Month: May 2018

Assessing our nation’s control of blood pressure: A Q&A

Photo by agilemktg1

Whenever you see a physician, an assistant probably takes your blood pressure. But does she tell you what the numbers mean?

The top number, called the systolic blood pressure (SBP), measures the maximum pressure your heart exerts while beating. The bottom number, called the diastolic blood pressure (DBP), measures the amount of pressure in your arteries between beats. Both are important. High systolic and diastolic blood pressure are associated with a higher risk of heart attacks, heart failure, stroke and kidney disease.

But what is considered high enough to treat? I was recently surprised to learn that physicians are still debating the national blood pressure clinical guidelines. To learn more, I spoke with Shreya Shah, MD, a clinical instructor of primary care and population health at Stanford.”

Why have clinical guidelines for blood pressure been controversial?

“Recommendations regarding optimal blood pressure control have shifted over the past decade. In 2003, the recommendations were to target a systolic blood pressure less than 140 for most patients and less than 130 for patients with certain risk factors. In 2014, new recommendations relaxed the blood pressure goals to a SBP less than 140 for most patients and less than 150 for those 60 and above. This was a big change in recommendations and thus sparked controversy.

Newer studies, especially the SPRINT trial, point towards the increased benefits of more intensive blood pressure control. This led to the recent set of guidelines in 2017.

At Stanford, we’re working to bring blood pressures down as close to normal as possible. We are targeting a SBP less than 140 and DBP less than 90 in all patients. But for those with certain risk factors, especially increased risk for heart disease, we may recommend lowering the goal to a SBP less than 130 and DBP less than 80.”

Are these goals being met? What did your latest study find?

“Using a national database, Randall Stafford, MD, and I analyzed patterns of blood pressure control for millions of patients who were treated for hypertension in 2016.

Our study, which appears in the Journal of General Internal Medicine, found that we’re not doing a great job with blood pressure control: 43 percent of hypertension patients had a SBP of 140 or higher and 24 percent of patients had a SBP of 150 or higher.

There were also higher rates of uncontrolled blood pressure among certain demographic groups — blacks, Hispanics and patients with Medicaid. These groups may have had less intensive attention to their high blood pressure for a number of reasons, including less access to high quality care and an inability to afford some medications.”

What can be done?

“Studies have demonstrated that team-based care leads to better improvements in blood pressure when compared to traditional models of primary care. Team-based care for hypertension involves the patient and their primary care physician, as well as other health professionals such as pharmacists, nurses, dieticians, case managers and social workers. Especially for treatment strategies involving health behavior change, physicians may not be as effective as other people whose training focused on these skills.

Stanford has already implemented this team-based care model in our primary-care clinics. And we are looking at other strategies, including helping our patients to be more involved in managing their high blood pressure. For instance, I encourage patients to regularly measure their blood pressure at home. The American Heart Association has resources available with information about choosing a home blood pressure monitor and using the correct home blood pressure technique.

I also encourage my patients to adopt a largely plant-based diet, lose weight and become more physically active. These non-medication strategies can be helpful for preventing high blood pressure, but are also as an integral part of treating high blood pressure.”

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.

New understanding of cellular signaling could help design better drugs, Stanford study finds

Photo by scanrail/Getty Images

An effective drug with minimal side effects — the dream of all drug companies, physicians and patients. But is it an impossible dream?

Perhaps not, in light of new research led by Ron Dror, PhD, an associate professor of computer science at Stanford. IN collaboration with other researchers, Dror used computer simulations and lab experiments to better understand G-protein-coupled receptors, which are critical to drug development.

G-protein-coupled receptors (GPCRs) are involved in an incredible array of physiological processes in the human body, including vision, taste, smell, mood regulation and pain, to name just a few. As a result, GPCRs are the primary target for drugs — about 34 percent of all prescription pharmaceuticals currently on the market target them. Unfortunately, despite all of this drug research, many of the underlying mechanisms of how GPCRs function are still unclear.

We do know that GPCRs act like an inbox for biochemical messages, which alert the cells that nutrients are nearby or communicate information sent by other cells. These messages symbolize a variety of signaling or pharmaceutical molecules. When one of these molecules binds to a GPCR, the GPCR changes shape — triggering many molecular changes within the cell.

Dror’s team investigated the relationship between these GPCRs and a key family of molecules inside cells called arrestins, which can be activated by GPCRs and can lead to unanticipated side effects from medications. Specifically, they sought to understand how GPCRs activate arrestin, so they can use this knowledge in the future to design drugs with fewer side effects.

“We want the good without the bad — more effective drugs with fewer dangerous side effects,” Dror said in a recent Stanford news release. “For GPCRs, that often boils down to whether or not the drug causes the GPCR to stimulate arrestin.”

Researchers know that GPCR is composed of a long tail and a rounder core, which bind to distinct locations on the arrestin molecule. Based on past studies, it was believed that only the receptor’s tail activated the arrestin — causing it to change shape and begin signaling other molecules on its own.

However, Dror’s new study demonstrated that either the tail or core can activate arrestin, as recently reported in Nature. And the core and tail together can activate the arrestin even more, Dror said.

Using this new understanding, the researchers hope in the future to design drugs that activate arrestin in a more selective way to reduce drug side effects.

Dror concluded in the release:

“These behaviors are critical to drug effects, and this should help us in the next phase of our research as we try to learn more about the interplay of GPCRs and arrestins, and potentially, new drugs.”

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.

%d bloggers like this: