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DR. MOSER: I would like to present several casesand review management problems. The first is a 56-year-old woman with a negative family history fordiabetes and high blood pressure (BP). She is a non-smoker, is not obese, is active physically, and is asym-ptomatic. A routine exam showed a BP of 155/95mm Hg. This was repeated three times at the firstvisit, with no variability. Cholesterol was 225 mg/dL,low-density lipoprotein (LDL) cholesterol 120mg/dL, and high-density lipoprotein (HDL) choles-terol 52 mg/dL. Blood urea nitrogen was 18 mg/dL,creatinine 1.2 mg/dL, uric acid 6 mg/dL, and glucose82 mg/dL. Urine was negative for protein on a dip-stick, and otherwise negative. The electrocardiogram(ECG) was normal.

Dr. Black, what additional procedures wouldyou like to perform before you treat this patient?Tell us how you would classify her as to risk andthe immediacy of intervention.

DR. BLACK: I wouldn’t do anything further,except perhaps to look into her history to makesure that the BP has been gradually increasing overtime.

DR. MOSER: The last time she had a BP takenwas 4 years ago.

DR. BLACK: And what was it?DR. MOSER: No record.DR. BLACK: Typical. The reason I ask is that

this is a very typical history of someone with essen-tial hypertension.

DR. MOSER: Okay...you decided not to do anyprocedures. Would you just tell her to come back

in 2 months and check the BP again?DR. BLACK: Well, I would assume she had had

a careful physical exam.DR. MOSER: Yes.DR. BLACK: And she did not have abdominal

masses or abdominal bruits, nor anything like arapid pulse rate to suggest thyroid disease or anyother secondary causes.

DR. MOSER: Nothing at all.DR. BLACK: I would certainly see her again in

about 1 month to check her pressure, although thatis a little sooner than recommended. After that, Iwould probably see her again in 1 month. If theaverage of the pressures on those visits is >140mm Hg systolic and/or >90 mm Hg diastolic, Iwould classify her as a stage I hypertensive. If itwere between 130 and 139 mm Hg and 85 and 89mm Hg, I would classify her as high-normal. Ineither case, since she has no risk factors other thana borderline age criterion, I would consider her alow-risk individual to whom I would unambigu-ously recommend lifestyle modification.

DR. MOSER: But she doesn’t smoke, she’sactive and thin... what lifestyle changes might behelpful?

DR. BLACK: One cannot do much, other thanperhaps reduce salt intake if she’s a salt user.

DR. MOSER: Again, she has told you, “I don’tuse any salt; I never use it in cooking, and I don’tuse it at the table.”

DR. BLACK: Then I would actually considertreating her with the drug class that has the fewest

Roundtable Discussion: Problems in the Management of Hypertension

Marvin Moser, MD; George L. Bakris, MD; Henry Black, MD

Following a symposium on hypertension sponsored by the National Heart, Lung, and Blood Institute in Chicago, ILon October 3, 2001, a panel was convened to discuss various aspects of hypertension treatment. Moderating thepanel was Dr. Marvin Moser, Clinical Professor of Medicine at The Yale University School of Medicine. Panel mem-bers included Dr. George Bakris, Professor of Preventive Medicine and Director, Hypertension/Clinical ResearchCenter at the Rush-Presbyterian-St. Luke’s Medical Center in Chicago, Illinois and Dr. Henry Black, Professor ofMedicine, Associate Vice President for Research, and Chairman of the Department of Preventive Medicine at Rush-Presbyterian.

THE JOURNAL OF CLINICAL HYPERTENSION VOL. IV NO. III MAY/JUNE 2002208

side effects. Here is someone who really is asymp-tomatic and feels well. I would not want to makeher feel worse with treatment. Now, what medica-tion would that be? That is an important question.

DR. MOSER: You tell me.DR. BLACK: Well, I think there are two

options. She’s white. A low dose of a diuretic orperhaps an angiotensin receptor blocker (ARB)would be the medication I would choose. Anangiotensin-converting enzyme (ACE) inhibitoralso would be an option. The problem with anACE inhibitor is that older women in particular,(although she is not really old), have a higher inci-dence of cough than do any other demographicsubgroups. But these would be my choices.

DR. MOSER: Okay, you would check her BPover 2−3 months, you would treat her if the BPstayed above 140 mm Hg.

Dr. Bakris, what about home BPs and ambula-tory monitoring? Why not obtain an echocardio-gram? The ECG was negative, but maybe she hasearly left ventricular hypertrophy (LVH) that canbe picked up on an echo. Isn’t this important?

DR. BAKRIS: Before I answer that question, letme ask you a question. Does she have anyretinopathy?

DR. MOSER: Unfortunately, the world is suchthat very few doctors look at the retina.

DR. BAKRIS: Well, they should.DR. MOSER: However, as you know, if she is

not a diabetic and has stage I or grade I hyperten-sion, her fundi may show some arteriolar narrow-ing, but that probably will not be very helpful indetermining the urgency of treatment. We all lookat fundi, but in a patient like this, it is very hard todetect definite changes.

DR. BAKRIS: Correct.DR. MOSER: Dr. Bakris, what difference would it

make? What if we saw some arteriovenous nicking?That is possible in a patient this age with this type ofBP. Would that change your approach?

DR. BAKRIS: Yes, it would change myapproach somewhat. It would tell me that she hashad an elevated pressure for a fairly long period oftime. And it might lead to earlier treatment.

DR. MOSER: You would not wait 2 or 3months to treat her?

DR. BAKRIS: I would basically do two things. Iwould bring her back, as Dr. Black suggested, in 1month and recheck her pressures. If they were sim-ilar or a little lower, I would either do 24-hour BPmonitoring or suggest investing in a home BPmachine and have her check her BPs at home, thentake a look at the pressures over time. When shereturns in another month, I would not expect

lifestyle changes to have impacted her pressurevery much. If we did a 24-hour monitor, we wouldget a quicker response, but the home BPs give us anongoing picture. If her morning BPs at home con-tinued to hover around 140/90 mm Hg, even if atabout 138/80−85 mm Hg, I probably would treather. In the absence of edema, diabetes, and otherrisk factors, I probably would start her on an ARBas my first choice.

DR. MOSER: All right, there are a couple ofpoints. What happens if you do ambulatory moni-toring at considerable cost and possible annoyance,and you get a daytime reading of 130/82 mm Hgand a nighttime reading of about 126/80 mm Hg(some dipping, but not much)? These are definitelywithin the normal range, even for ambulatory mon-itoring. However, in your office, on two or threeoccasions, her pressures remain at 145−150/90−95mm Hg. Are you going to treat her, or are you goingto say that this is just white coat hypertension, for-get it, and go about your business?

DR. BAKRIS: It would change my aggressive-ness. It would not change what I would do, but itwould change how quickly I do it. Based on datafrom the recent article in The New EnglandJournal of Medicine on mortality in people withhigh-normal pressures, I would definitely want herpressures somewhat lower.

DR. MOSER: As an aside, how do you feelabout home BPs in general?

DR. BLACK: I’m an outlier; I don’t use them. Ifpeople want to use them, I don’t stop them, but Ialmost never pay any attention to them.

DR. MOSER: In other words, if I brought in 20readings at 130−120 mm Hg and in your office it wasalways 150 mm Hg, you would use the office pres-sures for guidelines in therapy.

DR. BLACK: We need to educate people that whatis normal at home is not what is normal in the office.The average difference is about 12/7 mm Hg. Forsomebody who is 135/80−85 mm Hg at 10 p.m., afterhaving two drinks and just waking up from a boringbaseball game, to say the pressure is normal is wrong.I think it gives misinformation, it makes some people abit neurotic about their pressure, and I pay almost noattention to it.

DR. MOSER: Then the studies that appear toindicate that outcomes are improved when homeBPs are telephoned into a computer and storedmay not be important?

DR. BLACK: That is a little different. One ofmy concerns about home readings is the biaspatients have about telling you what they want youto know.

DR. MOSER: There are some data that claim


that this may not be true.DR. BLACK: Well, there are old papers that did

describe biased reporting, and I am concernedabout this.

DR. MOSER: The computer readout reports 20readings that are below 140/90 mm Hg, but youstill get readings higher than 145/95 mm Hg in theoffice.

DR. BLACK: I am simply not impressed, I donot particularly care what happens at home, unlessBPs are too low.

DR. MOSER: Dr. Bakris, you agree?DR. BAKRIS: No, I disagree. I think that if you

tell people to monitor home pressures and don’tgive them any guidance, then it’s meaningless. Iwouldn’t do that. What I do first is insist that thepatient bring the machine in and we calibrate it. Itell patients that the only BPs we are interested inare the ones in the morning, because of the highercardiovascular event rate at that time. They canmeasure it at any time they want—preferablybetween 6 a.m. and 10 a.m., and not after they’vehad drinks or eaten a full breakfast or anythinglike that—and they should always do it twice.These are the readings that I consider.

