ACC/AHA Guidelines: Not a Replacement for Clinical Contemplation

On May 19th the Journal of the American College of Cardiology published an illuminating paper by Pant et al. examining the impact of a dramatic change in one of the Cardiac Guidelines. The paper was entitled “Trends in Infective Endocarditis Incidence, Microbiology, and Valve Replacement in the United States from 2000 to 2011”. In 2007 the ACC/AHA Guidelines were radically shifted, advocating an enormous reduction in sub-acute bacterial endocarditis prophylaxis (SBEP) precautions. The rationale for the dramatic shift from an aggressive to a conservative stance emanated from two findings: a lack of RCT evidence for the need for SBEP precautions under most circumstances, and the growing problem of antibiotic resistance. Without claiming prescience or any other such miraculous gift, I will tell you that at the time I predicted a significant future rise in endocarditis. My belief was that the guidelines overshot their intentions. Some individuals, I surmised, have valvular heart disease that predisposes them to developing SBE yet fails to be “significant” enough to make them candidates for the revised SBEP recommendations.

For several years I bucked the system and continued my aggressive prophylaxis. Then I buckled. I followed the guidelines to a tee. Though none of my patients has developed SBE, I now question my decision to cave under the pressure of the guidelines. I have always been one to try to think through issues, to treat patients outside any preordained box and beyond an overly simplified algorithmic construct. But in this case I felt perhaps I should just go with the flow. In truth, it was just easier to do so. My liability was lessened and my decision-making efforts were simplified. Yet, in retrospect, seeing the predictable rise in streptococcal SBE, I have been forced to re-examine my decision. In doing so, once again I am confronted with our current fixation on RCTs as proof positive “evidence,” with all other levels of understanding being “non-evidence”.

The absence of RCTs in this construct is tantamount to a lack of evidence. This paradigm is of course false. Many levels of valid evidence exist and oversimplification, though appealing, is inherently flawed and theoretically dangerous. We see this now in eight years of follow up after the change in ACC/AHA SBEP Guidelines. We also see this in many other aspects of everyday practice. Though I chose an easier and perhaps idler path in this circumstance, I will now reverse my position and once again give greater thought to each SBEP recommendation I render. It will take longer to do so; more complex doctor-patient discussions will be required; and larger liability will fall upon my shoulders. But these are the elements required to be a better physician. I owe it to my patients, and equally importantly to myself, to do so. Having said this, pragmatic issues remain. How do we practice medicine in an efficient, cost-effective, economically sound, intellectually stimulating, personalized, high-level fashion, while adhering to the mounting pressure of regulatory changes and requirements? This is the question that requires our most focused attention yet typically receives short shrift. For modern American Medicine to enjoy the future we all believe it deserves, this question, along with its counterparts, deserves our full and undivided attention.

Learn more about preventive cardiology at www.preventivecardiologyinc.com.

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From the Ivory Tower to the Trenches: A Practical Approach to the 2013 ACC/AHA Cholesterol and Risk Assessment Guidelines

The distillation of well over one hundred pages of two guidelines into a pragmatic and accessible tool for the practicing clinician is of course a monumental task. It is essential to do so though. Clinicians require clear guidance in helping them manage patients in harmony with scientific developments. To think though that science is simply and solely a regurgitation of large randomized double blind placebo-controlled trials would be foolhardy to say the least. Science – especially medical science – is so much more. The fast-paced evolution of science keeps us all on our toes. And there are so many levels to consider: clinical trials of all forms, basic science of multiple disciplines, clinical acumen borne of clinical experience, and of course good old-fashioned common sense. So the Guidelines’ authors’ use of just a single facet of science, the Randomized Clinical Trial (RCT), a priori limits the utility of the recent guidelines. Still, they must be addressed and reckoned with. Indeed like most other things in life, they are not “all bad.” Before distilling the Guideline’s into a practical approach that I personally intend to follow, let’s first put the premise of the RCT as “King” in a real-world context by examining a typical doctor’s approach to patients.

