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    Old 08-07-2002, 07:25 PM   #16
    ARIZONA73
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    Gooba,

    I have read your most recent reply directed towards me. In it, you have referred to angiograms, stents, and narrowed arteries. Now that I have a much clearer perspective of where you are coming from, I do have one question for you. Have you ever considered undergoing chelation treatments?
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    Old 08-11-2002, 04:48 PM   #17
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    Just thought I would jump in here. I have high cholesterol and I refuse to take any statin drugs. The only way I would ever consider it would be to take CoQ10 with it because I read that statin drugs lower your CoQ10 and if you don't have enough CoQ10 you can have a heart attack. Instead, I take a lot of antioxidants. I would take L-Carnitine and other things but they are all so expensive. I have to pick and choose. Good luck.

     
    Old 08-11-2002, 08:39 PM   #18
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    Dora:

    You sound like a very intelligent person. You are absolutely correct when you stated that statin drugs cause the depletion of coenzyme Q-10. However, the real danger in this is not that you will suffer a heart attack, but that your odds of developing congestive heart failure would be substantially increased. In fact, there has been a significant increase in the incidence of congestive heart failure since these drugs were introduced. And furthermore, did you know that Merck applied for, and obtained a patent to include up to 1000mg of coenzyme Q-10 in their statin drugs over 10 years ago? Why? Because they were well aware of the dangers of coenzyme Q-10 depletion associated with the use of these drugs. But have they taken any measures so far in this direction? No, they haven't. Have they bothered to inform physicians of the potential dangers of coenzyme Q-10 depletion? No, they have not. And so have the physicians in turn been informing their own patients of these potentially fatal consequences? Of course not. My advice to you is to simply stay away from this garbage. My own father has gone through hell on these drugs. Please, don't make the same mistake. Keep doing what you are doing. Keep up the good work with the antioxidant supplements. I know what you mean by the high cost of L-Carnitine. But just continue doing whatever you can. You are on the right track. Good luck to you!
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    Old 08-12-2002, 06:30 AM   #19
    Gooba
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    Dora,
    Arizona73 is only partially correct.The statin drugs can cause a depletion of CoQ10 in your system.This will not result in a heart attack.Where he is incorrect is in the stating that it will cause heart failure.That is incorrect.The facts are that if a person who has an EF of less than 40% and have parts of their hearts enlarged due to the other number of causes,have CHF.Now,these patients can see a benefit from the addition of this enzyme into their system.It will bring their EF up and help their heart function better than it had prior.There is NO evidence that it is causal for CHF.

     
    Old 08-12-2002, 12:36 PM   #20
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    On May 24,2002, Dr. Julian M. Whitaker, M.D. filed a Citizen Petition with the Department of Health and Human Service Food and Drug Administration in Washington, D.C requesting that the FDA act immediately to require that the labeling for all HMG Co-A reductase inhibitors(statins), include the following warning statement:

    Warning: HMG Co-A reductase inhibitors block the endogenous biosynthesis of an essential co-factor, coenzyme Q-10, required for energy production. A deficiency of coenzyme Q-10 is associated with impairment of myocardial function, with liver dysfunction and with myopathies(including cardiomyopathy and congestive heart failure). All patients taking HMG Co-A reductase inhibitors should therefore be advised to take 100 to 200mg per day of supplemental coenzyme Q-10.

    Attached to this petition is a 20 page report written by Dr. Peter H. Langsjoen. In the introduction to the Citizen's Petition on Statins, Dr. Langsjoen stated:

    "Statins kill people-lots of people-and they wound many, many more. All patients taking statins become depleted in coenzyme Q-10(CoQ10), eventually- those patients who start with a relatively low CoQ10 levels(the elderly and patients with heart failure)begin to manifest signs/symptoms of CoQ10 deficiency relatively rapidly- in 6 to 12 months. Younger, healthier people who's only 'illness' is the non-illness 'hypercholesterolemia' can tolerate statins for several years before getting into trouble with fatigue, muscle weakness and soreness(usually with normal muscle enzyme CPK tests)and most ominously-heart failure. In my practice of 17 years in Tyler, Texas, I have seen a frightening increase in heart failure secondary to statin usage, 'statin cardiomyopathy'. Over the past five years, statins have become more potent, are being prescribed in higher doses, and are being used with reckless abandon in the elderly and in patients with 'normal' cholesterol levels. We are in the midst of a CHF epidemic in the U.S. with a dramatic increase over the past decade. Are we causing this epidemic through our zealous use of statins? In large part I think the answer is yes. We are now in a position to witness the unfolding of the greatest medical tragedy of all time- never before in history has the medical establishment knowingly(Merck & Co., Inc. has two 1990 patents combining CoQ10 with statins to prevent CoQ10 depletion and attendant side effects)created a life threatening nutrient deficiency in millions of otherwise healthy people, only to then sit back with arrogance and horrific irresponsibility and watch to see what happens- as I see two to three new statin cardiomyopathies per week in my practice, I cannot help but view my once great profession with a mixture or sorrow and contempt."
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    Old 08-12-2002, 03:07 PM   #21
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    I have seen that petition and subsequent articles.It is currently theory and conjecture.In the current literature available when you look up causes of CHF,that is not listed as a cause.What has been left out of the article is the status of the patients.CAD is a cause of CHF. What was the progression of the CAD in the patients and what was their EF? How was their heart functioning prior to the statin?


