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Background The appropriate timing to administer antithrombotic therapies in ST-elevation myocardial infarction (STEMI) remains uncertain. This study aims to evaluate the role of antithrombotic therapy administration at first medical contact (FMC) compared with the administration in the Cathlab. Methods We conducted a "before-after" observational study enrolling STEMI undergoing primary percutaneous coronary intervention (PCI). Outcomes were evaluated during two successive periods, before (control group: aspirin only at FMC) and after (pretreated intervention group: heparin, aspirin plus ticagrelor at FMC) the introduction of a new regional pretreatment protocol. Results A total of 537 consecutive patients (300 in control vs. 237 in intervention group) were enrolled. The pretreated compared with no pretreated population showed better basal reperfusion, expressed as basal Thrombolysis in Myocardial Infarction (TIMI)-flow (p for trend p < 0.001). Pretreated population showed lower frequency of TIMI 0 (56.5% vs. 73.7%, odds ratio [OR]: 0.46, 95% confidence interval [CI]: 0.32-0.67, p < 0.001) and higher frequency of TIMI 2-3 (33.3% vs. 19.3% OR: 2.0, 95% CI: 1.38-2.00, p < 0.001) and TIMI 3 (14.3% vs. 9.7%, OR: 1.56, 95% CI: (0.92-2.65), p = 0.094). Pretreated compared with no pretreated population showed reduced infarct size expressed as Troponin Peak (20,286 (8726-75,027) versus 48,676 (17,229-113,900), p = 0.001), and higher left ventricular ejection fraction at discharge (53% (44-59) vs. 50% (44-56), p = 0.027). In-hospital BARC >= 2 bleeding were similar (2.1% vs. 2.0%, p = 0.929, in pretreated versus no pretreated population, respectively). Conclusion This study provides support for an early pretreatment strategy in STEMI patients and confirmed the importance of an efficient organization of STEMI networks which allow initiation of antithrombotic treatment at FMC.

Antithrombotic therapy is the cornerstone of pharmacological treatment in patients undergoing primary percutaneous coronary intervention (PCI). However, the acute management of ST elevation myocardial infarction (STEMI) patients includes therapy for pain relief and potential additional strategies for cardioprotection. The safety and efficacy of some commonly used treatments have been questioned by recent evidence. Indeed a concern about morphine use is the interaction between opioids and oral P2Y(12) inhibitors; early beta-blocker treatment has shown conflicting results for the improvement of clinical outcomes; and supplemental oxygen therapy lacks benefit in patients without hypoxia and may be of potential harm. Other additional strategies remain disappointing; however, some treatments may be selectively used. Therefore, we intend to present a critical updated review of complementary pharmacotherapy for a modern treatment approach for STEMI patients undergoing primary PCI.

Early recanalization of the infarct-related artery to achieve myocardial reperfusion is the primary therapeutic goal in patients with ST-elevation myocardial infarction (STEMI). To decrease the duration of ischaemia, continuous efforts have been made to improve pre-hospital treatment and to target the early period after symptom onset. In this period the platelet content of the fresh coronary thrombus is maximal and the thrombi are dynamic, and thus more susceptible to powerful antiplatelet agents. There have been substantial advances in antiplatelet therapy in the last three decades with several classes of oral and intravenous antiplatelet agents with different therapeutic targets, pharmacokinetics, and pharmacodynamic properties. New parenteral drugs achieve immediate inhibition of platelet aggregation, and fast and easy methods of administration may create the opportunity to bridge the initial gap in platelet inhibition observed with oral P2Y12 inhibitors. Moreover, potential future management of STEMI could directly involve patients in the process of care with self-administered antiplatelet agents designed to achieve rapid reperfusion. However, the potential anti-ischaemic benefits of potent antiplatelet agents will need to be balanced against their risk of increased bleeding. This study presents a comprehensive and updated review of pre-hospital antiplatelet therapy among STEMI patients undergoing primary percutaneous intervention and explores new therapies under development.

We thank Fernández–Fernández et al. for their interest in our manuscript and for raising the question about the potential use of midodrine in patients with decompensated and worsening chronic heart failure.

