TAG: "Heart"

Kareem Abdul-Jabbar undergoes coronary bypass surgery


UCLA alum, NBA Hall of Fame member, has surgery at Ronald Reagan UCLA Medical Center.

UCLA Health is issuing this statement at the request of Kareem Abdul-Jabbar, the NBA’s all-time leading scorer and member of the Basketball Hall of Fame:

Kareem Abdul-Jabbar was admitted to Ronald Reagan UCLA Medical Center this week with cardiovascular disease, and he underwent quadruple coronary bypass surgery on April 16. The operation was performed by Dr. Richard Shemin, UCLA’s chief of cardiac surgery.

Shemin said the surgery was successful and he expects Abdul-Jabbar to make a full recovery.

At this time, Abdul-Jabbar would like to thank his surgical team and the medical staff at UCLA, his alma mater, for the excellent care he has received. He is looking forward to getting back to his normal activities soon.

He asks that you keep him in your thoughts and, most importantly, cherish and live each day to its fullest.

For those wanting to send well wishes, he thanks you in advance and asks that you support those in your own community who may be suffering from various health issues.

There will be no media interviews or additional information from Abdul-Jabbar, his physician or his spokesperson. However, news media planning stand-ups at the hospital must park news vans in the southbound lane of Westwood Boulevard, south of Westwood Plaza, between Le Conte Avenue and Med Plaza Circle (in the far right lane).

Media contact:
UCLA Health Sciences Media Relations
(310) 794-0777
UCLAHSmedia@mednet.ucla.edu

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Genetics overlap found between Alzheimer’s, cardiovascular risk factors


Inflammation, high blood lipids may play role in dementia risk, also offer therapeutic targets.

By Scott LaFee, UC San Diego

An international team of scientists, led by researchers at the UC San Diego School of Medicine, have found genetic overlap between Alzheimer’s disease (AD) and two significant cardiovascular disease risk factors: high levels of inflammatory C-reactive protein (CRP) and plasma lipids or fats. The findings, based upon genome-wide association studies involving hundreds of thousands of individuals, suggest the two cardiovascular phenotypes play a role in AD risk – and perhaps offer a new avenue for potentially delaying disease progression.

The findings are published in current online issue of Circulation.

“For many years we have known that high levels of cholesterol and high levels of inflammation are associated with increased risks for Alzheimer’s disease,” said study co-author Paul M. Ridker, M.D., M.P.H., the Eugene Braunwald Professor of Medicine at Harvard Medical School and director of the Center for Cardiovascular Disease Prevention at Brigham and Women’s Hospital. “The current work finds that specific genetic signals explain a part of these relationships. We now need to characterize the function of these genetic signals and see whether they can help us to design better trials evaluating inflammation inhibition as a possible method for Alzheimer’s treatment.”

The researchers used summary statistics from genome-wide association studies of more than 200,000 individuals, looking for overlap in single nucleotide polymorphisms (SNPs) associated with clinically diagnosed AD and CRP and the three components of total cholesterol: high-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides (TG). SNPs are fragments of DNA sequence that commonly vary among individuals within a population.

They found up to a 50-fold enrichment of AD SNPs for different levels of association with CRP, LDL, HDL and TG, which then lead to identification of 55 loci – specific locations on a gene, DNA sequence or chromosome – linked to increased AD risk. The researchers next conducted a meta-analysis of these 55 variants across four independent AD study cohorts, encompassing almost 145,000 persons with AD and healthy controls, revealing two genome-wide significant variants on chromosomes 4 and 10. The two identified genes – HS3ST1 and ECHDC3 – were not previously associated with AD risk.

“Our findings indicate that a subset of genes involved with elevated plasma lipid levels and inflammation may also increase the risk for developing AD. Elevated levels of plasma lipids and inflammation can be modified with treatment, which means it could be possible to identify and therapeutically target individuals at increased risk for developing cardiovascular disease who are also at risk for developing Alzheimer’s disease,” said Rahul S. Desikan, M.D., Ph.D., research fellow and radiology resident at the UC San Diego School of Medicine and the study’s first author.

If so, the research may have significant ramifications. Late-onset AD is the most common form of dementia, affecting an estimated 30 million persons worldwide – a number that is expected to quadruple over the next 40 years. The societal costs, from medical to lost productivity, are staggering. The 2010 World Alzheimer Report estimated total annual costs at $606 billion.

