January 27th, 2014
Prevention Guidelines in Practice: Vignette 3
Siqin Ye, MD
This vignette is the third in our series “Making Sense of the New Prevention Guidelines — The View from Clinical Practice”
A 41-year-old African-American woman presents to clinic. She has a total cholesterol of 165 mg/dL, HDL of 40 mg/dL, and SBP of 145 mm Hg. She is a smoker and is not taking medical treatment for hypertension. Her Pooled Cohort Equations estimated 10-year CVD risk is 4.2%.
A week later, she presents to the clinic again for a repeat blood-pressure check. Her SBP is now 166 mm Hg, which changes her estimated 10-year CVD risk to 8.4%.
- Would you start this patient on a statin?
- Would you measure her BP again or use the average of the two SBPs already obtained to calculate estimated 10-year CVD risk?
- Would you assess other risk markers, as recommended by the new AHA guideline for cardiovascular risk estimation, such as family history, hs-CRP, CAC scores, or ABI? If so, how would these results guide your recommendation for or against statin initiation?
8 Responses to “Prevention Guidelines in Practice: Vignette 3”
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Kye, we know that shes “atherosclerosing” her arteries at a fairly rapid rate: she has all the risk factors for it and she smokes. We know statins modify diseases progression, and have few side effects. Why not practice “personalized” medicine here and start her on one rather than waiting for a threshold based on population data. Its not like the plaques will start forming exactly once you hit that threshold. Also, as you pointed out, these tools might not be very precise or accurate when you’re dealing with individual patients whose risk factor values might vary.
First you have to investigate why she had this change in blood SBP in one week. Any new factors like medications, change of diet, etc. any issues with taking the blood pressure. What about the diastolic blood pressure and differential. Do you have a significant difference between the osculatory and palpatory blood pressure. What about the smoking issue? You have to deal with it and stop it, at this moment is more important issue. A total cholesterol of 160 mg/dl and HDL 40 then she has a non HDL chol of 120 mg/dl, not bad. At this level, I would prefer a compleat lipid panel, I don’t recommend Statin for the moment. You have to many basic question to answer before you consider more sophisticated risk factors.
Interesting how the new risk predictor depends continuously on SBP, a measurement fraught with variability, different techniques (office, home, ABPM), and likely different risks for a given SBP ( average ABPM and home assessments may yield higher risk for a given SBP than an office reading).
I recommend statins for nearly all smokers over 40 yo and reevaluate after 3-5 yrs of cessation.Her hypertension strengthens the recommendation. Her blood pressure will be treated with a CCB, possibly in combination with an ACEU or ARB if there is proteinuria.Lifestyle changes and/or treatment of OSA will hopefully reduce medical requirements in the future.
Assuming the patient is on board with the above guidance, the utility of CRP and CAC score decreases, as a commitment to statin therapy and RX of HTN has already been made. I do not need more lipid values to make a decision.
I would specifically use a moderate statin potency, like atorvastatin 20 mg. I would check lipids once in about 2 weeks for adherence and response, but I would not feel obligated to reach a certain “goal”. I would not recheck lipids or LFTs for at least a year for adherence purposes.
she is relatively young. sudden increase in b.p is to
be confirmed. i would prefer to do ABPM to establish hypertension and emphasize more on stopping smoking. that is more important than stating on statins, lifestyle modification and cessation of smolking is more important than anyother treatment
Neat case
If her TG is 100, reasonable for an AA woman even with a low HDL, then her LDL is 105 mg/dl
I tried treating her BP and if her systolic BP dropped to 140, risk did not change – actually slightly higher – but if I went to 130 with rx, her risk fell to 5.9% (interesting how sensitive the score is to syst BP with no RX)
When I left her untreated for BP and syst 166 but she stopped smoking, her risk when to 4.3
If I don’t do anything else but give her a statin and assuming her HDL and TG don’t change (likely), but her LDL drops to 60, TC drops to 120 I cannot even get a score so if I make her TC 130 on statin, her risk is 3.4% – but it doesn’t matter if that is her natural or her statin induced risk (I don’t know?)
If I saw her, I would focus on BP and smoking (even me) rather than the statin – but I would do a CAC and that might change my mind
Thanks everyone for your responses! It’s fascinating to see the different takes on this case.
The patient presented was an actual NHANES III participant used as an example in our manuscript on how SBP variability can affect cardiovascular risk estimation (http://www.ashjournal.com/article/S1933-1711%2813%2900214-3/fulltext). I was motivated to present the case (and to look at the study question) because too often we approach risk estimation as a “black box”, with little thought given to what’s driving the risk and how stable/reliable the estimate is.
I agree with everyone’s comments that smoking is a big component of modifiable risk for this patient. If she were not a smoker, her estimated risk would be reduced dramatically (by about half). Interestingly, blood pressure variability is itself a risk marker, and the variability demonstrated by this patient places her at higher risk—though how to incorporate the different risk markers we have available into the decision-making process can be challenging (except for maybe CAC).
