Spotlight: Jeffrey Olgin, MD, Celebrating 15 Years as Division Chief

Build, Discover, Lead: 15 Years as Division Chief

Fall 2024 marks the 15^th anniversary of the appointment of Jeffrey Olgin, MD, as chief of the UCSF Division of Cardiology. Under his steady leadership, the division has experienced unprecedented clinical growth, made pioneering discoveries in many areas of heart health, and developed one of the nation’s premiere training programs for future cardiologists. He has also pursued his own vibrant research programs in atrial fibrillation and digital health.

Growing up, Jeffrey Olgin, MD, found medicine to be an ideal blend of using science to help others. He was especially drawn to cardiac electrophysiology – the study of the heart’s electrical system. “I’ve always found it fascinating,” he said. “It’s a very logical field – it’s physics. And from a clinical standpoint, you can actually cure people with very high rates.”

After earning his bachelor’s degree in biopsychology and his medical degree from the University of Pennsylvania, Dr. Olgin was drawn to UCSF because of its trailblazing discoveries in the area of electrophysiology. In 1981, Melvin Scheinman, MD, performed the first cardiac ablation in a human, strategically burning a small area of the heart to cure an abnormal heart rhythm, also known as a cardiac arrhythmia. “Dr. Scheinman made UCSF the ‘epicenter’ for innovation in electrophysiology,” he said. At UCSF, he completed his internal medicine residency, fellowships in general cardiology and cardiac electrophysiology, and a year as a research fellow at the UCSF Cardiovascular Research Institute (CVRI).

Dr. Olgin then served on the faculty of the Krannert Institute of Cardiology at Indiana University for seven years. In 2003 he was recruited back to the UCSF Division of Cardiology as chief of the Section of Cardiac Electrophysiology and Melvin M. Scheinman, MD Endowed Chair in Electrophysiology. During that time, Dr. Olgin also directed the Clinical Cardiac Electrophysiology Fellowship Program and served as medical director of the Cardiac Electrophysiology Lab at UCSF Medical Center. As section chief, he grew the electrophysiology faculty, established a broad outreach network to other hospitals and cardiology practices in San Francisco, and brought novel cardiac electrophysiology techniques and procedures to UCSF.

In 2009, Dr. Olgin was appointed chief of the UCSF Division of Cardiology and Ernest Gallo-Kanu Chatterjee Distinguished Professor in Clinical Cardiology, and also serves as co-director of the UCSF Heart and Vascular Center and as a CVRI investigator.

Illuminating Causes of Atrial Fibrillation

As a physician-scientist, Dr. Olgin has spent his career discovering more about the underlying causes of atrial fibrillation – the most common cardiac arrhythmia. It occurs when the atria, or the upper chambers of the heart, quiver rapidly and in a chaotic manner instead of squeezing in a coordinated way. “If you were to look at the atrium during atrial fibrillation, it looks like a bag of worms,” said Dr. Olgin, wiggling his fingers to imitate the disorganized muscular movement rather than the concerted pumping action of a healthy heart.

Although atrial fibrillation is not usually fatal by itself, the condition compromises the efficient pumping of blood to the rest of the body, which can lead to shortness of breath, fatigue and other symptoms. The sluggish flow of blood through the heart can also increase risk of blood clots, which can travel to the brain and cause a stroke. “We believe that atrial fibrillation is a late manifestation of a disease process,” said Dr. Olgin. “It may take years to develop the necessary changes in the atria that ultimately result in atrial fibrillation.” His lab seeks to better understand this disease process, so it can be diagnosed and treated earlier.

Some patients go in and out of atrial fibrillation; others experience this arrhythmia for longer periods, or even constantly. According to the U.S. Centers for Disease Control and Prevention, as many as 6 million Americans may have atrial fibrillation. Its prevalence is projected to increase significantly in the coming decades, since aging, high blood pressure, diabetes and obesity are all risk factors.