“Currently, there are no disease modifying therapies and much attention has been focused upon prevention and early diagnosis,” said Ole A. Andreassen, M.D., Ph.D., a senior co-author and professor of biological psychiatry at the University of Oslo in Norway. “Delaying dementia onset by even just two years could potentially lower the worldwide prevalence of AD by more than 22 million cases over the next four decades, resulting in significant societal savings.”

Senior author Anders M. Dale, Ph.D., professor of neurosciences and radiology and director of the Center for Translational Imaging and Precision Medicine at UC San Diego, said further research will be needed: “Careful and considerable effort will be required to further characterize the novel candidate genes detected in this study and to detect the functional variants responsible for the association of these loci with Alzheimer’s risk. It will also be important to understand whether these genes, in combination with other known markers such as brain imaging, cerebrospinal fluid measurements and APOE E4 status, can improve the prediction of disease risk in AD.”

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1 in 4 atrial fibrillation patients receives unnecessary blood thinners


Researchers believe cardiology specialists may be unaware of risk.

An electrocardiogram reading traces irregular, rapid and chaotic atrial activity, seen in lead V1 (the top squiggly line).

By Heather Buschman, UC San Diego

About one quarter of all atrial fibrillation patients at the lowest risk for stroke receive unnecessary blood thinners from cardiology specialists, according to a new study by researchers at the UC San Diego School of Medicine and UC San Francisco, and these health care providers must be made aware of the resulting potential health risks. The findings are published online today (April 13) by JAMA Internal Medicine.

“Clinicians who prescribe blood thinners need to be diligent about weighing the risks and benefits of these medications,” said lead author Jonathan C. Hsu, M.D., cardiologist and assistant clinical professor of medicine at UC San Diego. “In those who have no risk factors for stroke, the risk of bleeding likely outweighs the benefit of stroke reduction. The fact that blood thinners were prescribed to so many patients with no risk factors for stroke is a wakeup call that we need to do better for our patients.”

In atrial fibrillation, electrical impulses are triggered from many areas in and around the upper chambers of the heart instead of just one area. This activity is chaotic, and the atrial walls quiver rather than contract normally in moving blood to the lower chambers.

For atrial fibrillation patients at risk for blood clots, anticoagulation therapies such as warfarin or other drugs reduce the risk of illness and death. But because their use carries a bleeding risk, they are not recommended for atrial fibrillation patients at a particularly low risk for stroke.

In fact, current guidelines do not recommend oral anticoagulation in patients under age 60 without heart disease or other known risk factors for blood clots or in atrial fibrillation patients without any established risk factor for stroke. What’s more, the previous guidelines, which were in place at the time the data for this study were collected, contained a very strong recommendation specifically to avoid anticoagulants in that population.

To examine the prevalence of inappropriate anticoagulant prescriptions in young and healthy patients at the lowest risk for blood clots, Hsu and team used a large national registry of cardiovascular patients. From this, they reviewed nearly 11,000 patients age 60 and under and found that roughly 25 percent were prescribed oral anticoagulant therapy contrary to contemporary guideline recommendations. Further, they found that males with atrial fibrillation at the lowest risk of stroke were more likely to be prescribed oral anticoagulation than females, as were older patients and overweight patients without stroke risk factors.

“The irony is that there is a general push to get providers to prescribe these drugs, and they are also generally under-prescribed among many atrial fibrillation patients who actually need them,” said senior author Gregory Marcus, M.D., director of clinical research at UC San Francisco. “Our study suggests people are trying to do the right thing but, due to a lack of understanding of some of the critical nuances, go too far in that direction in low-risk patients.”

Co-authors of this study also include Paul S. Chan, Fengming Tang, St. Luke’s Mid America Heart Institute and the University of Missouri, Kansas City; and Thomas M. Maddox, Veterans Affairs Eastern Colorado Health Care System/University of Colorado School of Medicine.

This research was funded, in part, by the National Heart, Lung and Blood Institute, part of the National Institutes of Health, (grant K23HL102224), U.S. Department of Veterans Affairs, Medtronic and SentreHeart Inc.

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Patients with heart stents face similar risks from bleeding, heart attacks


Results show importance of treating cardiac patients based on personalized risk factors.

By Scott Maier, UC San Francisco

In patients who received a stent to treat coronary artery blockage, those who experienced bleeding requiring hospitalization in the years after the procedure faced an increased risk of death that was similar to the risk faced by those who subsequently had heart attacks, according to a study of nearly 33,000 patients by UC San Francisco and Kaiser Permanente.

