BP elevations during pregnancy may raise risk for metabolic syndrome


Pregnant women who have persistent BP rises in the upper ranges of normal may face increased risk for developing metabolic syndrome and higher CV risk after giving birth, according to findings published in Hypertension.

“Our findings underscore an important issue that has long been ignored in clinical practice — the fact that criteria for hypertension in pregnancy are derived from the general population,” Jian-Min Niu, MD, department of obstetrics, Guangdong Women and Children Hospital, China, said in a press release. “We anticipate that if reaffirmed in further research, our study could spark a change in what we currently deem healthy [BP] in pregnant women.”

Researchers sought to study the associations between pregnancy BP strata and the development of metabolic syndrome.

They analyzed data from a cohort of 507 women from Guangzhou, China. Among the requirements were that the women had normal BP levels (< 140 mm Hg systolic/90 mm Hg diastolic); had normal glucose and lipid profiles; had no history of vaginal bleeding, alcohol or substance abuse; and were nonsmokers.

The original 507 participants each underwent seven or more BP evaluations during pregnancy. The cohort eventually shrank to 309 women due to data-permission issues and a 60.9% postpartum follow-up rate over 1.6 years. In addition, glucose and lipid levels were evaluated from study entry through follow-up.

Researchers stratified the cohort according to three diastolic BP trajectory categories: a low J-shaped group (34.2%; 62.5 ± 5.8 mm Hg to 65 ± 6.8 mm Hg); a moderate U-shaped group (52.6%; 71 ± 5.9 mm Hg to 69.8 ± 6.2 mm Hg); and an elevated J-shaped group within the range of hypertension (13.2%; 76.2 ± 6.7 mm Hg to 81.8 ± 4.8 mm Hg).

The researchers found that the hypertension-range group had a 6.5 greater odds of developing postpartum metabolic syndrome than the low J-shaped group (adjusted OR = 6.55; 95% CI, 1.79-23.92).

Niu and colleagues also developed a model for prediction of postpartum metabolic syndrome that included diastolic BP (membership in the elevated J-shaped group), fasting glucose > 4.99 mmol/L and triglycerides > 3.14 mmol/L at term, which showed good calibration and discrimination (C statistic, 0.764; 95% CI, 0.674-0.855; P < .001).

They wrote, “Pregnancy is a known, long-term CV risk for women. The presence of hypertensive disorders in pregnancy is generally recognized as a maladaptation to pregnancy-induced hemodynamic and metabolic alterations.”

In the release, Niu said, “Early identification of metabolic risk factors and implementations of lifestyle modifications may help delay the onset of CVD that would present itself 20 to 30 years after [childbirth].” – by James Clark

Licorice overload may cause seizures


Overconsumption of candies with licorice is associated with tonic clonic-seizures and hypertension in a case study.

The report involved a 10-year-old boy who was admitted to a hospital in Bologna, Italy following generalized tonic-clonic seizures. The boy had an elevated blood pressure. A brain magnetic resonance scan showed a localized vasogenic oedema. [Pediatric Neurology 2015;52:457-459

A follow-up examination offered the clue:  the boy’s teeth had black stains.  He later admitted to have consumed 20 licorice toffees per day in the past 4 months. This amounts to 2.88 mg/kg of glycyrrhizic acid, which gives licorice its sweet taste, and exceeds the WHO’s maximum recommendation of 2 mg/kg. This partly explained the reason for his hypertension, said the authors.

The risk of seizures from licorice is of particular concern in children with low body weight, they added. Licorice consumption is also linked to posterior reversible encephalopathy syndrome in children.

 

Vit D supplementation ineffective for hypertension


Vitamin D supplements are ineffective at controlling blood pressure (BP) and should not be used as an antihypertensive agent, according to a meta-analysis of randomised controlled trials (RCTs).

