Simply having a high cholesterol, and treating it with statins, has been disputed:
Researchers infused HDL cholesterol into a group of individuals and reversed heart disease:
A synthetic form of “good cholesterol” has been shown by researchers to quickly shrink blockages clogging coronary arteries, offering for the first time the possibility of a drug that could actually rapidly reverse heart disease.
In a small, preliminary study, the laboratory-made substance, which mimics HDL cholesterol, significantly reduced in just six weeks the amount of plaque narrowing arteries of heart attack and chest pain patients, the researchers reported.
Because the approach attacks the underlying source of many heart attacks, the results could mark a milestone in the search for new ways to treat the nation’s No. 1 killer, researchers said.
In addition, research reveals that inflammation is a major culprit. A recent study showed a 15% reduction in cardiac events in persons taking an anti-inflammatory medicine.
That is why the blood testing outlined at the end has a number of tests for inflammation–both in the blood and of cholesterol.
The inflammation of a subset of cholesterol, LDL cholesterol, turns into a “foam cell” which is the main problem in the development of heart disease. Of note, statins (the most common first line treatment for a high LDL cholesterol) have anti-inflammatory effects. The best way to treat for oxidized LDL is to measure LP (a)–a degenerative form of cholesterol.
We now look at a much more sophisticated picture of inflammation interacting with the subsets of cholesterol and lipids (fats or triglycerides), and newer risk factors in the blood to give a more sophisticated and predictive picture of your cardiovascular health or risk:
- Cholesterol- is a participant, not the cause of cardiovascular disease.
- HDL – the [good] lipoprotein that carries cholesterol away from the heart back to the liver. The higher the more protective.
- ApoA — a liver marker for HDL
- LDL – the [bad] lipoprotein that carries cholesterol to the heart from the liver. The lower the better.
- ApoB — a liver marker for LDL
- Triglycerides – neutral fats, elevated by increased carbohydrate intake, which has its own risk consequence.
- LDL particle sizing – small heavy dense vs large fluffy particles. This has lead to a new risk profile type called Pattern B or Pattern A. (see below)
- LDL and HDL isoforms – both can be fractionated into five separate and more distinct components.
The New 21st Century Risk factor profile
- Lp(a) – (lipoprotein a) – a degenerative form of the LDL that aggressively promotes atherosclerosis (hardening of the arteries).
- Homocysteine – newer risk factor — from incomplete conversion of the amino acid homocysteine to methionine that may be irritating to blood vessels. This inflammatory response is a risk for vascular disease.
- hsCRP – high sensitivity C-Reactive Protein – a sensitive, but non-specific, measure of inflammation — showing newer notions of cardiovascular disease as inflammatory in nature. This is much closer to revealing the cause of cardiovascular disease. Remember, cholesterol does not cause heart or vascular disease.
- Fibrinogen Levels – as above, the higher the fibrinogen levels the greater likelihood of forming small blood clots that can lead to blocked arteries. Blocked arteries can eventually cause strokes and heart attacks. This may have the most prognostic significance (predictor) of any of above and is least likely to be tested by routine or even “advanced” workups
- Lp-PLA2 – (lipoprotein-associated phospholipase A2) – levels — the newest and most sophisticated measurement of the effects of this enzyme on oxidized LDL causing the entire cascade that leads to atherosclerotic changes. This is reputed to be one of the first markers for cerebrovascular (stroke) risk and a surrogate for endothelial dysfunction, leading to heart disease.
Look above at LDL particle sizing. There is an increasingly recognized, but infrequently and poorly diagnosed syndrome of high triglycerides and low HDL which is a surrogate marker for these small dense LDL particles. Termed Pattern B or ALP (Atherogenic Lipoprotein). Look at the following illustration. See how these small dense particles “leak” into the vascular wall and the larger LDL particles don’t?
This leak is the beginning of atherogenesis, or atherosclerosis — hardening of the arteries. The end result: high blood pressure and blocked arteries eventually leading to strokes and heart attacks.
Why is this important? Because routine testing will not measure any of this. A Normal LDL level might actually be quite dangerous. You need to go to more sophisticated testing and understanding.
So the story is a lot more than just Cholesterol. Cells need a certain amount of cholesterol as a lubricant for healthy cell membranes. It is also the biochemical source of all sex, stress and blood pressure regulating steroids — so that it is necessary for functioning.
