A case for exercise

Did you miss me?  Various things have kept me away from the blog for a while, but I thought I’d come back with a case.

You have a 58 year old white male patient who you’ve seen 4-5 times in your continuity clinic.  He has diabetes (uncontrolled, with HbA1c 9.5%), HTN (typically reads low 150s/90s in clinic), and hyperlipidemia (guess what?  He refuses medicines).  Oh, and his BMI is 36.

You’ve been harping on the miraculous benefits of diet and exercise all this time, and he’s finally decided to give it a try. He tells you that he’s joined Crossfit and is ready to start exercising, once you give the OK.

He wants to know:

  1. Don’t I need to have a stress test or something?  My dad got one every year before his last heart attack.
  2. How much exercise should I doing?  WHAT should I be doing? Can I just jump right in on the Workout of the Day?
What do you think? How would you answer him? If you aren’t sure what to say, vent about your patients like this (in a HIPAA compliant way, of course), or strategize how to get patients to exercise in the first place.  Or just tell me hello- let me know you are out there.  Any comments are appreciated.  And stay tuned,  some resolution and some more questions to come later this week.
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Drops of Jupiter

CRP: not just for osteomyelitis any more

Ever have a patient ask you about something they saw on Dr. Oz?

It says right there, it’s all about me!  What agenda could there possibly be?

This post comes from something that has gotten a good deal of media attention, but not so much attention in our training programs.  Here’s my take on high resolution CRP.

So high resolution CRP is NOT the same test that you might order on someone with a FUO or chronic infection. The typical CRP assay that you might order in that situation doesn’t do a great job at distinguishing low levels. The values on the order of 1-3mg/mL is what becomes important in coronary disease.

Several observational studies have demonstrated that there is a relationship between CRP and coronary disease, that persists when adjusting for other traditional CV risk factors. The OR for the various studies are 1.4-1.9, meaning those with higher CRP levels have 40-90% relative risk of developing coronary disease compared to those with lower CRP levels.  There have been at least 2 other large observational studies which didn’t show much incremental change in risk stratification above more traditional cardiovascular risk factors.

Another issue with CRP is what is “normal.”  Typically patients are stratified into three groups:

low risk <1.0
intermediate risk 1-3
high risk >3

Levels higher than 10 are generally due to infectious or inflammatory states and shouldn’t be used to risk stratify anyone.

How to use the hr-CRP is hotly debated, and as usual, depends on who you ask.  Some cardiology societies recommend that we check CRP on everyone at the same time you check a lipid profile. Others recommend using it more for the intermediate risk patient- those with a Framingham risk score in the 10-20% range and already at their cholesterol goal without medicine.  I find this more helpful as it may actually change management.

So speaking of management, what do you do if you check the CRP and it is high?  It can be lowered with the typical lifestyle modifications:  Mediterranean diet, exercise, stop smoking. Medicines may also help- TZDs, ACE-I/ARBs, and Statins can all lower the CRP.

The JUPITER trial studied patients with normal LDL and CRP of >2– they were randomized to Rosuvastatin vs Placebo.  The trial was stopped early for benefit in the Rosuvastatin arm– OR for the primary endpoint of MI, Stroke, Revascularization, and Death was 0.77.  NNT for the composite outcome was 169.

Unfortunately, the risk of diabetes also increased in the patients on rosuvastatin.  NNH was 167 (hmm, awfully close to the NNT). So, the jury is out on the risk/benefit here, and you should talk with your patients about the potential for both before treating them.

Other statin studies have been done for primary prevention, with positive results, but nothing as great as the magnitude of JUPITER, despite the fact that JUPITER enrolled lower risk patients. Maybe this is because Rosuvastatin is a more potent statin (lovastatin and pravastatin were in the other big trials), or maybe it’s because they stopped the trial early.  Our favorite EBM guru would remind us that trials stopped early are more likely to overestimate benefit. Here is another takedown of the trial, pointing out several sources of bias.

So I would say the jury is out on CRP.  I really don’t find it helpful in the high or low risk Framingham patient. It might be useful in the intermediate (10-20%) Framingham risk category, if they already have goal lipids.  If you found a CRP over 3, it might be motivating to encourage lifestyle modifications (perhaps Mediterranean diet?) to lower it.  I’m not convinced that we need to medicate all of these people with anything, although I’m sure I could find someone to disagree with that.

This is real.  Look.

Hollenhorst Plaque

Thanks, Zarjou for your answer- you are right on.

A hollenhorst plaque is evidence of a cholesterol embolus in the eye. It is one finding of cholesterol crystal embolism syndrome. Simplified- a piece of cholesterol flicks off of an unstable plaque and causes trouble upstream.    Manifestations can be seen in kidneys, skin (blue toe syndrome), GI, and CNS- including the eye, as in our patient.  This can be a result of instrumentation- such has a cath or CEA, or can be spontaneous.

Hollenhorst plaques tend to originate from the carotid artery, and just over half of patients are symptomatic ranging from amarosis fugax, pain, or blurred vision.  Incidental discovery of a plaque, such as in our patient, happens about a third of the time, and may represent an old event, or may be significant of something serious. Certainly, if there is a sign of occlusion in other vascular beds, then you can assume something important is going on.

Evaluation should include non invasive imaging of the vascular bed in question- for a Hollenhorst Plaque, look at the carotid arteries.  You should treat other risk factors for vascular disease- quit smoking, control blood pressure, and diabetes.  You should certainly also take a look at the lipid profile and treat aggressively. Many would say that this is a coronary risk equivalent, with concomitant lipid and blood pressure goals.

Statins also may stabilize the plaque in question, with anti-inflammatory effects mentioned by Zarjou. There is not much data on anticoagulation, as this is not thrombus per say. In fact, anticoagulation with warfarin or heparin may actually increase the risk for recurrent cholesterol embolism.  Anti-platelet therapy seems to be reasonable based on other coronary risk goals, but doesn’t do much to help the cholesterol embolic syndrome.

Thanks for playing along-  You know I love games. Expect more in the future.