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Ozone & cholesterol combine to cause heart disease

Lessons are slowly learnt.  In April of 79 Scientific American ran an article on plaque formation which solidly supported the conclusion below.  It showed that reactive chemicals in the blood which initiated a response that resulted in the build up of plaque in artery walls.  Among the chief culprits was carbon monoxide—thus the tie in with tobacco smoke.  The role of reactive chemicals is now widely accepted—jk. 

 

 

At the bottom is a necropsy study which shows that atheriosclorsis development is a lifelong process.   

 

Scientific American on line, May 2006 at www.sciam.com.

 

Ozone and Cholesterol Combine to Cause Heart Disease

Numerous studies have linked heart disease and air pollution, particularly smog. Smog--a toxic brew of chemicals and molecules such as ozone--seems to exacerbate heart disease, leading to an increase in heart attacks and fatalities. But researchers have yet to discover the pathway by which smog impacts the cardiovascular system. Now a new study shows how ozone's byproducts in the body can harden arteries and cause heart disease.

Chemist Paul Wentworth, Jr., of the Scripps Research Institute and his colleagues tested such byproducts--known as atheronals--in vitro. These molecules form when ozone and cholesterol interact. "Cholesterol makes up 40 percent of most of your membranes, including those in your lungs," Wentworth explains. "If you inspire smog, there directly is the interaction."

The team's previous research had shown that the white blood cells responsible for inflaming arterial walls also produce ozone and, ultimately, the atheronals: atheronal-a and atheronal-b. These compounds are present in the plaque removed from clogged arteries. The new research shows that when the atheronals interact with various blood cells, they produce some of the effects known to lead to heart disease, such as causing a malfunction in the cells that line arterial walls. "The atheronals can actually cause all the relative aspects that are known to promote cardiovascular disease," Wentworth notes.

 

It remains unclear whether the atheronals typically derive from interactions in the bloodstream or in the lungs. "My sense is that it's a combination of both," Wentworth says. And more research will be needed to determine whether atheronal levels in the blood speed the onset of heart disease such as atherosclerosis. Nevertheless, the scientists write: "the atheronals may be a heretofore unrecognized chemical player in the known linkage between environmental pollution and cardiovascular disease." The research will appear in the June 13 issue of Biochemistry. --David Biello

 

 

From a similar article May of 03:

The researchers also detected one of the atheronal compounds in blood taken from patients suffering from late-stage atherosclerosis. Because the molecule is not present in healthy individuals, the scientists suggest that it could one day form the basis of a new diagnostic test for coronary artery disease. --Sarah Graham

 

For related articles:  on arterocsclerosis, health consequences of tobacco, carbon monoxide and tobacco, and chemical causes of coronary disease.

 

 

American Heart Association

http://circ.ahajournals.org/cgi/content/abstract/103/22/2705

 

Taken from Circulation 2001;103:2705-2710,

 

High Prevalence of Coronary Atherosclerosis in Asymptomatic Teenagers and Young Adults

Evidence From Intravascular Ultrasound

E. Murat Tuzcu, MD; Samir R. Kapadia, MD; Eralp Tutar, MD; Khaled M. Ziada, MD; Robert E. Hobbs, MD; Patrick M. McCarthy, MD; James B. Young, MD; Steven E. Nissen, MD

From the Departments of Cardiology (E.M.T., S.R.K., E.T., K.M.Z., R.E.H., J.B.Y., S.E.N.) and Cardiothoracic Surgery (P.M.M.), The Cleveland Clinic Foundation, Cleveland, Ohio.

Correspondence to E. Murat Tuzcu, MD, Cleveland Clinic Foundation, F25 9500, Euclid Ave, Cleveland, OH 44195. E-mail tuzcue@ccf.org

 

Background—Most of our knowledge about atherosclerosis at young ages is derived from necropsy studies, which have inherent limitations. Detailed, in vivo data on atherosclerosis in young individuals are limited. Intravascular ultrasonography provides a unique opportunity for in vivo characterization of early atherosclerosis in a clinically relevant context.

Methods and Results—Intravascular ultrasound was performed in 262 heart transplant recipients 30.9±13.2 days after transplantation to investigate coronary arteries in young asymptomatic subjects. The donor population consisted of 146 men and 116 women (mean age of 33.4±13.2 years). Extensive imaging of all possible (including distal) coronary segments was performed. Sites with the greatest and least intimal thickness in each CASS segment were measured in multiple coronary arteries. Sites with intimal thickness 0.5 mm were defined as atherosclerotic. A total of 2014 sites within 1477 segments in 574 coronary arteries (2.2 arteries per person) were analyzed. An atherosclerotic lesion was present in 136 patients, or 51.9%. The prevalence of atherosclerosis varied from 17% in individuals <20 years old to 85% in subjects 50 years old. In subjects with atherosclerosis, intimal thickness and area stenosis averaged 1.08±0.48 mm and 32.7±15.9%, respectively. For all age groups, the average intimal thickness was greater in men than women, although the prevalence of atherosclerosis was similar (52% in men and 51.7% in women).

Conclusions—This study demonstrates that coronary atherosclerosis begins at a young age and that lesions are present in 1 of 6 teenagers. These findings suggest the need for intensive efforts at coronary disease prevention in young adults.

 

 

 

 

 

 

Those who have a financial interest in the outcome manipulate the results, Major study finds that all 37 journal articles positive effects over stated; the average was 32%. Statins cause erectile dysfunction, cognitive imparement, and cancer.  

Lipitor (2011) lifetime sales $131 billion, tops all drugs.  Plavix at $60 billion is second.

 

STATINS CANCER Link

52% short term

 

LA Times, Health section, July 21, 2008  --  excerpts

Vytorin, the combination drug (simvastatin (better known by its commercial name Zocor) and ezetimibe--known as Zetia) prescribed to lower cholesterol, sustained another blow today, when the author of a major clinical trial announced that the medication had failed to drive down hospitalization and death due to heart failure in patients with narrowing of the aortic valve. In the process, researchers in Norway detected a significant blip in cancers in the 1,800 subjects they followed

Today's findings suggested something more ominous: the incidence of cancer -- and of dying of cancer -- was significantly higher in the patients taking Vytorin. Altogether, 67 patients on placebo developed cancer during the trial. Among subjects on Vytorin, 102 developed cancers of various kinds.*  This is the second adverse press—the first being in March 08, when the ENHANCE trial found that Vytorin fared no better than a placebo at reducing plaque buildup on the walls of patients' arteries.* *

Comments by jk

Simvastatin (Zocor) is off patent.  Thus in a scramble for profits a combination drug (on patent) was introduced.  Direct to consumer market cost $155 in 07—mainly TV ads. 

*  The pressing issue is that since the development  of Statins, the very first animal studies in the 60s it has been known that Statins increase the incidents of cancer.  However, nearly all studies done thereafter have not included cancer. 

*  Several studies have failed to find a reduction in the build of plaque, even thought the statins including Zocor, reduce LDL and cholesterol.  Few studies include the principle reason for taking a statin, namely a reduction in the death rate.  Claims for such reduction probably entail a failure to control the contravening variable, aspirin usage.  Given a pile of evidence, including the very mechanism of plaque formation, which involves inflammation process, I must conclude that the use of statins is highly suspect.  Given the harm done including cognitive impairment, weakness, and cancer, if my skepticism is born out, the harm done by statins as a course of treatment will far surpass that of VIOXX which killed over 200,000 people world wide by accelerating atherosclerosis. 

 EXTENDED RELEASE NIACIN IS A SAFER, AND A MORE EFFECTIVE WAY TO LOWER MI RISK!