Describing Unique Traits of the Atrium

Dr. Olgin’s lab has made pivotal discoveries about the biology of atrial fibrillation. His group discovered that scarring in the heart, also known as fibrosis, is not merely a result of atrial fibrillation, but actually produces disruptions in the flow of electrical impulses through the heart which lead to atrial fibrillation. They also found that TGF-β signaling is key to this fibrotic process in the atrium.

Not all heart tissue is created equal. Dr. Olgin has also been trying to discover which characteristics of the atria make them particularly vulnerable to developing fibrosis, compared with the ventricles – the lower two chambers of the heart. “Certain stimuli, such as sleep apnea or heart failure, cause fibrosis in the atrium in a very profound way, but don’t have much effect in the ventricle,” he said. “As with a lot of things in biology, it’s not caused by one single factor.”

Other researchers had found that a family of proteins called natriuretic peptides serve as a system of “brake pedals” for the inflammatory and fibrotic processes which occur after a heart attack or other cardiac injury. The Olgin Lab identified a protein called the natriuretic peptide clearance (NPR-C) receptor, which is abundantly expressed in the atria but comparatively scarce in the ventricles. “NPR-C works by removing one of the ‘brake pedals’ from the fibrotic process,” said Dr. Olgin. Because NPR-C is so plentiful in the atria, it is easier for fibrosis to occur in the atrium than the ventricle. His group is also investigating other pathways that appear to regulate TGF-β-mediated fibrosis differently in the atrium than the ventricle.

They hypothesize that this difference in the physiologic makeup of the atrium and ventricle is related to their distinct functions. The atria have a relatively easier job, since they are only responsible for pumping blood to heart chambers directly below them. “The atrium is a thin-walled chamber,” said Dr. Olgin. “It’s built to have some amount of normal collagen deposition. If it didn’t have biological processes for some amount of baseline fibrosis, it would blow up like a balloon under those pressures. Because that fibrotic process is already revved up, as soon as you tip that scale just a bit, it’s amplified, leading to abnormal fibrosis (scarring from deposition of excess collagen).”

By contrast, the ventricles have a heavier lift. They are the powerhouse chambers of the heart, pumping blood from the heart to the entire rest of the body. “The ventricle has a lot of muscle thickness, so it’s not as prone to blowing up as the atrium, and doesn’t need as much of that fibrosis backbone to keep it functioning,” said Dr. Olgin.

His lab’s most recent work, using RNA sequencing, has also revealed that the fibroblasts (the cells that produce collagen) of the atrium and ventricle have entirely different cellular populations and RNA expression patterns, matched to their distinct biological functions. They also found that the right ventricle, which is relatively thin-walled, has a fibroblast population that is more similar to its atrial neighbors than the left ventricle.

Trigger Sites and Border Zones

Dr. Olgin’s lab has also learned more about the origins of the rogue electrical signals that trigger atrial fibrillation. Many of these signals originate in the pulmonary veins, which carry oxygenated blood from the lungs back to the heart. In an animal model, they found that the areas where the pulmonary veins connect into the left atrium may have some variation of electrical conduction speeds and other alterations that make them vulnerable to generating abnormal electrical signals. They also hypothesize that the circular shape of the pulmonary vein could amplify the tendency for these rogue signals to loop around and around, rather than petering out.

“The pulmonary veins are just the triggers, and if that trigger doesn’t occur in a vulnerable substrate, then they’re just extra beats,” said Dr. Olgin. “But if they occur in a vulnerable substrate after remodeling, then it will induce atrial fibrillation, and that atrial fibrillation will be longer and longer lasting.”

Dr. Olgin has also made important discoveries about how to reduce the likelihood of a potentially life-threatening arrhythmia called ventricular tachycardia. In an animal model, his lab found that while a dense scar develops around the affected area to prevent the heart from developing a hole, interstitial fibrosis (less dense scar intermingled with normal heart cells) may also develop in the immediate area around the acutely injured part of the heart. “This secondary remodeling appears as little tentacles of collagen between cells, and they can cause ventricular tachycardia,” he said.

