There has been so much published and spoken about in doctors’ offices about heart health, and I often see and hear patient’s misinformed and confused about how to best address optimum heart health.

Here is a quick summary of our current understanding:

  • Blood lipids, generally tracked by “Total cholesterol”, “Triglycerides”, “HDL cholesterol” (aka “good cholesterol”), and “LDL cholesterol” (aka “bad cholesterol”), are used by physicians and their patients to gauge the risk of plaque forming in arteries and contributing to the development of Coronary Artery Disease (CAD).
  • In general, patients are asked to lower their LDL cholesterol and triglycerides and raise their HDL cholesterol through diet and exercise, and, if not controlled with diet and exercise, with the addition of supplements and/or drugs.
  • Family (or past) medical history of CAD is valuable in assessing risk in conjunction with blood lipids, but the biggest risk factor for CAD is one’s age. Like a barnacle on the hull of a boat, the odds are generally increased for the formation of either with time in the water.
  • Triglycerides are more broadly interpreted and affected, can lead to accretion of fat, and are generally best kept low.

A few problems with our current understanding:

  • Often, the measurements of blood lipids, particularly LDL cholesterol, are not direct, but instead are “calculated” using other assays that theoretically can be used to derive LDL cholesterol. This is inherently less precise and accurate.
  • Cholesterol is necessary for life, so monikers of “good” and “bad” cholesterol are misleadingExcess (“elevated” or “high”) LDL cholesterol – that which is directed toward that which is needed in, eg, cell walls for proper functioning – are thought to increase risk of plaque formation. Because HDL cholesterol is that which is directed back from the blood (to the cell walls, eg) to the liver where it is not available to be deposited as plaque in arterial walls, it is considered “good” because it is countering the effect of excess LDL cholesterol to potentially become arterial plaque.
  • Excess LDL cholesterol is associated with an increased risk of CAD and stroke, BUT, while LDL cholesterol is necessary for formation of plaque, the presence of excess LDL cholesterol does not guarantee that plaque will be formed, nor does the presence of low (“optimal”) LDL cholesterol guarantee that plaque will not be formed.
  • There are many components involved with plaque formation, so to place all or most of our attempts to limit the risk of CAD and stroke on the modulation of LDL cholesterol is seriously misguided and misplaced.

Assaying and tracking Lp(a) and/or LDL-P are much more valuable in evaluating CAD and stroke risk, especially when taken in conjunction with other assays such as inflammatory markers, but the current “Standard of Care” has yet to latch on to the most recent research regarding cardiovascular disease. Combined with an EKG, resting and/or with exercise stress, and an echocardiogram, resting and/or with exercise stress, we have more information to evaluate risk. While these assays are much better markers for consideration, and the EKG and Echocardiogram as well as one’s own and family history provide more insight, we are still making an educated guess as to whether plaque is indeed extant.

One additional measure is to use a non-invasive technique that use ultrasound to visualize the carotid (neck) arteries, because there is a 95% correlation between what is found in these arteries and what is found in the coronary (heart) arteries.

The “Gold Standard” for evaluating CAD is through imaging of the heart via Computed Tomography (CT) to obtain an angiogram. This gives us a complete extremely detailed, three-dimensional image of the heart and coronary arteries that allows us to determine the extent (if any) of plaque formation as well as type (calcified, fibrous, or soft). Until fairly recently (and still today in most practices), this CT – Angiogram (CTA) was reserved for patients that appeared to have the most risk of developing CAD, mainly over fear that the irradiation involved with the imaging had to be justified by the need to better quantify the CAD risk.

However, as with the technological improvements with x-ray technology in other areas like dentistry, eg, that limit exposure to irradiation to the point where x-rays are used much more ubiquitously, CTA’s for the average adult only expose one to about 5 millisieverts of irradiation. To put that into perspective, we (here in Los Angeles at sea level) receive about 3.5 millisieverts of irradiation annually just for living here. And, the recommended maximum exposure PER YEAR is 50 millisieverts. A good deal, especially if you consider that in evaluations of higher risk patients, the protocol might typically include a perfusion study with nuclear tagged dye or obtaining a “Calcium Score” (aka Coronary Artery Calcium or CAC score) which entail similar or more irradiation.

So, what to do?

As with all medical decisions, the individual’s risk factors as well as preferences should be taken into account in evaluating CAD and stroke risk. Risk factors include both the good and bad contributions that include not only age, blood assays, and family and personal history, but lifestyle and habits. Preferences include one’s mental as well as physical health, goals, and finances.

The “bottom line” is that current knowledge regarding measurement of risk for CAD is not pervasively distributed in clinical practice yet. Direct (as opposed to calculated) measures of assays that include more relevant markers of CAD risk should be made part of a standard panel of laboratory assays for CAD. If warranted, further evaluation beyond lab assays should start with a “Bilateral Carotid Doppler Ultrasound” – a non-invasive imaging of the arteries in the neck and strongly correlated with the coronary arteries that is quick and does not involve irradiation.

If plaque or flow disruption is thus visualized, then moving the gold standard, CTA, is the most efficient and effective means for evaluating CAD. Note that I am not advocating eschewing the use of EKG’s or echocardiograms for evaluation of heart health, BUT, neither of these measures rules out CAD. Ie, these measures may detect an abnormality, but typically only in an advanced stage, and, even in advanced stages may not provide evidence of CAD.

NB: There is no doubt in the medical community that statins can be used to slow, stop or even reverse coronary artery disease. I borrow from my friend and cardiologist colleague, Dr. Peter Pelikan who joked with me that “the web page that states that statins don’t work for CAD are right next to the web pages that say no Jews were killed by Nazis in WWII or that we haven’t landed on the moon.” But, would you necessarily give antibiotics to one who didn’t have an infection just because they were surrounded by bacteria? My answer is NO. Especially when we have identified side effects to them, and, in the case of lowering LDL cholesterol, why should we necessarily do so if we don’t have evidence of extant CAD, and we are not convinced that doing so will PREVENT formation of plaque.

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