January 16th, 2014
Co-Chairs of JNC8 Hypertension Guidelines Address a Challenging Case
Justin Sadhu, MD, Paul James and Suzanne Oparil, MD
Washington University in St. Louis cardiology fellow Justin Sadhu presents a challenging case to the co-chairs of the JNC8 hypertension guidelines: Paul James, Professor and Chair of the Department of Family Medicine at the University of Iowa, and Suzanne Oparil, Professor of Medicine and director of the vascular biology and hypertensive program at the University of Alabama at Birmingham’s School of Medicine.
Sadhu: My patient is a 76-year-old black male who presents to the cardiology clinic for routine follow-up. His medical history includes hypertension, coronary artery disease (CAD) with prior stenting several years ago for anginal symptoms but no history of myocardial infarction (MI), and stage II chronic kidney disease (CKD) without proteinuria (estimated GFR 68 mL/min/1.73 m2 by the CKD-EPI equation). His current medications include aspirin (81 mg), atorvastatin (20 mg), hydrochlorothiazide (25 mg), lisinopril (40 mg), and metoprolol succinate (25 mg), all taken once daily.
The patient reports overall good quality of life without any angina or dyspnea and denies any adverse symptoms related to medications. Specifically, he denies any orthostatic lightheadedness. He remains reasonably active with housework and social activities, although he does not exercise regularly.
On exam, heart rate is 67 and blood pressure (BP) is 108/62. Body-mass index (BMI) is 24 kg/m2.
How would you proceed with further management of this patient? Would you consider discontinuing any of his antihypertensive medications?
James and Oparil: This case is important because it is similar to what many clinicians see frequently. It also highlights some of the important elements of the new 2014 Hypertension Guidelines.
Our comments are intended to address the clinical problem of hypertension, though it is difficult to separate BP elevation from other cardiovascular risk factors.
Set Goal BP
First we must address the characteristics of the patient that are decision points in assessing and recommending BP goals and then address the appropriate choices of medications.
To set goals for BP, we must know a patient’s age and whether he has diabetes or chronic kidney disease. The patient, at age 76, is older than age 60. The case report identifies a history of CKD without proteinuria, apparently based on the estimated GFR of 68 ml/min/1.73 m2. There is no reported history of diabetes, so the question before us is: Does this gentleman actually have CKD? Much of the discussion about his care will hinge on how we answer this question.
The clinical challenge is that the estimating equations for GFR were not validated in individuals over age 70 and we do know that an age-related decline in the estimated GFR is to be expected. Our recommendation is to individualize therapy and we do not have evidence to guide us here. If this gentleman had proteinuria, that would confirm the presence of CKD. Given his age, we would not label this patient with the diagnosis of CKD and would attribute this laboratory value to age-related decline.
Based on strong evidence in support of Recommendation 1 in our guideline, and his age being over 60, we would set a goal BP target of less than 150/90. If we were more convinced of CKD, the goal would be less than 140/90. Since his BP is 108/62, this does not appear to be a clinically significant distinction.
Is he “overtreated”? What medications should he be taking?
The patient’s BP today is 108/62. We would recommend that his BP be measured again after standing for one minute, as he may not remember if he has orthostatic symptoms at home. If there is any evidence that he is orthostatic, we would discontinue the metoprolol and reduce the dosage of the lisinopril.
There is not an evidence-based answer to the question about whether BP can be too low in a patient who is taking antihypertensive medications if he/she is asymptomatic, though many of us have a concern about a J curve at systolic BP < 120 mm Hg.
Other reasons to adjust his medications would be to improve adherence, reduce the costs of his therapy, and reduce the potential for adverse effects or drug-drug interactions. The benefit of lowering BP with medications to any goal below 150/90 mm Hg in this age group remains unproven. It would be important to assess the patient’s perception of the burden of his medication regimen and compare this to the potential benefits of drug treatment and make a shared decision about therapy moving forward.
Rationale:
The patient is on three medications that could be considered anti-hypertensives. He is on a diuretic (hydrochlorothiazide 25 mg daily), an angiotensin converting enzyme (ACE) inhibitor (lisinopril 40 mg daily) and a beta blocker (metoprolol 25 mg daily). His race is reported as black and, thus, based on Recommendation 7 of our guideline, we would recommend a diuretic or calcium channel blocker as initial therapy. He is on a diuretic at a dosage that has been demonstrated to improve health outcomes (see Table 4 of the guidelines). He is not on a calcium channel blocker — this would be a consideration if his BP were not controlled.