“Every year, 600,000 patients in the United States receive a coronary stent and are given drugs that prevent the formation of clots within the stent. These drugs prevent heart attacks but increase the risk of internal bleeding,” said lead author Dhruv Kazi, M.D., M.Sc., M.S., an assistant professor of medicine at UCSF. “These bleeds are often written off as a side effect, but it turns out that they may be just as bad for patients as the heart attacks we’re trying to avoid.”

The study in the April 14 issue of the Journal of the American College of Cardiology is the first to show that the two risks are of comparable magnitude.

Kazi said that the results underline the importance of treating cardiac patients based on personalized risk factors, instead of using what he called a “one-size-fits-all” approach based on population statistics. This study points toward the possibility of using other information about patients that may help identify the antiplatelet drug that is most likely to be the most safe and effective for individual patients in the long run.

The study authors analyzed the records of 32,906 patients in the Kaiser Permanente Northern California health care system who received stents between 1996 and 2008 and were followed for four years. They found that both post-procedure heart attack and episodes of bleeding requiring hospitalization were associated with a greater relative risk of death (91 percent and 61 percent, respectively) over the same time span. The risks in the two groups were not different statistically, so the researchers could not say the risk for one was greater than the other.

Senior author Alan S. Go, M.D., of the Kaiser Permanente Division of Research, noted that the study results “highlight the need for and value of high-quality outcomes research using data from patients treated in the real world to inform patients and doctors about the consequences of treatments.”

Randomized trials, Go observed, “can tell us whether or not a drug, such as an antiplatelet medication, works. But patients enrolled in these trials are highly selected and may not really be like the patients we treat in the clinical practice and are usually followed for a short period of time.”

In contrast, Go said, when rigorously evaluated, data collected in everyday clinical practice can yield valuable insights about long-term effectiveness and safety that complement what is learned from randomized clinical trials.

“We’ve known for some time that bleeds that occur during the stent procedure are bad for the patient, so we increasingly take steps to reduce those bleeds, such as giving drugs with lower bleeding risk and using the radial artery to perform the procedure instead of the femoral artery,” Kazi said. “This is the first study to show that bleeds that occur in the months and years after discharge are also bad for the patient, emphasizing the need for long-term strategies that reduce a patient’s risk of bleeding.”

Other co-authors are Thomas K. Leong, M.P.H., and Matthew D. Solomon, M.D., Ph.D., of Kaiser Permanente, and Tara I. Chang, M.D., M.S., and Mark A. Hlatky, M.D., of Stanford University.

The study was supported by funds from the American Heart Association, Kaiser Permanente Northern California Division of Research, Stanford University and UCSF.

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Heart pouch may explain potentially important cause of strokes


UC Irvine findings could lead to new therapeutic strategies for preventing stroke.

By Tom Vasich, UC Irvine

A pouchlike structure inside the heart’s left atrial chamber in some people may explain strokes that otherwise lack an identifiable cause, according to UC Irvine School of Medicine researchers.

Dr. Mark Fisher, a professor of neurology and pathology & laboratory medicine, and colleagues evaluated 75 stroke patients at UC Irvine Medical Center to learn whether this left atrial septal pouch could be a potent source of stroke-causing blood clots.

Of the 23 patients who had experienced a stroke of undetermined origin (a “cryptogenic” stroke), 30 percent possessed the left atrial septal pouch. It was present in only 10 percent of the 52 patients who’d had a stroke with an identifiable trigger.

Stroke is the leading cause of long-term severe disability and the fourth-most-common cause of death in the U.S. About 80 percent of the 700,000-plus strokes that occur annually in this country are due to blood clots blocking a brain artery. In up to a third of these cases, the clots’ origin cannot be determined.

UC Irvine cardiologists first discovered this pouchlike structure inside the heart’s left atrial chamber in a 2010 study.

“The cul-de-sac nature of this heart pouch may promote stagnation of the blood, forming clots that can travel into the brain and cause a stroke,” Fisher said.

“This finding points to a potentially important cause of strokes,” he added. “The presence of this pouch could change how neurologists treat these patients and lead to new therapeutic strategies for preventing strokes.”

Fisher said that large-scale studies are necessary to verify the results of this study, which appears online in Frontiers in Neurology at http://journal.frontiersin.org/article/10.3389/fneur.2015.00057/abstract.

