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Resumen Introduccion y objetivos Esta por clarificar el valor pronostico de la troponina T de alta sensibilidad tras una intervencion coronaria percutanea en pacientes con enfermedad coronaria estable. Esta cuestion clinicamente relevante se ha investigado en 3.463 pacientes consecutivos a los que se practico una intervencion coronaria percutanea. Metodos En este estudio se incluyo a pacientes con enfermedad coronaria estable y un valor basal de troponina T de alta sensibilidad menor que el limite superior de referencia del percentil 99 (0,014 μg/l). Se determino la troponina T de alta sensibilidad antes de la intervencion y luego al cabo de 6, 12 y 24 h. El objetivo principal fue la mortalidad por cualquier causa. Resultados Se clasifico a los pacientes en un grupo con un valor maximo de troponina T tras la intervencion ≤ percentil 99 (n = 742), un grupo con un valor maximo de troponina T tras la intervencion entre > percentil 99 y 5 veces el percentil 99 (n = 1.928) y un grupo con un valor maximo de troponina T tras la intervencion > 5 veces el percentil 99 (n = 793). La edad avanzada, el indice de masa corporal mas bajo, el valor de troponina basal, las lesiones complejas, las lesiones en bifurcacion y la longitud del stent se asociaron de manera independiente a concentraciones de troponina T aumentadas despues de la intervencion. La mediana de seguimiento fue de 15,5 meses. Hubo 56 muertes: 5 pacientes (1,7%) con valor maximo de troponina T tras la intervencion ≤ percentil 99, 35 (4,5%) con valor maximo de troponina T tras la intervencion entre > percentil 99 y 5 veces el percentil 99, y 16 (4,3%) del grupo con valor maximo de troponina T tras la intervencion > 5 veces el percentil 99 (hazard ratio = 1,50; intervalo de confianza del 95%, 1,01-2,25; p = 0,047). Tras el ajuste, el valor maximo de troponina T tras el procedimiento no mostro asociacion independiente con la mortalidad tras la intervencion coronaria percutanea (p = 0,094). Conclusiones En los pacientes con enfermedad coronaria estable y sin elevacion basal de la troponina T de alta sensibilidad, la elevacion de esta despues de una intervencion coronaria percutanea no se asocio a mayor mortalidad tras el procedimiento.

Introduction and objectives The prognostic value of high-sensitivity troponin T after percutaneous coronary intervention in patients with stable coronary artery disease is unclear. We investigated this clinically relevant question in 3463 consecutive patients undergoing percutaneous coronary intervention. Methods This study included patients with stable coronary artery disease and baseline high-sensitivity troponin T below the 99th percentile upper reference limit (0.014 μg/L). High-sensitivity troponin T was measured before and at 6, 12 and 24 hours after the procedure. The primary outcome was all-cause mortality. Results Patients were divided into a group with peak postprocedural troponin T ≤ 99th percentile (n = 742), a group with peak postprocedural troponin T > 99th to 5 × 99th percentile (n = 1928), and a group with peak postprocedural troponin T > 5 × 99th percentile upper reference limit (n = 793). Advanced age, smaller body mass index, baseline troponin level, complex lesions, bifurcation lesions and stented length were independently associated with elevated troponin T levels after the procedure. The median follow-up was 15.5 months. There were 56 deaths: 5 deaths (1.7%) among patients with peak postprocedural troponin T ≤ 99th percentile, 35 deaths (4.5%) among patients with peak postprocedural troponin T > 99th to 5 × 99th percentile and 16 deaths (4.3%) among patients with peak postprocedural troponin T > 5 × 99th percentile upper reference limit (hazard ratio = 1.50; 95% confidence interval, 1.01-2.25; P = .047). After adjustment, peak postprocedural troponin T level was not independently associated with mortality after percutaneous coronary intervention ( P = .094). Conclusions In patients with stable coronary artery disease and without elevated baseline high-sensitivity troponin T, elevated high-sensitivity troponin T level after percutaneous coronary intervention was not associated with postprocedural mortality.