Vitamin D had no effect on systolic BP and diastolic BP (p=0.97 and p=0.84, respectively for RCTs and p=0.27 and p=0.38, respectively for individual patients). [JAMA Intern Med 2015;doi:10.1001/jamainternmed.2015.0237]

“The results do not support the use of vitamin D or its analogues as an individual treatment for hypertension or as a population-level intervention to lower BP,” said lead author Dr. Miles Witham from the University of Dundee, Dundee, Scotland.  “The lack of efficacy of vitamin D treatment on BP also argues against routine measurement of25-hydroxyvitamin D [25OHD] levels in patients with hypertension.”

The analysis included studies that used vitamin D for a minimum of 4 weeks for any indication, published between January 1966 and March 2014. Nearly 7,600 participants were involved in the study.

Subgroup analysis did not reveal any baseline factors predictive of a better response to treatment. There were also no significant differences between patients with or without diabetes, those taking or not taking angiotensin-converting enzyme (ACE) inhibitors, irrespective of BP, parathyroid hormone, and 25OHD levels.

Witham however said there are a few caveats to the study, among them inclusion of single-centre trials and background cardiovascular medications. Other potential confounders are ageing, obesity, smoking, and inactivity, which could have influenced the results.

Previous studies have linked low levels of vitamin D with elevated BP and future cardiovascular events. Intervention studies however yielded conflicting findings.

Renal Denervation: Revived for Hypertension?


Renal denervation may yet have a role in the treatment of resistant hypertension, as greater improvements in blood pressure were seen at 1 year than were seen at 6 months in the SYMPLICITY HTN-3 trial, researchers reported here.

With 12-month follow-up of originally denervated patients from the trial and 6-month follow-up of crossover patients who had the procedure 6 months after having had a sham procedure, reductions in office and 24-hour ambulatory blood pressure measurements, respectively, were:

  • Renal denervation: 18.9 mmHg systolic, 7.8 mmHg diastolic and 7.6 mmHg systolic, 4.7 mmHg diastolic
  • Crossover: 17.7 mmHg systolic, 7.1 mmHg diastolic and 9.2 mmHg systolic, 4.9 mmHg diastolic

The 6-month decrease in systolic blood pressure among the crossover population from baseline was statistically significant (P<0.001), reported George Bakris, MD, director of the American Society of Hypertension Comprehensive Hypertension Center at the University of Chicago, and colleagues.

In contrast, results in a noncrossover group — patients who never had the procedure — were not significant for change from baseline, with reductions in office blood pressure of 21.4 mmHg systolic and 8.2 mmHg diastolic. Decreases in 24-hour ambulatory blood pressure in that group were 6.1 mmHg systolic and 2.9 mmHg diastolic.

In the original trial, the mean change in systolic blood pressure at 6 months was -14.13 mmHg for patients who had renal denervation and -11.74 mmHg for patients who had a sham procedure. The difference between the groups did not meet the superiority margin of 5 mmHg.

“Renal denervation is a work in progress,” Bakris stated at a press conference at theEuropean Society of Cardiology meeting. “It definitely is not dead. I would say it is out of the ICU now and probably onto the floor.”

Bakris and colleagues also reported that the 12-month data indicated that renal denervation was safe “with no difference in major adverse events between the treated and original sham procedure groups out to 12 months.”

With 1-year follow-up of originally denervated patients and 6-month follow-up of crossover patients, there was no significant difference between the groups in the rate of a composite safety endpoint: 6.8% in the original renal denervation group, 5.3% in the crossover group, and 7.2% in the noncrossover group.

The composite endpoint consisted of death, vascular complications, new-onset end-stage renal disease, embolic events resulting in end-organ damage, renal artery reintervention, and hypertensive emergency or crisis.

While there was a worsening of blood pressure after 6 months in the control patients who remained on medical therapy throughout 1 year, the authors attributed this to changes in therapeutic adherence.

They acknowledged that “possible confounding factors including the population studied, drug prescription changes, variable adherence to therapy, and procedural variability all remain unresolved at 12 months.”

Carlo Di Mario, MD, who was not involved in the study, called the new results “very encouraging.” He pointed out that one advantage of denervation is that the results are permanent and not dependent upon a patient’s lifestyle choices.