The research was conducted at UC Irvine Medical Center by members of the Department of Neurology (Fisher and Dr. Annlia Paganini-Hill), the Division of Cardiology (Drs. Dawn Lombardo, Nathan Wong, Ailin Barseghian, Jashdeep Dhoot, Harkawal Hundal and Jonathan Salcedo) and the UCI School of Medicine (Dr. Jonathan Wong, who is now with the California Pacific Medical Center). It was supported by the American Heart Association.

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Necklace and smartphone app can help people track food intake


UCLA-developed app could help battle obesity, heart disease and diabetes.

WearSens rests loosely above the sternum and uses highly sensitive sensors to capture vibrations from the action of swallowing.

By Bill Kisliuk, UCLA

A sophisticated necklace developed by researchers at the UCLA Henry Samueli School of Engineering and Applied Science can monitor food and drink intake, which could help wearers track and improve their dietary habits.

The inventors of the WearSens device say it could help battle obesity, heart disease, diabetes and other problems related to nutrition.

Majid Sarrafzadeh, a distinguished professor of computer science and co-director of UCLA’s Wireless Health Institute, led a team that created the device and an algorithm that translates data from the necklace, and tested it on 30 people who ate a variety of foods.

The researchers found that WearSens can differentiate between solids and liquids with 87 percent accuracy, between hot drinks and room-temperature drinks with 90 percent accuracy, and between food items with different textures with 80 percent accuracy. Researchers say those figures will improve as users calibrate the device based on their eating habits.

The research was published online by the IEEE Sensors Journal.

“Today, many people try to track their food intake with journals, but this is often not effective or convenient,” Sarrafzadeh said. “This technology allows individuals and health care professionals to monitor intake with greater accuracy and more immediacy.”

WearSens rests loosely above the sternum and uses highly sensitive piezoelectric sensors to capture vibrations from the action of swallowing. Piezoelectric sensors produce voltage based on the mechanical stress — or movement or pressure — that is applied to them.

When the wearer eats or drinks, skin and muscle motion from the lower trachea trigger the sensors, and the necklace transmits the signals to a smartphone, where the UCLA-developed algorithm converts the data into information about the food or beverage. The phone displays data about the volume of food or liquid consumed and can offer advice or analysis; for example, that the wearer is eating more than in previous days or that the person should drink more water.

With the WearSens device, the sensor information is translated using a spectrogram, which offers a visual representation of vibrations picked up by the sensors. Spectrograms are often used in speech therapy and seismology, among other applications.

“The breakthroughs are in the design of the necklace, which is simple and does not interfere with daily activity, and in identifying statistical measures that distinguish food intake based on spectrogram images generated from piezoelectric sensor signals,” said Nabil Alshurafa, a graduate student researcher at UCLA who is a co-inventor of the device and the first author of the research.

The study’s other authors are co-inventor Haik Kalantarian, a graduate student researcher; Shruti Sarin and Behnam Shahbazi, also graduate student researchers; Jason Liu, who was a UCLA graduate student at the time he worked on the research; and postdoctoral researcher Mohammad Pourhomayoun.

The team is continuing to refine the algorithms and the necklace’s design. The researchers hope WearSens will be available to the public later this year.

The technology is available for licensing via the UCLA Office of Intellectual Property and Industry-Sponsored Research, which facilitates the conversion of UCLA research to benefit the public.

The research was supported by the National Science Foundation.

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Infant leaves UCLA’s Mattel hospital for home with a transplanted heart


Drayvn is the hospital’s second youngest heart transplant recipient.

Drayvn Johnson got a heart transplant when he was 23 days after he was born with a heart defect and only one coronary artery. Now 5 weeks old, he left Mattel Children's Hospital UCLA for home today with his mother, Nicole Eggleston. (Photo by Reed Hutchinson, UCLA)

By Amy Albin, UCLA

Staff at Mattel Children’s Hospital UCLA witnessed a happy ending today (March 11) instead of what could have easily been a tragic one  when they bid farewell to 5-week-old Drayvn Johnson, who went home with his mother, Nicole Eggleston, and two older brothers after becoming the hospital’s second youngest heart transplant recipient. He was only 23 days old when he received his new heart, which was the size of a strawberry.