     
    Old 08-26-2002, 09:41 PM   #22
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    I have read all the different views here and have very little to comment which is: yes Cholesterol is what clogs the arteries:yes any type of arterficial drug has pros and cons.
    My husband has had open heart surgery and died 4 times during this so I tend to agree that your oulook is different in retrospect of this.
    I take zocor. my cholesterol was 273 until I was placed on it and it slowly decreased to 119 over a six month time frame then stress hit which makes your body creat more and it raised back to 220 in a three month time frame.
    I do not exercise,I do watch my diet now after my husbands ordeal so to sum up,yes cholesterol is dangerous,yes the drugs are needed by some of us,yes they do help some of us,yes they have risk,yes diet is important in control,but the most important thing is to exercise and minimize stress as much as possible.
    Truthsearcher the folks coming here for support are not here to argue with others, they are here to be able to discuss their problems with others who are going through the same thing they are and to benefit from their experience through their circumstances.
    This is all I have to say on the matter.
    God Bless each of you here.
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    Old 08-29-2002, 05:13 PM   #23
    Gooba
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    The Importance of Lipid Evaluation and Management in the Prevention and Treatment of Acute Myocardial Infarction


    from Preventive Cardiology
    Posted 08/16/2002
    Monte Malach, MD; Pascal James Imperato, MD, MPH & TM

    Abstract and Introduction
    Abstract
    There is an obvious need to measure low-density lipoprotein cholesterol in all patients with acute myocardial infarction and coronary artery disease. The recent guidelines of the National Cholesterol Education Program have established the desired level for low-density lipoprotein cholesterol for such patients at <100 mg/dL. However, several studies have demonstrated a lack of low-density lipoprotein cholesterol measurement and lipid-lowering therapy with statins in patients with acute myocardial infarction and coronary artery disease. These findings point to a need for quality of care improvement efforts to foster both lipid measurement and statin use in such patients. Many studies have demonstrated the numerous beneficial effects of statin use. In addition to lipid lowering, these include plaque stability and antiplatelet, antimacrophage, and antiatherothrombotic activities as well as enhanced endothelial activity. As a class of drugs, the statins have been shown to offer significant benefits with little in the way of associated risks.

    Introduction
    There are five components to early, aggressive therapy for the treatment of acute myocardial infarction (AMI). These include aspirin, blockers, and "clot busters" -- reperfusion by thrombolytics or primary angioplasty (ABC),[1] angiotensin-converting enzyme (ACE) inhibitors for congestive heart failure (CHF) or any large anterior AMI,[2] and now lipid-lowering therapy (LLT).

    The benefits of ABC on morbidity, mortality, and recurrent events at 30 days and 1 year are impressive. It has been found that aggressive therapeutic intervention within 12-24 hours with aspirin and blockers in the emergency room and 30-minute door-to-needle time for thrombolysis are workable and extremely effective, as noted in the Guidelines for the Management of Patients with Acute Myocardial Infarction issued by the American College of Cardiology/American Heart Association.[2] Primary angioplasty for AMI has increasingly been adopted as the intervention of choice at a growing number of large medical centers.[3] The suggestion of fewer hemorrhagic strokes in angioplasty patients than in patients treated with thrombolytics also makes it an attractive choice.[4]

    The report of the Heart Outcomes Prevention Evaluation (HOPE) study[5] drew attention to the protective benefit of the ACE inhibitor ramipril in patients with AMI without CHF. This study demonstrated that its use resulted in a 22% decrease in death and stroke. Previous reports have indicated the favorable effect of ACE inhibitors on remodeling of the newly infarcted wall, thus yielding a less flabby myocardium and a smaller heart in patients with an ejection fraction <40%.[2]

    The fifth therapeutic modality for patients with AMI is the use of statins for LLT. In addition to an absolute reduction in fatal AMI and recurrent events, there is significant prevention of initial events. This report focuses on the use of statins as early LLT in patients with AMI and coronary artery disease (CAD).

