The role of alexithymia in predicting incident depression in patients at first acute coronary syndrome

Objective Alexithymia has been considered both to predispose to depression and to worsen cardiac prognosis after an acute coronary syndrome. Nonetheless, no studies have evaluated its role as a risk factor for incident depression, in patients with acute coronary syndrome. Methods In 251 consecutive patients, the presence of a first-ever depressive episode was evaluated with the Primary Care Evaluation of Mental Disorders at baseline and 1, 2, 4, 6, 9, 12 and 24 months after their first acute coronary syndrome. At baseline, patients completed the Toronto Alexithymia Scale (TAS-20) and the Hospital Anxiety and Depression Scale. Results Out of 251 subjects (80.9% males), a first-ever depressive episode was diagnosed in 66 patients. Depressed and never-depressed patients differed in female gender, living status, alexithymic scores at TAS-20 and depressive symptoms. Nonetheless, nor the TAS-20 factors nor its total score were predictive of developing a depressive episode in a Cox regression. Moreover, baseline differences in TAS-20 scores between the two groups, disappeared after controlling for anhedonic symptoms. Conclusion Our results do not support the hypothesis that alexithymia at TAS-20 is a risk factor for incident depression after acute coronary syndrome

Risk factors for incident depression in patients at first acute coronary syndrome

The association between depression and acute coronary syndrome (ACS) is well-established and the first seems to impact meaningfully on cardiac prognosis. Nonetheless only a few studies have evaluated the relationship between incident depression, defined as new cases in patients with no history of depression, and ACS. Therefore the aim of this study is to analyse the risk factors of incident depression in a sample of patients who were presenting their first ACS. 304 consecutive patients were recruited. The presence of major (MD) and minor (md) depression was assessed with the Primary Care Evaluation of Mental Disorders (PRIME-MD), whereas its severity was evaluated with the Hospital Anxiety and Depression Scale (HADS). Evaluations were collected both at baseline and at 1, 2, 4, 6, 9 and 12 month follow ups. Out of 304 subjects (80.6% males), MD was diagnosed in 15 (4.9%) and md in 25 patients (8.2%). At baseline risk factors for a post-ACS depressive disorder were being women (MD only), widowed (md only) and having mild anhedonic depressive symptoms few days after the ACS. Clinicians should keep in mind these variables when facing a patient at his/her first ACS, given the detrimental effect of depression on cardiac prognosis

Effect of Abciximab on Prothrombin Activation and Thrombin Generation in Acute Coronary Syndromes Without ST-Segment Elevation

Background — Abciximab is very effective in reducing major cardiac events in patients undergoing interventional procedures. Its antithrombotic effect is primarily attributable to the blocking of platelet glycoprotein IIb/IIIa receptors, but recent evidence suggests that it may have a direct antithrombin effect. No data are available concerning the effect of abciximab on the in vivo markers of prothrombin activation and thrombin generation in patients with acute coronary syndromes without ST elevation. Methods and Results — We measured the plasma levels of prothrombin fragment 1+2 (a marker of prothrombin activation) and the thrombin/antithrombin complex (a marker of thrombin generation) in 167 patients with acute coronary syndromes without ST elevation enrolled in the GUSTO IV ACS trial who were randomized to receive abciximab for 24 hours (52 patients), abciximab for 48 hours (59 patients), or placebo (56 patients) in addition to heparin. Blood samples were obtained at baseline (before any treatment), after 24 and 48 hours (before study drug discontinuation), and 1 month later. There was a significant increase in the plasma levels of prothrombin fragment 1+2 after 48 hours and after 1 month in all 3 groups, placebo ( P =0.0001), 24-hour abciximab ( P =0.0002), and 48-hour abciximab ( P =0.0001). The plasma thrombin/antithrombin complex levels were similar in the 3 groups at all time points and did not change during the study drug infusions. Conclusions — Abciximab does not decrease prothrombin activation and thrombin generation in patients with acute coronary syndromes without ST elevation not undergoing interventional procedures