“I think that renal denervation will be resurrected,” said DiMario, professor of clinical cardiology at Royal Brompton and Harefield Hospital in London. “I don’t think that patients could become resistant to their medication, and they don’t necessarily become noncompliant with medication. But they could become noncompliant with their diet or with their exercise regimen. They may have begun using tobacco or alcohol. The advantage of denervation is that it is permanent.”

Di Mario also told MedPage Today that the denervation devices are also improving, making the procedure easier to perform with better and more predictable results.

“I think it is a shame that there has been an over-reaction to the initial results of SYMPLICITY as well as over-enthusiasm,” he said. “There are nonresponders to renal denervation, but most people do well with it. We do not have good medication for resistant hypertension.”

Exploration of devices to treat resistant hypertension in progress


Despite recent setbacks, research and development on device therapy for treatment-resistant hypertension is proceeding, a hypertension expert said at the Cardiometabolic Health Congress.

See Also

Baroreceptor activation therapy and renal denervation are not yet approved for use in the United States, but both are approved in other countries and have demonstrated benefit in patients whose hypertension cannot be controlled by diet, lifestyle and medication, George L. Bakris, MD, FAHA, FASN, professor of medicine and director of the University of Chicago Medicine Comprehensive Hypertension Center, said during a presentation.

George L. Bakris

Baroreceptor activation therapy

Baroreceptor activation therapy works via electrodes around the carotid sinus and carotid baroreceptors that are activated by a battery-operated device, Bakris, a Cardiology Today Editorial Board member, said. “That stimulates the baroreceptors and, in a dose-dependent fashion, amplifies the response to the brain and lowers [BP]. Over time, when you turn the device on, you can see a very nice drop in [BP] as well as a drop in sympathetic tone. It is very reproducible.”

One advantage, according to Bakris, is that “unlike with renal denervation, you know in the [operating room], before you have even sewn up a patient what the response is.” Another is that the voltage can be titrated to lower BP and heart rate by different degrees, he said.

The first version of the device, the Rheos (CVRx), had a battery that lasted 6 months and a pair of glove-like extensions that wrapped around each carotid bifurcation, and required a procedure that took about 90 minutes, he said. That sufficed for proof-of-concept, but was too cumbersome for commercialization. So, a new version, the Barostim Neo, was developed.

“[The Barostim Neo] has a single electrode because the engineers figured out that [more than] 80% of the response was actually coming from the right carotid baroreceptor, not the left,” he said. The new version has a battery that lasts 3 or 4 years and requires 45 to 60 minutes to implant, he said.

In a pivotal trial, baroreceptor activation therapy reduced systolic BP by –32 mm Hg to –36 mm Hg at 12 months, he said. A recent analysis showed that reduction was sustained at 5 years, he added. Another trial of the therapy is to begin soon.

Baroreceptor activation therapy is also being studied for a possible indication for patients with HF. It is already documented to reduce left ventricular mass, Bakris said. In a substudy of 60 patients from the pivotal trial, LV mass was reduced by a mean of –15 g/m2 after 12 months of baroreceptor activation therapy.

The therapy has not yet been approved by the FDA because of the acute safety profile of the original device; for example, it has been associated with increased rates of hematoma at 30 days, Bakris said. He noted that most observed complications were related to the anatomy of the vessel as opposed to the device. However, at 2 years to 5 years, rates of system- and procedure-related complications, MI and stroke are very low, he said.

Renal denervation

Renal denervation was considered a highly promising therapy for treatment-resistant hypertension because “we have surgical data from the 1950s that clearly show that it works,” Bakris said. “If you do studies that suggest it is not working, then either you have a procedural issue or you have missed something along the way.” For example, he said, one small pilot study of renal denervation had a range of norepinephrine spillover of 0% to 90%.