    Lipid Levels As Risk Factors
    Public awareness of the connection between cholesterol, lipids, and CAD has increased dramatically in recent years,[6] and in particular because of the updated report of the National Cholesterol Education Program (NCEP).[7] A major focus of the NCEP report is on low-density lipoprotein cholesterol (LDL-C), which is the primary target of therapy. LDL-C has also been the focus of major clinical trials, and "...as a result, the primary goal of therapy and the cut points for initiating treatment are stated in terms of LDL."[7] Indeed, the outcome benefits in terms of morbidity and mortality in CAD are related to the reduction of LDL-C. Frequently, there are also concomitant decreases in total cholesterol (TC) levels and modest elevations of high-density lipoprotein (HDL) levels.

    Currently, optimal levels for LDL have been set at <100 mg/dL, while those for TC and HDL have been set at <200 mg/dL and >60 mg/dL, respectively. Risk assessment has been based on a history of CAD, family history of CAD, diabetes (now considered the risk equivalent of existing CAD), hypertension, cigarette smoking, HDL <40, LDL >160, men >/=age 45 and women, >/=age 55. Multiple risk factors increase the need to lower LDL to <100.

    Need for Increased Measurement of LDL-C
    In addition to recognizing risk factors, there is also a need to increase measurement of LDL-C. Three recently published studies have focused on this issue,[8-10] and two of them have demonstrated inadequate lipid measurement in patients hospitalized with AMI.

    A study undertaken by IPRO, the federally funded quality improvement organization (QIO) for New York State, demonstrated serious in-hospital deficiencies in simply ordering lipid levels on Medicare patients with AMI.[8] In this study, 20 hospitals participated in a collaborative quality improvement effort. The baseline data consisted of rates of lipid level measurement, dietary counseling, and LLT for 406 hospitalized Medicare patients with documented AMI. The intervention consisted of forming multidisciplinary teams within hospitals (medicine, nursing, laboratory, pharmacy, and social service) in order to identify gaps in the process and needed modifications, with a focus on accomplishing uniform ordering of lipid levels on admission or during hospitalization. Educational meetings, site visits, and teleconference calls were conducted with team leaders and hospital opinion leaders, who were also provided with the recent relevant medical literature. A provider user-friendly protocol and a written plan were also requested from each hospital.

    Postintervention data demonstrated much improved LDL-C measurement on admission to the hospital, from a baseline of 32/406 (8%) to 161/498 (32%), and LDL-C measurement during hospitalization from a baseline of 57/406 (14%) to 241/498 (48%) (p<0.001). In addition, the prescribing of LLT for LDL-C >130 mg/dL rose from 0 to 22/48 (46%) (p<0.001). Dietary intervention was unchanged, from 204 (50%) to 245 (49%) of the patients. The inclusion of LDL-C on admission blood specimen panels was both a goal and an achievement. The results of this study indicate that a focused, user-friendly method, protocol, or preprinted order sheet can enhance the ordering of LDL-C and LLT for elevated LDL-C. While there was significant improvement as a result of this quality improvement intervention, performance levels are still well below the ideal in terms of LLT.

    The National Registry of Myocardial Infarction (NRMI) study involved a national sample of 138,001 patients with AMI in 1470 US hospitals.[9] It showed that LLT was ordered on discharge from the hospital in only 37.7% of patients. This is a disturbing finding, in view of the dramatic benefits of early statin therapy on morbidity, mortality, and recurrent events requiring rehospitalization and the existence of readily available guidelines.

    The Cardiac Hospitalization Atherosclerosis Management Program (CHAMP) study undertook improvement in initiating medical therapy in patients discharged after AMI.[10] The increase in statin use rose from 6% to 86%, LDL levels were reduced to <100 mg/dL in 58% vs. a baseline of 6%, and there was a significant reduction in 1-year mortality. There was also concomitant significant improvement in the use of aspirin, blockers, and ACE inhibitors as a result of a program to increase the use of all of these medications prior to hospital discharge.

    The three cited studies demonstrate that physicians are failing to order lipid levels on admission for an AMI and that LLT is not ordered for the majority of patients with AMI. Yet the role of statins in LLT has clearly been demonstrated for primary and secondary prevention of CAD, as well as stroke prevention. Thus, there is a need to utilize techniques that not only increase the regular measurement of LDL-C but also initiate LLT during hospitalization for AMI or CAD.

