20 research outputs found
Guidelines and protocols for cardiovascular magnetic resonance in children and adults with congenital heart disease: SCMR expert consensus group on congenital heart disease
Microvascular obstruction assessed by 3-tesla magnetic resonance imaging in acute myocardial infarction is correlated with plasma troponin I levels
Role of Coronary Microcirculation in No-Reflow Phenomenon in Myocardial Infarction with ST Segment Elevation
Defining Post-release ‘Success’: Using Assemblage and Phenomenography to Reveal Difference and Complexity in Post-prison Conceptions
Respiratory Training Late After Fontan Intervention: Impact on Cardiorespiratory Performance
Parenting practices and prospective levels of hyperactivity/inattention across early- and middle-childhood
This study examined specific parenting practices as predictors of prospective levels of children’s hyperactivity/inattention across early- and middle-childhood. Participants were a mixed-sex community cohort (N = 976; 52 % boys) aged 4–10 years (M = 6.5, SD = 1.3). Measures of parenting practices, hyperactivity/inattention, conduct problems, and maternal education were collected at baseline, and hyperactivity/inattention re-assessed at 12-month follow-up. Analyses examined predictors of 12-month hyperactivity/inattention while controlling for levels at baseline. High levels of parental involvement were associated with reduced levels of hyperactivity/inattention, but only across early childhood. Conversely, increases in child age were associated with increased levels of hyperactivity/inattention across middle-childhood, but only among children exposed to high levels of inconsistent discipline. Inconsistent discipline and parental involvement appear to be uniquely associated with prospective hyperactivity/inattention across childhood, independent of associated conduct problems. Our results further suggest some developmental specificity with regard to the effects of these distinct dimensions of parenting on hyperactivity/inattention at different points in childhood
Hemorrhage promotes inflammation and myocardial damage following acute myocardial infarction: insights from a novel preclinical model and cardiovascular magnetic resonance
Abstract Background Myocardial hemorrhage is a frequent complication following reperfusion in acute myocardial infarction and is predictive of adverse outcomes. However, it remains unsettled whether hemorrhage is simply a marker of a severe initial ischemic insult or directly contributes to downstream myocardial damage. Our objective was to evaluate the contribution of hemorrhage towards inflammation, microvascular obstruction and infarct size in a novel porcine model of hemorrhagic myocardial infarction using cardiovascular magnetic resonance (CMR). Methods Myocardial hemorrhage was induced via direct intracoronary injection of collagenase in a novel porcine model of ischemic injury. Animals (N = 27) were subjected to coronary balloon occlusion followed by reperfusion and divided into three groups (N = 9/group): 8 min ischemia with collagenase (+HEM); 45 min infarction with saline (I-HEM); and 45 min infarction with collagenase (I+HEM). Comprehensive CMR was performed on a 3 T scanner at baseline and 24 h post-intervention. Cardiac function was quantified by cine imaging, edema/inflammation by T2 mapping, hemorrhage by T2* mapping and infarct/microvascular obstruction size by gadolinium enhancement. Animals were subsequently sacrificed and explanted hearts underwent histopathological assessment for ischemic damage and inflammation. Results At 24 h, the +HEM group induced only hemorrhage, the I-HEM group resulted in a non-hemorrhagic infarction, and the I+HEM group resulted in infarction and hemorrhage. Notably, the I+HEM group demonstrated greater hemorrhage and edema, larger infarct size and higher incidence of microvascular obstruction. Interestingly, hemorrhage alone (+HEM) also resulted in an observable inflammatory response, similar to that arising from a mild ischemic insult (I-HEM). CMR findings were in good agreement with histological staining patterns. Conclusions Hemorrhage is not simply a bystander, but an active modulator of tissue response, including inflammation and microvascular and myocardial damage beyond the initial ischemic insult. A mechanistic understanding of the pathophysiology of reperfusion hemorrhage will potentially aid better management of high-risk patients who are prone to adverse long-term outcomes
