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A New Window into the Heart and Cardiovascular Circulation

Physiology and anatomy interface at the inner (intima-media) thickness of our great vessels.  It is within the intima-media that abnormalities in vascular biochemistry layer out soft, vulnerable plaque.  It is within the IMT that vascular disease first progresses and it is within the IMT that vascular disease first regresses.  The IMT is the leading edge of cardiovascular disease.  CIMT measurement allows us to quantify, and then follow, your overall plaque generating status in a manner that is non-invasive, quantitative, and reproducible.  CIMT is moderate in price and does not expose you to ionizing radiation.  We will use CIMT to determine risk, guide our preventive efforts, and then gauge the effectiveness of these maneuvers, with greater precision than our current best methods can provide.

Clinical Cardiology, the discipline in which I was trained, focuses on “flow-limiting”, “surgical disease”, 70-90% narrowings that compromise flow to the heart with exercise.  We diagnose these “lesions” when exercise/chemical stress EKG, echo, or nuclear studies demonstrate “flow disparity” between “diseased” and normal vessels, or “ischemia” (impaired cardiac energy production due to insufficient supply of oxygenated blood).  We address these focal lesions by rendering blood flow sufficient, either with bypass surgery or stent placement.  If revascularization is not possible we will carry out EECP to generate a collateral circulation, or we might prescribe drug therapy to lower your HR and BP, to decrease your heart’s requirement for oxygenated blood (if we can’t increase supply then we must decrease demand).  Following revascularization blood flow is restored, your symptoms resolve, and your stress studies normalize.  Revascularization can prevent a heart attack (or stroke when lesions compromise blood flow to the brain) and save your life – but it doesn’t prevent most heart attacks, strokes, and cardiovascular deaths, as
       the initial manifestation of vascular disease in 50% of afflicted Americans is sudden death!

That’s right; these people never knew what hit them.  Many had no symptoms, most did not have flow-limiting narrowings, and some had recently passed a stress test.  They didn’t die because a 90% narrowing closed off (when a 90% narrowing closes you typically experience a small heart attack or none at all as a protective collateral circulation has formed).  You die of a heart attack when a 30-60%, “non-surgical” narrowing closes off abruptly – there is no pre-existent collateral protection and an entire wall of the heart is lost.  The same principle holds true within the cerebral circulation – only 10% of strokes are due to closure of a vessel with a high-grade narrowing.  The rest of our strokes and heart attacks occur when the immature or “vulnerable” plaque within a non-flow restrictive narrowing cracks, spasms, or clots.  Relying of the presence of symptoms or an abnormal stress test to protect you from cardiovascular calamity, to prompt you and your doctor to take pre-emptive or corrective action, will likely be a failed policy – as Clinical Cardiologists we would not even have seen you.

OK; we all know this, and that is why we practice Preventive Cardiology.  Let’s work on your risk factors before you develop your first “lesion”.  Sounds sensible, but who are we to treat with prevention – all 240 million of us?  At what age should we start?  How aggressive should we be?  Should we put asymptomatic 30 years-olds on a statin?  We should if they have early disease, a high CRP, and oxidative stress.  But if their vasculature is pristine and no other risk factors are present, if  they really aren’t at any risk, and we then begin them on life-long therapy with potent drugs, then we are going to hurt a lot of people to prevent heart disease in just a few, and we are going to spend a lot of money.  Knowing when to prevent and how hard to prevent is a challenge to Preventive Cardiology and to the resources of our society.  Also difficult is determining whether a specific preventive measure is successful or not in a given individual.  If we focus only on cholesterol – well, 50% of heart attack victims have normal cholesterol, so cholesterol reduction is not the magic answer.  What we need is a risk-free, reproducible, quantifiable measure of your “plaque status” that can be repeated over time to tell whether your plaque volume is receding or progressing, whether your preventive program is succeeding or failing. 

CIMT is this measure.

CIMT measures, in micrometers, the thickness of the inner wall of your carotid artery, the intima (the endothelial cells that line the artery and soft plaque that is accumulating within and behind it), and the media (the smooth muscle layer of the vessel).  The intima-media segment of a vessel (IMT) is the interface between physiology and anatomy.  An abnormal IMT is the site of soft plaque (and soft plaque tends to be vulnerable plaque) accumulation and it is associated with endothelial dysfunction (inability of the endothelial cells to make protective nitric oxide).  We know what the average CIMT value is for a man or women of your age, for smokers and for non-smokers, for diabetics and non-diabetics, etc.  If your CIMT is significantly above average for your age and gender, then you are in some trouble.  CIMT progresses in the average American at a rate of 0.014 mm/year.  If your IMT is progressing faster, than you are depositing soft plaque in all of your arteries at an above average rate; you are now in big trouble and you are at increased risk of heart attack or stroke.  Conversely, if our preventive efforts stabilizes or regress your CIMT value (yes – here we are melting away soft plaque) then your risk of an adverse event is minimal.  We can lower cholesterol and BP with drugs, but this doesn’t guarantee that we are regressing or stabilizing plaque, but if we regress your CIMT, we confirm that our preventive efforts are really working. 

Which sound better to you – cholesterol control or plaque control?

Conversely, if your CIMT is progressing rapidly despite control of your standard risk factors, then we must look deeper into the potential causes of atherosclerosis that you might bear.