    Primary Prevention
    Increasing numbers of large, randomized, controlled clinical trials have demonstrated the value of LLT in high-risk patients with or without symptoms.[11,12] The Lipid Research Clinics Program-Coronary Primary Prevention Trial (LRC-CPPT), published in 1984,[13] reported on the use of cholestyramine. It was found that in 3806 men with hypercholesterolemia who were followed for 7 years, the drug reduced TC by 13.4%, LDL-C by 20.3%, and CAD events by 19%. Another primary prevention trial using the fibrate gemfibrozil in 4081 asymptomatic men with elevated lipid levels demonstrated a 34% decrease in CAD events during a 5-year follow-up.[14]

    In the West of Scotland Coronary Prevention Study (WOSCOPS), reported in 1995,[15] 6595 men <65 years of age with no history of myocardial infarction (MI) and elevated TC were treated with pravastatin over a 4.9-year follow-up. There were reductions of 33% in CAD deaths, 22% in all-cause mortality, and 11% in strokes, associated with a decrease in TC of 20% and LDL-C of 26%.

    Another primary prevention trial was the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS), which involved 6605 individuals, amongst which were 997 women and 1416 people aged 65-73, who were at low to average risk and had average LDL-C and TC levels. The statin (lovastatin) was given for 5+ years and reduced LDL-C by 25% and first CAD event or death by 36%.[16]

    Secondary Prevention
    Many providers have historically paid little attention to the lipid levels of older patients, based on a now-dated belief that intervention would not affect either cardiovascular morbidity or mortality.[17] The Long-Term Intervention With Pravastatin in Ischaemic Disease (LIPID) study, published in 1995,[18] involved 9014 patients aged 65-75 years with known CAD and normal or only slightly elevated TC. There were decreases in mortality (24%), all cause-mortality (22%), and stroke (19%). LDL-C decreased 25% among the treatment group. An updated review of the LIPID study, published in 2001,[19] focused on patients up to age 80 and found the absolute benefit of treatment to be significantly greater in older patients as a form of secondary prevention.[20] It has thus been suggested that high levels of LDL-C may cause CAD in the absence of other risk factors in the elderly.

    The Cholesterol and Recurrent Events (CARE) trial found that in 1283 older patients (65-75 years) with an AMI and TC and LDL levels in the average range (<240 mg/dL and 115-174 mg/dL, respectively), pravastatin (40 mg/day) reduced major coronary events.[21] These events occurred in 28.1% of the placebo group and in 19.7% of the pravastatin group. Stroke incidence was 7.3% in the placebo group vs. 4.5% in the pravastatin group. About 75% of deaths from AMI occurred in patients over age 65, the group that has been less likely to receive statin therapy.[21]

    The Scandinavian Simvastatin Survival Study (4S), published in 1994,[22] involved 4444 high-risk men and women (827) and included a 5-year follow-up. All of the individuals, who were recruited from 94 clinical centers, had angina or a prior AMI and hypercholesterolemia, and were placed on a lipid-lowering diet and randomized to simvastatin or placebo. There were reductions in all-cause mortality (30%), CAD deaths (42%), stroke (30%), TC (28%), and LDL-C (35%). The conclusion of the investigators was that the drug was effective and safe. Of interest, there were seven violent deaths in the placebo group and six in the drug group. One case of rhabdomyolysis occurred in a patient taking 20 mg/day of simvastatin, with recovery after discontinuance of the drug. Six patients had a 10-fold creatine phosphokinase elevation on the drug; 20 had alanine aminotransferase and 49 aspartate aminotransferase elevations, without muscle symptoms.

    A Canadian study[23] compared the use of statin LLT in 42,628 elderly patients (>/=65 years) after AMI, both before and after publication of the 4S study. They found a 3.6-fold increase in statin use after the 4S study. Cardiologists and internists increased their use of statins twice as much as general physicians.

    Aggressive LLT was compared with angioplasty in patients with stable CAD and LDL-C of at least 115 mg/dL in the Atorvastatin Versus Revascularization Treatment (AVERT) study.[24] During an 18-month period, atorvastatin, 80 mg daily, reduced the incidence of ischemic events by 36%. The patients on atorvastatin also had a significantly longer time to a subsequent ischemic event.

    There has been an extension of LLT to acute coronary syndromes, which now include unstable angina and non-Q wave MI. Thirty-day mortality rates, with or without LLT, were 0.5% and 1.0%, respectively, and 6-month mortality rates were 1.7% and 3.5%, respectively.[25]

    The Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial was a randomized clinical trial that assessed the benefit of early, high-dose (80 mg/day) atorvastatin initiated within 24-72 hours of an acute coronary syndrome or unstable angina in 3086 patients in 122 clinical centers. It was found that atorvastatin reduced recurrent symptomatic ischemia requiring emergency hospitalization by 16% in a 16-week follow-up.[26] Also, there were only 12 strokes in the atorvastatin group, compared to 24 in the nontreatment group. While this was a very short-term study, the implications strongly point to a decrease in subsequent clinical cardiac events.

