What Should your blood pressure targets be?

Adults treated at a target blood pressure level lower than commonly recommended had a reduced risk of cardiovascular disease and death.

While there were some adverse effects with the lower target, study results suggest that the benefits outweighed the risks.

High blood pressure, or hypertension, causes no direct symptoms, but can lead to serious health problems if left untreated.Brand X Pictures/Stockbyte/Thinkstock

Blood pressure is the force of blood pushing against the walls of the arteries. High blood pressure, or hypertension, occurs when this force is too high. About 1 in 3 U.S. adults has hypertension. The condition itself usually causes no symptoms, but it can damage the heart, blood vessels, kidneys, and other parts of the body if left untreated.

Blood pressure is typically given as 2 numbers, such as 110/70 millimeters of mercury (mm Hg). The first number is systolic pressure, which is measured as the heart beats to pump blood. The second is diastolic pressure, which is measured when the heart is at rest between beats.

NIH’s National Heart, Lung, and Blood Institute (NHLBI), along with other NIH components, sponsored a large clinical study to determine whether treating people with hypertension to a target systolic blood pressure of less than 120 mm Hg (intensive treatment) would be more beneficial than targeting a level of 140 mm Hg (standard treatment).

Researchers enrolled more than 9,300 participants, age 50 and older, from 102 medical centers and clinical practices throughout the U.S. and Puerto Rico. The participants had increased cardiovascular risk, but didn’t have diabetes. About 36% were women, 58% were white, 30% were African-American, and 11% were Hispanic. Approximately 28% were 75 or older, and 28% had chronic kidney disease.

Participants who were randomly assigned to the target of less than 120 mm Hg received 3 medications on average, while those whose target was less than 140 mm Hg received about 2. The researchers monitored a variety of cardiovascular disease outcomes.

NIH stopped the intervention in August 2015—a year earlier than planned and after a median follow-up of about 3 years—when it became apparent that the more intensive intervention was beneficial. The findings were published online in the New England Journal of Medicine on November 9, 2015.

The researchers found that targeting a systolic blood pressure of less than 120 mm Hg reduced rates of cardiovascular events, such as heart attack and heart failure, as well as stroke, by 25% compared to the 140 mm Hg target. The more intensive treatment also reduced the risk of death by 27%.

Certain types of serious consequences were more common in the group undergoing the intensive treatment. These included low blood pressure, fainting, electrolyte abnormalities, and acute kidney damage. However, rates of other serious adverse events that may be associated with lower blood pressure—such as slow heart rate and falls with injuries—were similar in both groups.

“Although the study provides strong evidence that a lower blood pressure target saves lives in people who are at higher risk for cardiovascular events, patients and their health care providers may want to wait to see how guideline groups incorporate this study and other scientific reports into any future hypertension guidelines,” says study co-author Dr. Lawrence Fine of NHLBI. “In the meantime, patients should talk to their health care providers to determine whether this lower goal is best for their individual care.”

The researchers are continuing to assess the effects of the treatments on kidney disease, cognitive function, and dementia.

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Structure of a Key Blood Pressure Regulator

About 1 in 3 American adults has high blood pressure. This increases their risk of many conditions, including heart attack, heart failure, and stroke.

Angiotensin receptor blockers are used to treat high blood pressure, but can have other effects. Understanding the receptor’s structure and how medications interact with it will help in the design of more effective drugs. Image credit: AlexRaths/iStock.

One of the ways the human body regulates blood pressure is through a molecule called the angiotensin II type 1 receptor (AT1R). When the hormone angiotensin II binds to this receptor, it activates a pathway involving signaling molecules called G-proteins that constricts blood vessels and raises blood pressure. AT1R also activates other signaling pathways with different functions. For example, it can activate a pathway involving beta-arrestin proteins that reduces blood pressure and has other cardiovascular benefits.

High blood pressure is often treated with drugs called angiotensin receptor blockers (ARBs), which include losartan, candesartan, valsartan, irbesartan, telmisartan, and eprosartan. These drugs reduce blood pressure by blocking the G-protein pathway, relaxing and widening blood vessels. But they can also block the beneficial effects of AT1R and cause negative side effects, such as dizziness and headache. Designing drugs that block only the harmful G-protein pathway would allow the beneficial pathways to continue working as blood pressure is reduced. Creating such drugs would require detailed knowledge of AT1R’s molecular structure, which has been difficult to figure out.

A team of researchers led by Dr. Vadim Cherezov at the University of Southern California used a novel X-ray crystallography technique called serial femtosecond crystallography to reveal the receptor’s structure. Extremely bright, brief pulses of an X-ray free-electron laser allowed the researchers to obtain structural information from tiny micron-sized crystals at room temperature and without radiation damage.

The researchers were able to determine the structure of AT1R when bound to an angiotensin receptor blocker called ZD7155. They specifically identified the components that make up the receptor’s binding pocket, where the blockers bind to cause their effects. Mutating these parts of the protein revealed which specific amino acids in the receptor were critical for binding. The researchers used this information to develop simulations of what happens in the binding pocket when other angiotensin receptor blockers bind to it.

Of current drugs, Cherezov says, “It’s like using a 2-by-4 to kill a fly. Yes, it works, but perhaps a more refined approach could achieve the positive results without many side effects by only blocking the G-protein pathway while keeping the arrestin pathway active. To do so, you need to understand exactly how and where drug-like molecules bind to the receptor and what conformational changes they produce.”

The researchers expect that their findings could lead to more effective drugs that cause fewer side effects.

—by Brandon Levy

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