DR. MOSER: Would these readings changeyour approach?

DR. BAKRIS: Well, it changes my approachonly if I get dramatically low readings at home anddramatically high readings in the office. But to tellyou the truth, I’ve never seen that, except in onepatient whom I sent for biofeedback.

DR. BLACK: It is also interesting that we berateourselves for not taking BP in the office accurately,but we have no quality control at all about BPstaken in the home.

DR. BAKRIS: That’s right.DR. MOSER: I agree that home pressure may

have limited value, but there are some patientswho want to know what their pressures are and inthose cases, its important that they be encouragedto measure them. These readings also serve as rein-forcement if they are controlled. Also, in some sit-uations patients will complain of dizziness whentheir pressures are high rather than low, so there isprobably some benefit to home BP recordings.

DR. BLACK: I base my therapeutic decisions onoffice readings because that is what we know.

DR. BAKRIS: And, by the way, so do I.DR. MOSER: All right. Three months pass by

and our patient’s BPs are still over 145/90−95 mmHg, but you now have this 24 hour reading thatsays let’s wait a minute, the BPs are normal. Whatdo you do?

DR. BLACK: I think you are in a very common

dilemma. We ought to follow on our own rules.She is classified as stage I and is below 60 years ofage. We can go for 6−12 months without specificpharmacologic treatment. If she had normal ambu-latory pressures, I would feel much more confidentdoing that than if her pressures were high. If theywere high—especially if she had retinopathy—Iwould treat much sooner. I think our rules arewise. If, at the end of 3 months, BPs are not high-er, I would wait. At 6 months, if they are higher,i.e., >160 or >100 mm Hg—stage II—treatment isindicated. If not, we can wait for 12 months andthen begin specific medication. These are reason-ably well considered guidelines.

DR. MOSER: I’m not so certain that I agree.Both of you are vigorous therapists who believe intreating hypertension before microproteinuria isnoted and before there is evidence of LVH. Are yougoing to wait for 1 year and possibly risk furthervascular changes before beginning therapy? I amaware that the odds of developing clinical evidenceof a cardiovascular event within 1 year in a low-risk patient are very low, but what about slow pro-gressive changes that we cannot detect clinically?

DR. BLACK: Because she is at such low risk,with no risk factors other than hypertension, thelikelihood of her having an event within 1 year,while I sit and watch, is slim to none. However, ifthat were my BP, I would reduce it.

DR. MOSER: You would treat yourself after amonth or two?

DR. BLACK: Hypertension is not an asympto-matic disease. There is a series of very subtle butclearly definable effects on the quality of life.

DR. MOSER: Then why would you not treatthis woman the way you would treat yourself?

DR. BLACK: Well, because I cannot prove ben-efit in this type of case, and you propose a scenarioin which I have to use my gut, not my brain.

DR. MOSER: Okay. Well, medicine is intu-itive—why not use a gut feeling based on knowl-edge but not definitive data?

DR. BLACK: That’s right, it’s an art, not a science.DR. MOSER: What do you believe? There are data

on people who have so-called “white coat hyperten-sion” in the office and normal BPs at home who showincreased vascular resistance, left ventricular dysfunc-tion, and some of the metabolic changes noted inhypertensive patients. We do not have long-term treat-ment outcome data on these patients, but I intuitivelybelieve that they should be treated.

DR. BLACK: My approach to this is probablythe same as yours. I consider white coat hyperten-sion a way station between normotension and def-inite hypertension. There is clear evidence from


many sources that these people are not the same asnormotensives. These are the people we treat withlifestyle modifications if we’re concerned aboutpossible side effects or cost, but we treat with med-ication if BPs remain elevated.

DR. MOSER: George, would you go along withtreating this patient if, after 2 months of checkingpressures with or without an ambulatory monitor,her pressures remained elevated?

DR. BAKRIS: Well, I think what Henry says isunfortunately the truth.

DR. MOSER: Why unfortunate?DR. BAKRIS: Because I would do exactly what he

said. If I were in this situation, I would treat myself. Ifyou follow present national guidelines, you would nottreat this woman for 6 months to 1 year. You wouldsimply follow her, without specific medications.Admittedly, studies that I have seen that describe thiskind of patient in terms of natural history suggest thatthe probability of something happening to her is aboutequal to the probability of lightning striking me.