    The early implementation of statin treatment in patients with AMI in the Swedish Registry of Cardiac Intensive Care[27] resulted in a significant reduction in 1-year mortality. After adjusting for other risk factors, there was a relative risk reduction of 20% in favor of the statin-treated patients. This was evident regardless of age, sex, prior disease manifestation, or medications. This study involved 137,262 admissions to 58 coronary care units of unselected survivors of a documented AMI from 1995-1998. The conclusion from the foregoing trials is that a statin should not only be given, but started as soon as possible after an AMI or acute coronary syndrome.

    The progression of CAD has reportedly been brought to a standstill with the combination of simvastatin and niacin, both of which raise HDL and lower LDL.[28] Despite concern about the side effects of niacin, 90% of patients remained on combination therapy at the end of 3 years. In addition, there was a 70% reduction in clinical events at 3 years from combined therapy, compared to a 35% reduction on simvastatin alone. HDL increased 30% above baseline with combination therapy, as opposed to 10% on a statin alone.

    Other Benefits of Statins
    Other significant actions of statins merit attention because of marked benefits in coronary and cerebrovascular disease that may be related to the non-lipid-lowering effects of these drugs. Plaque stability is probably an equal or greater benefit of statin use by virtue of prevention of macrophage activity at the site of lipid-filled atheromas.[29] This action may prevent acute occlusion of vessels where there may be little or no actual luminal narrowing, but unstable intramural atheromas. In a study of 42 patients who had coronary arteriography before or up to 1 month after an AMI, it was found that there was stenosis of 50% or less in the affected vessel.[30] Another study revealed that AMI frequently developed in myocardium perfused by arteries with noncritical stenosis.[31] Thus, a vulnerable plaque in a vessel without a high-grade stenosis may produce an acute event. This may be preventable by statin-induced plaque stabilization and antimacrophage activity.

    Plaque disruption is a macrophage-dependent process.[29] Macrophages are attracted to the atheroma, causing the release of metalloproteinases, which lyse the thin, fibrous cap of atheromas, resulting in an occluded blood vessel that promotes thrombosis. Hypercholesterolemia has been shown to be associated with increased platelet-dependent thrombosis generation. Pravastatin has been shown to normalize the generation of thrombin.[32] As a supplement to the effect of statins on macrophages, it has been demonstrated that long-term exercise also decreases the atherogenic activity of the blood mononuclear cells in persons at high risk of developing ischemic heart disease.[33]

    Statins also have antiplatelet activity. Patients with elevated LDL-C have platelets that are also more sensitive to aggregation than patients who have normal LDL-C or TC levels. Simvastatin and pravastatin have both been shown to reduce platelet aggregation. Statins also maintain a favorable balance between prothrombotic and fibrolytic mechanisms, resulting in a decrease of coronary artery thrombosis.[34] Indeed, the membrane cholesterol content of platelets is reduced by pravastatin, which alters platelet membrane fluidity, thus making platelets less likely to provoke thrombosis.[34,35]

    The antithrombotic actions of statins are multifactorial. They include reversal of blood hypercoagulability by reduction of oxidized LDL-C, improved blood flow, decreased vasospasm, improved endothelial function, improved fibrinolysis, and plaque stability.[35] Statins reduce the progression of carotid intima-media thickening. In addition, statin-enhanced plaque stability has also been reported in the carotid arteries.[35] Retardation of carotid artery plaque formation has been shown to result from the use of blockers, ACE inhibitors, and calcium channel blockers.[36] In peripheral artery disease, among 11 atherothrombotic biomarkers assessed at baseline, TC, HDL-C, and C-reactive protein (CRP) were found to be the strongest predictors of the development and prognosis of peripheral arterial disease.[37]

    Pravastatin has been shown to improve endothelial activity by limiting acetylcholine-induced vasoconstriction. It thereby inhibits stasis-induced increases in thrombosis and spasm and promotes vasodilatation and antithrombosis. Up-regulation of nitric oxide synthesis by statins preserves nitric oxide, which inhibits macrophage and platelet adhesion and thereby maintains thrombosis resistance on the endothelial wall. Oxidized LDL inhibits nitric oxide. Statins reduce oxidation of LDL, thus enhancing an active endothelium.[29,35] This is a mechanism whereby statins decrease acute obstructive coronary and carotid artery disease, AMI, and stroke. A study by Raitakari et al.[38] demonstrated that oxidized LDL in high concentration exhibits injurious effects on the coronary vascular bed.