“One of the possible reasons that renal denervation did not work [in the SYMPLICITY HTN-3 trial] is that the procedure, while reproduced from earlier studies, was restrictive and not as extensive as could have been done,” Bakris said. “We now know from animal studies that were done subsequent to the presentation of these data that if you fully denervate, not just one renal artery, but [other renal arteries] and the branches, the standard deviation for norepinephrine spillover falls dramatically and you have a [more than] 90% reduction in norepinephrine spillover. Future studies … will probably have to short-circuit every main and branch artery in sight.”

Although the SYMPLICITY HTN-3 trial (Medtronic) failed to show benefit of renal denervation for the primary efficacy endpoint of change in office systolic BP as compared with a sham procedure, at least three companies have developed new catheters for renal denervation, and there will be studies in the future, he said. – by Erik Swain

Are Your Medications Causing or Increasing Incontinence?


If you are struggling with urinary incontinence or your existing incontinence is getting worse, take a look at the medications you are taking. They may contribute to the problem.

There are four groups of medications doctors commonly recommend that can cause or increase incontinence. If you are taking any of these, you should let your doctor know about your incontinence and discuss your medications (both prescription and over-the-counter) to see if there is another approach to control or eliminate the problem.
The most common incontinence problems arise from medications in the following four categories:

1. Diuretics to reduce excess fluid

Diuretics, also known as “water pills,” stimulate the kidneys to expel unneeded water and salt from your tissues and bloodstream into the urine. Getting rid of excess fluid makes it easier for your heart to pump. There are a number of diuretic drugs, but one of the most common is furosemide (Lasix®).

According to urologist Raymond Rackley, MD, approximately 20 percent of the U.S. population suffers from overactive bladder symptoms.

“Many of those patients also have high blood pressure or vascular conditions, such as swelling of the feet or ankles,” he says. “These conditions are often treated with diuretic therapies that make their bladder condition worse in terms of urgency and frequency.”

A first step is to make sure you are following your doctor’s prescription instructions exactly. As an alternative to water pills, Dr. Rackley recommends restricting salt in your diet and exercising for weight loss. Both of these can reduce salt retention and hypertension naturally.

2. Alpha blockers for hypertension

Another class of drugs used to reduce high blood pressure or hypertension by dilating your blood vessels can also cause problems. These medicines are known as alpha blockers. Some of the most common are Cardura®, Minipress® and Hytrin®.

These are usually more of an issue for women. Again, discuss this with your physician, because there are alternative drugs you may be able to take.

Men typically take these to treat an enlarged prostate (benign prostatic hyperplasia or BPH) which can restrict urination by putting pressure on the urethra. By relaxing the muscles in the bladder neck, they allow smoother urine flow for those patients.

3. Antidepressants and narcotic pain relievers

Some antidepressants and pain medications can prevent the bladder from contracting completely so that it does not empty. That gives rise to urgency or frequency or voiding dysfunction. They can also decrease your awareness of the need to void.

“Some of these drugs can also cause constipation,” Dr. Rackley says. “Constipation, in turn, can cause indirect bladder incontinence because being constipated takes up more room in the pelvis that the bladder needs to expand.”

4. Sedatives and sleeping pills

Using sedatives and sleeping pills can present a problem, especially if you already have incontinence. They can decrease your awareness of the need to void while you are sleeping.

The best way to address this situation, Dr. Rackley says, is to take other steps to relax and improve your sleep. Getting more exercise to make you tired, for example, can help. It’s also important to maintain a regular bedtime and wake-up schedule. Dr. Rackley says finding other ways to relax before bed — meditation, reading a book or listening to soothing music or sound effects (e.g., rain or waves) — can also help you sleep better.

 

Losartan plus hydrochlorothiazide improves BP control in diabetics with hypertension


Combination therapy using losartan plus hydrochlorothiazide improves blood pressure control in patients with type 2 diabetes mellitus (T2DM) complicated with hypertension, according to a Japanese study.

