - 6.29). When patients were subdivided according to abciximab use, MPV was a marker of worse outcome but only in patients who did not receive abciximab (HR 3.67, CI 95% 1.13 - 11.49).

Conclusion

An increased MPV is an independent predictor of both a patent IRA (TIMI flow 2 or 3 before PPCI) and 30-day mortality. This marker may be able to identify patients requiring more aggressive antiplatelet therapy.     

Incidence and predictors of subacute thrombosis in patients undergoing primary angioplasty for an acute myocardial infarction

Subacute thrombosis (SAT) is a major concern in patients undergoing percutaneous coronary intervention (PCI). So far, only little data has been available on characteristics and outcome of patients with SAT after primary PCI for ST elevation myocardial infarction (STEMI). From 1997-2001, 1,548 unselected consecutive patients underwent primary PCI for STEMI as part of a randomized controlled trial stenting vs. balloon angioplasty. All patients received acetylsalicylic acid (500 mg i.v.) and heparin (5,000 IU) before the procedure. After stenting, all patients received ticlopidine 250 mg daily (before July 1999) or clopidogrel 75 mg daily (after July 1999) for one month. Five percent of patients received glycoprotein IIb/IIIa blockers. We prospectively recorded incidence and characteristics of patients with SAT during one year follow-up. SAT occurred in 4.1% (63/1548) and reinfarction in 6.0% of patients. The incidence of SAT did not change over time (1997: 8/175[4.6%],1998: 8/325 [2.5%],1999: 13/358 [3.6%], 2000: 22/426 [5.2%], 2001: 12/264 [4.5%]). SAT occurred in 39/63(62%) patients during hospital stay. The incidence did not differ between patients after ticlopidine 23/681 (3.4%) or clopidogrel 40/867 (4.6%, p = 0.222). Univariate predictors of SAT were: patients with an LAD stenosis (5.4% vs. 2.9%, p = 0.016), with Killip class >1 at presentation (8.6% vs. 3.7%, p = 0.007) and in patients who received a stent (5.1% vs. 2.7%, p = 0.022). After multivariate analysis, Killip class >1 on admission was the only independent predictor of SAT(OR 2.26, 95% CI 1.14-4.47, p = 0.019). SAT was associated with a higher mortality at long-term follow-up (15% vs. 7%, p = 0.026). In a prospectively recorded, unselected consecutive series of patients undergoing PCI for STEMI, SAT occurred in 4.1% of patients at one-year follow-up. Signs of heart failure on admission, anterior myocardial infarction and stenting were predictors of SAT.     

Impaired bioavailability of clopidogrel in patients with a ST-segment elevation myocardial infarction

Recent data has indicated that interindividual variability of intestinal absorption is an important determinant of the wide response variability to clopidogrel. We hypothesised that the physiological state of STEMI influences the intestinal absorption of clopidogrel. To evaluate this, we determined the pharmacokinetic response to a high loading dose of clopidogrel and the absolute ADP induced change in aggregation from baseline in STEMI patients and healthy volunteers. We found a significantly impaired bioavailability in STEMI patients as compared to healthy volunteers and a strong correlation between the reduction in platelet aggregation and the maximal plasma concentration of the active metabolite of clopidogrel. Although large clinical trails have clearly demonstrated the effectiveness of clopidogrel in the setting of STEMI, this small observational study encourages further research based on clinical endpoints to define the optimal dosing of clopidogrel in STEMI patients.     