“All of our heart transplant patients are special, but I think this one was special because we knew there was a risk we might not find a donor in time,” said Dr. Juan Alejos, professor of pediatric cardiology and director of the Pediatric Heart Transplant Program at Mattel Children’s Hospital UCLA

Dravyn was born with a condition called pulmonary atresia in which the pulmonary valve does not form properly. It was discovered during Eggleston’s pregnancy in a sonogram performed at 22 weeks. Doctors had thought initially that his heart could be repaired with a series of corrective surgeries performed over the first few years of Dravyn’s life.

However, when he was born in early February at an Orange County hospital, doctors found that he had only one coronary artery instead of two and determined that surgery would be too risky for the baby.

At 5 days old, Drayvn was airlifted to Mattel where doctors confirmed that the only hope for his survival was an urgent heart transplant. Miraculously, within two days after Drayvn’s name went on a list for a transplant, a donor was found. And Drayvn got his new heart. The hospital’s youngest heart recipient was a 16-day-old infant who received a transplanted heart in 1994.

The UCLA Pediatric Heart and Heart-Lung Transplant Program is one of the major referral centers for the western United States. The team has performed more than 300 pediatric heart transplants since 1984 when it did its first such surgery. The program is a coordinated effort among pediatric cardiologists, cardiothoracic surgeons, dentists, nurse practitioners, transplant coordinators, nutritional specialists, social workers and child developmental specialists. For more information, visit http://transplants.ucla.edu/heart.

The family has set up a website to help raise funds for Drayvn’s care.

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Bioengineers put human hearts on chip to aid drug screening


Chips ultimately could replace use of animals to screen drugs for safety, efficacy.

By Sarah Yang, UC Berkeley

When UC Berkeley bioengineers say they are holding their hearts in the palms of their hands, they are not talking about emotional vulnerability.

Instead, the research team led by bioengineering professor Kevin Healy is presenting a network of pulsating cardiac muscle cells housed in an inch-long silicone device that effectively models human heart tissue, and they have demonstrated the viability of this system as a drug-screening tool by testing it with cardiovascular medications.

This organ-on-a-chip, reported in a study published today (March 9) in the journal Scientific Reports, represents a major step forward in the development of accurate, faster methods of testing for drug toxicity. The project is funded through the Tissue Chip for Drug Screening Initiative, an interagency collaboration launched by the National Institutes of Health to develop 3-D human tissue chips that model the structure and function of human organs.

“Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy,” said Healy.

The study authors noted a high failure rate associated with the use of nonhuman animal models to predict human reactions to new drugs. Much of this is due to fundamental differences in biology between species, the researchers explained. For instance, the ion channels through which heart cells conduct electrical currents can vary in both number and type between humans and other animals.

“Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans,” said Healy. “It takes about $5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market.”

The heart cells were derived from human-induced pluripotent stem cells, the adult stem cells that can be coaxed to become many different types of tissue.

The researchers designed their cardiac microphysiological system, or heart-on-a-chip, so that its 3-D structure would be comparable to the geometry and spacing of connective tissue fiber in a human heart. They added the differentiated human heart cells into the loading area, a process that Healy likened to passengers boarding a subway train at rush hour. The system’s confined geometry helps align the cells in multiple layers and in a single direction.

Microfluidic channels on either side of the cell area serve as models for blood vessels, mimicking the exchange by diffusion of nutrients and drugs with human tissue. In the future, this setup also could allow researchers to monitor the removal of metabolic waste products from the cells.

“This system is not a simple cell culture where tissue is being bathed in a static bath of liquid,” said study lead author Anurag Mathur, a postdoctoral scholar in Healy’s lab and a California Institute for Regenerative Medicine fellow. “We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs.”

Within 24 hours after the heart cells were loaded into the chamber, they began beating on their own at a normal physiological rate of 55 to 80 beats per minute.

The researchers put the system to the test by monitoring the reaction of the heart cells to four well-known cardiovascular drugs: isoproterenol, E-4031, verapamil and metoprolol. They used changes in the heart tissue’s beat rate to gauge the response to the compounds.

The baseline beat rate for the heart tissue consistently fell within 55 to 80 beats per minute, a range considered normal for adult humans. They found that the responses after exposure to the drugs were predictable. For example, after half an hour of exposure to isoproterenol, a drug used to treat bradycardia (slow heart rate), the beat rate of the heart tissue increased from 55 to 124 beats per minute.

The researchers noted that their heart-on-a-chip could be adapted to model human genetic diseases or to screen for an individual’s reaction to drugs. They also are studying whether the system could be used to model multi-organ interactions. A standard tissue culture plate could potentially feature hundreds of microphysiological cell culture systems.

