To determine the impact of the Hospital Value-Based Purchasing (HVBP) program-the US pay for performance program introduced by Medicare to incentivize higher quality care-on 30 day mortality for three incentivized conditions: acute myocardial infarction, heart failure, and pneumonia.
Financial barriers to health care are associated with worse outcomes following acute myocardial infarction (AMI). Yet, it is unknown whether the prevalence of financial barriers and their relationship with post-AMI outcomes vary by sex among young adults.
The original 1992 Atlanta Classification System for acute pancreatitis was revised in 2012 by the Atlanta Working Group, assisted by various national and international societies, through web-based consensus. This revised classification identifies two phases of acute pancreatitis: early and late. Acute pancreatitis can be either oedematous interstitial pancreatitis or necrotizing pancreatitis. Severity of the disease is categorized into three levels: mild, moderately severe and severe, depending upon organ failure and local/systemic complications. According to the type of pancreatitis, collections are further divided into acute peripancreatic fluid collection, pseudocyst, acute necrotic collection, and walled-off necrosis. Insight into the revised terminology is essential for accurate communication of imaging findings. In this review article, we will summarize the updated nomenclature and illustrate corresponding imaging findings using examples.
The incidence rates of ischemic stroke and ST-segment elevation myocardial infarction (STEMI) have decreased significantly in the United States since 1950. However, there is evidence of flattening of this trend or increasing rates for stroke in patients younger than 50 years. The objective of this study was to examine the changes in incidence rates of stroke and STEMI using an age-period-cohort model with statewide data from New Jersey.
To assess associations between different antidepressant treatments and rates of three cardiovascular outcomes (myocardial infarction, stroke or transient ischaemic attack, and arrhythmia) in people with depression.
Abundant, indirect epidemiological evidence indicates that influenza contributes to all-cause mortality and cardiovascular hospitalisations with studies showing increases in acute myocardial infarction (AMI) and death during the influenza season.
Physical exertion, anger, and emotional upset are reported to trigger acute myocardial infarction (AMI). In the INTERHEART study, we explored the triggering association of acute physical activity and anger or emotional upset with AMI to quantify the importance of these potential triggers in a large, international population.
Quality collaboratives are widely endorsed as a potentially effective method for translating and spreading best practices for acute myocardial infarction (AMI) care. Nevertheless, hospital success in improving performance through participation in collaboratives varies markedly. We sought to understand what distinguished hospitals that succeeded in shifting culture and reducing 30-day risk-standardised mortality rate (RSMR) after AMI through their participation in the Leadership Saves Lives (LSL) collaborative.
Myocardial injury is common in patients without acute coronary syndrome, and international guidelines recommend patients with myocardial infarction are classified by aetiology. The universal definition differentiates patients with myocardial infarction due to plaque rupture (type 1) from those due to myocardial oxygen supply-demand imbalance (type 2) secondary to other acute illnesses. Patients with myocardial necrosis, but no symptoms or signs of myocardial ischaemia, are classified as acute or chronic myocardial injury. This classification has not been widely adopted in practice, because the diagnostic criteria for type 2 myocardial infarction encompass a wide range of presentations, and the implications of the diagnosis are uncertain. However, both myocardial injury and type 2 myocardial infarction are common, occurring in more than one-third of all hospitalised patients. These patients have poor short-term and long-term outcomes with two-thirds dead in 5 years. The classification of patients with myocardial infarction continues to evolve, and future guidelines are likely to recognise the importance of identifying coronary artery disease in type 2 myocardial infarction. Clinicians should consider whether coronary artery disease has contributed to myocardial injury, as selected patients are likely to benefit from further investigation and in these patients targeted secondary prevention has the potential to improve outcomes.
Following stroke, the damaged tissue undergoes liquefactive necrosis, a stage of infarct resolution that lasts for months, although the exact length of time is currently unknown. One method of repair involves reactive astrocytes and microglia forming a glial scar to compartmentalize the area of liquefactive necrosis from the rest of the brain. The formation of the glial scar is a critical component of the healing response to stroke, as well as other central nervous system (CNS) injuries. The goal of this study was to evaluate the toxicity of the extracellular fluid present in areas of liquefactive necrosis and determine how effectively it is segregated from the remainder of the brain. To accomplish this goal, we used a mouse model of stroke in conjunction with an extracellular fluid toxicity assay, fluorescent and electron microscopy, immunostaining, tracer injections into the infarct, and multiplex immunoassays. We confirmed that the extracellular fluid present in areas of liquefactive necrosis following stroke is toxic to primary cortical and hippocampal neurons for at least 7 weeks following stroke, and discovered that although glial scars are robust physical and endocytic barriers, they are nevertheless permeable. We found that molecules present in the area of liquefactive necrosis can leak across the glial scar, and are removed by a combination of paravascular clearance and microglial endocytosis in the adjacent tissue. Despite these mechanisms, there is delayed atrophy, cytotoxic edema, and neuron loss in regions adjacent to the infarct for weeks following stroke. These findings suggest that one mechanism of neurodegeneration following stroke is the failure of glial scars to impermeably segregate areas of liquefactive necrosis from surviving brain tissue.