A research team led by investigators from Massachusetts General Hospital (MGH) and collaborators has shown, for the first time, that it may be possible to non-surgically treat or even prevent the damage to a major heart valve that often occurs after a heart attack. In their report the investigators – including co-senior authors at Boston Children’s Hospital and Brigham and Women’s Hospital – describe how treatment with the antihypertension drug losartan reduced mitral valve damage in an animal model of heart attack.
“Our study supports a new concept transforming how we think about heart valves,” says Robert Levine, MD, of the Heart Valve Program and the Cardiac Ultrasound Laboratory in the Corrigan Minehan Heart Center at MGH, co-senior author of the report. “They are not just passive tissue flaps, as previously thought, but are biological battlegrounds where medicines can be used to help patients. Patients with heart valve disease are currently treated with interventions – surgery or implanted devices – late in their illness when the heart is failing. We aim to prevent disease progression at an early stage and keep our patients’ hearts healthy.”
When blockage to a coronary artery causes the death of heart muscle, the body responds by sending immune cells and other inflammatory factors to the site of the damage. Co-lead author Jacob Dal-Bianco, MD, also of the MGH Heart Valve Program, explains, “A heart attack is like a fire in the heart;  inflammation triggered by damage to the heart muscle attracts cells to clear up the damage and form a healed scar. The mitral valve can be caught up as an innocent bystander in this process and become inflamed and scarred, eventually becoming shorter, stiffer and less able to close effectively.”
Located between the left atrium, which receives oxygenated blood from the lungs, and the left ventricle, from which blood is pumped out to the body, a healthy mitral valve keeps blood flowing in the right direction. But if the valve tissues called leaflets don’t close properly after the heart beats, blood can leak back towards the lungs – a process called mitral valve regurgitation – reducing the efficiency of the heart and placing additional stress on the already-damaged organ. While it had been thought that post-heart-attack damage to the mitral valve was caused only by physical forces exerted by the scarring and stretching of damaged heart muscle, recent research by MGH team members found that the valve itself becomes thicker and stiffer, further reducing its ability to close.
Among the factors released by immune cells in an attempt to heal damaged heart muscle is transforming growth factor (TGF)-beta. While it is an important regulator of processes involved in growth, development and the immune response, excess levels of TGF-beta can overactivate other cells, leading to further scarring and stiffening of the mitral valve. Surgical repair of a damaged mitral valve fails within two years in 60 percent of patients, leading to shortness of breath and eventual heart failure.
The hypertension drug losartan is known to inhibit the effects of TGF-beta, and the current study was designed to see whether it could reduce post-heart-attack mitral valve damage in an animal model. For two months, daily doses of the drug were given to sheep in which a heart attack had been surgically induced. A control group of animals that did not receive the drug had surgical mesh sutured to their left ventricular walls to restrict the stretching that typically follows a heart attack and keep the size of the ventricle the same as in the drug-treated animals. At the end of the study period, significantly less inflammation, thickening and scarring had developed in the mitral valves of the losartan-treated animals, compared with the control group. Another study by the same group is investigating whether losartan treatment actually can reduce mitral valve regurgitation.

Massachusetts General Hospital
www.massgeneral.org/about/pressrelease.aspx?id=2141

