Cardiology

Written by

 

 

Ronald G Victor MD

The New 2017 ACC/AHA Hypertension Guidelines

The new 2017 ACC/AHA Hypertension Guidelines were presented last week at a special session the AHA Meeting in Anaheim, CA, and published simultaneously in over 400 pages of text in Hypertension, with a 200-page version in JACC and an excellent synopsis and editorials in JAMA. The writing committee and the task force members are to be congratulated on a comprehensive and outstanding set of evidence-based practice guidelines. Kudos! These new guidelines are the antithesis of the 2014 JNC 8 Report, which was not comprehensive, not endorsed by any medical society, and, based on insufficient data. JNC 8 got it backwards by relaxing the blood pressure (goal) for patients ≥60 years of age—the very group that stands to benefit the most from intensive BP control. In contrast, the new guidelines are heavily influenced by SPRINT (Systolic Blood Pressure Reduction Intervention Trial), a groundbreaking NIH-funded trial (first published in NEJM in 2015) which showed that intensive systolic BP reduction targeting <120 mm Hg was superior to standard reduction targeting <140 mm Hg in reducing the risk of CVD events and all-cause mortality in high-CVD risk patients without diabetes, prior stroke, or advanced CKD. This is the first set of US hypertension guidelines to be risk-based (finally!).

The new document lowers the definition of hypertension by 10 mm Hg to address under-treatment of hypertension, which is all too common in general medical practice, and it places unprecedented emphasis on home and ambulatory BP monitoring for clinical decision making. The new guidelines were widely endorsed by multiple medical societies, including the American Society of Hypertension, the Association of Black Cardiologists, the National Medical Association, the American Pharmacists Association, the Preventive Cardiovascular Nurses Association, and the American Academy of Physicians Assistants—all of which had representatives on the writing committee. Remarkably, the new guidelines were not endorsed by the American College of Physicians/American Academy of Family Practitioners, which earlier this year sided with the relaxed JNC 8 systolic BP goal of 150 mm Hg for patients ≥60: in my view, a misinformed decision by professional general medicine guideline writers who are not hypertension specialists.  

The major new recommendations by the new 2017 guidelines are summarized as follows:

1. Hypertension is now defined as a usual BP of ≥130/80 mm Hg. The conventional cut-off value of 140/90 mm Hg is now redefined as Stage 2 (ie, severe) hypertension, which previously was reserved for values ≥160/100 mm Hg.
2. The 130/80 mm Hg cut-off value for establishing the diagnosis of hypertension can be based on repeated careful office-based measurements or by home BP monitoring or daytime ambulatory BP monitoring. This daytime value of 130/80 roughly corresponds to a nighttime BP as low as 110/65 and a 24-hour average BP of 125/75 mm Hg by ambulatory monitoring. Home and ambulatory BP monitoring are important to prevent over-treatment of white coat hypertension and under-treatment of masked hypertension.
3. Non-drug lifestyle modification (DASH diet, exercise, weight loss, moderation in alcohol) is heavily recommended for everyone, including those with elevated BP in the 120-129/>80 mm Hg range.
4. Recommended medication treatment thresholds are based on both the BP level and global CVD risk, as estimated by the updated ACC ASCVD Risk Calculator. For patients with Stage 1 hypertension in the 130s/80s with an estimated 10-year CVD risk ≤10%, give lifestyle modification alone 3 to 6 months to lower BP into the 120s/70s; if not, add BP medication. For patients with Stage 1 hypertension with an estimated 10-year CVD risk >10% and for patients with Stage 2 hypertension—regardless of their risk score— start BP medication simultaneously with lifestyle modification.  
5. The same treatment algorithm applies to patients with common comorbidities including those with stable ischemic heart disease, metabolic syndrome or full-blown diabetes, or CKD. For secondary stroke prevention, the guidelines are more conservative, making <140/90 mm Hg the initial goal with <130/80 mm Hg being recommended as a stretch goal, especially for patients with prior lacunar strokes for which the RCT evidence is strongest.
6. Medication non-adherence is emphasized as a major cause of apparent drug-resistant hypertension.
7. Finally, evidence overwhelmingly shows that the best way to control hypertension in general practice is with a team-based approach, which includes a pharmacist or other mid-level provider.

The recommended first-line drugs for hypertension are the same as in many other sets of guidelines and include a thiazide-type diuretic, an ACEI or ARB, and a CCB. Compelling indications for comorbid conditions are the same as in many other sets of guidelines.    

 In addition to these extensive and carefully evidenced-based guidelines, I offer some practical tips about achieving optimal BP control in outpatient practice.