Efficacy and safety of enoxaparin in unselected patients with ST-segment elevation myocardial infarction

In randomized clinical trials the low-molecular-weight heparin enoxaparin has been shown to reduce ischemic complications in patients with acute ST elevation myocardial infarction (STEMI) treated with fibrinolysis. Little is known about the use and efficacy of enoxaparin in unselected patients with STEMI in clinical practice. In a retrospective analysis of the prospective ACOS registry we compared the outcomes of patients with STEMI treated with enoxaparin or unfractionated heparin. A total of 6,299 patients with STEMI < 12 hours were included in this analysis, 609 (10%) were treated with enoxaparin and 5,690 (90%) with unfractionated heparin. In the multivariable propensity score analysis enoxaparin was associated with a reduction in the combined endpoint of death and non-fatal reinfarction in the entire group (odds ratio 0.59; 95% CI 0.43-0.80) and the subgroups of patients treated without early reperfusion (odds ratio 0.65, 95% CI 0.43-0.97), fibrinolysis (odds ratio 0.64; 95% CI 0.33-1.26) and primary percutaneous coronary intervention (odds ratio 0.33; 95% CI 0.15-0.72). There was no significant increase in severe bleeding complications with enoxaparin (6.5% versus 5.5%, p = 0.4). In clinical practice in unselected patients with STEMI treated with or without early reperfusion therapy early treatment with enoxaparin compared to unfractionated heparin is associated with a significant reduction of the combined endpoint of inhospital death and reinfarction without a significant increase in severe bleeding complications.     

Prothrombotic markers and early spontaneous recanalization in ST-segment elevation myocardial infarction

We tested the hypothesis that selected prothrombotic biomarkers might be associated with early spontaneous coronary recanalization in patients with ST-segment elevation acute myocardial infarction (STEMI). We prospectively enrolled 123 patients with STEMI including 53 patients with spontaneous coronary recanalization (cases) and 70 patients with persistent occlusion (controls) at the time of emergent coronary angiography and before angioplasty. All had received aspirin and heparin. Blood samples were collected immediately before angioplasty to measure soluble P-selectin, circulating microparticles originating from platelets (PMPs), granulocytes (GMPs), endothelial cells (EMPs); tissue factor-associated MP (TF-MP); soluble platelet glycoprotein V (sGPV) and prothrombin F1 + 2; tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1) and plasmin-antiplasmin (PAP). A sub-group of 70 patients (35 cases, 35 controls) was available for flow cytometry analysis of platelet P-selectin and activated GPIIb-IIIa. Baseline clinical characteristics did not differ between groups except for more frequent hypertension and dyslipidemia in controls. Platelet activation markers and PMP did not differ between the two groups. Controls had higher numbers of EMPs and GMPs compared to cases, but the difference was no longer significant when corrected for risk factors. Controls differed from cases by higher plasma levels of sGPV [64 (47-84) ng/ml vs. 53 (44-63) ng/ml] and PAP [114(65-225) ng/ml vs. 88 (51-147) ng/ml]. The difference persisted after adjustment for risks factors (p = 0.031 and 0.037, respectively). Persistent occlusion of the infarct related artery is associated with some markers related to higher thrombin (sGPV) and plasmin (PAP) production but is not associated with markers of platelet activation.     

Frequency of naturally-occurring regulatory T cells is reduced in patients with ST-segment elevation myocardial infarction

BACKGROUND: Naturally-occurring regulatory T cells (Treg) constitute a mature T-cell population characterized phenotypically by co-expression of CD4 and CD25(high) surface molecules. We investigated here the frequency of circulating Treg in patients presenting with STEMI in comparison with subjects without coronary artery disease (CAD). The effect of primary percutaneous coronary intervention (PCI) with implantation of a bare (BS) or paclitaxel-eluting stent (PES) on peripheral Treg distribution was also examined. METHODS: Peripheral blood mononuclear cells were isolated from 30 consecutive patients presenting with STEMI and from 30 age-matched control subjects with angiographically normal coronary arteries. Treg were detected by flow cytometry according to their characteristic CD4+ CD25(high) membrane phenotype, and their frequency was assessed before PCI and at 48 h and at 6 days after PCI. CD27 expression identifying a highly suppressive Treg subset was also analysed. RESULTS: The percentages of both (CD27+)Treg and (CD27-)Treg were significantly lower in patients with STEMI in comparison with controls. In addition, the (CD27+)Treg/(CD27-)Treg ratio was skewed toward the CD27- population. The frequency of both Treg subsets significantly increased 48 h after either BS or PES implantation, remaining elevated for up to at least 6 days after PCI. CONCLUSIONS: Our data suggest that the percentage of circulating Treg is significantly reduced in patients with STEMI, suggesting that this immunosuppressive T-cell subset is compartmentalized within the acutely ischemic myocardium to limit the ongoing inflammation associated with this condition, and that coronary revascularization is associated with partial reconstitution of peripheral Treg pool.     