    Further evidence that statins may enhance circulation is that vasospasm is decreased, as shown by improved forearm blood flow in hypercholesterolemic patients treated with statins for 4 weeks.[39] In addition, LDL apheresis increases forearm blood flow. After 3 months of statin therapy, coronary artery perfusion increases, which conceivably is related to decreased vasospasm in addition to regression of plaques.[35]

    Stroke prevention is a clear benefit of statin use, and studies support the role of lowered blood lipids in the prevention of subsequent stroke and transient ischemic attack in patients with established CAD.[40] There is growing evidence for the reversal of carotid artery thickening and unstable plaques. It was shown that pravastatin reduced the incidence of stroke by 11% in the WOSCOPS study,[15] 31% in the CARE study,[18] and 19% in the LIPID study.[21] The 4S study demonstrated a 30% reduction of stroke with simvastatin.[22]

    There are increasing suggestions that atherosclerosis is an inflammatory process.[41,42] Elevation of CRP has been demonstrated in unstable angina and non-Q wave MI. The Pravastatin Inflammation/CRP Evaluation (PRINCE) study[43] evaluated the effect of pravastatin on CRP as a marker for coronary artery disease and atherosclerosis. Pravastatin lowered CRP, TC, and LDL-C within 12 weeks of treatment. As further enhancement of the concept that atherosclerosis is an inflammatory process, it has been reported that lovastatin therapy reduces CRP, an acute-phase reactant, in patients with relatively low lipid levels.[44] Thus the primary prevention of CAD events may require CRP measurement in addition to that of lipids. As a caution, it should be noted that statins do not reduce all acute-phase reactants; since fibrinogen and plasminogen activator inhibitor type 1 are unaffected.[45] In addition, an immunomodulating benefit of statins unrelated to lipid lowering has been noted after cardiac transplantation, along with improved survival.[46]

    The evidence linking the above factors to CAD is discussed in a recent review by Mawhorter and Lauer.[47] By the process of recruitment and attraction of macrophages into the intima of coronary arteries in the presence of oxidized LDL-C, these macrophages become foam cells and are the basis of an atheroma. The association of infection and seropositivity with certain specific organisms -- Chlamydia pneumoniae, cytomegalovirus, Helicobacter pylori, Coxsackie B virus, herpes virus, and others -- can transform infected monocytes into foam cells, and this may be documented by seropositivity.[36] Many trials are underway in patients with CAD to evaluate the benefit, if any, of antibiotic therapy.[47]

    The standard risk factors for atherosclerosis and CAD include hyperlipidemia, hypertension, diabetes, smoking, and family history. Aside from the conventional risk factors for the development of atherosclerosis, other factors have emerged: homocysteine, fibrinogen, impaired fibrinolysis, increased platelet reactivity, hypercoagulable states, and possibly infectious and inflammatory markers (CRP).[41]

    The multifactorial effects of statins, in addition to lipid lowering, all speak to the benefits of these drugs in preventing new and recurrent CAD and stroke. In Great Britain, The National Institute of Clinical Evidence has endorsed the widespread use of statins for patients who have had an AMI.[48] The new NCEP Guidelines suggest the same.[7] As stated by LaRosa et al.,[49] after a careful meta-analysis, "...the cholesterol controversy is no more." Indeed, in another study, the reduction of LDL-C with statin therapy decreased the risk of CAD and all-cause mortality for men, women, the elderly, and the middle-aged.[27]
    Comparative Efficacy of Statins
    It seems certain that the effects of statins are a drug class effect. Long-term studies have shown that pravastatin, simvastatin, and atorvastatin are all effective for the primary and secondary prevention of CAD events. They all show relative equivalency of effect in different doses in the long term.

    The Comparative Dose Efficacy Study of Atorvastatin Versus Simvastatin, Pravastatin, Lovastatin, and Fluvastatin in Patients With Hypercholesterolemia (CURVES)[50] compared dose-related efficacy of the four agents in 518 patients. Milligram for milligram, atorvastatin proved to be most potent. All of the drugs had similar tolerability, and no instances of persistent elevation of serum transaminase or myositis were noted.

    The safety and effectiveness of simvastatin in achieving United States and European guideline LDL-C levels was reported in the GOALLS Study in patients with established CAD.[51] The pharmacokinetic properties of statins, however, do vary. As reported by Bottoroff and Hansten,[52] lovastatin, simvastatin, atorvastatin, and cerivastatin are chiefly metabolized by CYP3A4. This has the potential of side effects that are more toxic and increased blood levels when combined with diltiazem, erythromycin, clarithromycin, itraconazole, ketoconazole, cyclosporine, nefazodone, and many human immunodeficiency virus protease inhibitors.[53] In patients on simvastatin and lovastatin, which are lipophilic agents, myotoxic effects are more likely to occur, including rhabdomyolysis.[51] However, this is rare when the drugs are administered as monotherapy. Pravastatin is not primarily metabolized by CYP3A4 and causes no concern with coadministered drugs metabolized by this pathway.[52]

    The concomitant administration of lovastatin, simvastatin, or fluvastatin with oral anticoagulants may increase hypoprothrombinemia and the risk of bleeding. According to a Medical Letter report,[53] there was no increase in the incidence of breast cancer after 6 years of treatment. After 7 years of follow-up of patients treated with lovastatin, pravastatin, and simvastatin, there was no increase in the overall incidence of cancer.

