Abstract Background A delayed presentation of patients with ST-segment elevation myocardial infarction (STEMI) has been reported globally after the outbreak of coronavirus disease-19 (COVID-19). However, it remains unknown whether differences already exist at the time of pre-hospital electrocardiograms (ECGs). Purpose We therefore compared pre-hospital ECGs of STEMI patients hospitalized in Italy after the first reported case of COVID-19 on February 21, 2020 with data from the same period in 2019 to identifying potential changes between the two periods. Methods We analyzed prehospital ECGs of patients with a final diagnosis of STEMI from February 21, 2020, to April 16, 2020. Data were divided in two periods, before and after the first confirmed case of COVID-19 in Italy. Pathological Q-waves and the Anderson-Wilkins acuteness score, which estimates the acuteness of ischemia, were independently assessed by two reviewers. Results 167 (5.15%) of out 3,239 ECGs qualified for STEMI and were included in the analysis. ECGs recorded during the COVID-19 pandemic showed more frequently pathological Q-wave complexes compared with the control period (54.5% vs. 22.1%, risk difference 32.3%, 95% confidence intervals [CI], 21.2 to 43.5 percentage points) and presented a higher number of pathological Q-waves (1.4±1.6 vs. 0.5±1.2; p<0.001). The Anderson-Wilkins acuteness score was significantly lower during the COVID-19 period (2.4±0.9 vs. 2.8±0.7; p<0.001), suggesting a lower probability of acute ischemia. Conclusions Pre-hospital ECGs of patients with a final diagnosis of STEMI presented more frequently the signs of late ischemia during the COVID-19 pandemic. Funding Acknowledgement Type of funding sources: None. Figure 1
During development we transition from coregulation (where regulatory processes are shared between child and caregiver) to self‐regulation. Most early coregulatory interactions aim to manage fluctuations in the infant's arousal and alertness; but over time, coregulatory processes become progressively elaborated to encompass other functions such as sociocommunicative development, attention and executive control. The fundamental aim of coregulation is to help maintain an optimal ‘critical state’ between hypo‐ and hyperactivity. Here, we present a dynamic framework for understanding child–caregiver coregulatory interactions in the context of psychopathology. Early coregulatory processes involve both passive entrainment, through which a child's state entrains to the caregiver's, and active contingent responsiveness, through which the caregiver changes their behaviour in response to behaviours from the child. Similar principles, of interactive but asymmetric contingency, drive joint attention and the maintenance of epistemic states as well as arousal/alertness, emotion regulation and sociocommunicative development. We describe three ways in which active child–caregiver regulation can develop atypically, in conditions such as Autism, ADHD, anxiety and depression. The most well‐known of these is insufficient contingent responsiveness, leading to reduced synchrony, which has been shown across a range of modalities in different disorders, and which is the target of most current interventions. We also present evidence that excessive contingent responsiveness and excessive synchrony can develop in some circumstances. And we show that positive feedback interactions can develop, which are contingent but mutually amplificatory child–caregiver interactions that drive the child further from their critical state. We discuss implications of these findings for future intervention research, and directions for future work.
Recently, the cardiovascular outcomes for people using anticoagulation strategies (COMPASS) trial demonstrated that dual therapy reduced cardiovascular outcomes compared with aspirin alone in patients with stable atherosclerotic disease.We sought to assess the proportion of patients eligible for the COMPASS trial and to compare the epidemiology and outcome of these patients with those without COMPASS inclusion or with any exclusion criteria in a contemporary, nationwide cohort of patients with stable coronary artery disease. Among the 4068 patients with detailed information allowing evaluation of eligibility, 1416 (34.8%) did not fulfil the inclusion criteria (COMPASS-Not-Included), 841 (20.7%) had exclusion criteria (COMPASS-Excluded), and the remaining 1811 (44.5%) were classified as COMPASS-Like. At 1 year, the incidence of major adverse cardiovascular event (MACE), a composite of cardiovascular death, myocardial infarction, and stroke, was 0.9% in the COMPASS-Not-Included and 2.0% in the COMPASS-Like (P = 0.01), and 5.0% in the COMPASS-Excluded group (P < 0.0001 for all comparisons). Among the COMPASS-Like population, patients with multiple COMPASS enrichment criteria presented a significant increase in the risk of MACE (from 1.0% to 3.3% in those with 1 and ≥3 criteria, respectively; P = 0.012), and a modest absolute increase in major bleeding risk (from 0.2% to 0.4%, respectively; P = 0.46).In a contemporary real-world cohort registry of stable coronary artery disease, most patients resulted as eligible for the COMPASS. These patients presented a considerable annual risk of MACE that consistently increases in the presence of multiple risk factors.
Re-induction of fetal genes and/or re-expression of postnatal genes represent hallmarks of pathological cardiac remodeling, and are considered important in the progression of the normal heart towards heart failure (HF). Whether epigenetic modifications are involved in these processes is currently under investigation. Here we hypothesized that histone chromatin modifications may underlie changes in the gene expression program during pressure overload-induced HF. We evaluated chromatin marks at the promoter regions of the sarcoplasmic reticulum Ca2+ATPase (SERCA-2A) and β-myosin-heavy chain (β-MHC) genes (Atp2a2 and Myh7, respectively) in murine hearts after one or eight weeks of pressure overload induced by transverse aortic constriction (TAC). As expected, all TAC hearts displayed a significant reduction in SERCA-2A and a significant induction of β-MHC mRNA levels. Interestingly, opposite histone H3 modifications were identified in the promoter regions of these genes after TAC, including H3 dimethylation (me2) at lysine (K) 4 (H3K4me2) and K9 (H3K9me2), H3 trimethylation (me3) at K27 (H3K27me3) and dimethylation (me2) at K36 (H3K36me2). Consistently, a significant reduction of lysine-specific demethylase KDM2A could be found after eight weeks of TAC at the Atp2a2 promoter. Moreover, opposite changes in the recruitment of DNA methylation machinery components (DNA methyltransferases DNMT1 and DNMT3b, and methyl CpG binding protein 2 MeCp2) were found at the Atp2a2 or Myh7 promoters after TAC. Taken together, these results suggest that epigenetic modifications may underlie gene expression reprogramming in the adult murine heart under conditions of pressure overload, and might be involved in the progression of the normal heart towards HF.
Endovascular treatment of below-the-knee region disease is often challenging because of the involvement of arterial bifurcations. Several cases have been reported on the use of coronary stents for the treatment of these patients, but limited evidence is available on the use of dedicated coronary bifurcation devices. We here report the endovascular treatment of a symptomatic bifurcation lesion in below-the-knee region, using a self-expanding Biolimus A9–eluting stent in combination with a “conventional” coronary drug-eluting stent.