They conducted experiments to dial down the interstitial fibrosis in the border zone between the dense scar tissue and healthy cells, showing that it helped prevent development of arrhythmias after a heart attack. They also found that the signaling pathways that produced the interstitial fibrosis were different than those that produced the dense scar, so they could target just the weak signals that produced the ventricular tachycardia without interfering with the protective formation of dense scar in the part of the heart most impacted by a heart attack. Dr. Olgin believes those lessons learned about muting interstitial fibrosis signals may have some utility for preventing atrial fibrillation.

Creating a New Research Platform

In addition to his lab research, Dr. Olgin leads a clinical research program which is pursuing new ways to better detect and treat cardiac arrhythmias.

One clinical dilemma is that heart attack survivors whose hearts have decreased ejection fraction, or the ability to pump blood, have a high risk of experiencing sudden death in the first few months after their heart attack. Implantable cardioverter-defibrillators (ICDs) can shock a patient’s heart out of a life-threatening arrhythmia, but current guidelines require patients to wait up to three months before becoming eligible to receive an ICD.

Dr. Olgin and his colleagues led the Vest prevention of Early Sudden death Trial (VEST), a multicenter, international randomized clinical trial to determine whether patients who used a wearable cardioverter-defibrillator during this high-risk period between having a heart attack and becoming eligible for an implantable ICD would reduce their risk of sudden death. The study results, published in the New England Journal of Medicine, demonstrated that the defibrillator vest did reduce overall mortality in the first three months after a significant heart attack, provided it was worn.  However, many patients found it difficult to wear the vest consistently.

“It had been very hard to recruit patients to VEST and other clinical trials I have been involved with, and it seemed like we ought to be able to use technology to make enrollment and follow-up easier,” said Dr. Olgin. In 2012, he partnered with Gregory Marcus, MD, MAS, now associate chief of research for UCSF Cardiology, and Mark Pletcher, MD, MPH, now chair of the Department of Epidemiology and Biostatistics, to start the Health eHeart Study.

His work leverages the internet, mobile technology, sensors and biomarkers to follow more than 200,000 participants who complete periodic questionnaires from their smartphone, tablet or computer. Participants are also invited to join various substudies, based on their particular health characteristics. Because they are enrolled through this central study and research can usually be conducted without the need for in-person visits, it allows for rapid enrollment, low overhead, and the ability for participants to easily contribute data streams from wearable sensors as well as their electronic health records.

Dr. Olgin and his colleagues received funding from the National Institutes of Health (NIH) to build out this pilot, creating the Eureka digital research platform. It allows investigators across UCSF and nationally to conduct direct-to-participant research studies. Eureka has now enrolled more than 500,000 participants across nearly 70 studies focusing on health conditions ranging from diabetes to inflammatory bowel disease, cancer and Parkinson’s disease. Most studies are funded by the NIH or the Patient-Centered Outcomes Research Institute (PCORI).

Eureka also helps investigators like Dr. Olgin develop novel mobile health tools for both research and clinical care. For example, he and his colleagues developed a novel algorithm for atrial fibrillation detection using Apple watches.

Predicting and Preventing Atrial Fibrillation

Dr. Olgin leads BEAT-AFib Study, which uses the Eureka platform to find ways to prevent atrial fibrillation. “The idea is to try to identify it before someone develops atrial fibrillation,” he said. “Right now, we have no way to do that, but we’re looking at very early markers of atrial myopathy, atrial remodeling, blood-borne signals of atrial fibrillation, and very high-resolution ECG signals of atrial conduction abnormalities to see if we can predict who will develop atrial fibrillation.”

