By: Dr. Brett Wisniewski and Dr. Jaclyn Suffi

Our quest for optimal cardiovascular health is never-ending. First, it was the low-fat diet, now it’s the liberal prescription of statin drugs. Tomorrow, it will be a 3D printed heart replacement. As medicine advances, heart disease continues to rise. We clearly do not have a good handle on this disease…or maybe we are missing something that has been right in front of our faces. Albert Einstein defined insanity as: “doing the same thing over and over again, expecting different results.” We can clearly see that we have been attacking cholesterol all this time, getting the same poor outcomes, yet continuing to try and lower cholesterol. Insanity.

I have my suspicions when drugs are constantly pushed for diseases that they obviously are not curing (see Vaccine article). In 2014, I wrote an article about cholesterol profiles and expanding our diagnostic view for heart disease (What do my cholesterol numbers REALLY mean?). The overall theme remains: a standard cholesterol profile, that is routinely run, is nearly useless in assessing your current risk or the state of your cardiovascular system. That’s right, the “lipid panel” you have had run for years is one of the worst tests to base your cardiovascular therapy off of.

The total amount of cholesterol is not our concern; some individuals have higher total cholesterol and have almost zero risk of any kind of cardiovascular event. A recent study that looked at over 100,000 patients in 500 hospitals found that almost half the patients admitted to the hospital for cardiac events had LDL levels BELOW 100mg/dL and 17.6% of the patients even had LDL BELOW 70mg/dL! How many more people/studies do we need to prove the point that lower LDL cholesterol does not stop heart attacks? How low can we go with LDL? I had one patient tell me his doctor wanted to see his LDL at 20!! Yes, 20! When he came in to see me his LDL was at 60 and he was already feeling the negative effects: confusion, muscle burning, fatigue and short-term memory issues.

If we are still seeing so many cardio events, even with normal or low cholesterol levels, then obviously this is not the marker we should continue to use as a sole predictor of mortality. If your car is running strangely and the mechanic replaces the entire transmission, yet the car continues not to run right, do we continue to keep changing transmissions, repeatedly? Or would you maybe investigate another part of the car?

Lowering cholesterol for cardiovascular disease is not only ineffective, but can be dangerous. For example, a patient last year, we’ll call him “Bob,” was starting to get his life back in order. He dropped the fast food and soda, began packing his lunch for work and adding in more colorful veggies. He had also started an exercise routine with a fully qualified trainer. 

About the same time, his other doctor threatened him with statins, stating that if he did not take them that he would die this year from a heart attack. This, coming from a doctor, could scare anyone into taking any medication. Well, fast-forward 3 weeks and “Bob” starts to complain of his muscles aching, especially after training. He chalks it up to working out more and his body trying to recover. One Tuesday morning “Bob” enters the gym at 5:30, he loads the squat bar with lightweights and begins warming up while waiting for his trainer to start his workout. About 3 squats in he hears a loud crunching, and a pop in his ankle along with his thigh muscle and hits the floor with the weight bar on his chest. He immediately made an appointment with his other doctor who was reluctant to say that he had statin-induced myopathy. In other words, the statins he was prescribed created an environment in his body in which his muscles could no longer function properly. If caught in time, and with the proper therapy, this is reversible. However, many aren’t as lucky as “Bob” to have such quick and significant signs. They go years creating damage without even knowing it.

Cholesterol is also important for numerous other processes in the body and an increase may be an important sign that something else is happening. Let’s think about normal physiology for a second: If I see a post-menopausal woman enter the office complaining of hormonal issues and her cholesterol comes back high, what is one of my first thoughts? Well, since sex/steroid hormones (estrogen, DHEA, testosterone, etc.) are all made from cholesterol, one may deduce that her body is manufacturing more cholesterol to try and balance out her hormonal fluctuations. Lowering this person’s cholesterol may actually make her feel WORSE. 

Of course, the proper markers for cardiovascular disease risk should be run, but my point is that the knee-jerk reaction should not be to lower the cholesterol. That is, unless you have definitive proof that it needs to be done. For some reason, we have developed this tunnel vision that cholesterol is only related to the vascular system, thus leading us down the rabbit hole of lowering the number and watching people’s health decline and continue to die of heart disease.

The analogy of sticky cholesterol floating down your arteries and clogging it up like a dirty bathroom drain is, frankly, false. The specific details of how exactly cholesterol affects the arteries and its role in CVD is beyond this article, but suffice it to say that inflammation in the muscular layer of your arteries is the feature we are interested in. An inflamed arterial wall not only narrows the tunnel in which blood flows (think about pinching down on a straw) it also forms the risk of a thrombus or blood clot. For accurate assessment, you need to look at the INFLAMMATORY response, such as reactions from the immune system.

70% of those who are admitted to a hospital due to CVD have normal or low cholesterol.

