Prehypertension Boosts Stroke Risk

We've long known that high blood pressure is a primary risk factor for stroke, but new research suggests that blood pressure on the high end of normal can be a threat, too. This condition, called prehypertension, is diagnosed when the top blood pressure number (systolic) is between 120 and 139 mmHg and the low number (diastolic) between 80 and 89 mmHg. The new information follows a review of 12 studies that included data on more than 518,000 participants in the United States, Japan, China and India taken from studies that lasted from 2.7 to 32 years. The researchers, from the University of California, San Diego, found that people with prehypertension were 55 percent more likely to have a stroke compared to individuals whose blood pressure was normal.

The review also revealed that people younger than 65 with prehypertension had a stroke risk that was 68 percent higher than normal, and that regardless of age those whose blood pressure was in the range of 130 to 139 had a stroke risk 79 percent higher than normal. In the United States, one-third of adults have prehypertension. The study was published online on September 28 in Neurology.

My take? We've known for some time that prehypertension can raise the risk of cardiovascular disease. Although the studies this report was based on encompassed a lot of people, it was only an analysis, not a study, and the authors appropriately noted that their findings must be confirmed before deciding upon the best approach to treatment. In the meantime, if your blood pressure has been edging up, lifestyle changes - losing weight, getting more exercise, giving up smoking, learning to relax and cutting back on salt, alcohol and caffeine - may help bring it down.

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Eating Potatoes Can Help Lower Blood Pressure

Of course, the potatoes in question can't be French fries or chips or loaded with butter, cheese or all the other high calorie trimmings that sometimes come with spuds. But if you're partial to potatoes and enjoy eating them steamed or boiled, in moderation, they could be good for your blood pressure, even if you're already taking medication for hypertension. Researchers performing a small study (only 18 participants, mostly overweight or obese) at the University of Scranton reported the results of eating six to eight purple potatoes twice a day. After a month, average diastolic blood pressure (the bottom number) among the study group dropped 4.3 percent while average systolic pressure (the top number) fell 3.5 percent. Researcher Joe Vinson, Ph.D., noted that plain potatoes are not particularly fattening (a single one contains about 110 calories), and they're loaded with beneficial phytonutrients, which may be responsible for the blood-pressure lowering effect seen in his study. In a statement he noted that earlier research showed that potatoes contain a substance similar to ACE inhibitors, a group of blood pressure drugs.

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Severe Pulmonary Hypertension May Be Reversed By Estrogen Treatment

UCLA researchers have found that the hormone estrogen may help reverse advanced pulmonary hypertension, a rare and serious condition that affects 2 to 3 million individuals in the U.S., mostly women, and can lead to heart failure.

The condition causes a progressive increase in blood pressure in the main pulmonary artery, which originates in the heart's right ventricle and delivers blood to the lungs. The rise in pressure impairs heart function by enlarging the right ventricle, potentially leading to heart failure.

Published in the American Journal of Respiratory and Critical Care Medicine, the preclinical study shows that in rats, estrogen treatment can reverse the progression of pulmonary hypertension to heart failure and can restore lung and ventricle structure and function.

The disease progresses slowly, so most patients don't seek treatment until major symptoms occur, such as shortness of breath, dizziness and fainting. According to researchers, current medication for pulmonary hypertension only temporarily reduces the disease's severity. For advanced pulmonary hypertension, there are fewer options, and the condition often necessitates a lung transplant.

"Unfortunately, up until now, there hasn't been an ideal pharmacological therapy to treat advanced pulmonary hypertension," said senior study author Mansoureh Eghbali, Ph.D., an assistant professor of anesthesiology at the David Geffen School of Medicine at UCLA who has a strong background in studying the role of gender and estrogen in cardiovascular diseases. "We hope that this early study may offer insight into new therapies."

The UCLA team found that by treating rats with severe pulmonary hypertension with low doses of estrogen, they were able to prevent the disease from progressing to right-ventricular heart failure; this did not happen in untreated rats.

Systolic blood pressure and ejection fraction - the volume of blood being pumped out of the heart's right chamber with each heart beat - also improved. Tests showed that lung weight, which can increase with the disease and resulting heart-ventricle enlargement, was also corrected. After 10 days of estrogen treatment, function returned to an almost normal state.

The researchers stopped the estrogen therapy after 10 days but continued to observe some of the treated rats. They tracked the continued improvement and found almost full restoration of systolic blood pressure and ejection fraction to normal levels after an additional 12 days.

"We were surprised to find this continued benefit, even after we stopped the estrogen treatment," said the study's first author, Dr. Soban Umar, a UCLA Department of Anesthesiology researcher who has studied pulmonary hypertension and right-ventricular heart failure and is a key member of Eghbali's laboratory team. "These findings suggest that even short-term estrogen therapy may suffice to reverse the disease."

All rats with severe pulmonary hypertension that were treated with estrogen survived by the study's end. Only 25 percent of the untreated rats survived.

The team also explored how estrogen could work in reversing the disease by studying several cellular and molecular mechanisms.

They found that the number of inflammatory cells in rats with pulmonary hypertension increased five-fold, compared with normal rats. In the animals treated with estrogen, this was reversed to normal. The team found that estrogen reduced regulation of a pro-inflammatory gene that also plays a key role in disease development caused by pulmonary hypertension. They also found that estrogen had an inhibitory effect on lung fibrosis.

In addition, the team observed that estrogen therapy restored blood vessels in the lungs and right ventricle whose loss is associated with the disease.

Further study identified that estrogen exerts its biological effects on pulmonary hypertension through a receptor called estrogen receptor beta, a protein that regulates estrogen's activity in the body.

"Estrogen appears to work through an interplay of several factors, including suppression of lung inflammation and fibrosis, as well as reversal of ventricle enlargement," Eghbali said. "We may be able to utilize estrogen receptor beta in the development of future therapies to stimulate estrogen activity to treat pulmonary hypertension."

Researchers had also tested estrogen receptor alpha, the other receptor that controls estrogen activity, but found that it wasn't as effective in treating pulmonary hypertension.

Eghbali added that estrogen receptor beta may prove to be a favorable therapeutic target, since this receptor may require only a short treatment duration and low dosage and has less pro-estrogenic effects on the breasts and uterus than estrogen receptor alpha.

Pulmonary hypertension affects mostly younger women, despite the fact that females in this age group should be under the protective benefits of natural estrogen produced by the body, Eghbali said.

"These patients may have a genetic mutation that is interfering in how estrogen receptor beta directs estrogen activity that is leading to pulmonary hypertension," she said.

Her team's next step is to explore these genetic questions. Currently, Umar and Eghbali are collaborating with UCLA pulmonary hypertension physicians to investigate gender-related issues and to define the role of estrogen in patients with this deadly disease.

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