Aims: To evaluate the prevalence and predictors of persistent sinus rhythm in a recent cohort of unselected patients undergoing electrical cardioversion for atrial fibrillation. Methods: We enrolled all consecutive patients undergoing elective electrical cardioversion for atrial fibrillation between January 2017 and December 2018. We analysed baseline clinical and echocardiographic data as well as pharmacological antiarrhythmic therapy. Primary endpoint was the maintenance of sinus rhythm at 12 months after electrical cardioversion. Results: Of the 300 patients enrolled, 270 (90%) had successful electrical cardioversion and among them, 201 patients have 12-month follow-up data (mean age 70 ± 10 years; 74% men). At 12 months, only 45.7% were in sinus rhythm. Patients without sinus rhythm compared with persistent sinus rhythm at 12 months had a lower baseline left ventricle ejection fraction (LVEF) (49.1 ± 16 vs. 59.7 ± 9%, P = 0.02) and had more frequently a history of atrial fibrillation more than 12 months (55 vs. 34% P = 0.003). At the multivariate analysis, only the duration of the disease beyond 12 months (OR 0.26, 95% CI: 0.08-0.88, P = 0.032), LVEF (OR 1.06, 95% CI: 1.01-1.12, P = 0.012) and the presence of sinus rhythm at 1-month follow-up (OR 18.28, 95% CI: 3.3-100, P = 0.001) were associated with the probability of maintaining sinus rhythm at 12 months. Conclusion: In unselected patients with atrial fibrillation undergoing elective electrical cardioversion, only 45.7% were in sinus rhythm at 12 months. The presence of sinus rhythm at 1-month follow-up emerged as an independent predictor of maintenance of sinus rhythm. This highlights that early re-evaluation of these patients appears useful for assessing longer term outcomes also from the perspective of a possible selective approach to ablation strategies.

The historical classification of heart failure (HF) has considered two distinct subgroups, HF with reduced ejection fraction (HFrEF), generally classified as EF below 40%, and HF with preserved ejection fraction (HFpEF) variably classified as EF above 40%, 45% or 50%. One of the principal reasons behind this distinction was related to presence of effective therapy in HFrEF, but not in HFpEF. Recently the expanding knowledge in the specific subgroup of patient with a LVEF between 41% and 49% and the potential benefit of new therapies and of those used in patients with LVEF below 40%, has led to rename this group as HF with mildly reduced EF (HFmrEF). In this review we discuss the reasons behind this modification, we summarize the main characteristics of HFmrEF the similarities and differences with the two other EF categories, and finally we provide a comprehensive overview of the current available evidence supporting the treatment of patients with HFmrEF.

Our understanding of the pathophysiology of acute coronary syndrome and of the vascular biology of coronary atherosclerosis has made enormous progress with the implementation of intravascular imaging. Intravascular imaging contributes to overcoming the known limitations of coronary angiography and allows for the in vivo discrimination of plaque morphology giving insight into the underlying pathology of the disease process. The possibility of using intracoronary imaging to characterize lesion morphologies and correlate them with clinical presentations may influence the treatment of patients and improve risk stratification, offering the opportunity for tailored management. This review examines the current role of intravascular imaging and describes how intracoronary imaging represents a valuable tool for modern interventional cardiology in order to improve diagnostic accuracy and offer a tailored approach to the treatment of patients with coronary artery disease, especially in the acute setting.

Background and aims: The optimal duration of dual antiplatelet therapy (DAPT) after myocardial infarction (MI) in patients treated with second-generation drug-eluting stent (DES) is unclear, therefore, we aim to evaluate the ischemic and bleeding risk according to DAPT duration using a pooled-analysis of two randomized trials. Methods: MI patients treated with durable-polymer second-generation DES from two randomized trials, SMART-DATE and DAPT-STEMI, were pooled. The primary endpoint was a composite of net adverse clinical events (NACEs) defined by all-cause mortality, any MI, stroke and BARC 3-5 bleeding, between 6 and 18 months after index percutaneous coronary intervention. Results: A total of 2016 patients were analyzed, 1014 were treated with 6-month DAPT versus 1002 patients with ≥12-month DAPT duration. The primary endpoint occurred in 2.7% vs 2.5% (HR 1.07; 95%CI 0.62–1.85, p = 0.80) of cases, in 6 vs ≥ 12-month DAPT, respectively. The composite of cardiac death, MI and stroke was similar (2% vs 1.6%, HR 1.24, 95%CI 0.65–2.4, p = 0.52). BARC 3-5 bleeding occurred more frequently in the ≥12-month DAPT (0.2% vs 0.9%, HR 0.22, 95%CI 0.05–1.02 p = 0.05, log rank p = 0.03). MI occurred more frequently in the 6-month DAPT (1.6% vs 0.6%, HR 2.66, 95%CI 1.04–6.79, p = 0.04). Stent thrombosis was similar in both arms (0.7% vs 0.5%, p = 0.26). Conclusions: Six vs ≥ 12-month DAPT, followed by aspirin alone, resulted in comparable NACEs in patients with event-free MI at six months after durable-polymer DES implantation. However, single therapy with aspirin beyond the 6 months reduced bleeding rates but was associated with a higher rate of MI compared to ≥12-month DAPT.