The CIMT procedure is simple.  An ultrasound study is carried out of the carotid arteries in your neck.  A specialized software program is used to precisely measure the mean and maximum IMT.  Standard carotid ultrasound is looking for “flow-limiting” stenoses, narrowings that could be addressed surgically.  This is not what we are interested in with CIMT testing - we will be measuring soft plaque accumulation in non-overtly diseased vessel segments (if plaque is identified we measure the CIMT at an adjacent, normal appearing segment).  While the presence of plaque obviously has significance, it is the IMT parameter that best predicts the presence and severity of atherosclerotic vascular disease elsewhere in your body, it’s risk of progression, and your risk of sustaining an atherosclerotic event (think of IMT as the “staging ground” for obstructive plaque – the higher the IMT, the greater the rate of IMT progression, the more rapidly will large, obstructive plaques form).  Over 2,000 studies (go to www.pubmed.gov and enter Carotid IMT) document the link between CIMT and current risk, and an even more powerful relationship between the rate of change in CIMT and future risk.  We will use CIMT to help us decide who should be treated with preventive measures and how aggressive our efforts should be.  We will use the rate of change of CIMT to gauge the success of the regimens that we construct for you.
                                                      
CIMT allows us to “keep score”.

The tables below list factors that have been associated with an increased CIMT and/or an increased rate of CIMT progression, as well as therapies that have been shown to delay or prevent CIMT progression.

We will be adding to these tables as more research comes out.  We are currently evaluating the interaction between metal detoxification, reverse cholesterol transport with unsaturated Phosphatidylcholine, and static magnetic field therapy on CIMT and other measures of disease activity in stable angina patients.

The cost of CIMT is $200.  While the value, and incremental value of CIMT above and beyond risk factor analysis has been conclusively demonstrated, neither Medicare nor the major commercial insurers in NW Ohio will cover the cost of CIMT (but not to worry, they will be happy to cover the cost of your heart attack, stent, bypass surgery, and cardiac transplantation that maybe we could have prevented).  They consider CIMT to be a “screening procedure” or “experimental”.  The 2,000 published studies on IMT testing are not enough.  Until the position of Medicare changes, the cost of CIMT will be your responsibility.  We can give you a receipt and you can turn it in to your insurer, but we will not write your insurer to request preauthorization (this never works and serves only to waste our time and your time).

We have already found undiagnosed, “surgical” narrowings during IMT testing of “normal” individuals.  If potentially obstructive plaque is identified, we will refer you for a formal carotid ultrasound, which involves blood flow velocity measurement to quantify the degree of vessel stenosis.

We are the only practice in NW Ohio to offer CIMT testing, so your personal physician and family members may not be aware of its value.  We are currently working on a DVD presentation covering CIMT (and brachial artery flow-mediated vasodilation, a direct measure of endothelial function). 

 Interpreting Your CIMT Findings

In individuals not known to have CV disease; CIMT testing is done to assess risk for CV disease and CV events.  In patients with known vascular disease, the current CIMT reflects your current plaque producing potential.  It serves as a baseline, such that future measurements can tell us whether the underlying plaque generating process has been stabilized or whether it is still progressing.

If you do not have known CV disease, we can use your CIMT (adjusted for age bracket), to predict your risk, and to help us decide whether you need preventive efforts, or how aggressive we should be.  For example, if you are 45 years of age and have a CIMT at the 90^th percentile for this age bracket, you have more soft plaque than do 90% of our colleagues; you are at risk for CV disease and CV events and we need to get to work.  Conversely, if you are 65 years of age and have a CIMT at the 10% percentile (for age) and no visible plaque, then you are probably home free as far as CV disease is concerned.  If we are treating you to decrease your CV risk, I will emphasize measures that have been shown to decrease or stabilize IMT, as measures that favorably affect CIMT also decrease event rates (for example, if your sugar is high and we treat you with Metformin, we will lower your sugar, favorably affect the CIMT, and lower your event risk; if we use a Sulfonylurea drug, we will lower your sugar, but we will not favorably affect your CIMT, nor will we decrease your event risk).  We can repeat your CIMT periodically, probably once a year (many therapies will affect the CIMT within 6 months).  If the CIMT is stable, your current program will be continued; if it is still progressing, then we need to work harder.

Reference group data is attached.  The top page contains mean CIMT values obtained from Brits who are ultra healthy or who have one or more risk factors.  The second page contains the ARIC (Atherosclerosis Risk in Communities) data describing mean and percentile CIMT findings recorded in 5,000 45-65 year old Americans.  Population values pertaining to young people and more senior Americans is not as firm. 

If your CIMT study demonstrates large, potentially obstructive plaque, then we will recommend a formal ultrasound, which includes blood flow velocity measurement to better quantify the narrowing.

At your next visit I will discuss with you your IMT value, in relation to your age bracket and current health status.  If appropriate, we will take a more aggressive aim at your risk factors or possibly initiate a program of anti-atherosclerotic therapy – but now we know what we are treating – not numbers but plaque buildup and plaque building potential, and now we have a real measuring stick, future CIMT determinations.

A formal, two hour presentation of CIMT, including factors that promote its progression and treatments that stabilize or regress the CIMT value, is in the works (and should be ready by late summer-early fall).