Not-high before-treatment platelet reactivity in patients with STEMI: prevalence, clinical characteristics, response to therapy and outcomes.

Platelet reactivity (PR) has been indicated as a pathophysiological key element for ST-Elevation Myocardial Infarction (STEMI) development. Patients with not-high before-treatment platelet reactivity (NHPR) have been poorly studied so far. The aim of this study is to investigate the prevalence, clinical characteristics, response to therapy and outcomes of baseline prior to treatment NHPR among patients with STEMI undergoing primary PCI.We analyzed the data from 358 STEMI patients with assessment of PR by VerifyNow before P2Y12 inhibitor loading dose (LD). Blood samples were obtained at baseline, and after 1 hour, 2 hours, 4-6 hours and 8-12 hours after LD. High platelet reactivity (HPR) was defined as Platelet Reactivity Unit values ≥208, while patients with values <208 at baseline were defined as having NHPR.Overall, 20% patients had NHPR. Age and male gender both resulted independent predictors of NHPR, even after propensity score adjustment. The percentage of inhibition of PR after ticagrelor or prasugrel LD was similar between HPR and NHPR patients at each time point. However, patients with HPR showed worse in-hospital clinical outcomes, and the composite adverse outcome endpoint of death, reinfarction, stroke, acute kidney injury or heart failure was significantly higher (10.0% vs 1.4%; p = .017) as compared with the NHPR group.In conclusion, a significant proportion of patients presenting with STEMI has a baseline NHPR that is associated with better in-hospital outcomes as compared with patients with HPR. Further studies are needed to better elucidate the potential therapeutic implications of NHPR in terms of secondary prevention.

Risk Stratification Using the CHA2DS2-VASc Score in Takotsubo Syndrome: Data From the Takotsubo Italian Network.

BACKGROUND: The CHA2DS2-VASc score predicts stroke in patients with atrial fibrillation and has been reported to have a prognostic role even in acute coronary syndrome patients. The Takotsubo syndrome is a condition that mimics acute coronary syndrome and may present several complications including stroke. We sought to assess the ability of CHA2DS2-VASc score to predict adverse events in Takotsubo syndrome patients. METHODS AND RESULTS: Overall, 371 Takotsubo syndrome patients were enrolled in a prospective registry. Patients were divided into 3 groups according to the CHA2DS2-VASc score: Group A (≤1), B (2-3), and C (≥4). The median CHA2DS2-VASc score was 3 (interquartile range: 2-4). Overall, 9%, 42%, and 49% were included in Group A, B, and C, respectively. Follow-up length was 26±20 months. The mortality rate was 6%, 7%, and 17% in Group A, B, and C, respectively (P=0.011). The stroke rate was 3% and not different among the 3 groups. Estimated major adverse cardiac and cerebrovascular events (the composite of death, myocardial infarction, and stroke) rates in the 3 groups were 6%, 9%, and 17% in Group A, B, and C, respectively (P=0.033). The CHA2DS2-VASc score resulted as a predictor of major adverse cardiac and cerebrovascular events (odds ratio 2.1, 95% confidence interval, 1.2-3.6; P=0.01) and all-cause mortality (odds ratio 1.5, 95% confidence interval, 1.2-1.9; P=0.001). CONCLUSIONS: In Takotsubo syndrome, the CHA2DS2-VASc score allows prediction of cardiovascular events and mortality at long-term follow-up.

APpropriateness Assessment in Antiplatelet THerapY (APATHY) registry: Insight from current clinical practice.

