BackgroundThe circadian clock influences a number of cardiovascular (patho)physiological processes including the incidence of acute myocardial infarction. A circadian variation in infarct size has recently been shown in rodents, but there is no clinical evidence of this finding. Objective To determine the impact of time-of-day onset of ST segment elevation myocardial infarction (STEMI) on infarct size. Methods A retrospective single-centre analysis of 811 patients with STEMI admitted between 2003 and 2009 was performed. Infarct size was estimated by peak enzyme release. The relationship between peak enzyme concentrations and time-of-day were characterised using multivariate regression splines. Time of STEMI onset was divided into four 6-hour periods in phase with circadian rhythms. Results Model comparisons based on likelihood ratio tests showed a circadian variation in infarct size across time-of-day as evaluated by peak creatine kinase (CK) and troponin-I (TnI) concentrations (p¼0.015 and p¼0.012, respectively). CK and TnI curves described similar patterns across time, with a global maximum in the 6:00enoon period and a local minimum in the noone18:00 period. Infarct size was largest in patients with STEMI onset in the dark-to-light transition period (6:00enoon), with an increase in peak CK and TnI concentrations of 18.3% (p¼0.031) and 24.6% (p¼0.033), respectively, compared with onset of STEMI in the 18:00emidnight period. Patients with anterior wall STEMI also had significantly larger infarcts than those with STEMI in other locations. Conclusions Significant circadian oscillations in infarct size were found in patients according to time-of-day of STEMI onset. The infarct size was found to be significantly larger with STEMI onset in the dark-to-light transition period (6:00enoon). If confirmed, these results may have a significant impact on the interpretation of clinical trials of cardioprotective strategies in STEMI.

In DM patients with coronary artery disease taking maintenance aspirin and clopidogrel therapy, impaired renal function is associated with reduced clopidogrel-induced antiplatelet effects and a greater prevalence of HPPR.

BACKGROUNDA polypill that includes key medications associated with improved outcomes (aspirin, angiotensin-converting-enzyme [ACE] inhibitor, and statin) has been proposed as a simple approach to the secondary prevention of cardiovascular death and complications after myocardial infarction. METHODSIn this phase 3, randomized, controlled clinical trial, we assigned patients with myocardial infarction within the previous 6 months to a polypill-based strategy or usual care. The polypill treatment consisted of aspirin (100 mg), ramipril (2.5, 5, or 10 mg), and atorvastatin (20 or 40 mg). The primary composite outcome was cardiovascular death, nonfatal type 1 myocardial infarction, nonfatal ischemic stroke, or urgent revascularization. The key secondary end point was a composite of cardiovascular death, nonfatal type 1 myocardial infarction, or nonfatal ischemic stroke. RESULTSA total of 2499 patients underwent randomization and were followed for a median of 36 months. A primary-outcome event occurred in 118 of 1237 patients (9.5%) in the polypill group and in 156 of 1229 (12.7%) in the usual-care group (hazard ratio, 0.76; 95% confidence interval [CI], 0.60 to 0.96; P = 0.02). A key secondaryoutcome event occurred in 101 patients (8.2%) in the polypill group and in 144 (11.7%) in the usual-care group (hazard ratio, 0.70; 95% CI, 0.54 to 0.90; P = 0.005). The results were consistent across prespecified subgroups. Medication adherence as reported by the patients was higher in the polypill group than in the usual-care group. Adverse events were similar between groups. CONCLUSIONSTreatment with a polypill containing aspirin, ramipril, and atorvastatin within 6 months after myocardial infarction resulted in a significantly lower risk of major adverse cardiovascular events than usual care. (Funded by the European Union Horizon 2020; SECURE ClinicalTrials.gov number, NCT02596126; EudraCT number, 2015 -002868 -17.

In patients with IE, the presence of diabetes, acute renal insufficiency, Staphylococcus aureus infection, supraventricular tachycardia, vegetation size ≥15 mm, and signs of persistent infection are associated with the development of SS.

Please cite this article as: Vivas D, Roldán V, Esteve-Pastor MA, Roldán I, Tello-Montoliu A, Ruiz-Nodar JM, Cosín-Sales J, María Gámez J, Consuegra L, Luis Ferreiro J, Marín F, Arrarte V, Anguita M, CequierÁ, Pérez-Villacastín J, Recomendaciones sobre el tratamiento antitrombótico durante la pandemia COVID-19. ABSTRACTThe new coronavirus SARS-CoV-2, which gives rise to the highly contagious COVID-19 disease, has caused a pandemic that is overwhelming health care systems worldwide. Affected patients have been reported to have a heightened inflammatory state that increases their thrombotic risk. However, there is very scarce information on the management of thrombotic risk, coagulation disorders, and anticoagulant therapy. In addition, the situation has also greatly influenced usual care in patients not infected with COVID-19.

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Background The coronavirus disease 2019 (COVID‐19) shows high morbidity and mortality, particularly in patients with concomitant cardiovascular diseases. Some of these patients are under oral anticoagulation (OAC) at admission, but to date, there are no data on the clinical profile, prognosis and risk factors of such patients during hospitalization for COVID‐19. Design Subanalysis of the international ‘real‐world’ HOPE COVID‐19 registry. All patients with prior OAC at hospital admission for COVID‐19 were suitable for the study. All‐cause mortality was the primary endpoint. Results From 1002 patients included, 110 (60.9% male, median age of 81.5 [IQR 75‐87] years, median Short‐Form Charlson Comorbidity Index [CCI] of 1 [IQR 1‐3]) were on OAC at admission, mainly for atrial fibrillation and venous thromboembolism. After propensity score matching, 67.9% of these patients died during hospitalization, which translated into a significantly higher mortality risk compared to patients without prior OAC (HR 1.53, 95% CI 1.08‐2.16). After multivariate Cox regression analysis, respiratory insufficiency during hospitalization (HR 6.02, 95% CI 2.18‐16.62), systemic inflammatory response syndrome (SIRS) during hospitalization (HR 2.29, 95% CI 1.34‐3.91) and the Short‐Form CCI (HR 1.24, 95% CI 1.03‐1.49) were the main risk factors for mortality in patients on prior OAC. Conclusions Compared to patients without prior OAC, COVID‐19 patients on OAC therapy at hospital admission showed lower survival and higher mortality risk. In these patients on OAC therapy, the prevalence of several comorbidities is high. Respiratory insufficiency and SIRS during hospitalization, as well as higher comorbidity, pointed out those anticoagulated patients with increased mortality risk.