No single solution exists for alleviating crowding in emergency rooms, but a new study identifies four key strategies that have reduced the problem.
The study concludes that engaged executive leadership can alleviate the problem when combined with a data-driven approach and coordination across the hospital from housekeepers to the CEO. Crowding in emergency rooms has been associated with decreased patient satisfaction and even death.
“Emergency department crowding can be dangerous for patients,” said senior author Benjamin Sun, M.D., a professor of emergency medicine in the OHSU School of Medicine. “We know, for example, that emergency department crowding can lead to delays in pain medications for patients with broken bones, as well as delays in antibiotics for patients with pneumonia. We know the risk of death is higher when the emergency department is more crowded than when it’s less crowded.”
The study identified groups of hospitals categorized as low, high or highest-improving in terms of lengths of stay and boarding times (the length of time an admitted patient must wait for an inpatient bed), as measured through statistics provided by 2,619 U.S. hospitals to the Centers for Medicare and Medicaid Services. The authors picked a representative sample of four hospitals in each of the three categories of performance, then systematically interviewed a broad range of stakeholders.
The researchers talked to 60 people at the 12 hospitals. Interviewees included nursing staff, emergency department directors, directors of inpatient services, chief medical officers and other executive officers.
The study identified four key strategies:
1) Involvement of executive leadership: The study noted that executive leaders in highperforming hospitals identified hospital crowding as a top priority complete with clear goals and resources to achieve those goals.
“In contrast, low performing hospital executive leadership did not prioritize crowding initiatives, despite acknowledging the causes,” the authors wrote. “Emergency department leadership often felt isolated in their struggle with significant boarding and lengths of stay.”
2) Hospital-wide coordinated strategies: High-performing hospitals performed as a cohesive system across departments to alleviate crowding, in contrast to low-performing hospitals that operated in silos. For example, one executive at a high-performing hospital developed strategies for improving bed turnaround times on inpatient rooms.
“Instead of waiting for the room to go from dirty to clean and then to book transportation for a patient to come, we started doing things in parallel so that we would cut down on waiting time,” the executive said in the report.
3) Data-driven management: High-performing hospitals gathered and used data to adjust operations in real time, provided immediate feedback to key personnel, and predicted patterns of flow in the emergency department and hospital, matching resources to meet expected demand.
“In contrast, at low-performing hospitals, data were most often available only retrospectively, and, if the data were used, they were discussed by executive leadership at monthly or quarterly meetings,” the authors wrote.
4) Performance accountability: High-performing hospitals held staff accountable and problems were addressed immediately to reduce crowding.
Sun described a typical scenario in one high-performing hospital: “If boarding in the ED exceeded the acceptable limit, the chief medical officer would physically get out of the office, go onto the ward floors, and start reviewing charts and asking, ‘What can we do to fix the problem?’” he said.
OHSU School of Medicine
http://tinyurl.com/y8bq3gvg

Human rhinovirus (HRV), the culprit behind most colds, is the leading cause of hospitalization for premature babies. However, in very preterm children, exactly how HRV causes severe respiratory disease — and which patients may need more intensive observation and treatment — is less well understood.
A new study led by Children’s National Health System research clinicians showed that in children who were born severely premature, HRV infections seem to trigger an airway hyper-reactivity (AHR) type of disease, which leads to wheezing and air-trapping (hyperinflation) and more severe respiratory disease. This, in turn, increases the risk for hospitalization.
The study found that other signs of respiratory distress, such as low arterial blood oxygen or rapid shallow breathing, were no more common in severely premature children (less than 32 weeks of gestational age) than in kids born preterm or full-term. The findings have implications for administering supportive care sooner or more intensively for severely premature children than for other infants.
“When it comes to how they respond to such infections, severely premature children are quite different,” says Geovanny Perez, M.D., a specialist in pulmonary medicine at Children’s National and lead study author. “We’ve known they are more susceptible to human rhinovirus infection and have more severe disease. However, our study findings suggest that severely premature kids have an ‘asthma’ type of clinical picture and perhaps should be treated differently.”
The study team sought to identify clinical phenotypes of HRV infections in young children hospitalized for such infections. The team theorized that severely premature babies would respond differently to these infections and that their response might resemble symptoms experienced by patients with asthma.
“For a number of years, our team has studied responses to viruses and prematurity, especially HRV and asthma,” Dr. Perez says. “We know that premature babies have an immune response to HRV from the epithelial cells, similar to that seen in older patients with asthma. But we wanted to address a gap in the research to better understand which children may need closer monitoring and more supportive care during their first HRV infection.”
In a retrospective cross-sectional analysis, the study looked at 205 children aged 3 years or younger who were hospitalized at Children’s National in 2014 with confirmed HRV infections. Of these, 71 percent were born full-term (more than 37 gestational weeks), 10 percent were preterm (32 to 37 gestational weeks) and 19 percent were severely premature (less than 32 gestational weeks).
Dr. Perez and his team developed a special respiratory distress scoring system based on physical findings in the children’s electronic medical records to assess the degree of lower-airway obstruction or AHR (as occurs in asthma) and of parenchymal lung disease. The physical findings included:

• Wheezing;
• Subcostal retraction (a sign of air-trapping/hyperinflation of the lungs), as can occur in pneumonia;
• Reduced oxygen levels (hypoxemia); and
• Increased respiratory rate (tachypnea).

The research team assigned each case an overall score. The severely premature children had worse overall scores — and significantly worse scores for AHR and hyperinflated lungs relative to children born late preterm or full-term.
“What surprised us, though, in this study was that the phenotypical characterization using individual parameters for parenchymal lung disease, such as hypoxemia or tachypnea, were not different in severe preterm children and preterm or full term,” says Dr. Perez. “On the other hand, our study found that severely preterm children had a lower airway obstruction phenotype associated with retractions and wheezing. Moreover there was a ‘dose effect’ of prematurity: children who were born more premature had a higher risk of wheezing and retractions.”
Among the implications of this study, Dr. Perez sees the potential to use phenotypical (clinical markers, such as retractions and wheezing) and biological biomarkers to better personalize patients’ treatments. Dr. Perez and his team have identified biological biomarkers in nasal secretions of children with rhinovirus infection that they plan to combine with clinical biomarkers to identify which patients with viral infections will benefit from early supportive care, chronic treatments or long-term monitoring.
ScienceDailyhttps://tinyurl.com/yd3mz3eu

Having a loved one go through a critical illness is a stressful and traumatic experience that may have lasting effects months after the patient is discharged from the intensive care unit (ICU). To improve the well-being of both patients and family during this vulnerable time, a set of new guidelines has been released, providing physicians with evidence-based strategies to optimize outcomes for the critically ill and those at their bedside.
“There is increasing awareness that support for family can also improve patient outcomes,” said Judy Davidson, lead author of the guidelines and a nurse at UC San Diego Health. “Families in the ICU aren’t visitors — they are an integral part of the care and the care team.”
Based on an analysis of more than 450 qualitative and quantitative studies, a multidisciplinary, international panel of 29 health care experts developed a series of recommendations for family-centred care, defined as an approach to healthcare that is respectful of and responsive to individual families’ needs and values. The experiences and perspectives of former ICU patients and family members from UC San Diego Health, the University of Maryland (UOM) School of Medicine, patient advocacy organizations and the LGBTQ community were used to develop the new guidelines.
The 23 recommendations grouped into five categories include: space for loved ones to sleep; educational programmes to teach family how to assist with care; encouraging family members to be part of the decision-making process; implementing ICU diaries to reduce a family’s anxiety and post-traumatic stress; and involving a multi-disciplinary team, such as psychologists, social workers and spiritual advisors. UC San Diego Health is among the first hospitals in the nation to embrace the concept of implementing a family diary in the ICUs.
“Structured interventions and approaches to support family members of critically ill patients are needed both to mitigate the impact of the crisis of critical illness and to prepare family members for decisionmaking and caregiving demands,” said Davidson. “Up to half of families with a critically ill loved one experience psychological symptoms. A robust programme built around family-centred care may decrease the negative impact surrounding critical illness. It is a matter of public health.”
The guidelines suggest that clinicians and institutions need to decide which intervention or combination of interventions are likely to be the most successful in specific circumstances.
“We have developed a self-analysis tool that ICUs can use to build a customized family-centered plan that will bring change,” said Robert El-Kareh, MD, MPH, hospitalist at UC San Diego Health and associate professor at UC San Diego of Medicine, who was instrumental in building translational tools to help ICUs move recommendations into practice.

University of California – San Diego http://tinyurl.com/y732jdfk