Identifying people in the earliest stages of atrial fibrillation could allow them to pinpoint biomarkers – such as signals that could be detected through blood draws or subtle findings in an echocardiogram or ECG – indicating someone is at high risk of developing atrial fibrillation.

Dr. Olgin hopes this approach will help identify potential interventions. “Once cholesterol levels were measurable and understood to be one of the most important risk factors for coronary disease, we’ve been able to treat people aggressively with statins and other medications to prevent them from developing coronary disease,” he said. “Could we do the same thing with atrial fibrillation? Is there a combination of markers that could indicate, ‘This person is at risk, and therefore we’re going to be super aggressive at weight loss, treating sleep apnea, hypertension management, and decreasing alcohol intake?’”

He would like to figure out a way to enrich his study population with people who are likely to develop atrial fibrillation, but then catch them early, before they’ve developed it. “That would allow us to power small trials of specific compounds to interrupt the fibrotic cascade,” said Dr. Olgin. “For example, we’d like to study whether approaches such as blocking NPR-C might delay progression of atrial fibrillation in at-risk people. Right now it would take thousands of patients [from the general population] to identify what interventions could produce an outcome of less atrial fibrillation.”

In addition to his own studies, Dr. Olgin’s lab also plays a supporting role for many other cardiac research projects because of their expertise in cardiac physiology. For example, his lab conducted molecular assays for studies led by Dr. Marcus on alcohol and the heart. They also completed high-resolution mapping and molecular studies in physiology for arrhythmia investigations led by Edward P. Gerstenfeld, MD, MS, chief of the Cardiac Electrophysiology and Arrhythmia Service and Melvin Scheinman Endowed Professor of Medicine.

Lowering Cost, Expanding Scale of Clinical Research

Dr. Olgin is also involved in three NIH-funded trials powered by the Eureka platform, serving as co-principal investigator of the digital coordinating center. The first is the REACT-AF Trial (Rhythm Evaluation for AntiCoagulaTion with Continuous Monitoring of Atrial Fibrillation), which is randomizing participants with atrial fibrillation to continue taking a daily oral anticoagulant to prevent strokes, or wear an Apple watch with a special Eureka algorithm which detects atrial fibrillation.

If the watch senses the participant is having an atrial fibrillation episode, it instructs the wearer to take an anticoagulant for the next 30 days. “This way, when participants are not in atrial fibrillation, they aren’t taking an anticoagulant,” said Dr. Olgin. “If effective, this approach could support a precision medicine approach, guiding patients to take a blood thinner as needed rather than every day for the rest of their lives. This could reduce side effects such as bleeding events, while also preventing stroke.”

REACT-AF seeks to enroll more than 5,000 participants at about 80 sites, and all follow-up is being done through Eureka. “We’re a year and a couple months in to the study, with a 90 percent compliance rate,” said Dr. Olgin. “The main innovation of REACT is that it’s a much cheaper study. We don’t need coordinators at our 80 sites calling every participant or conducting follow-up appointments. We have a centralized call center which reaches out to the 10 percent of participants who have not yet answered their outcome surveys in the Eureka app. This is a really interesting experiment in taking what would normally have been a very expensive study because of the personnel cost, and making it much less expensive.”

The second study is called HeartShare, focusing on a poorly understood condition called heart failure with preserved ejection fraction (HFpEF). Unlike heart failure with reduced ejection fraction (HFrEF), in which the heart’s ability to squeeze blood efficiently is compromised, the hearts of HFpEF patients retain their squeezing function but have difficulty relaxing, which interferes with the heart’s capacity to adequately fill with blood in between beats. Currently there are few effective treatments. “HFpEF is a hodgepodge disease, and we don’t understand what makes up the different groups,” said Dr. Olgin.

HeartShare is a longitudinal cohort study with two groups. The HeartShare Deep Phenotyping group will enroll up to 2,000 participants with HFpEF who come in person to undergo a number of tests, including magnetic resonance imaging (MRI) studies, echocardiograms and blood tests. They will return annually for follow-up visits and complete monthly surveys online or by phone. The HeartShare Registry group will enroll up to 10,000 participants with heart failure of any kind who participate entirely remotely, completing an intake questionnaire as well as periodic surveys, questionnaires and assessments via the Eureka app.