Background Patients with ST-segment elevation myocardial infarction (STEMI) undergoing drug-eluting stent (DES) implantation are at increased risk of late adverse events, partly explained by an exaggerated inflammatory reaction to durable-polymer stent coatings. Objectives We sought to investigate whether implantation of polymer-free DES would reduce this risk. Methods In the ISAR-TEST 5 (the Intracoronary Stenting and Angiographic Results: Test Efficacy of Sirolimus- and Probucol- and Zotarolimus-Eluting Stents) trial, patients were randomly allocated to receive a polymer-free sirolimus- and probucol-eluting stent or a new generation durable-polymer zotarolimus-eluting stent. We analyzed late clinical outcomes in the subgroup of patients presenting with STEMI. The primary endpoint was the combined incidence of cardiac death, target vessel-related myocardial infarction or target lesion revascularization at 5 years. Results 311 patients with STEMI were randomized to receive sirolimus- and probucol-eluting stents (n = 215) or zotarolimus-eluting stents (n = 96). At 5 years, there was no difference in the incidence of the primary endpoint in patients treated with sirolimus- and probucol-eluting stents versus zotarolimus-eluting stents (18.3% versus 20.1% respectively, hazard ratio = 0.87, 95% CI, 0.50–1.51; P = 0.62). Rates of the individual components of the primary endpoint were also comparable in both groups. The incidence of definite/probable stent thrombosis was 1.4% versus 1.0% respectively (hazard ratio = 1.35, 95% CI, 0.14–12.94, P = 0.80). Conclusions Long-term outcomes of patients with STEMI treated with polymer-free sirolimus- and probucol-eluting stents versus durable-polymer zotarolimus-eluting stents were similar. Stent thrombosis rates were low and comparable in both treatment groups, with no events beyond 12 months. Clinical Trial Registration: Registered at ClinicalTrials.gov (Identifier NCT 00598533) © 2016 Wiley Periodicals, Inc.

Objectives The aim of this study was to evaluate the late clinical performance of a polymer-free sirolimus- and probucol-eluting stent compared with a new-generation durable polymer-based zotarolimus-eluting stent. Background It was previously shown that polymer-free sirolimus- and probucol-eluting stents were noninferior to zotarolimus-eluting stents at 12 months. However, long-term follow-up of these devices is critical to evaluate late comparative efficacy. Methods In a clinical trial with minimal exclusion criteria, 3,002 patients were randomly assigned to treatment with polymer-free sirolimus- and probucol-eluting stents versus zotarolimus-eluting stents. The primary endpoint was the combined incidence of cardiac death, target vessel–related myocardial infarction, or target lesion revascularization. Results At 5 years, there was no difference in the incidence of the primary endpoint between sirolimus- and probucol-eluting stents and zotarolimus-eluting stents (23.8% vs. 24.2%, respectively; hazard ratio: 0.98; 95% confidence interval: 0.84 to 1.15; p = 0.80). The rates of the individual components of the primary endpoint were also comparable in both groups. The incidence of definite or probable stent thrombosis was low in both groups (1.3% vs. 1.6%, respectively; hazard ratio: 0.86; 95% confidence interval: 0.46 to 1.62; p = 0.64). The rates of any death, myocardial infarction, and revascularization were similar in both groups. Results were consistent across pre-specified subgroups of age, sex, diabetes, and vessel size. Conclusions Long-term outcomes of patients treated with polymer-free sirolimus- and probucol-eluting stents compared with a new-generation durable polymer-based zotarolimus-eluting stent were similar. Rates of stent thrombosis were low and comparable in both treatment groups, with few events beyond 12 months. (Efficacy Study of Rapamycin- vs. Zotarolimus-Eluting Stents to Reduce Coronary Restenosis [ISAR-TEST-5]; NCT00598533 )

