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Reflections on ASH 2013: Lessons in Quality Improvement

Reflections on ASH 2013: Lessons in Quality Improvement

The 2013 ASH annual meeting provided me a lot of food for thought. There were data galore poured out over less than a week, but some of the critical content—the surefire take home messages—warrants post-meeting reflection. If primary care practice addressed these points alone, the quality of care for patients with hypertension would experience a boost.
  
Diagnose Resistant Hypertension
There were 7 sessions that addressed various aspects of resistant hypertension. I think there is an important message in the time spent on and redundancy in covering this entity, which is increasing in prevalence. I would like to address 4 things that should be part and parcel of our practice.

1. Do not delay making a diagnosis of resistant hypertension. It is a critical diagnostic and therapeutic milestone in the patient’s course. From a diagnostic perspective, it is a time to consider: primary aldosterone syndromes, renal artery stenosis, and obstructive sleep apnea among other causes. Why did I begin with excess aldosterone? Because that immediately brings us to the therapeutic choice of spironolactone. It really works! Initiation should not be delayed when a bona fide diagnosis of resistant hypertension is made. Changing regimens like musical chairs is not a good substitute for adding spironolactone. Also remember, patients do NOT have to have an elevated aldosterone/renin ratio in order to benefit from spironolactone.

2. When a patient is identified as resistant, he or she should have already been on a 3-drug regimen that includes an ACEI or ARB + a calcium channel blocker + an appropriate diuretic (more on this to follow).  
    a. Dose the medications appropriately before diagnosing resistance! Ten mg of the typical ACEI or 12.5 mg of hydrochlorothiazide in a patient with a GFR of 30 mL/min does not cut it!
    b. When a patient is characterized as resistant, the thiazide diuretic of choice should be chlorthalidone.

3. Primary care clinicians appropriately worry about hyperkalemia. That concern, however, should not paralyze therapy. This is where “stacking” diuretics can help. 

There is a concern about adding spironolactone to the regimen because the patient is already receiving either an ACEI or an ARB. Both can raise potassium levels. Chlorthalidone is indicated and it lowers potassium in individuals with resistant hypertension. Why not stack spironolactone and chlorthalidone? The more places in the nephron that are affected, especially when combinations balance out K+ excretion/retention, the lower the BP without hyperkalemia. Conversely, if low potassium is the problem, combination K+ wasting/K+ sparing diuretics can be stacked. I used to treat the higher-dose hydrochlorothiazide/triamterene combination as a relic of days long gone by. The formulation was developed to permit a higher dose of hydrochlorothiazide without risking hypokalemia. Now that is what we need today—not yesterday.       

4. Don’t give up if the addition of spironolactone does not get the patient to target BP. You can add other medications. You can stack diuretics and calcium channel blockers (a dihydropyridine and diltiazem, for example). Seek consultation.

Soon there will be additional therapeutic assistance.

Consider Renal Denervation
The next innovation (presently under intensive study) to treat refractory hypertension is renal denervation therapy. Older practitioners (present company definitely included) remember guanethidine. The sympathetic blockade consequent to its use actually led to its obsolescence. It was so effective as a ganglionic blocker that orthostatic hypotension precluded its use. Decreasing sympathetic nerve activity to the kidney significantly lowers BP. Preliminary data have established that renal denervation can lower systolic and diastolic BP 32 and 12 mm Hg, respectively. Significant lowering has persisted for 6 months or longer. There has been no decline in GFR in subjects who have undergone renal denervation. Heart rate falls as a result of renal denervation.

If this novel therapy works as well as it has to date, and has few complications or side effects, it is another reason to identify resistance early. We may have more than medicine for those with refractory hypertension.     

Say No to Beta-Blockers

If the goal in adding medications is solely to lower BP, resist the urge to prescribe traditional beta-blockers. Atenolol is a specific “no-no.” Nontraditional beta-blockers are quickly becoming the “in” drugs. The two to consider are carvedilol (adds alpha-blockade) and nebivolol (adds nitric oxide to the mix). For example, in head-to-head comparisons, when metoprolol and carvedilol are compared, type 2 diabetes mellitus is more often a consequence of metoprolol and not carvedilol. Long-term use of traditional beta-blockers increases insulin resistance and diabetes. It is like trading one disease (hypertension) for another (diabetes). 

Discern Urgencies From Emergencies and Leave Inpatient Hypertension Alone

These may seem strange topics to combine, but bear with me. Remember that severe hypertension is defined BP 180/110 mm Hg or greater. When is such a pressure an emergency and not an urgency? When there is target organ injury it is an emergency. Evaluate the patient for target organ damage before choosing therapy. That same rule—evaluate carefully—also applies to inpatients with hypertension. Avoid overtreatment. Hydralazine may cause dangerous side effects. If target organ damage is absent, aggressive BP lowering is unreasonable, similar to the management of an urgency.

Haste can make waste.


 

 
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