What if there was a way we could visualize and measure the thickness of these arteries? Maybe look at the visual cues of inflammation and combine it with the biochemical markers? A technology such as this would allow us to see past total cholesterol numbers and actually assess the current state of inflammation in a particular artery. 

The carotid artery is a large branch of the vascular tree on either side of your neck. Ever take your pulse by placing two fingers near the corner of your jaw? The pulse you are feeling is from the carotid artery. It is also the main line from your heart to your brain. An ultrasound of the carotid artery has been shown to be most effective in measuring intima-media thickness (IMT) and establishing a more accurate projection of CVD risk. This simple procedure can be performed in just a few minutes and is painless. Results from the test include IMT, presence of plaque, and arterial age. Ideally, IMT should be less than 0.600 mm. If IMT increases to >1.000, greater care and concern should be given to the person’s CVD risk and health. Analysis including IMT, plaque and inflammation, is used to estimate the individual’s arterial age. On average, we find this to be, about 10 years older than a patient’s actual age. That, obviously, is not ideal.

How do we use this information?

The Carotid Scan alone provides significant value and coupling it with a few other non-invasive tests is optimal. One test you have probably had dozens of times is blood pressure. The accepted normal blood pressure value is around 120/80, although numbers may vary in athletes and the elderly. According to the American Medical Association, a blood pressure of 140/90 or over is considered hypertensive for an individual under the age of 60. 

Combining blood pressure testing with other methods can provide a clearer picture of cardiovascular health.

Hypertension causes increased stress on both vessels and the heart, itself. Increased blood pressure has a cyclical relationship with certain inflammatory markers such as high sensitivity C-reactive protein, hs-CRP. This means that high blood pressure elevates CRP and high CRP raises your blood pressure. This is a vicious cycle that needs to be broken. 

Blood pressure should also be relatively equal when measured and compared from one arm to the other and similar, in the upper extremities when compared to the lower. This is called ankle brachial pressure or ABI. Blood pressure cuffs are attached to your upper arm (the common area above the elbow) and right above your ankle. The blood flow is detected with a Doppler ultrasound. Normally, we should see slightly higher pressures on the lower extremities versus the upper. If not, there may be some sort of blockage or vascular disease. Current research has shown a high correlation of CVD risk projection associated with arterial wall thickness and low ankle brachial index (ABI). Tests for both are simple, quick, non-invasive, and are usually performed in less than 10 minutes.

Some of the Heart Disease and Stroke statistics from the American Heart Association for 2016 were reported as follows:

  • “Based on 2009 to 2012 data, 32.6% of US adults >/= 20 years of age have hypertension, which represents approximately 80 million US adults.”
  • “From 2003 to 2013, the death rate attributable to high blood pressure increased 8.2%, and the actual number of deaths rose 34.7%.”
  • “Yet in 2013, CVD still accounted for 30.8% (800937) of all 2596993 deaths, or approximately 1 of every 3 deaths in the United States.”
  • “In 2013, 35% of deaths attributable to CVD occurred before the age of 75 years, which is younger than the current average life expectancy of 78.8 years.”
  • “For the first time since 1983, more males (402851) died of CVD than females (398086).”

Clearly, CVD is plaguing our country. Combinations of stressors affecting the cardiovascular system tax the vessels and, over time, modify their structure as a physiological response. One such modification takes place within the intima and media layers of the blood vessels. After prolonged exposure to hypertension, abnormal inflammatory cholesterol levels, increased sugar, and other systemic inflammation, the intima and media layers begin to thicken. This can be due to inflammation or plaque. Therefore, a measurement taken of the intima media thickness (IMT) can give the practitioner a better idea of the person’s risk for CVD. This physiological response and the use of the IMT in projecting CVD risk is well-documented in current research. Many articles have shown the correlation between increased thickness and increased risk. This assessment is more valid in individuals above age 40 than in younger persons.

Patients should be aware of all the available methods for predicting CVD risk. Don’t let your cardiovascular health be falsely determined by the traditional lipid panel. Talk with your doctor about some of the more advanced, non-invasive and cost-efficient strategies that are currently out there. It is time routine medicine evolves. These advanced strategies are not only safe, but they are also extremely valuable and could literally save your life.

Heart Disease and Stroke Statistics—2016 Update A Report From the American Heart Association.” Circulation. 2016;133:e599. DOI: 10.1161/CIR.0000000000000409.

Dr. Jeffrey Boone, Atherosclerosis Imaging in Primary Preventive Cardiology: The Eradication of Heart Attack and Stroke

Adding low ankle brachial index to classical risk factors improves the prediction of major cardiovascular events. The REGICOR study. doi.org/10.1016/j.atherosclerosis.2015.05.017

2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults. JAMA. 2014;311(5):507-520. doi:10.1001/jama.2013.284427

Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines. American Heart Journal. 2009; Volume 57, 1.

Additional References available upon request.