Drs. Powell and Shaikh bring up the use of ABPM to determine her “true” BP. From a hypertension management perspective, I think ABPM could be useful in this and other cases where there is a lot of visit-to-visit SBP variability. It is however difficult to use ABPM determined SBP to calculate CVD risk, as the cohorts used to derive the Pooled Cohorts Equation (and other regression based risk prediction tools) uses SBP measured at clinic/home visits.
Finally, Dr. Ginsberg makes several interesting observations, including that if a patient is started on anti-hypertensive treatment but has only small improvement in SBP, the estimated CVD risk can actually go up as an artifact of the equation! As an aside, the Framingham equation (http://cvdrisk.nhlbi.nih.gov/calculator.asp) had similar problems. For example, for a 55 year-old woman, with total cholesterol of 220, HDL of 30, who is a smoker and on anti-hypertensive treatment, her calculated 10-year CHD risk would be 6.4% for SBP of 118 but would become 10.5% for SBP of 122. This is because of an interaction term in the Framingham equation for treatment and SBP>120. I actually think these are advantages of the new guideline/Pooled Cohort Equation that hasn’t been much commented on, because there are no interaction terms, and because there is only one single cut-off of 7.5%, both of which makes risk classification more stable.
Again, thanks for everyone’s interest and feedback!
yes, i would like to add a statin, Rosuva 5 mg / day.
before i start anti HTN, i would like to counsel her in view of LOW HDL, smoker, HTN – family h/o, ethnic risk for CV diseases. would keep her on observation and review the need for ANti HTN drugs.
yes i would like to have her detailed family history, no hs CRP, CAC scores etc.
The new guidelines call for a clinician-patient “risk discussion” in this woman and all primary prevention patients who would consider a statin. The basis of the risk calculation from the risk assessment work group is pooled data from several long-standing, community- based US cohort studies. These were used to develop new sex-specific and race-specific equations to predict 10-year risk for atherosclerotic cardiovascular disease (ASCVD). (see Risk Assessment guidelines) As noted in a Lancet editorial “These pooled cohort equations represent a major step forward for risk estimation, because, for the first time in a major guideline, they focus on estimation of risk for both heart attacks and strokes and provide estimates applicable to African American people.” Lancet Dec 2013 Lloyd-Jones D. et al. Thus this pooled equation could be valuable for her.
Her major risk factors for ASCVD are cigarette smoking, low HDL-C and hypertension. An acute exacerbation of blood pressure is crucial to address, but it shouldn’t change the risk decision as regards long-term statin therapy. The immediate targets of therapy are her cigarette smoking and her elevated blood pressure. That’s why the guidelines stressed that clinicians write statin prescriptions, not the risk calculator. Her HDL-C is not a target of therapy, but should improve if she stops her tobacco use.
I would like to point out for those new to the risk discussion concept several points you could make in the risk discussion.. You should note that one way to look at age is to consider it a surrogate for exposure to chronic risk factors. If she spent most of her life at a lower BP that’s very different than if she spent most of last 10 years at a much higher BP. On the other hand tobacco use is an immediate problem. It can increase her risk of ASCVD events in the short-term. The good news from the ASCVD standpoint is that if she can quit tobacco use, her ASCVD risk in 1-2 years can reflect that of a non-smoker. If she can substitute the habit of regular physical activity and a healthier diet for her cigarettes, she can improve her blood pressure as well as her lipid profile. She doesn’t need lipid drugs to raise the HDL-C, she and the clinician need to ask what it would take to get her off cigarettes and into a more healthy lifestyle. Resource allocation should focus here at the present, not on statin use.
This case illustrates why the guidelines insisted on a risk discussion in primary prevention (and also by thte way for those secondary prevention patients over 75) . Please note that risk assessment guidelines do suggest that family history, hs-CRP, CAC scores, ABI and lifetime risk can be used to inform the risk decision about statins. The cholesterol guidelines added LDL-C ≥ 160 mg/dl, so all of these factors could be used to inform the risk decision as the clinician felt appropriate.
Based on the data presented here, it seems reasonable that the decision regarding a statin can wait until she is re-evaluated for statin use downstream. Hopefully she will have good adherence to smoking cessation and her anti-hypertensive therapy.
In 12-18 months, if she has been successful plug in her prevention efforts with no tobacco use but on anti-hypertensive treatment, the potential for benefit from statin therapy would not exceed the potential for adverse effects . It would be hard to justify statin treatment at that time. On the other hand, if she can’t quit tobacco use, her risk of an ASCVD event may be high enough (depending on lipid values obtained in a steady state) and the potential benefit of a statin prescription is reasonable to discuss.
The new guidelines highlighted the need for proper intensity of statins added to lifestyle in high risk groups (secondary prevention, LDL-C ≥ 190, and diabetes 40-75) where the evidence strongly supported this strategy. In primary prevention, the focus turned to physician judgement and patient preference with a consideration of more than just the risk calculator score to guide clinical decision making. An article in Annals of Internal Medicine (it online and soon to be published) provides a good synopsis for interested readers.