“Linking heart and liver tissue would allow us to determine whether a drug that initially works fine in the heart might later be metabolized by the liver in a way that would be toxic,” said Healy.

The engineered heart tissue remained viable and functional over multiple weeks. Given that time, it could be used to test various drugs, Healy said.

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Researchers discover protein’s key role in heart failure


Better understanding of molecular mechanism could lead to new drug targets.

By Bonnie Ward, UC San Diego

Researchers at the UC San Diego School of Medicine have identified a key piece in the complex molecular puzzle underlying heart failure – a serious and sometimes life-threatening disorder affecting more than 5 million Americans.

In a study published in today’s (March 5) online issue of Cell Reports, Xiang-Dong Fu, Ph.D., and colleagues explored the heart’s progression from initial weakening to heart failure, and found that a protein, known as RBFox2, plays a critical role in this process.

Contrary to its name, heart failure does not mean the heart completely stops working, but rather that the heart muscle becomes weakened to the point that it can no longer pump enough blood for the body’s needs. Coronary artery disease, high blood pressure and heart defects are among various factors that can lead to heart failure, which has no cure and is currently treated with medications, lifestyle changes, oxygen and cardiac devices. In some cases, a heart transplant is required.

Fu and his team studied the cellular changes that occur during the weakened heart muscle’s transition from working harder to maintain proper blood flow, known as the compensatory stage, to failing to sustain adequate blood supplies, known as decompensation.

“Numerous signaling molecules have been shown to be part of the compensatory program, but relatively little was known about the transition to decompensation that leads to heart failure,” said Fu.

To answer this question, the research team explored RBFox2, a gene splicing protein known to be involved in the heart’s early development and ongoing function.

“We wanted to know how RBFox2 might contribute to decompensation, given its vital role in heart functions,’’ said Fu.

In their studies, the researchers restricted blood flow in mice to induce a condition similar to heart failure and then tested their RBFox2 protein levels over a period of weeks.

“Strikingly, we found that RBfox2 protein was largely diminished in the hearts of live mice five weeks after the procedure,” he said.

Fu and colleagues also tested the reduction of the RBFox2 protein in mice specially engineered to lack the protein. In these experiments, the mice lacking the RBFox 2 protein developed heart failure symptoms similar to those in the blood-restricted mice, suggesting a functional connection between the reduction of RBFox2 and decline of the heart muscle.

The research team then sought to determine why, from a mechanistic point of view, the loss of RBFox2 would weaken the heart. To study this, they examined RBFox2-controlled changes in gene expression, which refers to the biological actions taken by genes, during various scenarios of heart development in mice. Specifically, the scientists compared changes detected in the hearts of RBFox2-deleted or blood-restricted mice to those that occur during post-natal heart “remodeling.” Remodeling is the process of heart strengthening that begins at birth and continues throughout childhood.

“The RBFox2 deletion-induced genetic changes are similar to those that occurred during blood restriction-induced heart failure, but opposite to those taking place during heart remodeling,” said Fu. “This indicates that the normal developmental program for strengthening heart performance is reversed during heart failure.”

Fu said the finding could lead to new drug targets for heart failure.

“We’ve learned that the RBFox2 protein is very important in keeping the heart muscle strong,” he said.  “Our research shows its diminished expression coincides with the weakening of the heart muscle. This strongly suggests a causal role for this protein in heart failure. By understanding these mechanisms, we may be able to find a way to prevent the decreased expression of RBFox2, which may help in preventing heart failure.”

Co-authors include Chaoliang Wei, Jinsong Qiu, Yu Zhou, Yuanchao Xue, Jing Hu, Kunfu Ouyang, Indroneal Banerjee, Hairi Li, Ju Chen, all at UC San Diego; and Caimei Zhang, Biyi Chen and Long-Sheng Song, all at the University of Iowa Carver College of Medicine.

Funding for this research came, in part, from the National Institutes of Health (grants GM049369, HG004659, and HG007005).

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UC Irvine first in Orange County to use remote heart failure monitoring system


Implanted CardioMEMS sensor helps reduce heart failure-related hospital readmissions.

Pranav Patel, UC Irvine

UC Irvine Health is the first medical center in Orange County to offer heart failure patients a wireless system that allows cardiologists to remotely monitor their pulmonary artery pressure and heart rate measurements.