BACKGROUND: In clinical practice there is a gap between guidelines recommendation and antiplatelet strategies used for acute coronary syndrome (ACS). We sought to evaluate appropriateness of antiplatelet strategies employed in a tertiary center. METHODS AND RESULTS: From January to June 2014, 430 ACS were treated with percutaneous coronary intervention by 3 groups of interventional cardiologists. Aspirin and clopidogrel (52%) were the most commonly used antiplatelet therapies, being prasugrel associated with aspirin in 110 (25.5%) and ticagrelor in 97 (22.5%) ACS. Inappropriate use of prasugrel (Tia/Ictus) was found in 2 (1.8%) patients and not recommended use (>75years, without diabetes or previous myocardial infarction) in 11 (10%). Not recommended use of ticagrelor (plus warfarin) was found in 4 (4.4%). Switching from clopidogrel to prasugrel occurred in 29% [28 showing high residual platelet reactivity (HRPR: ADP 10µmol>70%), and 4 left main stenting], while from clopidogrel to ticagrelor occurred in 13.4% (all showing HRPR, but 1). The most powerful predictor for prescription of 3rd generation P2Y12 inhibitors was the HRPR (OR 5.473, 95%CI 2.41-12.43, p<0.0001), whereas the behavior of attending cardiologist (HR 0.674, 95%CI 0.573-0.847, p=0.001) and the older age reduced the probability of receiving it (OR0.963, 95%CI 0.943-0.984, p=0.001). CONCLUSIONS: Clopidogrel remained the most common P2Y12 inhibitor employed for ACS. Third generation P2Y12 inhibitor prescription was lower than the one expected by guidelines recommendations, and the switching was largely based on clopidogrel HRPR. These findings suggest the need for a greater effort to improve adherence of cardiology community to current guidelines.

Impact of anticoagulation strategy with bivalirudin or heparin on nonaccess site bleeding in percutaneous coronary interventions: A meta-analysis of randomized trials.

BACKGROUND: Transradial approach has significantly decreased the rate of access site bleeding in patients undergoing percutaneous coronary interventions (PCI), therefore potentially mitigating the benefits offered by bivalirudin in lowering major bleeding complications as compared to heparin. However, nonaccess site bleeding, that represent the majority of hemorrhagic complications, still carry negative prognostic consequences for these patients and no study has so far defined the exact impact of bivalirudin on nonaccess site bleeding, that was therefore the aim of present meta-analysis. METHODS AND STUDY OUTCOMES: Literature archives (Pubmed, EMBASE, Cochrane) and main scientific sessions were scanned comparing bivalirudin vs. heparin in patients undergoing PCI. Primary endpoint was the occurrence of nonaccess site bleeding within 30 days. Secondary endpoints were 30 days mortality and the occurrence of access-site bleeding. RESULTS: A total of nine randomized clinical trials were finally included, involving 32,587 patients, 55.8% randomized to bivalirudin. Bivalirudin significantly reduced the rate of nonaccess site bleeding (2.6 vs. 3.8%, OR [95% CI] = 0.68 [0.60-0.77], P < 0.00001, Phet = 0.10). However, the reduction of hemorrhagic events was more pronounced when bivalirudin was compared to heparin plus glycoprotein IIbIIIa inhibitors than when it was compared to heparin alone (r = -0.01 (-0.02; -0.001), P = 0.02). Similar results were observed for access-site bleeding (OR [95% CI] = 0.67 [0.57-0.79], P < 0.000001, Phet = 0.10), with a significant role of glycoprotein IIbIIIa inhibitors use (r = -0.02 (-0.04; -0.004), P = 0.017). Moreover, the observed benefits in hemorrhagic complications did not translate into mortality benefits (OR [95% CI] = 0.89 [0.76-1.05], P = 0.18; Phet = 0.12; r = 0.21 (-1.12; 1.53), P = 0.76). CONCLUSIONS: The present meta-analysis shows that bivalirudin can provide a significant reduction of both access and nonaccess site bleeding in patients undergoing PCI. However, these hemorrhagic benefits did not impact on survival, and moreover, were significantly conditioned by the association of heparin with potent antithrombotic strategies, such as glycoprotein IIbIIIa inhibitors, rather than by heparin or bivalirudin alone. Therefore, we could not provide any clinical evidence for the routine use of bivalirudin as preferred anticoagulation strategy for PCI. © 2017 Wiley Periodicals, Inc.

Early changes of left ventricular filling pattern after reperfused ST-elevation myocardial infarction and doxycycline therapy: Insights from the TIPTOP trial.

