Was it really just a "Mild" Heart Attack?

You may have seen the news a couple of weeks back - the President of the American Heart Association (AHA), John Warner, MD, noted interventional cardiologist was missing his national AHA conference because he suffered a "mild" heart attack. He has referenced how his family has no "old men" - they all die early of cardiovascular disease. It's that history that prompted him to enter the field of cardiology initially, and spurred him to volunteer with the AHA.

To suffer a heart attack for Dr Warner might seem like an inevitability to most. We certainly don't know what he was doing to avoid this eventuality, but if we were to assume that he was doing everything he would profess as the President of the AHA, then can we consider ANY heart attack as "mild"? What does it say about the odds for the general population if the TOP DOC has a heart attack?

Let's consider some of the guidelines to cardiovascular prevention as suggested by the AHA. Of note, the last guideline for primary prevention of heart attack was released in 2013. The most recent updates involved discussions of diet, activity, cholesterol and risk assessment. Fundamentally, the general approach is one of risk assessment - making a "best guess" as to the likelihood of having a heart attack in the next ten years. These calculations are population based, but virtually all of the recommendations are based on "expert opinions" - in other words, the AHA physician's "best guess." With more Americans learning that they have heart disease by having a heart attack than any other way, it seems to me we are missing far too many opportunities for early identification. This would require a fundamental shift in how we approach cardiovascular disease.

Many years ago I was introduced to the Bale Doneen Method and have been using the program ever since. The basic premise of the Method is establishing whether the prerequisite condition exists - in other words, is there atherosclerosis? Without the deposition of sufficient lipid in the arterial wall, the possibility of a heart attack is nearly nill. This is not, however, the method used as the standard of care.

Let's look at an analogous situation in gastroenterology. If a patient comes into the office and they are worried about colon cancer risk. Hypothetically, we give the patient advice to adjust their lifestyle (reduce red meat, etc.), and take an aspirin a day. This advice, while carrying some risk of side effects, also lowers a patient's lifetime risk of colon cancer by more than 50%. That's a really good result, so why isn't this the standard of care?

There's a very simple answer - the same result can be achieved by one thorough evaluation of the colon by colonoscopy. One colonoscopy lowers lifetime risk of colon cancer by 50%, and affords the opportunity to remove to remove a dysplastic growth before it becomes an actual cancer. Define the disease process, identify the precursor condition and eliminate it before it's a real problem. We don't do that with cardiovascular disease.

The standard of care in "primary prevention" of cardiovascular disease is to prevent the first heart attack. But that's not preventing the disease - that's preventing the first negative event! That's like saying if we can avoid an amputation, we've done a good job with diabetes!! What about everything else that's messed up?!

The Bale Doneen Method works to identify the underlying issue - the presence of excess lipid (usually oxidized LDL) in the artery. It is this atherosclerotic process that underlies the vast majority of cardiovascular events. An array of blood tests, extensive history and targeted physical findings establish the presence of disease (atherosclerosis), not an evaluation of risk. THIS IS PRIMARY PREVENTION - preventing the process that DRIVES the first event, not simply avoiding the first event. And 90+% of heart attacks are thus avoidable.

Assuming Dr. Warner was being treated with the standard of care, his life was essentially up to chance. Standard of care (N.B.: reimbursed by insurance) does not look at lipid size, broad evaluation of inflammation, genetic factors effecting statin sensitivity/responsiveness or dietary tendencies, nor does it investigate the character of identified lipid collections (plaques). These are all components that contribute to the development of atherosclerosis, ever increasing the risk of a future event. Remove the factors influencing the development of the disease process and you reduce or remove the disease process.

Even this, though, does not establish the status of the cardiovascular system. The majority of cardiovascular events are related to lipid driven conditions. Current cardiac evaluation still does not provide a comprehensive description of the patient's overall cardiac status. Most imaging is limited to large vessel evaluation, leaving a full 75-80% of the cardiac blood supply undefined. Historically, small vessel disease has been a diagnosis of exclusion, and is increasing in it's prevalence partly as a consequence of the rising diabetic and pre-diabetic population.

I have been utilizing an advanced cardiac evaluation tool in my practice for many years. The Multifunction Cardiogram (MCG) enables evaluation of the entire cardiac system while at rest and, in under ten minutes. Utilizing LaGrangian-Euler mechanics, artificial intelligence and machine learning, a systems biology approach establishes an extraordinarily accurate assessment of the physiologic status of the heart. Once the baseline status is established, disease is identified and can be aggressively managed. The beauty of the MCG is in its ability to quickly establish the status in real-time. Since physiology is what is being evaluated, real-time changes can be demonstrated. This means that shifts over minutes, hours, days and weeks are all visible.

Use of the MCG in clinical practice affords the physician the opportunity to evaluate a patient's cardiac status, get a near immediate result and know the level of heart disease present. From there, aggressive management can be supported by repeated studies demonstrating clear shifts in the function of the heart. Being able to reinforce patient's behavior with clear, demonstrable result improvement is essential to successful progress in the avoidance of bad outcomes.

​I certainly hope that Dr. Warner is recovering well and he'll continue to do his good work. I'd like to believe that this "mild" heart attack would prompt a refocusing of the cardiac prevention effort toward identification of cardiac dysfunction in its earliest forms and personalized attention to patients of all risk. After all, if 58% of Americans learn they have heart disease by having a heart attack, we are not doing a very good job of prevention.