Filed under: atherosclerosis

How Long Does it Take to Reverse Plaque?


A new analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) shows that changes in coronary artery calcium (CAC) (as measured by the heart scan) may lag behind changes in coronary disease risk factors. 

 

CAC is a common measure of subclinical coronary disease, but the association between changes in coronary disease risk factors and progression of CAC is not clear. So Arguelles and colleagues analyzed data from 6800 participants of the MESA study. All participants underwent a CAC imaging test with computed tomography at baseline and either 1.6 or 3.2 years later. A quarter of the study subjects also underwent a third CAC test at an average of 4.9 years after baseline.

 

Reason: Individuals who come in with a very high risk-factor profile and are the most likely to be placed on medications already have a very high underlying level of pathology that could be driving that calcification process independent of declines in risk factors, including blood pressure, lipid levels, and blood glucose. 

 

 

The authors analyzed if the changes in CAC over time were associated with changes in blood pressure and lipid levels. The analysis was adjusted for age, ethnicity, smoking status, family history of cardiovascular disease, total income as a marker of socioeconomic status, and previous use of hypertension, lipid, and glucose-lowering drugs.

 

Among men who had detectable CAC at baseline, CAC increased an average of 57 Agatston units/year. In women, CAC progressed by 39 Agatston units/year. In all patients, the risk-factor measures went up or down depending on whether they were taking antihypertensivse, statins, or other medications. 

 

The researchers said that CAC "occurs in a time-lagged fashion" such that a longer study would have eventually seen CAC progression stop or reverse many years after the reversal in risk factors in patients taking medication. Whether risk factors such as high blood pressure and hyperlipidemia are more important to the initiation of calcification--or if they have more of a role in the progression of existing disease--is not clear yet.

 

I like to use CAC for a baseline before treatment or to monitor progress. I aslo require all chelation patients to get one. I have seen this time lag in my practice many times now but it took me about three years to notice it. It typically takes two to three years to see a reversal of plaque after initiating aggressive treatment. This is a very important thing to explain to patients. I typically see less calcium deposition per year the above numbers because I use combination therapy.  A moderate to high risk patient in my office would typically be on some or all of the following: fish oil, Coenzyme Q10, statins, vitamin K2, vitamin D, blood pressure meds, antioxidants, superoxide dismutase, pomegranate, phosphatidylcholine, lipoic acid, vitamin C, niacin and tocotrienols. After all, the goal is to reverse plaque or stop its progression. Sometimes patients do intravenous treatments as well.

 

What is Better Than C Reactive Protein at Assessing Plaque at Risk of Rupture?

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Lipoprotein-associated phospholipase A2 (Lp-PLA2 or just PLA2) is an enzyme produced mainly by white blood cells that is more cardiospecific than CRP.  Lp-PLA2 levels are higher in atherosclerotic plaque than in surrounding tissues as well as in the fibrous cap of arterial plaque prone to rupture. Plaque rupture is the number 1 casue of heart attacks. Though still a relatively new marker it has gained ground as an independent risk factor for heart attack and stroke. In the bloodstream Lp-PLA2 is attached to LDL and HDL cholesterol.  Elevated Lp-PLA2 levels have been shown to be predictive of cardiovascular events in more than 25 prospective epidemiologic studies published since 2000. Lp-PLA2 is inactive until LDL undergoes oxidation. After LDL oxidation Lp-PLA2 reacts and forms two proathrogenic molecules that trigger a cascade of inflammatory events.

Lp-PLA2 strongly predicts the chance of a second cardiovascular event in patients with pre-existing CHD as well. It is an emerging independent risk factor even after taking into account other markers of inflammation, kidney function, and blood viscosity. People with levels in the top 25% had twice the risk of an event as compared with those in the bottom 25%.

Get your Lp-PLA2 tested today.

Strategies to reduce PLA-2 include:

·         ashwaganda ( Withania somnifera)

·         fish oil (marine omega-3 fatty acids)

·         the plant derived antioxidants quercetin and naringenin, and resveratrol

·         address liver stressors such as alcohol, acetaminophen (Tylenol).

Learn about more strategies in my new book Dare to Live.