The third study is called CINEMAS (Cardiac Imaging of Neuro-Embolic Mechanisms in Atriopathies causing Stroke). It focuses on patients who have had a stroke without a prior diagnosis of atrial fibrillation. The current methods for diagnosing atrial fibrillation include getting a 15 to 20 second electrocardiogram to record electrical activity of the heart and wearing a heart monitor for two weeks. However, since atrial fibrillation may come and go, these methods might not detect arrhythmia if it occurs outside the time when a patient is actively monitored. In addition to completing echocardiograms and MRIs, CINEMAS participants will wear smartwatches to continuously monitor them for atrial fibrillation. The Eureka platform and its smartwatch algorithm support collection of patient monitoring and outcomes data.

Supporting Continual Growth

In addition to his robust clinical and translational research, Dr. Olgin still sees patients in clinic and on the inpatient electrophysiology service. As division chief since 2009, he has led the division through an era of tremendous expansion. “When I took over the division from Bill Grossman, I was fortunate that the division was in very good shape, which allowed me to focus on areas that needed to be built,” said Dr. Olgin. “That’s a credit to Bill and the faculty we have.”

“His overall accomplishments have been supporting innovation and overseeing symmetrical growth within the division,” said William Grossman, MD, Charles and Helen Schwab Endowed Chair in Preventive Cardiology and Dr. Olgin’s predecessor as division chief. “He’s maintained our excellent relationship with the CVRI and made it better than ever. As UCSF Health has expanded, he’s done an exceptional job of recruiting high-caliber faculty, including 14 new faculty members this year. That requires constantly keeping your eyes open for talent, cultivating relationships, and putting together competitive recruitment packages with the help of philanthropy. Jeff has done a fantastic job.”

Since 2009, the division grew from about 35 faculty to more than 90 in 2024. Dr. Olgin and his colleagues have recruited a diverse faculty, including graduates of the UCSF Cardiology Fellowship program as well as outside recruits, a range of junior and senior faculty, and those focused on clinical excellence, teaching, basic and translational science, and clinical research.

In the last 15 years, clinic sites have expanded from Mission Bay and a small clinic on the Parnassus campus, to today’s broad network which includes a larger space at Parnassus, a clinic at Daniel Burnham Court in the Cathedral Hill neighborhood of San Francisco, and additional clinics in San Mateo and Berkeley. Clinic visits have expanded from approximately 12,000 annually to more than 64,000 this year.

Dr. Olgin has also helped build infrastructure to support faculty success in research. For example, the Cardiology Clinical Research Unit has more than tripled, now including more than 30 clinical research coordinators supporting more than 125 active clinical studies. He also helped establish a division-wide biobank a few years ago to facilitate collection of heart tissue and other biosamples. This investment has paid off, with outstanding levels of both NIH- and non-NIH grants awarded to UCSF Cardiology faculty.

Dr. Olgin has garnered substantial philanthropic support, which has fueled innovation in all areas, including novel clinical initiatives, research, recruitment of top-notch faculty, and helping make the UCSF Cardiology Fellowship Program one of the most prestigious in the country. Private donations have allowed him to create several internal granting mechanisms, providing seed money for faculty members’ most creative ideas. For example, the Cardiology Innovation Awards support high-risk, high-reward research, and the Cardiology Scholars Awards fund initiatives in clinical excellence, such as creating a remote monitoring program for patients who developed hypertension due to preeclampsia during pregnancy and are at higher risk of heart disease.

Building Excellence in Every Area

Behind the scenes, Dr. Olgin also spends much of his time ensuring the division’s long-term financial stability, and partnering with UCSF Health to expand existing programs and build new ones. “I have a good relationship with the health system, in part because every time we say we’re going to deliver, we do,” he said.