The 24-week study recruited 43 Japanese patients with T2DM complicated with treatment-resistant hypertension. Prior to the study, participants were given 12 weeks of continuous treatment with the maximum dosage of angiotensin II receptor blockers (ARBs) as recommended in Japan, but their blood pressure did not reach the target level of systolic ≤130mm Hg and diastolic ≤80mm Hg. [Hypertens Res 2009;32:3-107]

Study participants were assessed for changes in blood pressure and metabolism after switching their treatment plan from maximum dose ARB to a combination of losartan 50 mg/day and hydrochlorothiazide 12.5 mg/day. At the end of the study, participants had significantly lower systolic and diastolic blood pressure. The results also showed that combination therapy did not have any effect on lipid metabolism, serum uric acid and potassium levels. However, HbA1c levels were higher and urinary albumin-creatinine ratios lower, said the researchers. [Intern Med 2014;53:1283-9]

The study found that mean systolic blood pressure dropped from 147±11mmHg at baseline to 133±13 mmHg at the end of the study, while mean diastolic blood pressure fell from 79±8 mmHg to 72±10 mmHg. This significant reduction could be due to the fact that patients with diabetes have enhanced renal tubular reabsorption, leading to the formation of sodium-sensitive hypertension. Diuretics promote sodium excretion, thus increasing the antihypertensive effects of other drugs.

Another explanation for the improved antihypertensive effect is that hydrochlorothiazide probably enhances the antihypertensive effects of ARBs by reducing circulating blood volume and increasing plasma renin activity. As ARBs work by inhibiting the actions of angiotensin II, their effectiveness increases in parallel with plasma renin activity. [J Pharmacol Exp Ther 1990;252:726-32]

Most patients with diabetes complicated by hypertension require multidrug therapy to achieve target blood pressure. Combining a diuretic with ARB and regularly monitoring kidney function, electrolytes and glucose metabolism is a potentially effective option for patients who fail first-line therapy using ARBs. This is particularly apparent in diabetic Japanese patients with treatment-resistant hypertension, summarized the researchers.

 

Sleep Apnea Can Make Your Hypertension Harder to Treat .


A new study finds strong links between severe, untreated obstructive sleep apnea (OSA) and high blood pressure even for heart patients on blood pressure medication.

“The current findings suggest that severe OSA may contribute to poor blood pressure control despite aggressive medication use,” says sleep disorder specialist Harneet Walia, MD. She says the study suggests that better strategies to treat sleep apnea can improve blood pressure control. And, in turn, patients’ heart health should improve.

The study results are significant because patients were under the close care of heart specialists, Dr. Walia says. And these doctors were following national guidelines to treat cardiovascular risk.

“The results are of interest as severe levels of obstructive sleep apnea appear to be contributing to uncontrolled blood pressure.” And this leaves the patients more vulnerable to heart problems, she says.

Dr. Walia was the first author of the study, titled “Association of Severe Obstructive Sleep Apnea and Elevated Blood Pressure Despite Antihypertensive Use.” This was a part of the Heart Biomarker Evaluation in Apnea Treatment (HeartBEAT) trial.” The study appears in the American Academy of Sleep Medicine journal.

Apnea patients and poor blood pressure control

Sleep apnea is a serious sleep disorder that occurs when a person’s breathing is interrupted during sleep. People with untreated sleep apnea stop breathing repeatedly during sleep, sometimes hundreds of times during the night. Their upper airways are completely or partially blocked repeatedly during sleep.

During an apnea episode, the diaphragm and chest muscles work harder as the pressure increases to open the airway. Breathing usually resumes with a loud gasp or body jerk. These episodes can interfere with sound sleep, reduce the flow of oxygen to vital organs, and cause heart rhythm irregularities.

Of the 284 study subjects, those with serious apnea were four times more likely to have resistant elevated blood pressure – even though they were taking three or more medications, says Dr. Walia. All these patients either had or were at risk for cardiovascular disease.

Previous research has also linked obstructive sleep apnea to resistant hypertension, Dr. Walia says.

“Our study is different because these are folks who had cardiovascular disease, and who were followed by cardiologists, yet severe apnea may have contributed to suboptimal blood pressure control,” she says.