Evaluation of Coronary Atherosclerosis by Multislice Computed Tomography in Patients With Acute Myocardial Infarction and Without Significant Coronary Artery Stenosis

Background— It is known that 9% to 31% of women and 4% to 14% of men with acute myocardial infarction have normal coronary arteries or nonsignificant coronary disease at angiography. These patients represent a diagnostic and therapeutic challenge. Multislice computed tomography (CT) can noninvasively identify the presence of coronary plaques even in the absence of significant coronary artery stenosis. This study evaluated the role of 64-slice CT, in comparison with coronary angiography, in detecting and characterizing coronary atherosclerosis in patients with acute myocardial infarction without significant coronary artery stenosis. Methods and Results— Thirty consecutive patients with acute myocardial infarction but without significant coronary stenosis at coronary angiography underwent 64-slice CT. All coronary segments were quantitatively analyzed by means of coronary angiography (CA-QCA) and 64-slice CT (CT-QCA). Forty-seven (10.4%) of the 450 coronary segments were not evaluable by CT. The mean proximal reference diameters at CT-QCA and CA-QCA were, respectively, 2.88�0.75 mm and 2.65�0.9 mm; the overall correlation between CT-QCA and CA-QCA for quantification of reference diameter was r s =0.77; P <0.001. The mean percent stenosis was 14.4�8.0% at CT-QCA and 4.0�11.0% at CA-QCA and the correlation was r s =0.11; P =0.03. Overall CT-QCA showed the presence of 50 plaques, of which only 11 were detected by CA-QCA. CT-QCA identified 25 plaques in infarct-related coronary arteries. Positive remodeling was present in 38 of the 50 plaques (76%), with a higher prevalence in the coronary plaques not visualized by CA-QCA (82.1% versus 54.5%). Conclusions— CT-QCA correlates well with CA-QCA in terms of coronary reference diameter analysis, but not stenosis quantification. Multislice CT can detect coronary atherosclerotic plaques in segments of nonstenotic coronary arteries that are underestimated by CA and may have an incremental diagnostic value for the diagnosis of acute myocardial infarction in patients without significant coronary stenosis at CA

Thrombin generation in human coronary arteries after percutaneous transluminal balloon angioplasty

AbstractObjectives. The aim of this study was to investigate the relation between coronary atherosclerotic plaque injury and activation of the coagulation cascade.Background. Thrombus formation after atherosclerotic plaque disruption has been implicated in the pathogenesis of atherosclerosis, unstable angina and myocardial infarction.Methods. Biochemical markers of thrombin generation (prothrombin fragment F1+2) and thrombin activity (fibrinopeptide A) were measured in coronary blood before, during and immediately after percutaneous transluminal coronary angioplasty. After demonstrating that blood withdrawal through an angioplasty catheter does not artifactually elevate the plasma levels of these markers in patients after heparinization, coronary artery samples ware collected proximal and distal to the lesion before and distal to the lesion after baltoon inflation in 26 patients.Results. Plasma levels of F1+2measured proximal to the lesion before angioplasty (median 0.47 nmol/liter, 95% confidence interval [CI] 0.40 to 0.50) were significantly elevated after angioplasty (median 0.55 nmol/liter, 95% CI 0.46 to 0.72, p = 0.001). In contrast, plasma fibrinopeptide A levels measured proximal to the lesion before angioplasty (median 2.0 ng/ml, 95% CI 1.3 to 22) were similar to those measured after angioplasty (median 1.8 ng/ml, 95% CI 1.3 to 3.0, p = NS). After we defined a normal range of interassay variability on the basis of values obtained from samples drawn proximal and distal to the lesion before angioplasty, seven patients (27%) had a significant increase in F1+2plasma levels. A significant increase in plasma fibrinopeptide A occurred in five of these seven patients. Lesions with dissection, filling defects or haziness on postangioplasty angiography were associated with more thrombin generation than lesions without these features.Conclusions. Markers of thrombio generation and activity can be collected safely and assayed accurately in heparinized blood withdrawn through aa angioplasty catheter. Balloon dilation of coronary stenoses increases thrombin generation and activity within the coronary artery in a substantial subgroup of patients undergoing angioplasty