AIM: Metalloproteinases inhibition by doxycycline reduces cardiac protein degradation at extracellular and intracellular level in the experimental model ischemia/reperfusion injury. Since both extracellular cardiac matrix and titin filaments inside the cardiomyocyte are responsible for the myocardial stiffness, we hypothesized that doxycycline could favorably act on left ventricular (LV) filling pressures in patients after reperfused acute ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS: Seventy-three of 110 patients of the TIPTOP trial underwent a 2D-Echo-Doppler on admission, and at pre-discharge and at 6-month after a primary PCI for STEMI and LV dysfunction. From admission to pre-discharge, LV filling changed from a high filling pressure (HFP) to a normal filling pressure (NFP) pattern in 91% of the doxycycline-group, and in 67% of the control-group. Conversely, 1% of the doxycycline-group, and 37% of the control-group changed the LV filling from NFP to HFP pattern. Overall, a pre-discharge HFP pattern was present in 4 patients (11%) of the doxycycline-group and in 13 patients (36%) of the control-group (p=0.025). The evaluation of metalloproteinases and their tissue inhibitors plasma concentrations provide possible favorable action of doxycycline. On the multivariate analyses, troponine I peak (p=0.026), doxycycline (p=0.033), and on admission to pre-discharge LVEF changes (p=0.044) were found to be associated with pre-discharge HFP pattern. Independently of their baseline LV filling behavior, the 6-month remodeling was less in patients with pre-discharge NFP pattern than in patients with HFP pattern. CONCLUSIONS: In patients with STEMI and LV dysfunction doxycycline can favorably modulate the LV filling pattern early after primary PCI.

Clinical events beyond one year after an acute coronary syndrome: insights from the RECLOSE 2-ACS study.

AIMS: The optimal duration of dual antiplatelet therapy after an acute coronary syndrome (ACS) is still unknown and debated. We sought to assess the incidence of adverse clinical events beyond 12 months after an ACS in patients treated by percutaneous coronary intervention (PCI) and clopidogrel. METHODS AND RESULTS: Among 1,592 consecutive ACS patients treated by PCI enrolled in the RECLOSE 2-ACS study and without event within one year, 1,310 (82%) patients presented at least one risk factor such as age ≥65 years, diabetes, prior myocardial infarction (MI), chronic kidney disease and multivessel coronary disease. The primary endpoint rate (the composite of cardiac death, MI, stroke and any urgent coronary revascularisation) was 3.7% per year after the first 12 months. The adverse event rate beyond 12 months was higher in patients with at least one risk factor as compared with patients without (8.1% vs. 1.8%, p<0.001). Each additional risk factor was associated with a relative risk for long-term adverse events of 1.66 (95% CI: 1.41-1.96; p=0.0001). Independent predictors of late events were age ≥65 years (OR 2.11, 95% CI: 1.38-3.37, p=0.002), insulin-treated diabetes mellitus (OR 2.29, 95% CI: 1.41-3.71, p=0.001), chronic kidney disease (OR 1.93, 95% CI: 1.21-3.09, p=0.006), prior MI (OR 2.71, 95% CI: 1.85-3.97, p=0.0001), and multivessel coronary disease (OR 1.53, 95% CI: 1.18-1.97, p=0.01). CONCLUSIONS: Patients at risk of adverse events beyond 12 months after an ACS may be identified by simple clinical and angiographic characteristics such as age, diabetes, chronic kidney disease, prior MI and multivessel CAD. The risk of adverse events progressively increases with the number of these high-risk features.

Bleeding events and maintenance dose of prasugrel: BLESS pilot study.