In medical schools, residencies, and fellowships all physicians are trained how to diagnose and manage patients. Take a hypothetical case. A new patient awaits your expertise as you enter the exam room. The patient has dutifully completed a multi-page questionnaire, the modern-day equivalent of a Review of Systems (ROS), Past Surgical History (PSH), Past Medical History (PMH), List of Allergies and Current Medications, and History of Present Illness (HPI). You’ve read the document prior to entering the room but you spend time clarifying the issues and creating this patient’s cohesive medical story. Then you examine him; from his right, just as you were taught in medical school. Your exam has morphed of course, emphasizing those aspects relevant to your particular specialty but still incorporating features from other areas of interest. After all, it is a whole person you are seeing, and ailments oftentimes breach systems’ boundaries as they are not constrained by artificial barriers. You examine his blood work as well as any other pertinent tests that have been performed prior to the visit. Then you think. You place the pieces of his particular puzzle in an orderly fashion; you make diagnoses; and then you create a plan. Reflecting on every single aspect of this fundamental, age-old doctor-patient interaction, consider how much of it is truly based upon solid RCT evidence. I will spare you the agony of this exercise as I’ve already done it countless times. The answer is essentially none. Where are the RCTs validating our ROS, HPI, examination from the right…? They simply do not exist. Yet, this is how we all practice medicine. And, it has worked out rather well for our patients. None of us should be handcuffed by RCTs when we evaluate and treat patients; we are all free to use any and all of the countless tools at our disposal. And frankly, the more tools in our chest, the better off are our patients. So, rule number one in addressing the guidelines is, “Remember that they are not rules.” Guidelines are not a part of the Ten Commandments. Even the authors of the 2013 ACC/AHA Guidelines acknowledge this when they state, “Guidelines attempt to define practices that meet the needs in most circumstances and are not a replacement for clinical judgment. The ultimate decision about care of a particular patient must be made by the healthcare provider and patient in light of the circumstances presented by that patient.” Translation: You the doctor should treat each and every individual patient in the manner you deem most appropriate. You must not feel shackled by these or any other “Guidelines.” With this in mind, I will now review the Cholesterol and Risk Assessment Guidelines to present an approach I will utilize in my practice. The views that follow emanate from experience garnered through practicing Clinical Lipidology and Preventive Cardiology, in addition to my personal interpretation of the literature as a whole.

Four groups qualify for statin therapy in the new guidelines, and I agree; they should all be treated. They are:

  1.  Patients with clinical atherosclerotic cardiovascular disease (ASCVD), defined as acute coronary syndromes (ACS), myocardial infarction (MI), stable or unstable angina pectoris, coronary or other arterial revascularization, stroke, transient ischemic attack (TIA), or peripheral arterial disease (PAD) presumed to be of atherosclerotic origin. These patients are to receive high-intensity statins.
  2. Primary elevations of LDL-C > 190 mg/dL (consistent with Familial Hypercholesterolemia, or FH). These patients are to receive high-intensity statins.
  3. Diabetic patients between the ages of 40 and 75 with LDL-C 70 to 189 mg/dL and no history of ASCVD. Patients with 10 year risk > 7.5% receive high-intensity statins while others receive moderate-intensity statins.
  4. Patients without clinical ASCVD or Diabetes Mellitus between the ages of 40 and 75, having an LDL-C 70 to 189 mg/dL and 10 year ASCVD risk of > 7.5%. These patients are to receive moderate-to-high intensity statins.

A few problems with this construct are:

  1. The Risk calculator is still shrouded in uncertainty. Many issues remain to be resolved, not the least of which is the fact that a strong Family History of premature ASCVD fails to impact risk in this system. Also, only 24,000 patients were evaluated to construct this tool which sits at the center of these guidelines and is meant to be used to determine therapy for hundreds of millions of people. Therefore, for now, when I opt to do a 10 year risk assessment I will still use Framingham Risk Scoring. I do so with the understanding of the limitations of this scoring system and the concomitant need for methods to further risk reclassify patients.
  2. The intention is to treat patients with high-intensity statins and assume an LDL-C reduction of > 50%, and moderate intensity statins to achieve a reduction of 30 to 50%. LDL-C goals are now passé in this paradigm. However, we all know that each patient is unique. Some respond very well to statin therapy; others do not. I will therefore continue to measure LDL-C (as well as LDL-P) on drug and I will continue to get my patients to goals at least as stringent as those in ATP3. There are ample data supporting the “lower is better” hypothesis. For example, the Cholesterol Treatment Trialists (CTT) study showed in both phases one and two that lower is better. The fact that we do not have RCTs that have used titration of statins to LDL goals as a primary endpoint in no way negates the overwhelming body of literature showing better outcomes at lower LDL-C , apo B, and LDL-P levels across a range of different statins. I will continue treat to targets.
  3. The high-dose-statin-absent-adjunctive-therapy (or-even lipid/lipoprotein-follow-up) concept is to me “pie in the sky.” We all know that from an LDL-C – but even more so LDL-P or apo B – standpoint by prescribing statins alone we will fall woefully short of what we have been accustomed to achieve. We also know that lower is better. Thus, by adhering to the guidelines’ advice we will very possibly see worse future outcomes. Additionally, we know from several trials that statin-related Diabetes Mellitus is dose related. JUPITER found that 20 mg of Rosuvastatin reduced 2.5 ASCVD events or deaths for every one excess in DM. Thus there is a trade-off for uptitration of statins. For me, I will use statins as a base and other therapies such as cholesterol absorption inhibition and bile acid sequestration as adjunctive therapy.
  4. ASCVD includes the presence of PAD but it does not include the presence of subclinical disease in the coronary or carotid arterial trees. This is counterintuitive. There is ample evidence that the presence of a high Coronary Artery Calcium score (CAC) or age-and sex-inappropriate Carotid Intimal Media Thickness (CIMT) predicts higher risk of ASCVD events. Even absent the copious data we have accumulated, doesn’t it make physiologic sense to ascribe as much value to disease in the vascular beds that are direct culprits for the very events we are attempting to thwart as we do to distant arteries in the legs? I will continue to use CIMT and CAC (and coronary CT angiography) in intermediate risk patients as tools to risk reclassify patients.
  5. The age limits of 40 to 75 are problematic. What do we do with a 35 year old woman with no other ASCVD risks except an LDL-C of 180 mg/dL and a powerful family history of premature ASCVD? Her 10 year risk is only 1.6% but she is too young to be treated by the new guidelines regardless of her risk score. I would unequivocally treat this woman.
  6. The absence of a significant lipoprotein and triglyceride discussion relegates the guidelines to be strictly statin/LDL-C documents. They do not attempt to be comprehensive and the authors acknowledge this fact. Thus, we should not be misled to believe that lipoproteins and triglycerides are suddenly unimportant. They are not. I will continue to assess them and manage them in a patient-centric, individualized manner. Again, every patient is different. Each one deserves his or her unique assessment and management. “One size fits all” has no place in modern medicine.
  7. Biological markers like Lipoprotein Associated Phospholipase A2 (LpPLA2), myeloperoxidase (MPO), oxidized LDL, Lp(a), and urine microalbumin have numerous studies either validating their position as ASCVD risk factors or at least implicating them in ASCVD. Though de-emphasized in these guidelines, biological markers are helpful tools in understanding our patients’ risks as well as motivating our patients to adjust their lifestyles and take their medications. I will continue to utilize them in my practice of “Interventional Prevention.”

In summation let us remember that these guidelines are not law. They are based entirely upon a mere 25 “highest level” clinical trials, ignoring thousands of “lower level” trials, human biology and physiology, and clinical acumen. To some extent I would say they are so limited in scope by inappropriately-stringent data-entry criteria that they have become Ivory Tower, clinically-blind advice. Their very construct diminishes their real world relevance.  Ironically the system suggested in the guidelines has itself never been validated by the very type of RCT evidence demanded by the guideline authors. Something is surely wrong with that. Yet on a positive note the new guidelines are simpler than ATP3. Reliance more upon Global (Total) Risk rather than individual risk factors makes it easier for clinicians to make recommendations. Still, simple is not always good. As outlined above, I intend to use the guidelines as a foundation upon which to build a more dynamic and plastic way to approach the patients in my clinical practice. I refuse to await trials that may never appear. Instead, I will continue to avidly follow the literature, eagerly learn from my colleagues, and diligently incorporate a wide gamut of data to render the well-considered recommendations I ultimately share with my patients.

Please read more about preventive cardiology at www.preventivecardiologyinc.com.

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