LOS ANGELES, July 11: People living in under-resourced neighborhoods are more likely to develop high blood pressure – also known as hypertension – than those in wealthier areas, according to new research from Cedars-Sinai Health Sciences University. The study was published in the American Journal of Hypertension.
“The increased risk for people in the least healthy neighborhoods was similar to being a full decade older than their counterparts in the healthiest neighborhoods,” said Joseph Ebinger, MD, MS, associate professor of Cardiology and director of the Coronary Intensive Care Unit in the Smidt Heart Institute at Cedars-Sinai and senior author of the study. “Although such disparities in hypertension prevalence are known to occur, our study is notable because it demonstrates the persistence of these differences over time.”
Investigators tracked the blood pressure of more than 94,000 Cedars-Sinai patients between 2018 and 2023. They found that, over time, patients in neighborhoods in the lowest 25% of rankings on a scale that assesses education, job opportunities and other social conditions were 7% more likely to develop high blood pressure than patients in the top 75% of neighborhoods.
“Many people do not know they have hypertension and are not being treated for it,” Ebinger said. “Our findings suggest cliniciansmay consider targeting interventionsin the context of socioeconomic data to help preventat-risk patients from developing the condition, which increases their risk for heart disease, kidney disease and stroke.”
Additional Cedars-Sinai authors include Jonathan N. Le, MD; Tzu Yu Huang, MPH; Patrick G. Botting, MSHS; Ellie Albertson, MPH, PhD; Natalie A. Bello, MD, MPH; Christina Harris, MD; Alan Kwan, MD; and Susan Cheng, MD, MPH.
Other authors include Brian Claggett, PhD.
Funding: This study was supported by grant funding from the NIH/NHLBI (K23HL 153888-03) and by the Smidt Discovery Fund of the Smidt Heart Institute.
Study Links Angina Severity to Composition of Heart Plaque
About half of women who experience angina, chest pain presumed to be from obstructed blood flow to the heart, don’t have significant coronary artery blockage. And yet, these women have elevated risk for heart attacks and strokes. New research from Cedars-Sinai Health Sciences University, published in Communications Medicine, helps explain why.
Investigators found that buildup in the coronary arteries of women with severe angina was more likely to consist of soft plaque. Soft plaque, also known as noncalcified plaque, is more prone to rupture and trigger dangerous blood clots than its more stable counterpart, known as calcified or hard plaque.
The findings were based on artificial intelligence analysis of more than 100 CT coronary angiograms (noninvasive heart scans) performed on women with angina and coronary artery disease.
“Our findings expand our understanding of why angina occurs in women without significant artery blockages,” said Damini Dey, PhD, professor of Biomedical Sciences at Cedars-Sinai and corresponding author of the study. “The findings also suggest the need to consider treating these women with medications to prevent the buildup of plaques and reduce the risk of heart attacks and other cardiac events.”
Other Cedars-Sinai authors include Rafal Wolny, Guadalupe Flores Tomasino, Kajetan Grodecki, Joel Lenell, Caroline Park, Rebekah Park, Jacek Kwiecinski, Daniel S. Berman, Piotr J. Slomka, Janet Wei, Martha Gulati and C. Noel Bairey Merz.
Other authors include Osama Dasa, Vinicius Calsavara, Matthew J. Budoff, Eileen Handberg, Carl J. Pepine, Leslee J. Shaw and Balaji Tamarappoo.
Acknowledgements: This study was primarily supported by grants from the NHLBI R01HL151266 and 1R01HL148787. It was also supported by CDMRP-DoD W81XWH-17-2-0030 and McJunkin Family Foundation through funds distributed by the University of Florida, Department of Medicine, Clinical Research Consortium CDRN-1501-26692, the Edythe L. Broad and the Constance Austin Women’s Heart Research Fellowships, Cedars-Sinai Medical Center, Los Angeles, CA, the Barbra Streisand Women’s Cardiovascular Research and Education Program, Cedars-Sinai Medical Center, Los Angeles, the Linda Joy Pollin Women’s Heart Health Program, the Erika Glazer Women’s Heart Health Project, Cedars-Sinai Medical Center, Los Angeles, CA; and the VA Women’s Health Practice-Based Research Network VA HSR&D SDR 10-012. R.W. is supported by a Polish National Science Centre (grant number 2021/43/D/NZ5/02434) and Medical Research Agency (grant number KPOD.07.07-IW.07-0150/24).
Competing interests: Drs. Berman, Slomka, and Dey have received software royalties from Cedars-Sinai Medical Center and report equity in APQ Health.
How the Brain Influences Aging Throughout the Body
Cedars-Sinai Health Sciences University investigators are helping clarify the brain’s role in how the body ages. Their study, published in Nature Communications, identified a group of brain cells that become overactive with age and may impair the body’s ability to maintain consistent temperature, stay properly hydrated and efficiently convert food into energy.
“These age-related problems make the body more vulnerable to illness and often rob people of their independence,” said Celine Riera, PhD, associate professor of Biomedical Sciences and Neurology, research scientist in the Board of Governors Regenerative Medicine Institute at Cedars-Sinai, and senior author of the study. “We found that a group of brain cells that produce a hormone called vasopressin become overactive with age, contributing to these problems.”