We aimed to assess the association between arterial hypertension and bleeding in patients undergoing percutaneous coronary intervention (PCI).The impact of arterial hypertension on bleeding risk of patients with coronary artery disease undergoing PCI is unknown.This study included 14,180 patients who underwent PCI. Bleeding was defined using the Bleeding Academic Research Consortium (BARC) criteria. Arterial hypertension was defined as treatment with antihypertensive drugs or a systolic blood pressure>140 mm Hg and/or diastolic blood pressure value>90 mm Hg documented on at least 2 occasions. The primary outcome was bleeding rate within 30 days of PCI.Overall, 11,066 patients (78.0%) had arterial hypertension. Bleeding events occurred in 1,232 patients with arterial hypertension and 278 patients without arterial hypertension (11.1% vs 8.9%; odds ratio [OR] = 1.28, 95% confidence interval [CI] 1.11-1.46, P< 0.001). Access-site bleeding occurred in 730 patients with arterial hypertension and 175 patients without arterial hypertension (6.6% vs 5.6%: OR = 1.19 [1.01-1.41], P = 0.049). Non-access-site bleeding occurred in 502 patients with and 103 patients without arterial hypertension (4.5% vs 3.3%; OR = 1.39 [1.12-1.72], P = 0.003). After adjustment, arterial hypertension was significantly associated with any bleeding (adjusted OR = 1.41 [1.19-1.67], P< 0.001), access-site bleeding (adjusted OR = 1.36 [1.10-1.68], P = 0.005) and non-access-site bleeding (adjusted OR = 1.42 [1.09-1.83], P = 0.008). A history of arterial hypertension increased the risk of non-access-site bleeding (P = 0.002), whereas systolic blood pressure at the time of PCI increased the risk of access site bleeding (P = 0.018).Arterial hypertension is associated with increased risk of bleeding during PCI procedures. © 2015 Wiley Periodicals, Inc.

SummaryThe DAPT score is a recently-proposed decision tool for guiding optimal duration of dual antiplatelet therapy (DAPT). It showed modest accuracy in prior derivation and validation cohorts of patients with ≥12 months DAPT. This study was aimed to evaluate the validity of the DAPT score in a cohort of patients with 6 or 12 months DAPT after implantation of predominantly second-generation drug-eluting stents. We analyzed data of patients enrolled in the ISAR-SAFE trial. Patients were classified into low (

Patients with ST-segment elevation myocardial infarction (STEMI) undergoing drug-eluting stent (DES) implantation are at increased risk of late adverse events, partly explained by an exaggerated inflammatory reaction to durable-polymer stent coatings.We sought to investigate whether implantation of polymer-free DES would reduce this risk.In the ISAR-TEST 5 (the Intracoronary Stenting and Angiographic Results: Test Efficacy of Sirolimus- and Probucol- and Zotarolimus-Eluting Stents) trial, patients were randomly allocated to receive a polymer-free sirolimus- and probucol-eluting stent or a new generation durable-polymer zotarolimus-eluting stent. We analyzed late clinical outcomes in the subgroup of patients presenting with STEMI. The primary endpoint was the combined incidence of cardiac death, target vessel-related myocardial infarction or target lesion revascularization at 5 years.311 patients with STEMI were randomized to receive sirolimus- and probucol-eluting stents (n = 215) or zotarolimus-eluting stents (n = 96). At 5 years, there was no difference in the incidence of the primary endpoint in patients treated with sirolimus- and probucol-eluting stents versus zotarolimus-eluting stents (18.3% versus 20.1% respectively, hazard ratio = 0.87, 95% CI, 0.50-1.51; P = 0.62). Rates of the individual components of the primary endpoint were also comparable in both groups. The incidence of definite/probable stent thrombosis was 1.4% versus 1.0% respectively (hazard ratio = 1.35, 95% CI, 0.14-12.94, P = 0.80).Long-term outcomes of patients with STEMI treated with polymer-free sirolimus- and probucol-eluting stents versus durable-polymer zotarolimus-eluting stents were similar. Stent thrombosis rates were low and comparable in both treatment groups, with no events beyond 12 months.Registered at ClinicalTrials.gov (Identifier NCT 00598533) © 2016 Wiley Periodicals, Inc.

Although there is increasing evidence that blood-derived macrophages support tumor progression, it is still unclear whether specialized resident macrophages, such as brain microglia, also play a prominent role in metastasis formation. Here, we show that microglia enhance invasion and colonization of brain tissue by breast cancer cells, serving both as active transporters and guiding rails. This is antagonized by inactivation of microglia as well as by the Wnt inhibitor Dickkopf-2. Proinvasive microglia demonstrate altered morphology, but neither upregulation of M2-like cytokines nor differential gene expression. Bacterial lipopolysacharide shifts tumor-educated microglia into a classical M1 phenotype, reduces their proinvasive function, and unmasks inflammatory and Wnt signaling as the most strongly regulated pathways. Histological findings in human brain metastases underline the significance of these results. In conclusion, microglia are critical for the successful colonization of the brain by epithelial cancer cells, suggesting inhibition of proinvasive microglia as a promising antimetastatic strategy. © 2010 Wiley-Liss, Inc.