In fact, some studies have that very low cholesterol levels in men can increase risk of death.
Bottom line: you need the resources and expertise of health professionals who fully understand the more complex story of lipids and who have access to more advanced testing methods.
Choose from the most sophisticated, and non-invasive approaches to cardio-vascular problems available anywhere — from the comprehensive testing as explained above to a combination of the following modalities:
- CIMT is a noninvasive way to asses a patient’s cardiovascular health by measuring the thickness of the intima and media layers of the carotid artery.
- CIMT accurately measures the presence of disease, vascular inflammation, risk of events, and progression or stabilization of the identified disease state.
- there is a 96% correlation with findings from the CIMT and the presence of plaque in coronary arteries.
- CIMT characterizes plaque based on the likelihood of predicting events. “Soft” plaque is more vulnerable and more likely to rupture than calcified plaque. Consider pharmacological and lifestyle therapy goals to reduce LDL-C and control other factors that promote the vascular inflammation process.
- Repeat CIMT annually to monitor progression, stabilization, or regression of plaque and/or vascular inflammation.
- Endothelial Function (EF) is a noninvasive test to assess the function of the endothelial lining of the arterial wall.
- By temporarily occluding the blood flow through arm compression, EF measures the ability of the vasculature to normalize blood flow by a bio-sensor measurement of vascular compliance.
- Decreased vasodilation shows the initiation of an inflammatory state and endothelial dysfunction which can lead to or accelerate the development of plaque.
- Endothelial dysfunction is reversible through lifestyle therapy, lipid lowering medications, and disease state control like blood pressure and blood sugar. Repeat EF every six months to monitor changes in arterial endothelial function.
Other testing includes:
Treadmill Stress Testing for those who have symptoms suspicious for heart disease.
Carotid Ultrasound or CIMT (intimal media thickness) scans —
Superfast CT (EBT) HeartScans for coronary artery calcifications
An outstanding panel of tests for heart disease is from cardiovip.com: It includes
VASCULAR INFLAMMATION CHARACTERIZATION
Preface: Arterial inflammation is a significant component of atherosclerotic disease process. The inflammatory biomonitor and physical diagnostic tests described provide insight to the influence of atherogenic cofactors such as altered cholesterol metabolism, tobacco use, etc., and their impact on the inflammatory responses in the progression of atherosclerotic lesions. Evidence suggests that the chronic perpetuation of immune mediated vascular inflammation and cholesterol-induced atherosclerosis are key steps in atherogenesis.
- MPO is a strong predictor of short term risk for a cardiovascular event.
- MPO, an enzyme released from white blood cells, accumulates in lesions in the arterial
wall. MPO diminishes nitric oxide bioavailability and oxidizes LDL, increasing unstable
lipid deposits in the arterial wall. Lesions can rupture resulting in blockages downstream
or formation of a thicker endothelial layer.
- MPO measurements, combined with other inflammatory markers and CIMT, enhance
cardio- vascular risk prediction especially in patient subgroups associated with low risk.
- For individuals with increased MPO levels, consider more aggressive lipid lowering and
antiplatelet drug therapy and lifestyle changes that promote vascular health and reduce
- Repeat abnormal results every quarter until treatment goal is met, then annually for continuous monitoring of CVD risk.
- Lp-PLA2 is a strong predictor of short term risk for a heart attack or stroke.
- Lp-PLA2 is an enzyme released in the plasma as a part of the immune response to vascular injury. Lp-PLA2 hydrolyzes LDL, promoting lipid deposits and rupture prone plaque.
- High concentrations are found in advanced atherosclerotic lesions.
- Lp-PLA2 is generally not elevated in systemic inflammatory conditions, and therefore is a good marker of vascular specific inflammation and thrombosis.
- Lp-PLA2 combined with other test results aids in the decision for lipid lowering or anti-inflammatory therapy and intensified lifestyle changes.
- For abnormal Lp-PLA2 consider statins, niacin, or fenofibrate therapy. Consider aspirin therapy if not contraindicated. Assess blood pressure. If not at goal, consider anti-hypertensive therapy. Consider diet/exercise, smoking cessation and weight reduction efforts as appropriate.