Real-time access to this data enables doctors to proactively manage a patient’s condition, helping to reduce the rate of hospital readmission related to heart failure, the leading cause of hospitalization among adults 65 and older in the U.S., according to the American College of Cardiologists.

Heart failure refers to the progressive weakening of the heart muscle until it no longer pumps enough blood to meet the body’s needs. Advances in treatment allow more patients to survive hospitalization for heart failure, but more than 50 percent of them experience a new onset of symptoms and end up being readmitted within six months. Cardiologists hope the CardioMEMS Heart Failure System will help break this cycle.

Dr. Pranav Patel, chief of the UC Irvine Health Division of Cardiology, implanted the sensor in an 84-year-old male patient on Feb. 6.

“This technology will help change the way we manage heart failure patients,” said Patel. “Once the patient returns home, they must pay careful attention to changes in weight, ankle or abdominal swelling and shortness of breath. CardioMEMS monitors their heart rate and artery pressure daily, and transmits that information to a secure database at the hospital or clinic for review by a physician or a nurse. We can identify early warning signals before the patient feels any symptoms.”

The implantable sensor is about the size the size of a dime, with thin loops at each end, and is placed in the pulmonary artery during a right heart catheterization procedure. Once implanted, the patient cannot feel the sensor, and it does not interfere with other devices such as a pacemaker or defibrillator. The system wirelessly captures and transmits the patient’s data to a secure database for analysis.

CardioMEMS received FDA approval in May 2014 and is designed for use with patients who have been hospitalized the previous year with New York Heart Association Class III heart failure. The American Heart Association uses this classification system, which is based on how much a patient’s physical activity is limited by their heart condition.

“If the patient is experiencing rising pressure or any deterioration of their heart failure condition, we can immediately make changes to their medication, diet and daily activities,” Patel said. “Early detection is the key to preventing more serious complications, avoiding another emergency room visit or hospital stay, and enhancing the patient’s overall well-being.

The UC Irvine Health Heart Failure Program uses state-of-the-science equipment and technologies to identify the cause of heart failure, or cardiomyopathy. A multidisciplinary team then works with patients to stabilize their condition and develops a comprehensive treatment plan.

In each of the last four years, the program has received the American Heart Association’s Get With The Guidelines – Heart Failure Gold Plus Quality Achievement Award. The recognition signifies that UC Irvine Health has achieved the goal of treating heart failure patients according to prevention guidelines recommended by the American Heart Association/American College of Cardiology.

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Nerve regeneration therapy has potential to prevent arrythmias after heart attack


Findings could help in development of therapeutics for post-heart attack care.

A therapy currently under development for spinal cord injuries stimulates nerve regeneration in the heart and provides resistance to arrhythmias following a heart attack, according to a new study published today (Feb. 2) in the journal Nature Communications by researchers at Oregon Health & Science University (OHSU), Case Western Reserve University and UC Davis.

Millions of people have heart attacks each year, and those who survive have increased risks of arrhythmias — or abnormal heart rhythms — and sudden cardiac death. Recent clinical trials showed that the severity of nerve degeneration in the heart caused by heart attack predicts increased arrhythmia susceptibility. Surgical implantation of a cardioverter defibrillator (ICD), a device that tracks and restores heart rate, is one of the only effective therapies for treating arrhythmias following a heart attack.

“Our study initially sought a therapy that would stimulate nerve regeneration after a heart attack. It was a surprising and thrilling discovery that not only could this regeneration be achieved through both genetic and pharmaceutical approaches, but that it also decreases the heart’s susceptibility to arrhythmias,” said Beth Habecker, senior author and professor of physiology and pharmacology in the OHSU School of Medicine. “We are excited to use these findings to pursue the development of therapeutics for post-heart attack care.”

Habecker led a team of researchers in determining why nerves were excluded from cardiac scars after a heart attack. OHSU graduate student Ryan Gardner found that factors preventing nerve regrowth after a spinal cord injury were also present in the heart and that by blocking their actions in mice, via genetic knockout or pharmaceutical therapy, nerve regeneration occurred and arrhythmia susceptibility decreased. The therapy that proved successful was a chemical compound known as intracellular sigma peptide, which was developed for traumatic spinal cord injury by Jerry Silver and colleagues at Case Western Reserve University.