Comparison between ticlopidine and clopidogrel in patients with ST-segment elevation myocardial infarction treated with coronary stenting

Controversy still surrounds the question, which antiplatelet drug should be added to aspirin in patients undergoing coronary stent implantation. The aim of the current study was to compare ticlopidine and clopidogrel in a consecutive series of patients with ST-segment elevation myocardial infarction (STEMI) treated with primary stenting. Our population is represented by 883 consecutive patients with STEMI undergoing primary stenting from April 1997 to October 2001. All clinical, angiographic, and follow-up data were prospectively collected. A total of 523 patients on clopidogrel were compared with 360 patients on ticlopidine after primary stenting. Except for age and statin therapy, no difference in demographic and clinical characteristics was observed between the two groups. Patients on clopidogrel had a higher rate of successful reperfusion (80.7% vs 73.1%, p = 0.008). No difference was observed between the two groups at both 30-day and 1-year follow-up. These data were confirmed after correction for age, successful reperfusion and statin therapy. This study shows no difference in long-term clinical outcome between clopidogrel and ticlopidine as adjunctive antiplatelet therapy in patients with STEMI undergoing stent implantation.     

Advances in antithrombotic therapy as adjunct to reperfusion therapies for ST-segment elevation myocardial infarction

The treatment of ST-segment elevation myocardial infarction (STEMI) has improved over the past decades, mainly due to reperfusion therapies. The aim of this article is to provide an updated review of adjunctive antithrombotic therapy to reperfusion strategies for STEMI. As compared to unfractionated heparin (UFH), among patients treated with thrombolysis, low-molecular-weight heparins (LMWHs), mainly enoxaparin, fondaparinux and clopidogrel have been shown to improve outcome in terms of death and reinfarction, whereas GP IIb-IIIa inhibitors, mainly abciximab, and direct thrombin inhibitors have reduced reinfarction, but not mortality. Among patients undergoing primary angioplasty, early UFH should still be regarded as the gold standard in anticoagulation therapy. In addition to ASA, early GP IIb-IIIa inhibitors, especially abciximab, should be considered since it has been shown to provide further benefits in terms of preprocedural recanalization. Despite the positive results observed in the HORIZONS trial, additional studies are needed to investigate the role of bivalirudin as compared to abciximab administration. In our opinion, bivalirudin may be considered instead of GP IIb-IIIa inhibitors among STEMI patients at high risk for bleeding complications. Due to the very low mortality currently achieved by primary angioplasty, a further reduction in short- or medium-term mortality would be quite improbable to be observed. Thus, additional endpoints, such as infarct size and myocardial perfusion, may be considered in future randomized trials among patients undergoing mechanical revascularization for STEMI.     

P2Y12 platelet reactivity after thrombolytic therapy for ST-segment elevation myocardial infarction

Introduction

Thrombolysis, as reperfusion therapy for ST segment elevation myocardial infarction (STEMI), induces a pro-thrombotic status with enhanced platelet activity; this study aims to evaluate P2Y12 platelet reactivity and response to clopidogrel in the post-thrombolysis scenario.

Materials and Methods

Observational, prospective study, including consecutive patients with elective angiography after thrombolytic therapy for STEMI. Every patient received antiplatelet therapy with loading doses of 250 mg aspirin and 300 mg clopidogrel on admission followed by 100 mg aspirin and 75 mg clopidogrel daily. P2Y12-dependent platelet reactivity (expressed in P2Y12-Reaction Units, PRU) was assessed with VerifyNow® device on admission, daily after thrombolysis and pre-angiography.

