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.
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.
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.