    The Future
    The enticing possibility of identifying vulnerable plaques in coronary, carotid, and cerebral vessels represents the new horizon in preventive cardiology. A 360° side-view spectroscopic catheter to monitor the metabolic activity of an atherosclerotic plaque, and the detection of atherosclerotic vulnerable plaque using super paramagnetic iron oxide contrast medium, are under study.[54,55] Plaques that are both hot and acidic are considered to be more vulnerable to rupture.[56] These plaques may create no more than a 30%-50% vessel narrowing or, being in the vessel wall, may leave the vessel lumen open. It is the hot plaque that is filled with active macrophages that release metalloproteinase enzymes, which can erode the thin, fibrous cap, releasing the lipid-laden atheroma and causing occlusion and thrombosis. The addition of new techniques to the benefits of statin use for atherosclerosis permits an optimistic view for the prevention, early diagnosis, and treatment of this disease.
    Summary
    Current therapy for AMI requires the early, aggressive use of five specific therapies. These include: 1) aspirin; 2) a blocker in the first 12-24 hours; 3) clot buster therapy (a thrombolytic in <30 minutes or angioplasty in <90 minutes); 4) an ACE inhibitor for CHF with an ejection fraction of <40%; and 5) early statin therapy.

    Although the use of statins after AMI has increased since the publication of primary and secondary prevention trials, much more education needs to be undertaken to optimize their use.

    Very early statin treatment of patients with AMI and CAD has been shown to reduce both early and late morbidity and mortality. Early statin treatment is not limited by gender or age.

    Governmental agencies in the United States (NCEP) and Great Britain (National Institute of Clinical Evidence) now advocate statin therapy for AMI.

    The relative safety of statins has been demonstrated in all of the clinical trials. Early monitoring of liver enzymes and muscle pain is still necessary.

    Studies clearly show that a majority of patients who would greatly benefit from statin treatment do not even have their blood lipids measured, much less receive early prescription of the medication.

    The medical challenge is both early measurement of lipids and early treatment of patients when indicated.



     
    Old 08-30-2002, 05:59 PM   #24
    ARIZONA73
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    The one statistic which I would be most interested in knowing is what percentage of doctors are THEMSELVES taking these statin drugs compared to that of the general population.
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    Old 09-17-2002, 03:31 PM   #25
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    From the Department of Medicine, Division of Cardiology, and
    The Positron Diagnostic and Research Center of the
    University of Texas Medical School, Houston, Texas
    *Professor of Medicine

    Supported in part by NIH Grants RO1-HL26862, RO1-HL26885
    and RO1-HL28356

    Address for reprints:
    K. Lance Gould, M.D., Professor of Medicine, University of Texas Medical School, Room 4.256 MSB,
    6431 Fannin Street, Houston, Texas 77030, Phone: (713) 500-6611, Fax: (713) 500-6615


    --------------------------------------------------------------------------------


    Coronary heart disease remains widely prevalent and is the leading cause of mortality and morbidity in the United States, with an estimated half-million deaths and $56 billion expended for hospital, physician, and medical-surgical costs associated with this disease. In war casualties of Korea and Vietnam, 12% to 20% of young men averaging 26 years old had coronary artery stenoses of 50% diameter narrowing or greater. It is therefore a conservative current estimate that 10% to 13% of middle-aged individuals in the United States have coronary heart disease, with up to 60% of heart attacks or sudden death occurring without prior warning symptoms sufficient to incur medical evaluation or treatment.

    For diagnosis of coronary artery disease, current cardiovascular practice focuses principally on ECG exercise testing, stress perfusion imaging, and coronary arteriography. For treatment, current cardiovascular practice focuses principally on antianginal drugs, percutaneous transluminal coronary angioplasty (PTCA), or bypass surgery. This review analyzes the basis for an alternative, comprehensive, noninvasive management of coronary artery disease using positron emission tomography (PET) perfusion imaging and vigorous risk factor modification aimed at regression of coronary atherosclerosis and stabilization of plaque to prevent the clinical events of myocardial infarction, sudden death and unstable coronary syndromes requiring PTCA or bypass surgery. The diagnostic and therapeutic components of this approach, PET, and vigorous risk factor modification are analyzed separately and then integrated into a practical paradigm or protocol for the principally noninvasive management of coronary atherosclerosis as currently practiced by the author.