These brain cells are in the hypothalamus, at the base of the brain. In healthy amounts, the vasopressin they produce helps blood vessels constrict. It also helps the kidneys control the amount of water and salt in the body, which helps control blood pressure and urine output.
When investigators artificially activated these brain cells in young laboratory mice, the cells produced more vasopressin and the mice developed changes similar to those seen in aging mice. Conversely, when investigators reduced the activity of these brain cells in aging mice, the mice were better able to maintain body temperature, hydration and metabolism, Riera said.
The findings provide scientists with new context for understanding how the brain contributes to systemic aging. Future studies may explore whether therapies targeting these brain cells can reduce age-related health problems and improve quality of life in aging people, Riera said.
Additional Cedars-Sinai authors include Nancy Morones, Predrag Jovanovic, Anna Sanetra, Kaitlyn Jang, Nareg Keshishian, Zhihan Clay Cui, Edward Novinbakht, Joshua J. Breunig, Anders Berg, Tamar Pirtskhalava, Selim Chaib, S Ananth Karumanchi, Tamar Tchkonia, Katlin Silm, and James L. Kirkland.
Funding: This work was supported by the Larry L Hillblom Foundation startup grant (C.E.R.), the Cedars-Sinai Pilot Award from the Center on Aging and Diabetes (C.E.R.), the CIRM Scholar fund EDUC-12751 (N.M.), the National Institute of Aging grant RF1AG091203 (C.E.R.) and R37AG013925 (J.L.K., T.T.).
Possible Biomarker Linked to Aggressive Thyroid Cancer
Cedars-Sinai Health Sciences University investigators have found a possible way to identify which patients are at greatest risk of thyroid cancer recurrence and might benefit from more aggressive treatment. Their findings were published in Science Advances.
“The incidence of thyroid cancer has tripled over the past three decades and it is now the most common cancer in adolescents and young adults,” said Anthony T. Nguyen, MD, PhD, assistant professor of Radiation Oncology and Biomedical Sciences and first author of the study. “The biomarker we identified, if further validated, could help us identify patients likely to have more aggressive disease so that we can intensify their treatment.”
In five patients with locally advanced thyroid cancer, investigators used single-cell RNA sequencing to analyze gene expression patterns in individual cells of the tumor microenvironment, comparing primary thyroid tumors and matched lymph nodes to which cancer had spread. Their findings were confirmed in a separate group of 21 patients with thyroid cancer.
Among multiple differences between primary tumor and lymph node, investigators found that an increase in IL7 receptor protein expression on the surface of immune cells in the lymph nodes was linked to improved patient outcomes.
“Our study is one of the first to use single-cell RNA sequencing to identify a lymph node-specific biomarker for aggressive thyroid cancer,” said Allen Ho, MD, professor of Surgery and co-corresponding author of the study. “Low levels of IL7 receptor in the lymph node can potentially be used to identify patients with more aggressive disease who are candidates for treatment intensification.”
The other corresponding author is Stephen Shiao, MD, PhD, professor of Radiation Oncology and Biomedical Sciences and co-leader of the Cancer Therapeutics Program.
“This study is an example of the promise of single-cell RNA sequencing to assess the status of tumors for more targeted treatment,” said Robert Figlin, MD, interim director of Cedars-Sinai Cancer.
Additional Cedars-Sinai authors include Jolene Viramontes, Isaiah Vazquez, Catriona McWilliam, Vaishnavi Devarakonda, Regina Henson, Wendy L. Sacks, Jon Mallen-St Clair, Yufei Chen, Evan Walgama, Kevin S. Scher, Justin Moyers, Julie K. Jang, Zachary S. Zumsteg, and Wonwoo Shon.
Howard M. Sandler is also an author of the study.
Funding: This work was supported by: National Institutes of Health grant K08CA191139 (SLS), Conquer Cancer Young Investigator Award (ATN), American Society for Radiation Oncology Junior Faculty Award (SLS), Cedars-Sinai Precision Health Grant (ASH).
New Expert Consensus Aims to Improve Diagnostics in Emergency Care
Cedars-Sinai Health Sciences University investigators convened a panel of medical experts to develop new definitions to improve diagnostic quality and safety in emergency departments. The definitions – diagnostic excellence and missed diagnostic opportunity—address a longstanding gap in the field, as they recognize the role uncertainty plays in emergency care. Their findings are published in Annals of Emergency Medicine.
“Our new definitions can be used to guide investigations about the diagnostic process in emergency departments to identify opportunities for improvement,” said study first author Carl Berdahl, MD, MS, associate professor of Medicine and Emergency Medicine at Cedars-Sinai. “Future work should explore the integration of these definitions into diagnostic research and quality and safety programs, and evaluate the impact on patients’ health outcomes.”
A 2022 report from the Agency for Healthcare Research and Quality suggested about 1 in 18 patients visiting emergency departments each year receive a misdiagnosis that causes preventable harm or worsens their outcome. This report sparked controversy about what the emergency department’s role should be in assigning diagnoses.