Crystal Ripplinger and Lianguo Wang of UC Davis used high-speed optical imaging of whole mouse hearts in action to assess the effects of nerve regeneration on electrical activity, calcium handling and arrhythmia susceptibility. This technique, available at just a handful of labs in the U.S., allowed the investigators to precisely visualize the cellular events that triggered lethal rhythms and was key to understanding why nerve regeneration prevented arrhythmia.

“Arrhythmia is one of the most unpredictable and life-threatening outcomes of a heart attack,” said Ripplinger,  assistant professor of pharmacology at the UC Davis School of Medicine. “Until now, we had always assumed that arrhythmias were mainly due to damage and death of heart cells. Our study is the first to suggest that treatments targeting nerve regeneration can normalize electrical activity and prevent arrhythmias in heart attack survivors. This finding opens the door to an entirely new avenue of anti-arrhythmic therapy.”

Habecker and Ripplinger hope their research will be applied to future studies in humans and may one day lead to an alternative treatment to ICD therapy.

Additional authors of the study, titled ”Targeting Protein Tyrosine Phosphatase After Myocardial Infarction Restores Cardiac Sympathetic Innervation and Prevents Arrhythmias,” were Jared Cregg and Bradley Lang of Case Western Reserve University, and Cassandra Dunbar and Bill Woodward of OHSU.

This work was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under award numbers HL093056, HL068231 and HL111600; the National Institute of Neurological Disorders and Stroke of the National Institutes of Health under award number NS25713; the American Heart Association under award number 12SDG9010015; and an Oregon Brain Institute Neurobiology of Disease Fellowship.

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Tiny infant has big impact on his community


Tiny Smiles Half Marathon is scheduled for Feb. 7.

By Tricia Tomiyoshi, UC Davis

“Miles” Keiser, though nicknamed “Tiny” by his family, an infant treated at UC Davis Children’s Hospital in 2011, is having a big effect on the lives of children with congenital heart disease in Sacramento and on his community.

Born in Northern California in June 2011, Tiny would undergo the first of three planned surgeries to correct hypoplastic left heart syndrome 10 days after birth, and would be treated afterward in the UC Davis Children’s Hospital Pediatric Intensive Care Unit/Pediatric Cardiac Intensive Care Unit.

The infant received his diminutive nickname from his pre-adoptive parents, Rick and Jean Keiser of Galt, who already had adopted two of Tiny’s siblings and were in the process of adopting their brother.

Tiny would spend most of his young life with his family at the hospital, punctuated by short visits in the Keiser home. The Keiser family was always by his side. Despite the best efforts of his physicians, chief among them associate professor of surgery and pediatrics Gary Raff, in December of 2011 Tiny lost his struggle to survive at just 6 months of age.

“We made some great friends in the hospital, including Dr. Raff and his team, all of the physicians in the PICU/PCICU and his cardiologists Michael Choy and Mark Parrish,” Rick Keiser said. “Everyone was amazing, from the housekeeping staff to Dr. Raff. They were incredible.”

After struggling with the loss of their child, the Keisers decided to establish a commemorative race in Tiny’s honor, the Tiny Smiles Half Marathon – “the tiny half,” to give back to the Children’s Hospital and other pediatric cardiac organizations. This year, 2015, Tiny Smiles has made the Children’s Heart Foundation one of its beneficiaries.

The Tiny Smiles Half Marathon is scheduled for Saturday, Feb. 7. On-site registration starts at 6 a.m. and the event ends at noon. It will combine a half-marathon of 13.1 miles starting at 8 a.m.; a 5 kilometer and 10 kilometer race starting at 8:15 a.m.; and a kids’ fun run starting at 9 a.m.

The race starts at Civic Drive and Chabolla Avenue in Galt; it ends at the Galt Fairgrounds. The half-marathon registration fee is $70; the 5k and 10k registration fee is $40. Registration closes on Thursday, Feb. 7, and is available through this link.

Tiny Smiles already has had some fundraising successes, including holding multiple blood drives and raising more than $10,000 for the UC Davis Children’s Hospital Pediatric Intensive Care Unit/Pediatric Cardiac Intensive Care Unit. Race sponsors include Fleet Feet Sports of Stockton; Central Valley Physical Therapy; SMUD, UC Davis Children’s Hospital, The City of Galt, Pro Transport Ambulance, The Taylor Family Foundation, Spaans Cookies and more.

For additional information about the race, please contact Rick Keiser at rick@tinysmilesrace.org, or (209) 329-4692.

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