DR. MOSER: In the short run.DR. BAKRIS: Yes, in the short run.DR. BLACK: Yes, in the short term.DR. BAKRIS: If she were still at this BP level.DR. MOSER: However, as we have noted, there

may be changes in the endothelium over a year’stime that you cannot detect.

DR. BAKRIS: That is a self-fulfilling prophecybecause the more you look, the more you will find.

DR. MOSER: We have somewhat differingpoints of view on the time we would wait to begintherapy. Let’s get to specific therapy when we dodecide to treat. What about starting this woman ona low-dose diuretic?

DR. BLACK: There is nothing wrong with thatapproach.

DR. BAKRIS: That would be my alternative.DR. MOSER: This is an alternative that is well

tolerated and probably as effective as other agentsin a high percentage of patients.

DR. BAKRIS: No argument at all.DR. MOSER: Let’s say that didn’t work. She

takes 12.5 mg of hydrochlorothiazide and comesback in 3 months. Her BP is still about 140−145/90 mm Hg; would you wait another 3 monthsbefore changing therapy?

DR. BAKRIS: I wouldn’t wait. Three months isan adequate time to see a response. I would doublethe dose in this case.

DR. MOSER: Okay, you would go to 25 mg perday.

DR. BAKRIS: And if that didn’t work in a fewmonths, I would add a second agent.

DR. MOSER: And the second agent would

preferably be an ACE inhibitor or an ARB?DR. BAKRIS: It would be an ACE or ARB.DR. MOSER: How about a β blocker?DR. BAKRIS: Well, my feeling about β blockers

is that they are really not as well tolerated as ACEinhibitors or ARBs.

DR. MOSER: So this patient would probably beon a diuretic and may require an ACE inhibitor asan additional therapy—or may respond to an ACEinhibitor or an ARB and require the addition of adiuretic to be maintained at BP levels as close to120/80 mm Hg as possible. The odds are that goallevels of BP will be achieved and maintained withthis type of therapy, without any adverse reaction.

DR. MOSER: The second patient: a 76-year-oldfemale, 120 pounds, 5’5”, active, asymptomaticexcept for a dull morning headache. Father andmother both had hypertension but died at ages 85and 87. Her BP has been hovering at 170−175/80−85 mm Hg for the past 3 years, and there were somevoltage criteria for LVH on an ECG. It was inter-preted by her doctor as normal, and because she wasthin, the voltage was considered to be within normallimits. Urine was negative, cholesterol 244 mg/dL,HDL of 70 mg/dL, and LDL of 112 mg/dL. What doyou do? Any further workup, or do you haveenough information to warrant proceeding withtreatment?

DR. BLACK: What about her physical exam?DR. MOSER: Physical examination was nega-

tive except for a grade 1 systolic murmur at the leftsecond interspace.

DR. BLACK: I would do nothing further. Sheclearly needs treatment.

DR. MOSER: What about an echocardiogram?DR. BLACK: What are you going to learn that

would change what you do?DR. MOSER: You don’t think an echo should

be done?DR. BLACK: No, not at all.DR. MOSER: Dr. Bakris?DR. BAKRIS: I would agree, especially in light

of what you just said. How is this procedure goingto change a treatment approach?

DR. MOSER: We all know that ECGs are notvery sensitive in picking up early LVH. If you reallywant to detect LVH, you need an echo, don’t you?

DR. BLACK: Of course.DR. BAKRIS: That’s fine, but again, how is a

positive or a negative echo for LVH going tochange the approach to treatment?

DR. MOSER: It probably will not change whatI would do, but a lot of experts do it routinely.

DR. BLACK: If she is in stage II isolated systolichypertension, she needs treatment. The Losartan


Intervention for Endpoint Reduction in Hypertension(LIFE) study,* which is a comparative study of differ-ent drugs in patients with LVH suggests that an ARBbased regimen reduces strokes more than a β blockerbased program and fewer cases of new onset diabetesoccur in the ARB group. Most medications that lowerBP will regress LVH if it is present. (*The LIFE studywas published after this discussion was held).

DR. MOSER: Are you saying that any drug wechoose, except for a vasodilator, is going to have abeneficial effect on BP and LVH—that it probablydoesn’t make any difference whether or not wedetect early evidence of cardiac enlargement?

DR. BLACK: Right.DR. MOSER: Okay. I agree. Do we need stand-

ing BPs a couple of times to see whether she haspostural changes?

DR. BLACK: Only if she were dizzy, which has-n’t been mentioned.