Type D personality in never depressed patients at their first acute coronary syndrome

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Platelet gene expression profile in acute myocardial infarction

Acute myocardial infarction is a sudden event that is fatal in around one-third of patients. It is primarily due to coronary atherosclerotic plaque rupture with subsequent platelet (PLT) activation/aggregation and thrombus formation. PLTs have a key role in the genesis and progression of atherosclerosis and in thrombus formation1. PLTs are anucleated cells which retain mRNA from their megakaryocyte precursor, therefore PLT mRNA is unique in representing a nearly fixed transcriptome2. We tested the hypothesis that platelet transcriptome acts as a fingerprint indicating the development of a future myocardial infarction, with the final goal of identifying a specific STEMI gene-signature, able to discriminate patients with acute event from healthy donors (HD) and from patients affected by stable coronary artery disease (sCAD), the phenotypically closest clinical condition to STEMI. Peripheral blood samples (50mL) were collected in Na-citrate tubes from 20 myocardial infarction patients (MI), 20 sCAD and 20 HD. Highly purified platelets were obtained by leukocyte depletion as previously described3. Platelet RNA extraction were performed by TRIzolTM reagent according to the manufacturer’s protocol. Gene expression profile was analyzed using an Affymetrix GeneChip system (Cancer Genomics and Bioinformatics Laboratory Facility, Kimmel Cancer Center, Jefferson University. Philadelphia, US). The exploratory analysis of PLT transcriptome confirmed differences in gene expression between STEMI, sCAD and HD. Hence, the common differentially expressed genes (DEGs) derived from the STEMI vs sCAD and STEMI vs HD comparisons were obtained and tested by k-nearest neighbor classification and bootstrap. A set of 17 STEMI-related DEGs was identified, showing good sensitivity and specificity for the discrimination of STEMI patients. Overall, we described a STEMI-specific gene expression patterns, suggesting that PLT transcriptome allows to characterize a powerful fingerprint of STEMI theoretically able to predict a future acute event

Optimal Timing of Coronary Invasive Strategy in Non–ST-Segment Elevation Acute Coronary Syndromes

Background: The optimal timing of coronary intervention in patients with non–ST-segment elevation acute coronary syndromes (NSTE-ACSs) is a matter of debate. Conflicting results among published studies partly relate to different risk profiles of the studied populations. Purpose: To do the most comprehensive meta-analysis of current evidence on early versus delayed invasive treatment in NSTE-ACS. Data Sources: MEDLINE, PubMed Central, and Google Scholar databases; conference proceedings; ClinicalTrials.gov registry; and Current Controlled Trials registry through May 2012. Study Selection: Available randomized, controlled trials (RCTs) and observational studies comparing early versus delayed intervention in the NSTE-ACS population. Data Extraction: Data were extracted for populations, interventions, outcomes, and risk of bias. All-cause mortality was the prespecified primary end point. The longest follow-up available in each study was chosen. The odds ratio with 95% CI was the effect measure. Data Synthesis: Seven RCTs (5370 patients) and 4 observational studies (77 499 patients) were included. Early intervention was less than 20 hours after hospitalization or randomization for RCTs and 24 hours or less for observational studies. Meta-analysis of the RCTs was inconclusive for a survival benefit associated with the early invasive strategy (odds ratio, 0.83 [95% CI, 0.64 to 1.09]; P 0.180); a similar result emerged from the observational studies. With early versus late intervention, the odds ratios in the RCTs were 1.15 (CI, 0.65 to 2.01; P 0.63) and 0.76 (CI, 0.56 to 1.04; P 0.090) for myocardial infarction and major bleeding during follow-up, respectively. Limitation: Current evidence from RCTs is limited by the small overall sample size, low numbers of events in some trials, and heterogeneity in the timing of intervention and in patient risk profiles. Conclusion: At present, there is insufficient evidence either in favor of or against an early invasive approach in the NSTE-ACS population. A more definitive RCT is warranted to guide clinical practice. Primary Funding Source: None