- Repeat abnormal results every quarter until treatment goal is met, then annually to monitor cardiovascular risk.
- hs-CRP is a protein released during acute phase inflammation.
- hs-CRP is a well-documented clinical marker of general and cardiac related inflammation,
even in individuals with normal LDL.
- Research shows that healthy individuals with elevated hs-CRP are 4 times as likely to
experience CVD events.
- Elevated levels, along with other inflammatory bio-monitors and CIMT results, aids in the
decision for lipid lowering and lifestyle therapy, especially in apparently healthy
individuals. Rule out and treat other sources of systemic inflammation.
- For abnormal hsCRP levels consider statins, ezetimibe or combination therapy if not
contraindicated. Consider aspirin therapy if not contraindicated. Assess blood pressure.
If not at goal, consider initiating anti-hypertensive therapy. Consider diet/exercise/weight reduction efforts as appropriate.
- Repeat abnormal results every quarter until treatment goal is met, then annually.
- F2-IsoPs is a strong predictor of future risk for coronary artery disease.
- F2-IsoPs are compounds produced by free radical oxidation. They promote platelet activation and aggregation resulting in thrombosis or blood clots.
- F2-IsoPs levels are reduced with low saturated fat diets, regular exercise and smoking cessation. Consider drug therapy if lipids are not at goal or if other bio monitors are elevated.
- For abnormal F2-Isoprostane levels consider statins, ezetimibe or combination therapy if not contra- indicated. Consider diet/exercise, smoking cessation and weight reduction efforts as appropriate.
- Repeat abnormal results every quarter until treatment goal is met then annually to assess future risk of cardiovascular disease.
- Microalbumin appearing in the urine reflects glomerular endothelial dysfunction and loss of
micro- vascular integrity.
- Individuals with high urinary microalbumin levels are 3 times more likely to develop
- cardiovascular disease.
- Patients with inflammation or narrowing of the small arteries in the kidneys are also at risk
for endo- thelial dysfunction in the rest of their vascular system.
- Early identification and treatment of lipids, glucose and blood pressure can slow down the
disease progression. Measure endothelial function to determine vascular compliance.
- For abnormal Microalbumin/Creatinine levels consider initiating or titrating anti-hypertensive
therapy. Assess the presence of CAD with imaging techniques such as CIMT and consider aspirin therapy if not contraindicated.
- Repeat abnormal Microalbumin/Creatinine ratio every 3 – 6 months until controlled, then yearly for high risk individuals with kidney disease, hypertension, and diabetes.
- Vitamin D deficiency is associated with an increased risk for heart disease.
- Both forms of Vitamin D are measured; Vitamin D3 is three times as potent as D2.
- Two-thirds of US population has suboptimal levels of Vitamin D. Consider increasing time in sun, dietary sources, or supplementation.
- Often patients who have elevated percent body fat concentrations have low Vitamin D levels.
- When combined with other biomonitors, Vitamin D better defines an individual’s risk for heart disease.
- For insufficient Vitamin D levels, consider vitamin D-rich foods such as cheese, vitamin D-fortified milk, shitake and button mushrooms, or supplementation with vitamin D3
- Monitor abnormal Vitamin D measurements quarterly until treatment goal is met, then monitor annually.
- Oxidized LDL more accurately predicts the progression of heart disease and plaque formation
in the arteries before symptoms have presented themselves.
- OxLDL is formed when the ApoB protein on LDL particles becomes oxidized. OxLDL is
recognized by scavenger receptors on macrophages which engulf OxLDL, leading to foam cell
formation which in turn initiates artherosclerosis and enhances vascular inflammation.
- Individuals with high levels of OxLDL are 4 times more likely to develop metabolic syndrome
in the next 5 years.
- Increased OxLDL levels are associated with the presence of coronary heart disease, diabetes,
and acute myocardial infarction. For individuals with elevated OxLDL consider
cholesterol-lowering medications, CoQ10, Omega-3 fatty acids, vitamin E, and low glycemic foods.
- Consider diet/exercise, smoking cessation and weight reduction efforts as appropriate.
- The OxLDL test can be ordered in conjunction with standard/lipid testing or inflammation testing.
Micronutrient Tests Associated With Vascular Inflammation