The panel of 10 experts from emergency medicine and related specialties reviewed scientific evidence to arrive at the new definitions. It defined “diagnostic excellence” as using evidence-based practices to arrive at an accurate and timely explanation of a patient’s condition based on the information available at the time; communicating that diagnosis to patients and families; and providing equitable, patient-centered care. It defined a “missed diagnostic opportunity” as a measurable departure from evidence-based practice that may contribute to a delayed or inaccurate diagnosis, or a failure in communicating diagnostic information to patients and families.
Additional Cedars-Sinai authors include Sam S. Torbati, MD; Maxim P. Ptacek, BS; Nabeel Qureshi, PhD; and Teryl K. Nuckols, MD, MSHS.
Additional authors include Gordon D. Schiff, MD; Arjun K. Venkatesh, MD, MBA; Edward G. Seferian, MD, MS; and Johan Carrascoza-Bolanos, BS.
Members of the Multidisciplinary ED Diagnostic Excellence Panel include Adebisi Alli, DO, MS; Marie L. Crandall, MD, MPH; Anuj K. Dalal, MD; Kelly T. Gleason, PhD, BSN; Sachin Gupta, PhD, MBA; Aaryn K. Hammond, MD; Victoria Nash, MS; Michelle D. Lall, MD, MHS, Robert Sherwin, MD; Scott D. Steenburg, MD, MS.
Funding: This work was supported by the Emergency Medicine Foundation’s Diagnostic Excellence in Emergency Medicine Grant. Dr. Berdahl was also supported by K08HS029534 and the National Academy of Medicine Scholars in Diagnostic Excellence Program.
Preclinical Study: Novel CAR T-Cell Therapy Controls Bladder Cancer
Investigators at Cedars-Sinai Health Sciences University have discovered that delivering a specialized CAR T-cell therapy directly into the bladder could control bladder cancer and reduce the need for bladder-removal surgery. The preclinical study, published in the Journal of Experimental Medicine, identifies a strategy that, after further testing in humans, could improve management of organ-confined tumors.
“Current bladder cancer therapies are limited by drug shortages, severe side effects and high recurrence rates, often forcing patients to undergo life-changing bladder-removal surgery,” said Parwiz Abrahimi, MD, PhD, urologic oncologist in the Department of Urology at Cedars-Sinai and first author of the study. “This new strategy has the potential to dramatically reduce the necessity for bladder removal, preserving the patient’s quality of life while maintaining control of their cancer.”
In laboratory mice, investigators found this localized approach safely confined the treatment to the bladder and prevented the engineered cells from escaping into the bloodstream. The findings support the practice of delivering cellular therapies directly via a catheter to treat organ-confined bladder cancers.
Additional authors include Jonathan F. Khan, Alyssa Duren-Lubanski, Winson Cai, Yacine Marouf, Nan Chen, Daniel Hirschhorn, Renata Mammone, Ileana C. Miranda, Jacob E. Tallman, Alejandra Vela-Moreno, Mohamad Hamieh, Bishoy M. Faltas, Thomas M. Carroll, Micaela L. Everitt, Hari K.K. Subramanian, Hikmat A. Al-Ahmadie, Olivier Elemento, Benjamin D. Hopkins, Douglas S. Scherr, Renier J. Brentjens, Jedd D. Wolchok and Taha Merghoub.
Cedars-Sinai Scientists Identify New Driver of Inflammation
Investigators at Cedars-Sinai Health Sciences University have identified a previously unrecognized driver of harmful inflammation. The findings, published in Nature Communications, center around TRIM21, a protein also linked to autoimmune disease.
“Our findings suggest TRIM21 may be one reason some autoimmune and autoinflammatory diseases share similar features,” said Jessica Carriere, PhD, an assistant professor of Pathology and Laboratory Medicine at Cedars-Sinai and co-corresponding author of the study. “By targeting TRIM21, we may eventually be able to develop new treatments for a range of inflammatory diseases.”
Researchers discovered that TRIM21 helps build the inflammasome, an alarm-like structure inside immune cells that triggers inflammation. While this alarm helps protect the body from infection, it also can become overactive and trigger excessive inflammation that damages healthy tissue and contributes to disease.
The study, which looked at laboratory mice and human patient samples, showed that TRIM21 not only helps activate this inflammatory response but also enables inflammatory signals to spread from dying immune cells to nearby cells, potentially creating a chain reaction that drives inflammation throughout the body.
Additional Cedars-Sinai authors include Sana Ismaeel, Elisabeth Jäger, Vinicius Dantas Martins, Kaiden A. Sims, Huyen Nguyen, Justin Ruiz, Hemisha Khatri, Savita Devi, Andrea Dorfleutner and Christian Stehlik.
Additional authors include Chawon Yun, Sonal Khare, Lan H. Chu, Lucia de Almeida, Janset Onyuru, Jae Jin Chae, Daniel L. Kastner, Lori Broderick and Hal M. Hoffman.
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