OBJECTIVES: To investigate the potential association between early tirofiban treatment and N-terminal pro-B-type natriuretic peptide (NT-proBNP) level after primary percutaneous coronary intervention (PCI). BACKGROUND: Whether the use of adjunctive early glycoprotein IIb/IIIa inhibitors (GPIs) therapy, may affect the level of NT-proBNP after primary PCI is poorly studied. METHODS: Nine hundred and eighty four ST-elevation myocardial infarction (STEMI) patients undergoing primary PCI were randomized to either pre-hospital tirofiban administration or placebo. NT-proBNP levels were evaluated on admission before angiography (baseline) and 18-96 hr after PCI. RESULTS: There were 918 (93.3%) patients with NT-proBNP values available at baseline and 865 (87.9%) post-PCI. Post-PCI NT-proBNP level dichotomized with median value as cut-off (968.8 pg/mL, IQR 430.9-1970.0) was significantly lower in patients treated with early tirofiban as compared to placebo (45.5% vs. 54.2% P = 0.011). At multivariate logistic regression analysis, independent predictors of post-PCI NT-proBNP level above the median were: NT-proBNP baseline level (OR 5.19; 95% CI, 2.92-9.25, P I (OR 4.07; 95% CI 1.24-13.36, P = 0.021), anterior infarct location (OR 2.61; 95% CI 1.84-3.70, P

Latest statements from European and American societies recommend to rule out viral presence in endomyocardial biopsy (EMB) via polymerase chain reaction (PCR) analysis before starting immunosuppression or immunomodulation in acute lymphocytic myocarditis presenting with life-threatening scenarios. However, recommendations in myocarditis are mostly based on heterogeneous studies enrolling patients with inflammatory cardiomyopathies and established heart failure rather than acute myocarditis. Thus, definitive evidence of a survival benefit from immunomodulation guided by viral presence is currently lacking. Finally, distinguishing innocent bystanders from causative agents among EMB-detected viruses remain challenging and a major goal to achieve in the near future. Therefore, considerable divergence remains between official recommendations and clinical practice, including the possibility of starting immunosuppressive therapy empirically, without knowing viral PCR results. This review systematically discusses the unsolved issues of immunomodulation guided by viral presence in acute lymphocytic myocarditis, namely (i) virus epidemiology and prognosis, (ii) variability of viral presence rates, (iii) the role of potential viral bystander findings, and (iv) the main results of immunosuppression controlled trials in lymphocytic myocarditis. Furthermore, a practical approach for the critical use of viral presence analysis in guiding immunomodulation is provided, highlighting its importance before starting immunosuppression or immunomodulation. Future, multicentre studies are needed to address specific scenarios such as fulminant lymphocytic myocarditis and a virus-tailored management as for parvovirus B19.

Objective To explore the predictors of deferred lesion failure (DLF) in patients with diabetes mellitus (DM) and lesions with a fractional flow reserve (FFR) >0.80 and to examine whether a predictive relationship between negative FFR values (>0.80–1.00) and DLF exists. Background DM is associated with rapidly progressive atherosclerosis and predictors of DLF in FFR negative lesions in this high-risk group are unknown. Methods All DM patients who underwent FFR-assessment between 1/01/2010 and 31/12/2013 were included, and followed until 1/7/2015. Patients carrying ≥1 FFR negative lesion(s) were assessed for DLF, and multivariate models used to identify independent factors associated with DLF. Results A total of 205 patients with 252 FFR >0.80 lesions were identified. At a mean follow-up of 3.1 ± 1.4 years, DLF occurred in 29/205 (14.1%) patients, 31/252 (12.3%) lesions. Using marginal Cox regression multivariate analysis, insulin requiring DM [HR 2.24 (95%CI; 1.01–4.95), P = 0.046] and prior revascularization [HR 2.70 (95%CI 1.21–6.01), P = 0.015] were identified as being associated with a higher incidence of DLF. Absolute FFR values in FFR negative lesions in DM patients are not predictive of DLF (receiver operating characteristics curve analysis: area under the curve: 0.57 ± 0.06, 95%CI 0.46–0.69). Conclusions In DM patients with FFR negative lesions, insulin requiring DM and prior revascularization are predictors for DLF. In contrast to non-DM patients, no predictive relationship between absolute negative FFR values (ranging >0.80–1.00) and the risk of DLF exists in DM patients. © 2017 Wiley Periodicals, Inc.