“This is an important finding from a clinical perspective because patients with poor blood pressure control taking multiple anti-hypertensive medications are particularly vulnerable to increased cardiovascular risk. Strategies to treat obstructive sleep apnea should be strongly considered because the improved control in blood pressure could potentially lead to improvement in cardiovascular morbidity and mortality,” she says.

Should you be evaluated?

Dr. Walia suggests that patients who have high blood pressure, are on anti-hypertensive medication and who have signs of obstructive sleep apnea be evaluated. Snoring, pauses in breathing during sleep, restlessness during sleep, excessive daytime sleepiness and impaired concentration are all signs of OSA, says Dr. Walia.

“It’s an important finding, especially for people who are taking multiple blood pressure medications,” she says. “They may be at risk for cardiovascular disease, anyway. Future research is definitely needed to gain a better understanding of the mechanistic pathways of this link.”

She says more studies are also needed on how sleep apnea treatment relates to blood pressure control and how it impacts people on different types of blood pressure medications.

SYMPLICITY trial: Negative results for renal denervation in resistant hypertension.


Renal denervation with Medtronic’s SymplicityTM catheter has been shown to be safe but not more effective than a sham procedure for reducing blood pressure (BP) in patients with resistant hypertension.

In the SYMPLICITY HTN-3 trial, renal denervation reduced office systolic BP at 6 months (the primary efficacy endpoint) by 14.13 mm Hg vs 11.74 mm Hg for sham procedure (p<0.001 for both), for a difference of 2.39 mm Hg, short of the margin of 55 mm Hg needed to establish superiority. The difference in the 24-hour ambulatory BP was narrower at 1.96 mm Hg (p=0.98 with a superiority margin of 2 mm Hg). [American College of Cardiology (ACC) 2014 meeting Abstract 451-14-LB-12757; N Engl J Med 2014; doi:10.1056/NEJMoa1402670]

“Safety was established, but the overall trial did not meet its primary endpoint,” said lead investigator Dr. Deepak L. Bhatt of the Brigham and Women’s Hospital in Boston, Massachusetts, US. “I would be very cautious in recommending this procedure without compelling data to support actual clinical outcomes.”

SYMPLICITY HTN-3 was a prospective, blinded, randomized, sham-controlled trial involving 535 patients (age 18-80 years) with a sustained BP of 160 mm Hg or higher despite being on a stable drug regimen, including full tolerated doses of ≥3 antihypertensive medications, including a diuretic. Patients underwent renal denervation therapy or renal angiography as the sham control. The primary safety endpoint was a composite of adverse events.

The lack of a direct measurement to confirm whether the renal arteries were actually denervated posed a challenge in the trial, said Bhatt. Other limitations were the relatively short follow-up period and that drug adherence was not measured. Operator experience was also a factor.

Discussant Dr. Anthony DeMaria from the University of California, San Diego, California, US, and former editor of the Journal of the American College of Cardiology, said the negative findings surprised cardiologists, given the positive findings from previous uncontrolled studies of renal denervation. He added that 10 studies have been published in JACC showing BP reductions of 30-40 mm Hg with renal denervation, as well as improvements in left ventricular hypertrophy.

“There is some really tantalizing data out there that there can be a benefit, but we need to go back to anatomy, to physiology, and even pathophysiology, to be sure we’re effectively denervating, so we can assess the results of the procedure.”

In an accompanying editorial, Dr. Franz Messerli from Icahn School of Medicine and Dr. Sripal Bangalore from New York University School of Medicine, both in New York City, said the negative result from SYMPLICITY HTN-3 brings the renal denervation train to a grinding halt. “The time has come to turn the page on renal denervation for hypertension, but by all means, let’s not close the book.”

