Saturday, July 16, 2011

The New Galenism

The term Galenism in this essay has the usual pejorative sense of a pernicious influence, which grants that while Galen transformed medicine in late antiquity, he yet so dominated its thought that subsequent thinking and innovation was stifled by his authority.

In the defense of Galen, his own personal ideal of the physician is one that I can enthusiastically subscribe to, and is best captured by the title of his treatise "That the best Doctor is also a Philosopher" (Galen On The Ideal Physician. P Brain. South African Medical Journal, 52:936-938, 1977)(Original Source - Claudii Galeni Opera Omnia. ed. C.G. Kuhn, Lepzig Cnobloch. 1821-1833. Reprinted, 1964: Hildesheim, Olms. The work translated is in vol I, pp. 53-63.) 

However, the genesis of Galenism owed less to his own habits of thought and investigative methodologies than it did to the mindless acceptance of his successors of his results, and who then embraced him as the ultimate authority in medical practice.  

One can see the current infatuation with practice guidelines as the reintroduction of slavish conformity to 'expert' opinion akin to the forces that kept the western practice of medicine mired in antiquity until the renaissance. 

Take as an example a recent case referred to me by the "Performance Improvement" department in one of the locum tenens hospital sites I am currently working at. The patient was an elderly female who presented with atrial fibrillation with rapid ventricular rate, mild chest pain, focal and severe ST segment changes in the anterior lateral leads of her EKG. She had a troponin I elevation of a significant degree occurring several hours after her initial assessment. Once her heart rate was controlled and once she was back in normal sinus rhythm her chest pain resolved, but her troponin I elevation remained mildly elevated. She had no EKG evidence of transmural infarction, and once she had returned to normal sinus rhythm her focal EKG changes remained but were attenuated compared to those seen initially. 

By the Universal Definition of Acute Myocardial Infarction, (, this patient had a so-called Type II AMI , i.e., rather than the AMI being a consequence of plaque rupture and thrombotic occlusion occurring within the vessel causing focal myocardial injury, the pathophysiological etiology for the myocardial injury signal is due to increased myocardial oxygen demand in combination with inadequate myocardial supply of oxygen and nutrients. Common causes for this pathophysiological state are anemia, arrhythmia (as in this case), hyper- or hypotension, vasoconstriction or arterial spasm. 

I am referred the case, as I did not begin this young lady (75 years of age) on Statin drug therapy since it was a protocol item. The entire implication of a Type II AMI is that is not a consequence of unstable plaque occluding or severely obstructing an epicardial coronary artery. And as such, since it is not the consequence of unstable cholesterol plaque, it is not obvious to a clinical expert in cardiology (that is myself) that statin drug therapy is indicated in this case. That is simply put, anti-cholesterol therapy is not, nor should it be a protocol item for post MI care in the Type II infarct. However, the change in nomenclature and the emphasis on correct pathophysiological characterization of the mechanism of an acute myocardial infarction now threatens the mindless execution of ‘best practices.’

The effect of acute statin therapy on plaque stabilization and prevention of Type I AMI is clear cut and supported by decades of biologically congruent results with powerful clinical data endpoints. Furthermore, because the effects of statins are so immediate in the setting of plaque stabilization, a significant effect of their use is probably related to their anti-inflammatory effects with respect to the vascular system. Thus, the absolute risk:benefit ratio is so highly weighted to treatment that the decision to treat epicardial lesions is virtually axiomatic across all genders and ages of patients. The survival advantage for statin drug therapy with respect to plaque stabilization is immediate and profound and occurs within many studies as soon as 6 months post event.

While the thoughtful use of guidelines to enhance patient care and improve medical outcomes is highly desirable, the mindless pursuit of ‘core measure’ statistics is anathema to the thoughtful physician. By not treating this patient with statin drug therapy I have invoked in my hospital a ream of paperwork designed to ‘improve my practice.’

However, if I had simply followed the guideline my performance would have been ‘perfect’ but my practice thoughtless, flawed, and ‘Galen-istic.’ While statin drugs are for the most part among the safest of all drugs and drug classes there still remain real potential risks with their use.

Since in the patient under discussion the guideline does not apply as the patient has no evidence of unstable plaque as her pathophysiology, could an argument be made for statin drug therapy based on ATP III guidelines?

This particular patient had a lipid profile in which her HDL cholesterol was 54 mg/dl, HDL/Cholesterol ratio was 3.4, and her LDL cholesterol was 119  mg/dl. According to the National Cholesterol Education Program, this patient has a 10 year risk of developing symptomatic CVD (due to epicardial disease - not supply/demand mismatch) of <9%. Furthermore her ATP III LDL goal is <130 mg/dl. Thus, no argument for statin drug therapy can be made based on population normative data and conventional risk assessment.

The PROSPER study (The PROspective Study of Pravastatin in the Elderly at Risk) (Randomized trial of 5,804 seniors age 70-82 years of age) demonstrated an actual cardiovascular death rate of 3.3% among patient’s on statins vs a 4.2% in the placebo group, a 0.9% absolute difference in mortality rate in this age group, with an absolute all-cause mortality rate difference in treatment versus placebo group of 0.2%. As a consequence because of the absence of a clinically significant difference in mortality between treated groups and placebo groups, I find little data to support a cholesterol intervention in this patient based on survival advantage within her age group.

Furthermore, the current patient had advanced COPD, was on home oxygen and is essentially bed-ridden due to her need for continuous oxygen therapy. Echocardiography demonstrates severe pulmonary artery hypertension due to the magnitude of her COPD. Again, we see a patient who is not manifestly obviously directly comparable to or appropriate to treat with guidelines designed to mitigate the effects of elevated cholesterol levels on the survival of predominately middle aged males.

So, in summary, a patient without evidence of unstable coronary plaque, without indication for drug therapy related to a population derived risk assessment, in an age group controversial with respect to absolute survival advantages of statin drug therapy, and with severe co-morbid pulmonary conditions was not treated with statin drug therapy AND the ghost of Galen has pronounced my practice inadequate and deserving of ‘practice improvement.

What is going on here? It seems to me that the more thoughtful your practice, the more headaches will be brought to that practice by those who inexpertly and without art-fullness drive that practice to the 'best practices' if or if not that practice applies to the precise patient in front of you. I am tempted to draw an analogy between the effect of standardization in education methodologies to the attempted standardization in medical treatments. But I will leave that rumination to a future post.   

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