OBJECTIVE: To evaluate changes in residual platelet reactivity (RPR) over time, and bleeding and ischaemic events rate using 5 vs 10 mg maintenance dose (MD) regimens of prasugrel 1 month after acute coronary syndrome (ACS). BACKGROUND: The optimal level of RPR with prasugrel may change over time after an ACS. METHODS: After 60 mg loading dose of prasugrel (T0) followed by 10 mg/day for 1 month, patients were randomised to receive prasugrel 10 mg/day (n=95, group A) or 5 mg/day MD (n=98, group B) up to 1 year. RPR was assessed at T0, 37 (T1) and 180 days (T2). The primary end point was Bleeding Academic Research Consortium (BARC) bleeding events ≥2 between 1 and 12 months, and the secondary composite end point was cardiac death, myocardial infarction, stroke and definite/probable stent thrombosis. RESULTS: From T0 to T1, RPR significantly increased in both groups A and B and the increase was higher for group B (δ ADP 10 µmol: 13.8%±14.7% vs 23.5%±19.2%, p=0.001). At T2 a lower rate of high RPR patients were found in group A (2.6% vs13.3%; p=0.014). The BARC type ≥2 bleeding occurred in 12.6% of group A versus 4.1% of group B (OR 0.29, 95% CI 0.09 to 0.94) and secondary end point in 2.1% vs 1.0% (p=0.542), respectively, without stent thrombosis. CONCLUSIONS: RPR increases shifting from 60 mg loading dose to 10 mg/day prasugrel MD with a further increase of RPR reducing prasugrel MD to 5 mg 1 month after ACS. Clinical value of these pharmacodynamic findings should be proved in larger clinical trials. TRIAL REGISTRATION NUMBER: NCT01790854.

Prevalence of thrombophilic disorders in takotsubo patients: the (ThROmbophylia in TAkotsubo cardiomyopathy) TROTA study.

Takotsubo cardiomyopathy (TTC) pathophysiology is still unclear. A transient intracoronary thrombosis dissolved at the time of angiography has been hypothesized. We aimed to evaluate the prevalence of thrombophilic disorders in TTC patients. In 75 TTC women, 75 age- and sex-matched acute coronary syndrome (ACS) patients, both enrolled during the acute phase, and in 75 control subjects, we compared the prevalence of congenital and acquired thrombophilic alterations and the values of clotting and endothelial activation biomarkers. Some parameters were re-assessed 1 month after the acute phase in TTC patients. No significant difference between the three groups was observed in factor II (G20210A) and V (G1691A) polymorphisms prevalence. Homocysteine levels were significantly higher in ACS patients vs. TTC and control subjects. Lipoprotein(a) values trended to be higher in TTC patients vs. control subjects, though not significantly. Other thrombophilic alterations in TTC patients were similar to that previously reported in healthy women. Von Willebrand factor and plasminogen activator inhibitor-1 were significantly higher in TTC and in ACS patients than controls. Clotting activation biomarkers were not statistically different between TTC patients and controls. During follow-up, in TTC patients, endothelial damage indices significantly decreased while clotting activation biomarkers remained unchanged. In conclusion, our results, showing a rate of thrombophilic alterations in TTC patients similar to control subjects, do not support the transient intracoronary thrombus hypothesis. However, several endothelial damage markers and lipoprotein(a) were higher in TTC patients vs. controls suggesting a role of endothelial dysfunction and of other factors concurring to hyperviscosity, as recently hypothesized.

Morphine is associated with a delayed activity of oral antiplatelet agents in patients with ST-elevation acute myocardial infarction undergoing primary percutaneous coronary intervention.

BACKGROUND: Morphine is recommended in patients with ST-segment-elevation myocardial infarction, including those undergoing primary percutaneous coronary intervention. Suboptimal antiplatelet effect during and after primary percutaneous coronary intervention is associated with increased thrombotic complications. It was hypothesized a potential drug-drug interaction between morphine and antiplatelet agents. We sought to assess platelet inhibition after a loading dose of the currently recommended antiplatelet agents in ST-segment-elevation myocardial infarction patients according to morphine use. METHODS AND RESULTS: Three hundred patients undergoing primary percutaneous coronary intervention receiving either prasugrel (n = 95) or ticagrelor (n = 205) loading dose had platelet reactivity assessed by VerifyNow 1, 2, and 4 hours after loading dose. Patients treated with morphine (n = 95; 32%) had a higher incidence of vomit (15% versus 2%; P = 0.001). P2Y12 reactivity units 2 hours after the loading dose was 187 (153-221) and 133 (102-165) in patient with and without morphine (P < 0.001); the difference persisted after excluding patients with vomit (P < 0.0001). High residual platelet reactivity (P2Y12 reactivity units ≥ 208) at 2 hours was found in 53% and 29% patients with and without morphine (P < 0.001) and without difference between prasugrel and ticagrelor patients. The independent predictors of high residual platelet reactivity at 2 hours were morphine use (odds ratio, 2.91 [1.71-4.97]; P < 0.0001) and age (odds ratio, 1.03 [1.01-1.05]; P = 0.010). Morphine remained associated with high residual platelet reactivity after propensity score adjustment (c-statistic, 0.68; 95% confidence interval, 0.66-0.70; P = 0.879 for Hosmer-Lemeshow test). CONCLUSIONS: In patients with ST-segment-elevation myocardial infarction, morphine use is associated with a delayed onset of action of the oral antiplatelet agents. This association persisted after adjusting for the propensity to receive morphine and after excluding patients with vomit.

