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Background: The role of thrombus aspiration plus primary percutaneous coronary intervention in ST-segment elevation myocardial infarction remains controversial. Methods: We performed a meta-analysis of 25 randomised controlled trials in which 21,740 ST-segment elevation myocardial infarction patients were randomly assigned to thrombus aspiration plus primary percutaneous coronary intervention or primary percutaneous coronary intervention. Study endpoints were: death, myocardial infarction, stent thrombosis and stroke. Results: On pooled analysis, the risk of death (4.3% vs. 4.8%, odds ratio (OR) 0.90, 95% confidence interval (CI) 0.79–1.03; P=0.123), myocardial infarction (2.4% vs. 2.5%, OR 0.95, 95% CI 0.80–1.13; P=0.57) and stent thrombosis (1.3% vs. 1.6%, OR 0.80, 95% CI 0.63–1.01; P=0.066) was similar between thrombus aspiration plus primary percutaneous coronary intervention and primary percutaneous coronary intervention. The risk of stroke was higher in the thrombus aspiration plus primary percutaneous coronary intervention than the primary percutaneous coronary intervention group (0.84% vs. 0.59%, OR 1.401, 95% CI 1.004–1.954; P=0.047). However, on sensitivity analysis after removing the TOTAL trial, thrombus aspiration plus primary percutaneous coronary intervention was not associated with an increased risk of stroke (OR 1.01, 95% CI 0.58–1.78). The weak association between thrombus aspiration and stroke was also confirmed by the fact that the lower bound of the 95% CI was slightly below unity after removing either the study by Kaltoft or the ITTI trial. There was no interaction between the main study results and follow-up, evidence of coronary thrombus, or study sample size. Conclusions: In patients with ST-segment elevation myocardial infarction, thrombus aspiration plus primary percutaneous coronary intervention does not reduce the risk of death, myocardial infarction or stent thrombosis. Thrombus aspiration plus primary percutaneous coronary intervention is associated with an increased risk of stroke; however, this latter finding appears weak.

AIMS: Despite troponin assay being a part of the diagnostic work up in many conditions with acute chest pain, little is known about its frequency and clinical implications in acute aortic syndromes (AASs). In our study we assessed frequency, impact on diagnostic delay, inappropriate treatments, and prognosis of troponin elevation in AAS.METHODS AND RESULTS: Data were collected from a prospective metropolitan AAS registry (398 patients diagnosed between 2000 and 2013). Cardiac troponin test, using either standard or high sensitivity assay, was performed according to standard protocol used in chest pain units. Troponin T values were available in 248 patients (60%) of the registry population; the overall frequency of troponin positivity was 28% (ranging from 16% to 54%, using standard or high sensitivity assay respectively, p = 0.001). Troponin positivity was frequently associated with acute coronary syndromes (ACS)-like electrocardiogram findings, and with a twofold increased risk of long in-hospital diagnostic time (odds ratio (OR) 1.92, 95% confidence interval (CI) 1.05-3.52, p = 0.03). The combination of positive troponin and ACS-like electrocardiogram abnormalities resulted in a significantly increased risk of in-hospital delay/coronary angiography/antithrombotic therapy due to a misdiagnosis of ACS (OR 2.48, 95% CI 1.12-5.54, p = 0.02). However, troponin positivity was not associated with in-hospital mortality (OR 1.63, 95% CI 0.86-3.10, p = 0.131).CONCLUSIONS: Troponin positivity was a frequent finding in AAS patients, particularly when a high sensitivity assay was employed. Abnormal troponin values were strongly associated with ACS-like electrocardiogram findings and with in-hospital diagnostic delay but apparently they did not influence in-hospital mortality.

AimsThis study compared the clinical, functional, and haemodynamic characteristics and current era survival of subgroups of patients with pulmonary arterial hypertension associated with congenital heart disease (PAH-CHD): Eisenmenger syndrome (ES); PAH-CHD associated with systemic-to-pulmonary shunts (SPs); PAH with small defects (SDs); and PAH after defect correction (CDs).Methods and resultsData from consecutive PAH-CHD patients referred to our centre from 1 January 1998 to 31 May 2011 were collected. A contemporary group of idiopathic PAH patients was utilized for comparison. Treatment was per PAH guidelines, including combination therapy, with approved PAH-specific drugs. Survival was assessed with Kaplan-Meier analysis from the first invasive haemodynamic confirmation of PAH and compared across subgroups by log-rank test. Of 192 patients (mean age 41 ± 17 years; 61% female), 90 had ES (aged 41 ± 16 years); 48 SP (aged 47 ± 18 years); 10 SD (aged 25 ± 21 years); and 44 CD (aged 36 ± 17 years). Patients with ES had the highest baseline pulmonary vascular resistance and the lowest exercise capacity. Seventy-eight per cent were treated with approved PAH-specific drugs, and 44% were treated with combination therapy. Kaplan-Meier survival estimates (95% confidence interval) at 20 years for ES, SP, and CD were 87% (77-93%), 86% (60-96%), and 36% (12-72%, P = 0.0001 vs. ES; P = 0.004 vs. SP), respectively, and at 15 years for SD was 66% (16-91%, P = 0.015 vs. ES; P = 0.016 vs. SP). The survival of the 278 patients with idiopathic PAH appeared to be worse when compared with the PAH-CHD subgroups.ConclusionRelevant clinical, functional, haemodynamic, and survival differences were observed among subgroups. In particular, patients with CD and SD had the worst survival. These findings should be considered when planning medical or interventional treatment strategies in PAH-CHD patients.