Results

41 patients fulfilled the inclusion criteria. Median time between thrombolysis and angiography was 2,5 days (IQR 1,8-4,1). Post-treatment platelet reactivity (PPR) showed poor correlation with time on clopidogrel treatment (r2 = 0.04) and reached a maximum value of 274 ± 84 PRU during the first 24 h after thrombolysis (Day + 1 determination). After this, values showed a progressive reduction until the point of angiography (249 ± 82 PRU), without significant differences between consecutive time-points (p = 0,549).Inhibition of platelet aggregation (IPA) assessed as a percentage of P2Y12 receptor blockage was poor, increasing gradually from 0 ± 4% on admission to 11 ± 6% the day of the angiography (p = 0,001). 71,4% of patients showed PPR ≥ 208 PRU during angiography.

Conclusions

Platelet reactivity, as assessed by post-treatment P2Y12 mediated reactivity, is heightened after thrombolytic therapy during STEMI management. In this scenario, standard doses of clopidogrel did not achieve significant inhibition of ADP-mediated platelet reactivity.     

Prior simvastatin treatment is associated with reduced thrombin generation and platelet activation in patients with acute ST-segment elevation myocardial infarction

Background

It has been reported that statin therapy produces additional effects including impaired activation of blood coagulation. It is not clear whether statins can affect hemostasis in patients with acute coronary syndrome. The aim of this study was to investigate the effect of prior statin treatment on thrombin generation and platelet activation in patients with ST-segment elevation myocardial infarction (STEMI).

Methods

We studied 53 consecutive STEMI patients admitted within 12 hours of pain onset, including 19 treated with simvastatin (40 mg/d) (simvastatin group) at least one month prior to STEMI, and 34 not receiving any statins (no-statin group) on admission. Thrombin-antithrombin (TAT) complexes generation and soluble CD40 ligand (sCD40L) release were determined in 60-second blood samples collected at the site of microvascular injury.

Results

There were no significant intergroup differences with respect to clinical and laboratory variables, including plasma TAT and sCD40L levels, except lower total cholesterol and low-density lipoprotein cholesterol in the simvastatin group. The mean maximum rate of TAT generation was 47.5% lower (p = 0.0002) and sCD40L release 33.3% lower (p = 0.0006) in the simvastatin group. Total amounts of TAT (p < 0.0001) and sCD40L (p = 0.002) collected within 5 minutes of bleeding were lower in simvastatin-pretreated patients. By multivariate regression analysis, variables describing local TAT and sCD40L profiles in the whole group were independently associated with simvastatin pretreatment (p < 0.0001), but not with cholesterol, platelet count or troponin levels.

Conclusions

Prior simvastatin use is associated with lower thrombin generation and platelet activation following vascular injury in the early phase of STEMI.     

Soluble CD40 ligand:interleukin-10 ratio predicts in-hospital adverse events in patients with ST-segment elevation myocardial infarction

INTRODUCTION: The balance between pro-inflammatory and anti-inflammatory molecules is likely to modulate the processes that lead to atherogenesis and rapid coronary artery disease progression. We sought to compare the positive predictive values of serum soluble CD40 ligand (sCD40L)/interleukin-10 (IL-10) ratio, versus individual sCD40L, and IL-10 measurements regarding in-hospital events in patients admitted into the hospital with ST-segment elevation myocardial infarction (STEMI). METHODS: We recruited 96 patients with STEMI. sCD40L and IL-10 were measured at hospital admission in every patient. The composite of in-hospital death and heart failure represented the study end-point. Heart failure was defined as Killip class>1. Multivariable logistic regression analysis was performed to identify independent variables related to in-hospital events. RESULTS: Thirty two patients (33%) achieved the study end-point and 64 (67%) had no adverse events during hospital admission. IL-10 levels (pg/ml) were lower (28.2+/-9.8 versus 33.24+/-11.3, p=0.03) and sCD40L levels (pg/ml) higher (156.8+/-54.2 versus 135.4+/-38.70, p=0.02) in patients with events compared to those without events. Significantly higher odd ratios were found for sCD40L/IL-10 ratio (OR=2.10, 95% CI: 1.90 to 2.80, p=0.01) compared to individual sCD40L (OR=1.40, 95% CI: 0.90 to 2.20, p=0.08) and IL-10 (OR=0.70, 95% CI: 0.50 to 0.93, p=0.02) measurements. CONCLUSION: Our study showed that serum ratio of sCD40L/IL-10 is a better independent predictor of in-hospital adverse events than individual sCD40L and IL-10 measurements in patients with STEMI.     