One rationale for the ACE inhibitor is if the clinician believed that the patient does in fact have CKD — treatment with an ACE inhibitor or angiotensin II receptor blocker has been shown to improve kidney outcomes in this patient group. However, based on the discussion above, the evidence is not strong that this gentleman does have CKD and this would be an area where his medication regimen could be simplified by reducing the dosage or eliminating the medication if his BP remains well controlled. One argument for leaving this medication without change is that he is doing well without any perceived harms. However, if concerns about polypharmacy, adherence, or adverse effects were to present, this would be an opportunity to reduce his medication burden. We also emphasize that we do not see a history of previous MI or heart failure (HF) and this strengthens our resolve to suggest that an ACE inhibitor is not required to achieve the goals for treatment of hypertension.
The patient is also on a beta blocker (metoprolol 25 mg daily). Beta blockers are a proven treatment for hypertension but did not rise to the level of the other four classes recommended for the initial treatment of hypertension in the 2014 Guidelines (Recommendation 6). This gentleman does have a history of CAD, but no documented MI or systolic HF — both indications for use of a beta blocker to improve patient outcomes. He is status post-stent placement and it is unclear if this medication was added to achieve goals of treatment for CAD or for hypertension. In the absence of MI or HF, the evidence is less convincing for the benefit of adding beta blockers to the regimen. Our first recommendation would be to stop the metoprolol given that the systolic BP is less than 120 mm Hg. We found no evidence to suggest that a lower BP goal should be recommended for those with CAD than for the general population.
We should emphasize continued vigilance with life-style interventions. His BMI is acceptable, but maintaining physical activity would be important. He should continue his daily aspirin and statin therapy given his CAD.
This is a great example, as it brings up several issues and highlights areas where we may consider “fine-tuning” guidelines.
I know we have addressed this issue before in this forum, but my preference for a thiazide would be chlorthalidone due to its longer half life and more robust evidence base, at least in older trials not using ACE inhibitors. I imagine there was some debate on this issue, and wonder whether the major disruption caused by specifying chlorthalidone as the thiazide of choice was a consideration. I often do not change to this agent if it means increasing pill burden. Or I get an ABPM.
I agree with stopping the metoprolol.. With atenolol, there remains rampant overprescription.
Without proteinuria or CAD or HFREF, I do not prioritize ACE inhibitors in African-Americans, as their utility to slow the progression of CKD is much less robust, and there are greater side effects in this population. I agree that a GFR over 60 does not constitute CKD anyway, although I have not yet adapted to the EPI calculation (which I view as a “third generation” GFR estimator, and I am surprised by its major aforementioned limitation).
I agree with a prior erudite post discussing the better predictive validity of the ABPM compared with office BP measurements. Results of such testing often alters my recommendation, including the timing of administration. It may also lead to sleep study in the non -dippers. Some combination of cost considerations, availability, and absence of large clinical endpoint trials limited its general endorsement.
It is increasingly clear that guidelines should be old news for practitioners in the specialty. Old unless they are truly debatable … like new risk calculators and setting a different BP threshold for age as young as 60.
Sir
As I read there are no head to head trails comparing atenelol versus metaprolol retrospective studies show no benfit of metaprolol over atenlol
Recent guidelines advise betablockers as fourth drug so we will be combining vasodilators before using beta blockers. Augumenantation index bemfit of metaprolol appears probably less significant.
So should we really change to metaprolol from atenlol
JNC8 – reshuffling chairs on a Titanic of HTN guidelines show – latest installment…
With regard to the case:
-there are ZERO clinical outcome/MACE trials of HCTZ 25 mg once a day vs. placebo. What is so Evidence Based about it then?
-in ALLHAT Lisinopril in African American performed significantly worse with regard to BP and MACE, comparing with Amlo and Chlorthalidone. Depriving him of evidence based meds (like Amlo) and using clearly inferior ones – is…well, – questionable.
-Metoprolol, or any other beta blocker have no evidence of improvement in clinical outcomes/MACE in patients without MI and/or CHF. There is no data on improvement in MACE for post-stent patients either. There is limited effectiveness and no outcome data for MACE in African Americans.
His BP is so low, it is past the inflection point of J-curve, especially for his age. I am concerned about it.
This patients decreased GFR and “CKD stage 2” diagnosis is likely to go away if we wean off HCTZ which probably does not need anyway. He should have orthostatic BP checked and it will probably drop quite low… He is quite likely overdiuresed, with ACEI and ASA doing the rest of the job to slow down his GFR and metoprolol masking tachycardia…
So…leave him as is on medications that have zero outcome trial support only on the basis of the fact that they lower BP and still did not make him overtly sick?? I thought we are still under “promo no nocere” oath… I would wean off his meds one by one, assessing BP (including standing), vitality and any markers of HTN end organ damage like albuminuria and NTproBNP. If his vitality and kidney function is better, and no warning signs of any sort appear – let his SBP go into 140s, as JNC8 actually allows…this is definitely one positive change in the JNC8.
BTW, if we do nothing, than at least change his Metoprolol succ and Lisinopril to HS dosing on the basis of Hermida’s MAPEC study?