• I believe that manual cuff measurement of BP is old-school and the least accurate way to estimate a person’s usual BP. We have replaced it in our Hypertension Center Clinic with automated unattended office BP (AOBP) using a highly rated oscillometric monitor. For a new patient, we measure BP in both arms and while sitting and standing. Then, we leave the patient unattended and take 3 sequential measurements with the monitor set on STAT mode. If the average AOBP is ≥130/80, I start or intensify therapy if I cannot get accurate home readings or ideally a 48-hour ambulatory BP monitor (ABPM). An annoying practical barrier is that the only Medicare-approved reimbursable indication for ABPM, unfortunately, is suspected white coat hypertension (elevated BP without a diagnosis of hypertension); most private payors will approve and reimburse ABPM.
• I am not a big fan of frequent home BP monitoring because it is hard to get accurate data, it does not assess sleeping BP, which is arguably the most important value, and some patients become absolutely obsessed with their BPs, especially if their doctor has recommended additional doses of medication for very high self-measured values. The latter practice places far too much pressure on the patient and the family and it can be the source of a crippling anxiety. PRN clonidine is the “work of the devil,” creating BP lability with symptomatic transient dips in BP followed by scary rebound BP surges. The correct way to use home BP monitoring is to have the patient take 3 consecutive readings seated with a validated monitor (checked out at the office visit) every morning and every evening for 4 consecutive days and then stop. I discard the first day’s reading and the first reading of every set as being spuriously high and average all the rest. If the average home BP is ≥130/80, I start or intensify medication therapy. The home BP protocol can be repeated after giving the medication enough time to reach steady state.
• I try to get most of my patients’ average daytime systolic BP to ≤120 mm Hg, particularly if they have a high CVD risk, have a strong family history of premature CVD, and are robust. The biggest risks of intensive therapy are causing orthostatic dizziness in frail elderly patients and acute kidney injury in patients with long-standing diabetes with ≥Stage 3 CKD. Such patients need a more relaxed treatment target and I include the patient (and family) in shared decision making about setting a personalized target BP value. In contrast, intensive control of hypertension is key in patients with recent onset of diabetes to delay or hopefully prevent development of micro- and macro-vascular complications.  
• When I decide to treat a patient for even mild hypertension, I recommend lifestyle modification as a critically important adjunct but not as a replacement for life-saving medication. I start both simultaneously. The sizes of the BP reductions attributed to lifestyle interventions in the new guidelines are upper-level estimates from mainly short-term efficacy trials. Careful real-world implementation research has yielded lower values. A healthy diet and regular exercise are very hard to implement in low-income neighborhoods. And recidivism is the Achilles’ heel of all behavior modification. As a society, we need to follow the lead of other high-income countries by putting sufficient pressure on the US food industry to reduce the sodium content of processed food.
• A long-acting, once-daily generic CCB (amlodipine) plus a long-acting ARB (irbesartan or telmisartan) is my go-to low-dose combination drug regimen for initiating medical management of hypertension, regardless of a patient’s race/ethnicity or comorbidity. I reserve thiazide-type diuretics for my third drug, if needed, because large registry data show they are less well tolerated and thus have a higher discontinuation rate then CCBs and ARBs. After age 60, the incidence of significant thiazide-induced hyponatremia rises steeply.
• The long-acting potent thiazide-type diuretics—indapamide or chlorthalidone—are the go-to evidence-based diuretics for hypertension. Low-dose HCTZ is short-acting, ineffective, and has never been shown to reduce CVD risk. It should be taken off the market.
• I reassess BP two weeks after an ARB/CCB combination, which is ample time to reach steady state. I reassess BP 5-6 weeks after adding a thiazide-type diuretic, as these drugs take longer to exert a peak effect on BP. The peak BP-lowering effect of spironolactone occurs after 6-8 weeks whereas the peak effect of eplerenone occurs sooner (5-6 weeks).  
• Because our goal is to prevent CVD events, there is compelling evidence that statin therapy should be prescribed for most patients with hypertension. The recent HOPE-3 trial and the older ASCOT trial showed that BP lowering medication plus low-dose statin therapy (10 mg of rosuvastatin or 10 mg of atorvastatin) has additive effects on CVD risk reduction in patients with mild or moderate hypertension and intermediate CVD risk. Based on those RCTs, I recommend such low-intensity statin therapy for hypertensive patients with an LDL cholesterol of ≥130 mg/dL or an estimated 10-year risk score of ≥7.5% without diabetes or established CVD. I recommend a high-intensity statin (20-40 mg of rosuvastatin or 40-80 mg of atorvastatin) for patients with a 10-year CVD risk of ≥10%.  
• In closing, I want to make two comments about secondary (identifiable) hypertension.

1. I am not convinced that obstructive sleep apnea is an identifiable cause of daytime hypertension. In the only proper RCT, CPAP had no effect on daytime BP and showed no benefit on secondary prevention of any CVD event including atrial fibrillation.
2. Primary aldosteronism is by far the most common identifiable and correctable cause of hypertension. It is very important to screen for this condition in any patient with difficult hypertension (uncontrolled on first-line triple therapy) or hypertensive heart disease even in the absence of hypokalemia or an adrenal nodule on imaging. Most patients are not hypokalemic and the CT scan should not be trusted (too many false positives and false negatives). Atrial fibrillation is >12-times more common in patients with primary aldosteronism than in patients with equally severe primary hypertension. To avoid false negative screening, the serum aldosterone and plasma renin activity should be ordered for 8 AM (the peak of the diurnal variation in aldosterone secretion) and the serum K should be > 4.0 (using KCL supplementation if needed). Under these conditions, a serum aldosterone of ≥15 and a suppressed plasma renin activity of <1.0 is a positive screening (typically the plasma renin activity is very suppressed at <0.6). The patient should be referred to an experienced hypertension specialist for further evaluation and management.