国产雷帕霉素药物洗脱支架置入治疗急性ST段抬高心肌梗死：与进口药物支架比较其安全性和有效性

目的：比较国产雷帕霉素洗脱支架（Firebird支架）和进口雷帕霉素洗脱支架（CypherTM支架）置入治疗急性ST段抬高心肌梗死的安全性和有效性。 方法：选择2005-03/2007-02就诊于赣州市立医院心内科及深圳市孙逸仙心血管医院的急性ST段抬高心肌梗死患者121例，经患者及家属知情同意后进行临床观察，治疗过程经医院医学伦理委员会批准。其中CypherTM支架组59例，Firebird支架组62例。比较两组支架置入后冠状动脉造影结果、住院期间的临床结果；随访2~12个月，记录死亡率、靶血管重建率及主要心血管事件发生率。 结果：①121例患者支架置入均获得成功。62例梗死相关血管的62处病变置入64枚Firebird支架；另59支梗死相关血管的59处病变置入61枚CypherTM支架。②Firebird支架组1例术后第5天出现支架内亚急性血栓形成，再次行冠状动脉介入术获得成功。CypherTM支架组1例术后64 d发生急性左心衰竭而死亡，1例术后5个月在院外猝死。③两组比较支架置入后造影结果和临床结果差异无显著性意义。④对117例患者进行随访，CypherTM支架组死亡率、靶血管重建率和主要心血管事件发生率分别为3.4%、0%和3.4%；Firebird支架组死亡率、靶血管重建率和主要心血管事件发生率分别为3.2%、1.6%和4.8%，差异无显著性意义（P > 0.05）。 结论：国产雷帕霉素药物洗脱支架置入治疗急性ST段抬高心肌梗死患者是安全的,随访未发现管腔内出现血液及组织细胞的变化，无特殊生物相容性和安全性问题，与进口雷帕霉素药物涂层支架相比较各项指标差异不明显。     

The DD genotype of the angiotensin converting enzyme gene independently associates with CMR-derived abnormal microvascular perfusion in patients with a first anterior ST-segment elevation myocardial infarction treated with thrombolytic agents

Introduction

The role of the angiotensin converting enzyme (ACE) gene on the result of thrombolysis at the microvascular level has not been addressed so far. We analyzed the implications of the insertion/deletion (I/D) polymorphism of the ACE gene on the presence of abnormal cardiovascular magnetic resonance (CMR)-derived microvascular perfusion after ST-segment elevation myocardial infarction (STEMI).

Materials and Methods

We studied 105 patients with a first anterior STEMI treated with thrombolytic agents and an open left anterior descending artery. Microvascular perfusion was assessed using first-pass perfusion CMR at 7 ±1 days. CMR studies were repeated 184 ± 11 days after STEMI. The ACE gene insertion/deletion (I/D) polymorphism was determined using polymerase chain reaction amplification.

Results

Overall genotype frequencies were II-ID 58% and DD 42%. Abnormal perfusion (≥ 1 segment) was detected in 56% of patients. The DD genotype associated to a higher risk of abnormal microvascular perfusion (68% vs. 47%, p = 0.03) and to a larger extent of perfusion deficit (median [percentile 25 - percentile 75]: 4 [0-6] vs. 0 [0-4] segments, p = 0.003). Once adjusted for baseline characteristics, the DD genotype independently increased the risk of abnormal microvascular perfusion (odds ratio [95% confidence intervals]: 2.5 [1.02-5.9], p = 0.04). Moreover, DD patients displayed a larger infarct size (35 ± 17 vs. 27 ± 15 g, p = 0.01) and a lower ejection fraction at 6 months (48 ± 14 vs. 54 ± 14%, p = 0.03).

