3379 Quakerbridge Road, Hamilton, NJ 08618
Tel: 609-396-6363
A Benchmark Preventive Cardiology Practice
since 2001
Prevention Diagnosis and Treatment of Heart Disease
Our Advanced Medical Therapy
After knowing your calcium score and it is not ZERO, the next step is patient mentoring and setting the goals of your personalized medical therapy.
The intensity of treatment is based on the level of cardiac risk and patient's preference - the higher the risk, the more intense the treatment. Most patients seen in our office choose the maximum degree of prevention possible.
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Nearly all heart attacks are caused by sudden rupture of a vulnerable plaque. A vulnerable plaque is characterized by a thin cap and a large central lipid (cholesterol) core with active ongoing inflammation within.
Strengthening the fibrous cap to prevent plaque rupture is crucial in preventing an acute heart attack. The size of the plaque and intensity of inflammation can be diminished by reducing the amount of cholesterol influx into the plaque. It is the LDL particles that deliver cholesterol to the plaque and reducing the number of LDL particles circulating in the blood is essential.
How long does it take to start benefiting from the treatment? Not long.
The ASCOT-LLA trial demonstrated reduction of heart attack starts within just weeks from initiation of basic (not advanced) statin therapy compared to placebo. The longer the duration of the treatment, the greater the benefit. Our more intensive treatment provides greater benefit.
How long does it take to detect the earliest evidence of plaque regression? About 12 months by CT angiography as shown above, depending on the intensity of treatment.
The availability of non-invasive coronary CT angiography makes documentation of plaque regression much easier.
Several invasive IntraVascular UltraSound (IVUS) regression trials showed plaque regression occurred only when LDLc was reduced to below 70 mg/dL in the JUPITER trial. Even lower is even better.
This is a screenshot of a patient's chart with a calcium score of 3500. He is at extremely high risk for heart attack, stroke, and sudden vascular death and requires very aggressive medical treatment. At the bottom, are our treatment goals.
The screenshot of his tabulated lab tests confirms the intensity of his plaque-stabilizing, plaque-regressing therapy since 2015.
Maintaining low LDL particle numbers and very LDL cholesterol levels are the primary reason why he is doing as well as he has. All his plaques, not only in the heart but also in the brain, have stabilized and regressed, preventing both heart attack and stroke.
Stents and heart bypass were both averted. He has no evidence of ischemia on the treadmill nuclear stress test.
This composite slide puts together several vital clinical trials that answer the question - is lowering LDL cholesterol levels to very low levels (like those of a newborn baby) significantly lowers the risk of a heart attack? Yes.
Lowering LDL cholesterol in high-risk patients from 190 mg/dL to 30 mg/dL reduces heart attack risk from 30% (very high) to 5% (low risk) over time.
In this patient with a very high calcium score of 3500, lowering and keeping his LDL cholesterol in the 30's for years reduces his cardiac risk to the lowest possible.
For high-risk patients: lower LDLc and LDLp for longer and get there faster.
My calcium score is very high at 1200. Does that mean that my arteries are severely obstructed and that I should have cardiac catheterization? No.
A calcium score does not predict severe obstruction. Initiate medical therapy on the first visit. If you have no cardiac symptoms and your nuclear stress test is normal, there is no need for cardiac catheterization. And definitely, there is no need to have stents.
Does plaque regression mean that my calcium score will also regress? No.
Calcium is deposited as part of the cycle of inflammation and healing within the plaque itself. In the more mature plaques, these calcium deposits coalesce and form sheets as shown in the top slide.
The central lipid core, not the calcification, forms the bulk of the plaque and it is this component that gets depleted with treatment causing regression. Most of the calcium is tightly bound chemically and does not dissolve.
Without treatment, calcification may increase as much as 40% per year. With optimal treatment, we expect an increase of 15% per year or less over a five-year period.
Coronary CT angiography is rapidly evolving with the help of AI providing a detailed characterization of all the soft and hard plaques that was never before possible noninvasively and quickly. It will become a useful management tool once the health insurance decides to cover this test.
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LDL particle vs LDL cholesterol - why we choose to measure both.
LDL cholesterol is easily and cheaply calculated using an indirect method that has been available for over 50 years and is used in clinical trials. It is a measure of the amount of cholesterol carried by LDL particles in mg per deciliter. It has become the standard - cheap, widely available, even in a doctor's office.
LDL particle number is a measure of the number of particles carrying cholesterol in the blood. The LDL particle is a complex structure consisting of a very long chain protein (ApoB 100), phospholipids, and cholesterol esters.
Oxidation of its multiple components converts LDL particles into atherogenic particles - initiating and sustaining an inflammatory response leading to plaque formation.
LDL cholesterol is a surrogate for LDL particles when they are concordant. But in some cases they are discordant - LDL cholesterol level is 50 mg/dL while LDL particle number is still high at 1500 nmol/L.
Measurement of the LDLp has become available only in large commercial laboratories (LabCorp and QUEST) for just over a decade.
Clinical Cardiology
When a 40 or 50 year old patient comes in for heart attack prevention, the initial evaluation involves clinical cardiology expertise.
Preventive Cardiology
After or during the initial evaluation, preventive cardiology expertise determines how most accurately determine the risk for cardiovascular events within the next 5 to 10 years.
Once the severity of risk is known, medical therapy is optimized to the level of risk. Advanced lipid therapy is the foundation of prevention in high risk patients.