DR. MOSER: No, she’s not dizzy.DR. BLACK: Then I would ignore home pres-

sures. If these get her more involved in her treatment,that’s fine, but she seems like a compliant patient andmay not need this type of reinforcement.

DR. MOSER: You would treat this patient based onoffice BPs. We probably will agree that a low-dosediuretic would be a good initial choice, but that a goalBP, of <140 mm Hg, will probably not be achieved ina high percentage of patients with this therapy alone.Based on a large European study, a dihydropyridinecalcium channel blocker (CCB) might be anotherchoice. My own feeling is that a combination of a low-dose β blocker/diuretic, an ACE inhibitor/diuretic, oran ARB/diuretic would also be acceptable and effectivechoices. A caveat: although we advocate a goal pres-sure of <140 mm Hg in the elderly patient with isolat-ed systolic hypertension, this is not readily achievablein a large number of patients. Many times, it is onlypossible to reduce pressures from about 170−180 to150−160 mm Hg before a patient will “feel funny.” Inthese cases, it may be advisable to back off and keepthe patient on the same therapy for 3−6 months. Afterthat time, therapy can be increased in an attempt tolower BP further. We should remember that the bene-fits noted in the clinical trials were achieved with a sys-tolic BP reduction of about 12−15 mm Hg.

DR. BLACK or DR. BAKRIS: Any further com-ments about this case?

DR. MOSER: The last case is a 46-year-oldmale, 165 pounds, 5’4”, referred to you by hisdaughter to get another opinion. He is sedentary,and there is a family history of diabetes and hyper-tension. His father died at age 55 of a myocardialinfarction, and his mother at 79 of diabetes. Hehas been healthy, with no symptoms other than

occasional shortness of breath on activity. Heignores this. His BPs are 150−160/95−100 mm Hg.He has recently been started on a long-actingnondihydropyridine CCB, and his BPs have beenabout 140−145/85−90 mm Hg. The doctor hasassured him that the therapy is successful, and thathe is doing well. His physical examination is essen-tially negative. Fundi show grade I−II changes withsome arteriovenous nicking. Routine urine testingwas negative, blood urea nitrogen was 22 mg/dL,creatinine 1.4 mg/dL, and glucose 104 mg/dL. Heis on antidiabetic therapy with a glycosylatedhemoglobin of 7. The ECG is now normal but hadpreviously shown evidence of LVH.

DR. BAKRIS: So he is diabetic.DR. MOSER: He is a diabetic, and has been told

that he is under control. He has no obvious evidenceof progressive renal disease. His LVH hasimproved. He has been told that everything is fine,and his BPs are 140−145/85−90 mm Hg.

DR. BAKRIS: Well, first of all, he is not undercontrol with a hemoglobin of A1c of 7.

DR. MOSER: This, of course, should be about5.5 or 6.

DR. BAKRIS: Exactly.DR. MOSER: All right, what do you do? Any

further tests?DR. BLACK: None that I can see.DR. MOSER: Would you want a determination

of microproteinuria, Dr. Bakris?DR. BAKRIS: Definitely. You said his dipstick

was negative?DR. MOSER: Dipstick was negative.DR. BAKRIS: Well, I would like to know if there

is less than 300 mg/day of protein in the urine, butthat will not affect my therapeutic decisions.

DR. BLACK: I would do the same thing that Isuspect you, or almost anyone else would. I wouldadd a second agent, which would be an ACEinhibitor or an ARB. I have a different goal BP inthis case. I do not consider a 140−145-mm Hg sys-tolic BP controlled. I also would not consider the85−90-mm Hg diastolic controlled in a diabeticpatient. Accepting numbers like this, which are closeto goal, might appear to be the easy way out, espe-cially in someone on a single agent. But we know wecan do much better if we change or add medica-tions. Data indicate that this type of patient shouldbe controlled at 130−135/80−85 mm Hg.

DR. MOSER: Would you put him on an ARB oran ACE inhibitor, or doesn’t it matter?

DR. BLACK: Frankly, I would probably put himon an ACE inhibitor, in addition to his present thera-py. I don’t think there is much difference between anARB and an ACE inhibitor, but if I’m an evidenced-

based type, I will have to go with the evidence wehave. We have good data on benefits with renal diseasein diabetes, but few data thus far on coronary heartdisease outcome with ARBs. Other studies will proba-bly show us that ARBs do just as well in reducing car-diovascular disease morbidity/mortality, but these dataare not available at present.