Conclusions

The DD genotype associates to a higher risk of abnormal microvascular perfusion after STEMI.     

CRUSADE bleeding risk score validation for ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention

Introduction

The CRUSADE bleeding risk score (CBRS) accurately predicts major bleeding in non-ST segment elevation myocardial infarction NSTEMI patients. However, little information exists about its application in ST segment elevation myocardial infarction STEMI. We aimed to assess the ability of CBRS to predict in-hospital major bleeding in STEMI patients undergoing primary percutaneous coronary intervention (PPCI).

Materials and Methods

We prospectively analyzed consecutive STEMI patients undergoing PPCI. Baseline characteristics, in-hospital complications and mid term mortality were recorded. Major bleeding was defined by the CRUSADE definition. Predictive ability of the CBRS was assessed by logistic regression method and the area under the ROC curve (AUC).

Results

We included 1064 patients (mean age 63 years). Mean CBRS value was 24. Most of patients (740/1064 (69.6%)) were in the two lowest risk quintiles of CBRS. Incidence of in-hospital major bleeding was 33/1064 (3.1%). The rates of in-hospital bleeding across the quintiles of risk groups were 0.4% (very low risk), 2.6% (low), 4.6% (moderate), 7.2% (high), and 13.4% (very high) (p 0.001). AUC was 0.80 (95% CI 0.73-0.87 p 0.001). In patients with radial access angiography (n = 621) AUC was 0.81 (95% CI: 0.65-0.97). Mean follow up was 344 days. Patients with bleeding events had higher mortality during follow up (HR 6.91; 95% CI 3.72-12.82; p 0.001).

Conclusions

Our patients had a significantly lower bleeding risk as compared to CRUSADE NSTEMI population. CBRS accurately predicted major in-hospital bleeding in this different clinical scenario, including patients with radial artery approach.     

Effects of antidepressant medication on morbidity and mortality in depressed patients after myocardial infarction

BACKGROUND: Depression after myocardial infarction (MI) is associated with higher morbidity and mortality. Although antidepressants are effective in reducing depression, their use in patients with cardiovascular disease remains controversial. OBJECTIVE: To undertake a secondary analysis to determine the effects of using antidepressants on morbidity and mortality in post-MI patients who participated in the Enhancing Recovery in Coronary Heart Disease study. DESIGN: Observational secondary analysis. SETTING: Eight academic sites. PATIENTS: The Enhancing Recovery in Coronary Heart Disease clinical trial randomized 2481 depressed and/or socially isolated patients from October 1, 1996, to October 31, 1999. Depression was diagnosed using a structured clinical interview. This analysis was conducted on the 1834 patients enrolled with depression (849 women and 985 men). INTERVENTION: Use of antidepressant medication. MAIN OUTCOME MEASURES: Event-free survival was defined as the absence of death or recurrent MI. All-cause mortality was also examined. To relate exposure to antidepressants to subsequent morbidity and mortality, the data were analyzed using a time-dependent covariate model. RESULTS: During a mean follow-up of 29 months, 457 fatal and nonfatal cardiovascular events occurred. The risk of death or recurrent MI was significantly lower in patients taking selective serotonin reuptake inhibitors (adjusted hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.38-0.84), as were the risk of all-cause mortality (adjusted HR, 0.59; 95% CI, 0.37-0.96) and recurrent MI (adjusted HR, 0.53; 95% CI, 0.32-0.90), compared with patients who did not use selective serotonin reuptake inhibitors. For patients taking non-selective serotonin reuptake inhibitor antidepressants, the comparable HRs (95% CIs) were 0.72 (0.44-1.18), 0.64 (0.34-1.22), and 0.73 (0.38-1.38) for risk of death or recurrent MI, all-cause mortality, or recurrent MI, respectively, compared with nonusers. CONCLUSIONS: Use of selective serotonin reuptake inhibitors in depressed patients who experience an acute MI might reduce subsequent cardiovascular morbidity and mortality. A controlled trial is needed to examine this important issue.     