In patients presenting with acute coronary syndrome (ACS) the optimal duration of dual-antiplatelet therapy after drug-eluting stent (DES) implantation remains unclear. At 6 months after intervention, patients receiving clopidogrel were randomly assigned to either a further 6-month period of placebo or clopidogrel. The primary composite endpoint was death, myocardial infarction, stent thrombosis, stroke, or major bleeding 9 months after randomization. The ISAR-SAFE trial was terminated early due to low event rates and slow recruitment. 1601/4000 (40.0%) patients presented with ACS and were randomized to 6 (n = 794) or 12 months (n = 807) clopidogrel. The primary endpoint occurred in 14 patients (1.8%) receiving 6 months of clopidogrel and 17 patients (2.2%) receiving 12 months; hazard ratio (HR) 0.83, 95% confidence interval (CI) 0.41-1.68, P = 0.60. There were 2 (0.3%) cases of stent thrombosis in each group; HR 1.00, 95% CI 0.14-7.09, P = >0.99. Major bleeding occurred in 3 patients (0.4%) receiving 6 months clopidogrel and 5 (0.6%) receiving 12 months; HR 0.60, 95% CI 0.15-2.49, P = 0.49. There was no significant difference in net clinical outcomes after DES implantation in ACS patients treated with 6 versus 12 months clopidogrel. Ischaemic and bleeding events were low beyond 6-months. ispartof: Scientific Reports vol:6 issue:1 ispartof: location:England status: published

We aimed to assess the association between arterial hypertension and bleeding in patients undergoing percutaneous coronary intervention (PCI).The impact of arterial hypertension on bleeding risk of patients with coronary artery disease undergoing PCI is unknown.This study included 14,180 patients who underwent PCI. Bleeding was defined using the Bleeding Academic Research Consortium (BARC) criteria. Arterial hypertension was defined as treatment with antihypertensive drugs or a systolic blood pressure140 mm Hg and/or diastolic blood pressure value90 mm Hg documented on at least 2 occasions. The primary outcome was bleeding rate within 30 days of PCI.Overall, 11,066 patients (78.0%) had arterial hypertension. Bleeding events occurred in 1,232 patients with arterial hypertension and 278 patients without arterial hypertension (11.1% vs 8.9%; odds ratio [OR] = 1.28, 95% confidence interval [CI] 1.11-1.46, P 0.001). Access-site bleeding occurred in 730 patients with arterial hypertension and 175 patients without arterial hypertension (6.6% vs 5.6%: OR = 1.19 [1.01-1.41], P = 0.049). Non-access-site bleeding occurred in 502 patients with and 103 patients without arterial hypertension (4.5% vs 3.3%; OR = 1.39 [1.12-1.72], P = 0.003). After adjustment, arterial hypertension was significantly associated with any bleeding (adjusted OR = 1.41 [1.19-1.67], P 0.001), access-site bleeding (adjusted OR = 1.36 [1.10-1.68], P = 0.005) and non-access-site bleeding (adjusted OR = 1.42 [1.09-1.83], P = 0.008). A history of arterial hypertension increased the risk of non-access-site bleeding (P = 0.002), whereas systolic blood pressure at the time of PCI increased the risk of access site bleeding (P = 0.018).Arterial hypertension is associated with increased risk of bleeding during PCI procedures. © 2015 Wiley Periodicals, Inc.

Although there is increasing evidence that blood-derived macrophages support tumor progression, it is still unclear whether specialized resident macrophages, such as brain microglia, also play a prominent role in metastasis formation. Here, we show that microglia enhance invasion and colonization of brain tissue by breast cancer cells, serving both as active transporters and guiding rails. This is antagonized by inactivation of microglia as well as by the Wnt inhibitor Dickkopf-2. Proinvasive microglia demonstrate altered morphology, but neither upregulation of M2-like cytokines nor differential gene expression. Bacterial lipopolysacharide shifts tumor-educated microglia into a classical M1 phenotype, reduces their proinvasive function, and unmasks inflammatory and Wnt signaling as the most strongly regulated pathways. Histological findings in human brain metastases underline the significance of these results. In conclusion, microglia are critical for the successful colonization of the brain by epithelial cancer cells, suggesting inhibition of proinvasive microglia as a promising antimetastatic strategy.