DR. MOSER: If you did a dipstick for micro-proteinuria and it was positive—let’s say between30 and 300 mg/day—would you then say that anARB has to be used to prevent progression ofmicroproteinuria?

DR. BLACK: Well, we have several trials thatsupport this, but we have nothing negative aboutACE inhibitors. I think the mechanism is the same,and the results may be the same.

DR. MOSER: So you would leave him on aCCB and add an ACE inhibitor or possibly anARB. If, 3 months later, the BPs are still 140/90mm Hg, what would you do?

DR. BLACK: I would titrate up with the drugsthat he is being given. I would probably use a fixedlow-dose combination, so that he takes one pill.

DR. MOSER: Okay, 3 months later, his BPs arestill not at 130−135/80−85 mm Hg. Would youadd another drug?

DR. BLACK: Yes, I would add another drug; Iwould add a diuretic.

DR. MOSER: I agree that a diuretic is clearly indi-cated, and I would consider using a combinationARB/diuretic or ACE inhibitor/diuretic in addition tothe CCB, or I would stop the CCB and see if one ofthe combinations would work by itself.

DR. BAKRIS: I would agree with all that. WhatI would have done, though, is probably go to acombination of an ACE inhibitor/CCB somewhatearlier. I would also limit his sodium intake so asnot to blunt the effects of the ACE or ARB. How-ever, you can make the point that sodium reductionis not vital if I add a diuretic, which is what Iwould do.

DR. MOSER: Now, what if this patient had hada creatinine of 2.3 mg/dL and a definite 2+ proteinon a dipstick. He’s on a CCB. Would you stop itand use an ARB and a diuretic? Or would his man-agement be the same as it would be if there was lit-tle evidence of nephropathy?

DR. BAKRIS: Based on recent data, first I wouldwant to know if it is a dihydropyridine or nondi-hydropyridine CCB. I definitely would stop a dihy-dropyridine, but not a nondihydropyridine, and Idefinitely would add either an ACE inhibitor or anARB and a diuretic.

DR. MOSER: Would you do this on thepatient’s first visit to you as a consultant?

DR. BAKRIS: Right away. In fact, an ACEinhibitor/diuretic or an ARB/diuretic should bepart of the regimen. I would titrate to higher dosesfairly quickly and make sure I achieved BPs below130/80 mm Hg.

DR. MOSER: So, based on recent evidence indiabetics who already have definite proteinuria andeven a slight elevation in creatinine, you would usean ARB and a diuretic in an effort to achieve BPcontrol and slow down progression to end-stagenephropathy. But you would also continue theCCB if this had been used initially.

DR. BAKRIS: Yes. Actually, if BP were not wellcontrolled—if goal BP’s were not achieved—Iwould probably add a β blocker.

DR. BLACK: One of the things that’s so artificalabout trials, and we have to remember this, is that theymay prevent us from using drugs we would use inpractice. There is just so far that we can take trialresults with respect to how much they tell us. Youwould never manage a complicated patient like thiswithout using all the classes of medications at your dis-posal. Trials don’t let us do that.

DR. MOSER: Of necessity, trials involve rigidprotocols.

DR. BLACK: They have a lot of value, but they dorestrict us. So, in this patient, management maybecome complicated, but this will prove to be worth-while if BPs can be lowered to the 130−135/80−85 mmHg level. This will require multiple drugs.

DR. MOSER: Finally, another scenario. Dr.Bakris, what if our last patient came to you havingstopped all of his medication? The creatinine was1.8 mg/dL and the protein was 2+ on a dipstick.

DR. BAKRIS: You mean, he had been takingmedication and stopped before his family got himto come to me?

DR. MOSER: Yes. He was on a CCB and, 1year ago, on a β blocker. He stopped it all.

DR. BAKRIS: Because?DR. MOSER: He just got tired.DR. BAKRIS: Well, I would basically educate

him as to what these drugs should be doing forhim, what he can expect as an outcome if he does-n’t follow the program. I would talk about cardio-vascular risk reduction with ACE inhibitors andabout ARBs in diabetic patients with some evi-dence of kidney involvement.

DR. MOSER: Would you start him on anARB/diuretic?

DR. BAKRIS: I would start him on anARB/diuretic right away—something like Hyzaar100/25 mg or Avalide 300/12.5 mg.

DR. MOSER: All right. He doesn’t respond tothat in terms of getting BPs as close to 120/80 mm


roundtable discussion: problems in the management of hypertension

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