Lower tissue factor inhibition in patients with ST segment elevation than in patients with non ST elevation acute myocardial infarction

Introduction

Mechanisms to explain the different course of coronary thrombosis between ST elevation myocardial infarction (STEMI) and non-STEMI patients remain poorly defined. We hypothesize, however, that STEMI patients may present lower tissue factor plasma inhibition to partly account for their more persistent coronary thrombotic occlusion.

Materials and Methods

Total (t-TFPI ) and free tissue factor plasma inhibitor (f-TFPI), thrombin-antithrombin complex (TAT), plasminogen activator inhibitor 1 (PAI-1), von Willebrand factor (vWF), and fibrinogen were measured on admission and at 3 and 6 months in patients with a first STEMI (n:69) or non-STEMI (n:60). C reactive protein (CRP) was also measured on admission and at 3 months.

Results

STEMI patients showed lower admission levels of t-TFPI (p = 0.001), f-TFPI (p = 0.030) and fibrinogen (p = 0.022), and higher vWF levels (p = 0.005) than non-STEMI whereas TAT, PAI and CRP levels were comparable. At 3 and 6 months VWF, t-TFPI, f-TFPI, and TAT levels declined significantly in the 2 groups (p = 0.002) reaching similar values. CRP levels also declined at 3 months (p = 0.002). Moreover, the rate of cardiac mortality, non fatal MI or stroke during a 6 year follow-up were unrelated to admission coagulation parameters.

Conclusions

The lower inhibition of tissue factor and greater endothelial dysfunction in STEMI than in non-STEMI patients may enhance thrombosis at the culprit lesion and adjacent coronary plaques, and hence, account at least in part for their different pathophysiology. This condition, however, is limited to the acute phase.     

心肌声学造影评价自体骨髓单个核细胞移植急性心肌梗死后的心肌再灌注：与核素心肌灌注成像比较

背景：以往对干细胞移植治疗急性心肌梗死后心肌再灌注的评价主要采用核素显像、MRI显像等,但这类方法重复性较差,并具有放射性。 目的：分析经静脉心肌声学造影对急性心肌梗死行自体骨髓单个核细胞移植后心肌再灌注的评价。 方法：对24例急性心肌梗死患者于单个核细胞移植前后行经静脉心肌声学造影检查,测量平台期的心肌显像增大强度A、曲线上升平均斜率β及A与β之积在移植前后的变化,并与心肌核素显像随访结果相对照,判定心肌再灌注情况。 结果与结论：经静脉心肌声学造影显示,患者移植后相关心肌节段的A、β及A•β之积均较移植前显著增加(P < 0.01),其中血管开通后β值的变化幅度最大,随访6个月后A值变化幅度增大,说明血管开通即刻先有灌注速度加快,移植后6个月心肌灌注缺损明显改善。移植后6个月梗死区即刻和延迟相心肌核素摄取均较移植前增强,SPECT心肌灌注图像评分较移植前显著下降(P < 0.05)。说明经静脉心肌声学造影结果与核素心肌灌注显像基本一致,可床旁无创评估移植心肌细胞微循环灌注情况。     

Effects of adjunctive verapamil administration in chronic schizophrenic patients.

1. The efficacy of adjunctive verapamil on psychopathological symptoms and tardive dyskinesia was investigated in 22 chronic schizophrenic patients, who had partially responded to neuroleptics. 2. After 28 days verapamil administration (240 mg/day) a significant improvement was found in anxiety-depression, and in some positive and negative symptoms. Three of the 22 patients showed clinically pronounced global improvement. 3. The treatment was ineffective in tardive dyskinesia.