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Posted April 15, 2015: by Bill Sardi
So you’ve had your heart attack or heart scare and cardiologists have relieved your unremitting chest pain by placement of wire props called stents in any of your four coronary arteries that supply the heart with oxygenated blood.
By now you’ve probably been placed on blood thinners and cholesterol-lowering drugs. But don’t fall into the trap of believing modern medicine’s false paradigm that cholesterol accumulation in your coronary arteries resulted in arterial narrowing and eventually a blood clot that caused your heart attack.
Before you become cholesterol-phobic it might be time to learn what really caused a blood clot to form in a coronary artery.
There has been so much talk about lipoproteins (cholesterol particles bound to proteins) like HDL and LDL cholesterol over the past four decades but so little mention of lipoprotein(a), which is a far greater risk factor for heart attacks than LDL cholesterol.
Despite the dismissal of total cholesterol as a meaningful risk factor for heart disease, cardiologists keep beating the same drum. What cardiology now says is this: elevated LDL (low density lipoprotein) is a risk factor for heart disease and should be reduced in the blood circulation to concentrations less than 70 milligrams per deciliter (1/10th of a liter) of blood. [Archives Medical Science March 16, 2015]
Despite the indisputable fact 200 healthy individuals have to be treated with cholesterol-lowering statin drugs for 5 years in order to spare one patient from a non-mortal heart attack, researchers continue to say “lowering LDL cholesterol should be the primary goal.” [Cell March 26, 2015]
But in the highest risk group for a heart attack (age 70-90 years) elevated cholesterol has not been found to be a significant mortality factor. [Journal American Medical Directors Association Dec 2014]
Before I go any further, let’s ask an important question. We don’t have a stent deficiency, so what caused clots to form in your coronary arteries? Why do the four coronary arteries that supply the heart with oxygenated blood develop blockages and blood clots rather than other arteries? Answer: because the coronary arteries are under the most pressure and require constant maintenance and repair.
This is where another cholesterol particle called lipoprotein(a) comes in.
Before you develop false reliance upon stents to prevent formation of blood clots in your coronary arteries, the following study may be instructive. Among 240 patients who had undergone angioplasty where a balloon is inflated to break up a clot in a coronary artery, 40% of these patients (97) experienced recurrence. Patients who experience a recurring blockage had higher lipoprotein(a) levels than those who did not (29 versus 14). [Circulation March 1995] The underlying cause of your chest pain or heart attack is more likely due to lipoprotein(a) than LDL cholesterol.
The role of lipoprotein(a) in heart disease is vastly underestimated. [Clinical Research Cardiology supplement April 2015]
Blood plasma concentrations of lipoprotein(a) greater than 20 milligrams/deciliter double the risk for cardiovascular disease. [Cholesterol 2012]
Researchers in Germany compared with lipoprotein(a) levels above 110 mg/deciliter to those who lipoprotein(a) level fell below 30 mg/deciliter. About half (50.2%) of the high lipoprotein(a) subjects had 3 diseased coronary arteries versus 25.1% among those with lower lipoprotein(a) levels. [Clinical Research Cardiology Supplement April 2015] See chart below.
|Study of 31,274 Hospitalized Patients With Coronary Artery DiseaseSource: Clinical Research Cardiology Supplement April 2015|
|Lipoprotein(a) greater than 100 mg/deciliter||Lipoprotein(a) lower than 30 mg/deciliter|
|History of heart attack||34.6%||16.6%|
|Three diseased coronary arteries||50.2%||25.1%|
|Required heart surgery||40.8%||20.8%|
|Need for balloon angioplasty/stent||55.3%||33.6%|
Elevated lipoprotein(a) levels correlate with re-blockage of coronary arteries after placement of a stent. [Atherosclerosis April 2013]
Patients with at least three stents in coronary arteries are more likely to have high lipoprotein(a) levels (greater than 30 mg/deciliter). [Disease Markers 2013]
While LDL cholesterol may not be a significant factor in the development of heart attacks, LDL levels often do correlate with lipoprotein(a) levels, which may mislead cardiologists who are attempting to reduce levels of LDL without recognizing lipoprotein(a) as the real culprit. [Atherosclerosis Aug 2002]
Since there is no drug that lowers lipoprotein(a), and knowing of nothing else that can be done to lower lipoprotein(a) levels, cardiologists punt and vainly attempt to lower LDL cholesterol. [Disease Markers 2013] Lipoprotein(a) is not regulated by the same mechanism as LDL cholesterol. [Journal Swiss Medicine Dec 7, 1991.
There is no doubt that lipoprotein(a) apheresis (blood filtration) is effective. It reduced the annual rate of adverse cardiac events (heart attack) by 79.7% in one study. [Clinical Research Cardiology Supplement April 2015] But apheresis is expensive and problematic.
Recognize, if you don’t address the problem of lipoprotein(a) you will continually need more stents to prevent blockages in your coronary arteries.
To learn how to reduce lipoprotein(a) levels or reduce its clot-forming effects, read my prior report on this topic. [Knowledge Of Health] Start by supplementing your diet with vitamin C and IP6 rice bran.
©2015 Bill Sardi, Knowledge of Health, Inc.