AIMS: Few studies have systematically evaluated the value of intra-procedural parameters in predicting response to cardiac resynchronization therapy (CRT). We investigated whether intracardiac (electrogram) measurements of electrical delays between the positioned right ventricular (RV) and left ventricular (LV) leads at implantation could predict the mid-term CRT response. METHODS AND RESULTS: Fifty-two patients underwent CRT implantation according to standard techniques and clinical indications. The RV-LV interlead electrical delay measured during spontaneous rhythm and the difference between the pacing-induced (Deltap) RV-LV interlead electrical delays measured during RV and LV pacing were defined intraoperatively using the electrical depolarizations registered at the ventricular leads on the device programmer. At 6 months, a reduction of LV end-systolic volume > or = 15% was used to define CRT responders. Responders (62%), when compared with non-responders, showed a higher proportion of ischaemic aetiology (P = 0.007) and a lower value of DeltapRV-LV interlead electrical delay (22.1 +/- 18.4 vs. 46.3 +/- 15.0 ms, P = 0.0001). At multivariate analysis, the DeltapRV-LV interlead electrical delay was the only independent predictor of response to CRT (P = 0.001). For such a parameter, the receiving operating characteristic curve analysis identified a cut-off value of 42 ms corresponding with the highest accuracy: sensitivity 90.6%; specificity 70%; positive and negative predictive value 83% and 82%, respectively. Conversely, no difference was ascertained between responders and non-responders when RV-LV interlead electrical delay was measured during spontaneous rhythm (76.1 +/- 28.5 vs. 89.6 +/- 21.2, P = 0.078). CONCLUSION: Intraprocedural measuring of paced RV-LV interlead electrical delay obtained during RV and LV pacing predicts mid-term CRT response.

Aims To evaluate the predictive value of high sensitivity (hs) C-reactive protein levels on long-term survival in patients with ST-elevation myocardial infarction (STEMI) treated with primary PCI. Methods and results We conducted a retrospective analysis of 758 STEMI patients (from January 2003 to December 2005), with STEMI onset < 12 h and hs-C-reactive protein determination on admission. Patients were classified into four groups [I (hs-C-reactive protein < 0.48 mg/dL), II (hs-C-reactive protein ≥ 0.48 to < 1.2 mg/dL), III (hs-C-reactive protein ≥ 1.2 to < 3.1 mg/dL), IV (hs-C-reactive protein ≥ 3.1 mg/dL)] according to quartiles of hs-C-reactive protein serum level. The IV quartile hs-C-reactive protein group had a higher incidence of in-hospital mortality and cumulative adverse events. At a mean follow-up of 724 ± 376 days (range 0–1393), the IV quartile hs-C-reactive protein group showed lower estimated survival, lower estimated myocardial infarction-free survival and lower estimated event-free survival. At multivariable analysis hs-C-reactive protein appeared to be an independent predictor of long-term mortality (HR: 1.04, 95% CI: 1.01–1.07, P = 0.003), long-term mortality and re-infarction (HR: 1.03, 95% CI: 1.01–1.06, P = 0.008) and adverse events (HR: 1.03, 95% CI: 1.01–1.05, P = 0.03). Conclusion Evaluation of hs-C-reactive protein on admission in STEMI patients undergoing primary PCI allows reliable risk stratification of these patients.

Aims Treatment delay is a powerful predictor of survival in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI). We investigated effectiveness of pre-hospital diagnosis of STEMI with direct referral to PCI, alongside more conventional referral strategies. Methods and results From January 2003 to December 2004, 658 STEMI patients were referred for primary PCI at our intervention laboratory. Three predefined referral routes were compared: (1) for patients within 90 min drive of the PCI centre, pre-hospital diagnosis and direct transportation ( n =166), (2) diagnosis at the interventional hospital emergency department ( n =316), (3) diagnosis at local hospitals before transportation ( n =176). Pre-hospital diagnosis was associated with more than 45 min reduction in treatment delay ( P =0.001). No significant difference in in-hospital mortality was apparent in the overall study population. In the cardiogenic shock subgroup ( n =80), pre-hospital diagnosis was associated with a two-thirds reduction in in-hospital mortality ( P =0.019); mortality was only 6.2% in shock patients who underwent PCI in