For example, under the leadership of Liviu Klein, MD, MS, medical director of the Advanced Heart Failure Comprehensive Care Center, in partnership with the UCSF Division of Adult Cardiothoracic Surgery, the UCSF Heart Transplant Program has transformed into a high-volume service, performing nearly 90 heart transplants in 2024. Dr. Olgin recruited Javid Moslehi, MD, William Grossman, MD Distinguished Professor in Cardiology, to found the Section of Cardio-Oncology and Immunology, which has quickly become one of the best-known programs in the country. The UCSF Hypertrophic Cardiomyopathy Center of Excellence, under the direction of Roselle Abraham, MD, and Ted Abraham, MD, is similarly well-known.

Under the direction of Sammy Elmariah, MD, MPH, the Adult Cardiac Catheterization Laboratory is pioneering new treatments for valve disease. The Cardiovascular Genetics Program, led by Vasanth Vedantham, MD, PhD, provides tailored care to patients based on their genetic makeup, and conducts cutting-edge research on the genetic underpinnings of heart disease. The UCSF Cardiac Electrophysiology and Arrhythmia Service, led by Dr. Gerstenfeld, continues its tradition of pioneering work, dating back to the first cardiac ablation in humans performed by Melvin Scheinman, MD, in 1981.

Dr. Olgin has also overseen an expansion of the UCSF Cardiology Fellowship Program, led by Atif Qasim, MD, expanding the overall number of fellows and adding new subspecialty fellowship programs. “We are by far the largest fellowship program in the Department of Medicine, and at any one time we have about 40 fellows,” said Dr. Olgin.

‘Cultivating a Highly Collaborative Culture’

Looking ahead, Dr. Olgin sees many new opportunities for growth, including the recent acquisition of St. Mary’s Medical Center. “Most of our programs are space-constrained, and I look forward to figuring out how to leverage St. Mary’s to help ease our space and access constraints,” he said. “I’m also really excited about the new hospital building and renovations happening on the Parnassus Campus. Just like Mission Bay went from being an outpost to an incredible, vibrant campus, in 10 years Parnassus will have a similar feel. I’m excited to see that unfold and how it works for our division.”

He hopes these expanded footprints will help address the twin needs for clinical care volume growth, as well more consolidated academic space to enhance cohesion within the division.

As division chief, Dr. Olgin has learned valuable lessons about the importance of good processes. “My tendency, and perhaps that of a lot of physicians, is to get things done quickly,” he said. “I’ve learned to balance that with making sure there is stakeholder buy-in, being more thoughtful about identifying and defining problems, and making sure we implement the right solutions. It’s good to pause and be more deliberate about that process. It’s also been helpful to assume that people want to do the right thing, and then figuring out how to help them make the right decisions.”

“Jeff Olgin’s leadership in cardiology has been remarkable,” said Robert Wachter, MD, chair of the UCSF Department of Medicine, Holly Smith Distinguished Professor in Science and Medicine, and Benioff Endowed Chair in Hospital Medicine. “He has strengthened existing programs and built many new ones in areas such as structural heart disease, critical care cardiology, and cardio-oncology. He has energized and diversified the division’s research portfolio, including groundbreaking studies using novel digital tools. He has improved the culture of the division, and been exceptionally successful in fundraising. He is a model division chief.”

“One of the reasons I’m still doing this, 15 years later, is because it’s still really fun to build programs, support other faculty, and see their programs develop,” said Dr. Olgin. “We’ve also been very intentional in cultivating a highly collaborative culture in the division. People feel this is a place where they can grow, accomplish things, and access deep and broad expertise, both in research and clinically. Because of that, patients get really good care.”

Outside of medicine and science, Dr. Olgin enjoys mountain biking, hiking, and spending time with his wife and their two children.

-Elizabeth Chur