Diagnosis and Evaluation of Stent Thrombosis with Optical Coherence Tomography.

Stent thrombosis (ST) is a rare complication of percutaneous coronary interventions (PCI), especially with drug-eluting stents. ST presents as acute myocardial infarction requiring emergent repeat PCI; optimal reperfusion occurs in two-thirds of patients. As a result, ST has been associated with a high mortality rate and a high rate of recurrent thrombosis. We discuss the use of optical coherence tomography (OCT) for the diagnosis and evaluation of ST. OCT-guided ST management seems a feasible, safe, and appropriate approach. Intracoronary assesses the efficacy of coronary thrombus removal procedures and detects the prevalent stent-related factor that caused ST.

Effect of diabetes on scintigraphic infarct size in STEMI patients undergoing primary angioplasty.

BACKGROUND: It has been shown that among patients with ST-segment elevation myocardial infarction (STEMI), diabetes is associated with a significantly higher mortality, mainly because of impaired reperfusion. However, few data have been reported so far on infarct size as evaluated by well-refined techniques, such as nuclear imaging techniques. Therefore, the aim of the current study was to investigate the effect of diabetes in infarct size as evaluated by myocardial scintigraphy in a large cohort of STEMI patients undergoing primary PCI. METHODS: We included 830 STEMI patients undergoing primary PCI. Infarct size was evaluated at 30 days by technetium-99 m-sestamibi. A logistic regression analysis was performed to determine the relation between diabetes and infarct size (as above the median) after correction for baseline confounding factors. RESULTS: A total of 115 (13.8%) out of 830 patients suffered from diabetes. Diabetic patients were older (p < 0.001), with larger prevalence of female gender (p = 0.006) and hypertension (p = 0.001) but were less often smokers (p = 0.003). Diabetic patients had more often preprocedural thrombolysis in myocardial infarction grade 3 flow (p = 0.034) and less complete ST-segment resolution (p = 0.009). No difference was observed in scintigraphic infarct size between diabetes and control patients (p = 0.6)), which was confirmed at multivariate analysis after correction for baseline confounding factors (Adjusted OR [95% CI] = 0.87 [0.57-1.31, p = 0.51). CONCLUSION: Our study showed that among STEMI patients undergoing primary angioplasty, diabetes did not affect infarct size as compared with non-diabetic patients.

Residual platelet reactivity and outcomes with 5 mg prasugrel therapy in elderly patients undergoing percutaneous coronary intervention.

BACKGROUND: In acute coronary syndrome (ACS) patients older than 75 years old, prasugrel 10 mg maintenance therapy has shown less clinical efficacy and higher risk of bleeding. In patients older than 75 years, a prasugrel dose of 5 mg should be used if treatment is deemed necessary. OBJECTIVE: The aim of this study was to compare platelet reactivity and outcomes in elderly patients receiving prasugrel 5mg therapy with non-elderly patients receiving prasugrel 10 mg therapy. METHODS AND RESULTS: Consecutive ACS patients undergoing percutaneous coronary intervention (PCI) treated with prasugrel were included. Of 718 patients, 228 (32%) had ≥75 years and received prasugrel 5 mg/day. Residual platelet reactivity (RPR) was 47±18% and 36±16% in the elderly and non-elderly group, respectively (p=0.001). High RPR (≥70%) was found in 9% and 2% (p=0.0001) in elderly and non-elderly patients, respectively. In the 6-month follow-up, there was no difference in mortality, stent thrombosis, and reinfarction rates between the 2 groups but a higher rate of TIMI minor bleeding (7.9% vs 2.4%; p=0.001) in elderly as compared with younger patients. Age≥75 years was independently associated with bleeding events (HR 2.162 [1.105-4.229]; p=0.024). CONCLUSIONS: Elderly patients receiving prasugrel 5mg are more likely to experience high RPR than younger patients treated by prasugrel 10 mg. Despite the use of a reduced prasugrel maintenance dose and a higher level of RPR, elderly patients show increased risk of bleeding during prasugrel therapy as compared to younger patients.