Aims The purpose of this retrospective study was to assess the risk factors for the early and late outcome of the surgical treatment of acute type A aortic dissection, in terms of mortality and morbidity. Methods and results From 1976 to 2003, 487 patients with acute type A aortic dissection treated surgically were enrolled. Twenty-five pre-operative and intra-operative variables were analysed to identify conditions influencing early and late morbidity and early mortality. The in-hospital mortality rate including operative death was 22% (107 patients). Multivariable analysis indicated that pre-existing cardiac disease (RR=3.7, 95% CI=1.8–7.4) and cardiopulmonary resuscitation (RR=6.8, 95% CI=2.3–20.2) were independent predictors of in-hospital death. The causes of in-hospital mortality were low cardiac output in 32 patients (6.6%), major brain damage in 24 patients (5.9%), haemorrhage in 11 patients (2.2%), sepsis in nine patients (1.8%), visceral ischaemia in eight patients (1.6%), multiple organ failure in seven patients (1.4%), rupture of the thoracic aorta in six patients (1.2%), respiratory failure in six patients (1.2%), and four intra-operative deaths. The follow-up was 100% complete. The actuarial survival was 94.9±1.2% and 88.1±2.6%, at 5 and 10 years, respectively. Conclusions Patients' pre-operative co-morbidities and dissection-related complications significantly affect early and late survival and morbidity after surgical treatment of acute type A aortic dissection.

none 24 si Aim We sought to determine whether theoptimal dual antiplatelet therapy (DAPT) duration after drug-eluting stent (DES) placement varies according to clinical presentation. Methods and Results We performed an individual patient data pairwise and network meta-analysis comparing short-term (≤6-months) versus long-term (1-year) DAPT as well as 3-month vs. 6-month vs 1-year DAPT. The primary studyoutcome was the 1- year composite risk of myocardial infarction (MI)or definite/probable stent thrombosis (ST). Six trials were included in which DAPT after DES consisted of aspirin and clopidogrel. Among 11 473 randomized patients 6714 (58.5%) had stable CAD and 4758 (41.5%) presented with acute coronary syndrome (ACS), the majority of whom (67.0%) had unstable angina. In ACS patients, ≤6-month DAPT was associated with non-significantly higher 1-year rates of MIor ST compared with 1-year DAPT (Hazard Ratio (HR) 1.48, 95% Confidence interval (CI) 0.98-2.22; P = 0.059), whereas in stable patients rates of MI and ST were similar between the two DAPT strategies (HR 0.93, 95%CI 0.65-1.35; P=0.71; Pinteraction=0.09). By network meta-analysis, 3-month DAPT, but not 6-month DAPT, was associated with higher rates of MIor ST in ACS, whereas no significant differences were apparent in stable patients. Short DAPT was associated with lower rates of major bleeding compared with 1-year DAPT, irrespective of clinical presentation. All-cause mortality was not significantly different with short vs. long DAPT in both patients with stable CAD and ACS. Conclusions Optimal DAPT duration after DES differs according to clinical presentation. In the present meta-analysis, despite the fact that most enrolled ACS patients were relatively low risk, 3-month DAPT was associated with increased ischaemic risk, whereas 3-month DAPT appeared safe in stable CAD. Prolonged DAPT increases bleeding regardless of clinical presentation. Further study is required to identify theoptimal duration of DAPT after DES in individual patients basedon their relative ischaemic and bleeding risks. Palmerini, Tullio; Della Riva, Diego; Benedetto, Umberto; Bacchi Reggiani, Letizia; Feres, Fausto; Abizaid, Alexandre; Gilard, Martine; Morice, Marie-Claude; Valgimigli, Marco; Hong, Myeong-Ki; Kim, Byeong-Keuk; Jang, Yangsoo; Kim, Hyo-Soo; Park, Kyung Woo; Colombo, Antonio; Chieffo, Alaide; Sangiorgi, Diego; Biondi-Zoccai, Giuseppe; Généreux, Philippe; Angelini, Gianni D.; Pufulete, Maria; White, Jonathon; Bhatt, Deepak L.; Stone, Gregg W Palmerini, Tullio; Della Riva, Diego; Benedetto, Umberto; Bacchi Reggiani, Letizia; Feres, Fausto; Abizaid, Alexandre; Gilard, Martine; Morice, Marie-Claude; Valgimigli, Marco; Hong, Myeong-Ki; Kim, Byeong-Keuk; Jang, Yangsoo; Kim, Hyo-Soo; Park, Kyung Woo; Colombo, Antonio; Chieffo, Alaide; Sangiorgi, Diego; Biondi-Zoccai, Giuseppe; Généreux, Philippe; Angelini, Gianni D.; Pufulete, Maria; White, Jonathon; Bhatt, Deepak L.; Stone, Gregg W