Meanwhile, 6-month analysis from the first 1,000 patients with uncontrolled hypertension enrolled in the Global SYMPLICITY Registry showed significant reductions in office and ambulatory BP (11.9 and 7.9 mm Hg for all) and low rates of adverse events with renal denervation (using Symplicity catheter). Some differences with SYMPLICITY HTN-3 include randomization, blinding, sham control, BP inclusion criteria, antihypertensive drug treatment intensity and African-American inclusion in HTN-3. [ACC Abstract 403-14-LB-13135]

“Our study provides a significant contribution to the discussion about renal denervation when considering the procedure for high-risk patients who are suffering from uncontrolled hypertension and have exhausted all other options,” said lead investigator Dr. Michael Böhm from the University of Saarland in Homburg, Germany.

New Recommendations for Hypertension Management Released.


New recommendations published online in the Journal of the American Medical AssociationExternal Link aim to provide guidance on the management of patients with hypertension. More specifically, the recommendations focus on when medication should be started in patients, the best choices for medications to begin treatment; and communicating achievable blood pressure goals to patients.

“Patients want to be assured that blood pressure (BP) treatment will reduce their disease burden, while clinicians want guidance on hypertension management using the best scientific evidence. This report takes a rigorous, evidence-based approach to recommend treatment thresholds, goals, and medications in the management of hypertension in adults,” the report authors note.

The report, written by panel members appointed to the Eighth Joint National Committee, notes there is strong evidence to support treating hypertensive persons aged 60 years or older to a BP goal of less than 150/90 mm Hg and hypertensive persons 30 through 59 years of age to a diastolic goal of less than 90 mm Hg. However, given insufficient evidence in hypertensive persons younger than 60 years for a systolic goal, or in those younger than 30 years for a diastolic goal, the panel recommends a BP of less than 140/90 mm Hg for those groups. “The same thresholds and goals are recommended for hypertensive adults with diabetes or nondiabetic chronic kidney disease (CKD) as for the general hypertensive population younger than 60 years,” the report notes.

In general, the report authors note that the 140/90 mm Hg definition from Joint National Committee 7 “remains reasonable” and recommend that lifestyle interventions be used for everyone with blood pressures in this range. “For all persons with hypertension, the potential benefits of a healthy diet, weight control, and regular exercise cannot be overemphasized,” they said. “These lifestyle treatments have the potential to improve BP control and even reduce medication needs.”

Also in the report, the authors note there is moderate evidence to support initiating drug treatment with an angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, calcium channel blocker, or thiazide-type diuretic in the nonblack hypertensive population, including those with diabetes. In the black hypertensive population, including those with diabetes, a calcium channel blocker or thiazide-type diuretic is recommended as initial therapy. Additionally, there is moderate evidence to support initial or add-on antihypertensive therapy with an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker in persons with CKD to improve kidney outcomes.

Moving forward, the authors point out that an algorithm included as part of the recommendations will facilitate implementation and be useful to busy clinicians. They also suggest that “the strong evidence base of this report be used to inform quality measures for the treatment of patients with hypertension.”

Practice guidelines are traditionally promulgated by the government or by learned medical professional societies. The JAMA paper is a report of a group experts in the field of hypertension, but it does not carry the endorsement of any organized body. Moving forward, these recommendations will be taken into account in the coming year as the ACC/AHA Task Force on Practice Guidelines moves forward with developing the collaborative model to update the national hypertension guidelines in partnership with the National Heart, Lung, and Blood Institute (NHLBI). According to the ACC and the American Heart Association (AHA), once a writing group is appointed, there will be an extensive science and evidence review process, followed by draft recommendations that will undergo a peer and stakeholder review. Once the review process is complete, the ACC/AHA and partnering organizations will publish the guidelines in 2015 for clinicians to follow as the national standard for hypertension prevention and treatment.

The ACC, AHA and the Centers for Disease Control and Prevention released a scientific advisory on the effective approach to hypertension in November that encourages use of enhanced, evidence-based, blood pressure treatment systems for providers, including standardization of protocols and algorithms, incentives for improved performance based on achieving and maintaining patients at blood pressure goals, and technology-facilitated clinical decision support and feedback.