Comparison of double (360 mg) ticagrelor loading dose with standard (60 mg) prasugrel loading dose in ST-elevation myocardial infarction patients: the Rapid Activity of Platelet Inhibitor Drugs (RAPID) primary PCI 2 study.

UNLABELLED: In ST-elevation myocardial infarction (STEMI) patients, residual platelet reactivity soon after a loading dose (LD) of prasugrel or ticagrelor is higher than that reported for healthy volunteers or subjects with stable coronary artery disease; and the majority of primary percutaneous coronary intervention (PPCI) procedures with bivalirudin monotherapy are performed without proper platelet inhibition. However, ticagrelor LD is just the daily dose, whereas prasugrel LD is 6-fold the long-term daily dose. We hypothesized that an increased ticagrelor LD may result in a faster and more effective platelet inhibition as compared with the standard prasugrel LD. METHODS: Fifty patients with STEMI, pretreated with intravenous aspirin, undergoing PPCI were randomized to receive prasugrel 60-mg LD (n = 25) or ticagrelor 360-mg LD (n = 25). Residual platelet reactivity was assessed by VerifyNow at baseline and 1, 2, 4, and 12 hours after drug LD. RESULTS: At the time of LD, 90% of enrolled patients had an aspirin reactivity unit value <550. P2Y12 reaction units 1 hour after the LD (study primary end point) were 236 (129-289) and 248 (115-304) in the prasugrel and ticagrelor group, respectively (P = .899). High residual platelet reactivity (P2Y12 reaction units ≥240) was found in 43% and 56% of patients (P = .386) at 1 hour and in 30% and 32% of patients (P = .907) at 2 hours, respectively. There was no significant difference in bleeding, arrhythmias, or dyspnea episodes in the 2 groups. CONCLUSIONS: In patients with STEMI undergoing PPCI, double (360 mg) ticagrelor LD failed to achieve a faster and more intense platelet inhibition as compared with the standard prasugrel LD. Intravenously administered aspirin allowed to achieve a very early inhibition of acid arachidonic pathway.

Impact of multivessel disease on infarct size among STEMI patients undergoing primary angioplasty.

BACKGROUND: Although primary angioplasty achieves Thrombolysis In Myocardial Infarction (TIMI) 3 flow in most patients with ST-elevation myocardial infarction, epicardial recanalization does not guarantee optimal perfusion in a large proportion of patients. Multivessel disease has been demonstrated to be associated with impaired survival, however its impact on infarct size has not been largely investigated, that therefore is the aim of the current study. METHODS: Our population is represented by 827 STEMI patients undergoing primary PCI. Infarct size was evaluated at 30 days by technetium-99m-sestamibi. RESULTS: Multivessel disease was observed in 343 patients (41.5%). It was associated with older age (65 [57-74] vs 63 [53-71], p < 0.001), higher rate of previous MI (6.4% vs 2.5%, p = 0.005), longer ischemia time evaluated as continuous variable (210 [155-280] min vs 196 [145-270] min, p = 0.065) or percentage of patients with ischemia time >3 h (63.7% vs 56.4%, p = 0.038), and a trend in more cardiogenic shock (5.5% vs 2.9%, p = 0.055). Patients with multivessel disease received more often Abciximab (92.1% vs 88.4%, p < 0.001), Intra-aortic balloon pump (6.4% vs 1.9%, p < 0.001). No differences were observed in other clinical or angiographic characteristics. In particular, multivessel disease did not affect the rate of postprocedural TIMI 3 flow (90.9% vs 93.4%, p = 0.18) and ST-segment resolution (52.4% vs 54.9%, p = 0.48). Multivessel disease did not affect infarct size (12.7% [4.5%-24.9%] vs 12.3% [4%-24.1%], p = 0.58). Similar results were observed in subanalyses without any significant interaction for each variable (anterior infarct location (p int = 0.23), gender (p int = 0.9), age (p int = 0.7), diabetes (p int = 0.15)). The absence of any impact of multivessel disease on infarct size was confirmed when the analysis was conducted according to the percentage of patients with infarct size above the median, even after correction for baseline characteristics, such as age, previous MI, ischemia time, use of Gp IIb-IIIa inhibitors, cardiogenic shock, ischemia time (OR [95% CI] = 1.09 [0.82-1.45], p = 0.58). CONCLUSIONS: This study shows that among STEMI patients undergoing primary PCI multivessel disease does not affect infarct size.