Objective: We investigated, in the contemporary era of ST-elevation myocardial infarction (STEMI) treatment, the influence of diabetes mellitus (DM) on cardiovascular outcomes, and whether pre-hospital administration of ticagrelor may affect these outcomes in a subgroup of STEMI patients with DM. Background: DM patients have high platelet reactivity and a prothrombotic condition which highlight the importance of an effective antithrombotic regimen in this high-risk population. Methods: In toal 1,630 STEMI patients enrolled in the ATLANTIC trial who underwent primary percutaneous coronary intervention (PCI) were included. Multivariate analysis was used to explore the association of DM with outcomes and potential treatment-by-diabetes interaction was tested. Results: A total of 214/1,630 (13.1%) patients had DM. DM was an independent predictor of poor myocardial reperfusion as reflected by less frequent ST-segment elevation resolution (≥70%) after PCI (OR 0.59, 95% CI 0.43–0.82, P < 0.01) and was an independent predictor of the composite 30-day outcomes of death/new myocardial infarction (MI)/urgent revascularization/definite stent thrombosis (ST) (OR 2.80, 95% CI 1.62–4.85, P < 0.01), new MI or definite acute ST (OR 2.46, 95% CI 1.08–5.61, P = 0.03), and definite ST (OR 10.00, 95% CI 3.54–28.22, P < 0.01). No significant interaction between pre-hospital ticagrelor vs in-hospital ticagrelor administration and DM was present for the clinical, electrocardiographic and angiographic outcomes as well as for thrombolysis in myocardial infarction major bleeding. Conclusions: DM remains independently associated with poor myocardial reperfusion and worse 30-day clinical outcomes. No significant interaction was found between pre-hospital vs in-hospital ticagrelor administration and DM status. Further approaches for the treatment of DM patients are needed. CLINICAL TRIAL REGISTRATION: clinicaltrials.gov identifier: NCT01347580.

The aim of the study was to assess the clinical and prognostic impact of early functional mitral regurgitation (FMR) improvement on the outcome of patients with idiopathic dilated cardiomyopathy (IDC). The prevalence and prognostic role of FMR improvement, particularly at early follow-up, in patients with IDC are still unclear. From 1988 to 2009, we enrolled 470 patients with IDC with available FMR data at baseline and after 6 ± 2 months. According to the evolution of FMR, patients were classified into 3 groups: stable absent-mild FMR, early FMR improvement (downgrading from moderate-severe to absent-mild), and persistence/early development of moderate-severe FMR. At baseline, 177 of 470 patients (38%) had moderate-severe FMR. Patients with early FMR improvement had significantly better survival rate-free from heart transplant with respect to those with persistence/early development of moderate-severe FMR (93%, 81%, and 66% vs 91%, 64%, and 52% at 1, 6, and 12 years, respectively; p = 0.044). At 6-month follow-up multivariate analysis, FMR improvement was associated with better prognosis (hazard ratio 0.78, 95% confidence interval [CI] 0.64 to 0.96, p = 0.02); the other independent predictors were male gender, heart failure duration, and early re-evaluation of the New York Heart Association class and left ventricle systolic function. This model provided more accurate risk stratification compared with the baseline model (Net Reclassification Index 80% at 12 months and 41% at 72 months). In conclusion, in a large cohort of patients with IDC receiving optimal medical treatment, early improvement of FMR was frequent (53%) and emerged as a favorable independent prognostic factor with an incremental short- and long-term power compared with the baseline evaluation.

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To explore the predictors of deferred lesion failure (DLF) in patients with diabetes mellitus (DM) and lesions with a fractional flow reserve (FFR)0.80 and to examine whether a predictive relationship between negative FFR values (0.80-1.00) and DLF exists.DM is associated with rapidly progressive atherosclerosis and predictors of DLF in FFR negative lesions in this high-risk group are unknown.All DM patients who underwent FFR-assessment between 1/01/2010 and 31/12/2013 were included, and followed until 1/7/2015. Patients carrying ≥1 FFR negative lesion(s) were assessed for DLF, and multivariate models used to identify independent factors associated with DLF.A total of 205 patients with 252 FFR0.80 lesions were identified. At a mean follow-up of 3.1 ± 1.4 years, DLF occurred in 29/205 (14.1%) patients, 31/252 (12.3%) lesions. Using marginal Cox regression multivariate analysis, insulin requiring DM [HR 2.24 (95%CI; 1.01-4.95), P = 0.046] and prior revascularization [HR 2.70 (95%CI 1.21-6.01), P = 0.015] were identified as being associated with a higher incidence of DLF. Absolute FFR values in FFR negative lesions in DM patients are not predictive of DLF (receiver operating characteristics curve analysis: area under the curve: 0.57 ± 0.06, 95%CI 0.46-0.69).In DM patients with FFR negative lesions, insulin requiring DM and prior revascularization are predictors for DLF. In contrast to non-DM patients, no predictive relationship between absolute negative FFR values (ranging0.80-1.00) and the risk of DLF exists in DM patients. © 2017 Wiley Periodicals, Inc.

Because of concerns about the risk of bioresorbable drug-eluting scaffolds (BVS) damage, post-dilation was not recommended and applied in the existing randomized studies and most registries. Recent real world data suggest incomplete BVS expansion cause higher rates of thrombosis. In vivo

[Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4] A 17-year-old asymptomatic boy was referred to our hospital for family screening because of his father's unexplained left ventricular hypertrophy (LVH). The father received a pacemaker at 35 years of age for sick sinus syndrome