Switching from clopidogrel to prasugrel in patients having coronary stent implantation.

There are very few clinical data concerning the safety of switching from clopidogrel to prasugrel in patients undergoing coronary stenting. However, in the daily activity, clinicians face the decision of switching patients at high-risk of thrombotic events from clopidogrel to prasugrel. Thus, we sought to evaluate clinical events in patients undergoing coronary stent implantation and prasugrel therapy with (SWITCH group) or without (NAÏVE group) prior clopidogrel therapy. A total of 454 patients with stable or unstable coronary artery disease, aged 70 ± 10 years, underwent non-emergent stent implantation and received prasugrel therapy. Of these, 315 (69 %) patients received clopidogrel before switching to prasugrel therapy. In 239 patients with high residual platelet reactivity (HRPR) on clopidogrel, prasugrel decreased platelet aggregation from 72 ± 11 to 43 ± 16 % (p < 0.001). There was no difference in in-hospital major or minor TIMI bleeding (2.8 vs. 4.3 %; p = 0.411) between the SWITCH and NAÏVE groups as well as in mortality, acute stent thrombosis, reinfarction and stroke rates. At multivariable analysis, independent predictors of bleeding were female gender (OR 5.56 [1.41-19.88] p = 0.014) and chronic renal failure (OR 6.27 [1.59-21.65] p = 0.009), but switching therapy did not. This result was confirmed after switching propensity score adjustment (c-statistic 0.81; Hosmer-Lemeshow test p = 860). Switching from clopidogrel to prasugrel in patients undergoing non-emergent coronary stent implantation seems to be tolerated with no overt signs of increased bleeding.

Smoking and infarct size among STEMI patients undergoing primary angioplasty.

BACKGROUND: Prior studies have found that smokers with STEMI have lower mortality rates and a more favorable response to fibrinolytic therapy than nonsmokers, phenomenon defined as "the smoker's paradox". Still poorly explored is the impact of cigarette smoking in patients undergoing primary percutaneous coronary intervention. Aim of the current study was to evaluate the impact of cigarette smoking on scintigraphic infarct size in STEMI patients undergoing primary PCI. METHODS: Our population is represented by 830 STEMI patients undergoing primary PCI. Infarct size was evaluated at 30 days by technetium-99m-sestamibi. RESULTS: Smoking was associated with younger age (p < 0.001), a lower prevalence of female gender (p < 0.001), hypertension (p < 0.001), diabetes (p = 0.003), shorter ischemia time (p = 0.037), but higher rates of previous PCI (p = 0.016). No differences were observed in other clinical or angiographic characteristics. In particular, smoking did not affect the rate of postprocedural TIMI 3 flow. As shown in Fig. 1, smoking did not affect infarct size (12.5% [3.3%-23.7%] vs 12.7% [4.9%-25.9%], p = 0.12). Similar results were observed in subanalyses according to infarct location (anterior STEMI, p int = 0.33), gender (p int = 0.95) age, (p Int = 0.96), diabetes (p int = 0.85). The absence of any impact of smoking on infarct size was confirmed after correction for baseline characteristics, such as age, gender, hypertension, diabetes, previous PCI, ischemia time (OR [95% CI] = 0.80 [0.59-1.09], p = 0.15). CONCLUSIONS: This study shows that among STEMI patients undergoing primary PCI smoking status does not affect infarct size.