    New concepts introduced into scientific literature are by definition only partially validated. When completely documented by multiple confirmatory studies, extensive data and wide acceptance, the concept is no longer new or even publishable. Therefore, to some extent this analysis reflects the author's personal perspective on current medical literature, on some data not yet published, and on his personal experience in clinical practice. While a randomized clinical trial of the approach described here in comparison to mechanical revascularization would be ideal, it is germane to point out that the most widely used elective cardiology therapeutic procedure, PTCA, has never been subjected to randomized trial of its benefits in patients with stable coronary artery disease compared with medical therapy. In contrast, vigorous risk factor modification and/or lipid lowering in several randomized trials have demonstrated partial regression of stenoses and major reduction of cardiac events as detailed subsequently. This review goes beyond the traditional summary of what has been substantially proven. Rather, it is a rational synthesis of what is feasible, strongly supported by current medical literature, and demonstrated by the author's personal clinical practice as an example beyond mere academic conjecture. While many points will be challenged as inadequately validated, the purpose of this synthesis is to detail an alternative way of thinking about the primarily noninvasive management of coronary atherosclerosis that is as rational, clinically feasible, and no less validated than current more invasive practice paradigms.

    Pathophysiology
    The explanation for sudden death, myocardial infarction, or unstable coronary syndromes after a prolonged silent phase of coronary atherosclerosis is most commonly rupture of an atherosclerotic plaque associated with localized coronary thrombosis and/or spasm. Plaque rupture typically occurs at milder stenoses of 40% to 60% diameter narrowing or less that may not cause symptoms or ischemia on treadmill testing, which, therefore, may not predict future coronary events.

    Quantitative coronary arteriography of the entire coronary vascular tree indicates that patients with segmental coronary artery narrowing, even mild narrowing, have coronary artery lumen diameters that are diffusely 30% to 50% smaller than normal subjects' for the size of the regional distal myocardial mass. Quantitation of focal stenoses on coronary arteriograms does not account for the cumulative effects of diffuse coronary atherosclerosis or multiple stenoses on the maximum perfusion capacity of the integrated arterial/arteriolar vascular system. Intracoronary ultrasound also demonstrates in vivo the presence of diffuse coronary atherosclerosis in patients with risk factors, even in the absence of segmental stenoses by arteriography. Thus, either with or without significant or symptomatic segmental coronary artery stenoses, coronary atherosclerosis is a diffuse process in the entire epicardial coronary artery tree, subject throughout to the risk of plaque rupture and associated coronary events in the absence of vigorous risk factor management.

    Functional vasomotor abnormalities of the coronary arteries appear with both early and established coronary atherosclerosis and with or without hemodynamically significant segmental coronary narrowing. In experimental animals and in humans, coronary artery disease and/or hypercholesterolemia alone impair coronary arterial and distal arteriolar vasodilation mediated by endothelium, commonly in a regionally heterogeneous pattern. Atherosclerosis of proximal conduit epicardial coronary arteries impairs endothelium-mediated vasodilation of the distal microcirculation. Thus, the functional endothelium-mediated vasomotor abnormalities of epicardial coronary arteries also extend into the microcirculation despite absence of anatomic atherosclerosis in the coronary microcirculation. In both experimental animals and humans, cholesterol lowering improves the endothelium-mediated dilatory capacity of both coronary arteries and distal arterioles. In women with coronary artery disease, estrogens acutely improve abnormal coronary vasomotor response to intracoronary acetylcholine.

    Reversal of Coronary Atherosclerosis
    In recent randomized trials, vigorous cholesterol-lowering by moderate low fat diet and cholesterol lowering drugs or intensive lifestyle change resulted in stopping progression or partial reversal of coronary artery disease in up to 80% of treated subjects. The regression in these recent trials was only modest, 3% to 10% diameter stenosis units, depending on stenosis severity at baseline, but was consistently observed and statistically significant. There was a proportionately larger, major decrease in clinical events of myocardial infarction, death, bypass surgery, or balloon angioplasty in up to 80% of the treatment groups undergoing vigorous cholesterol lowering compared with control groups in several of these studies, including patients with severe coronary artery stenoses. The reason for proportionately greater clinical benefit than extent of anatomic regression appears to be plaque stabilization and reduction in the risk of plaque rupture, which leads to acute unstable coronary syndromes, particularly at sites of relatively mild narrowing in diffusely atheromatous coronary arteries. There is also a marked decrease in angina pectoris in parallel with decreased coronary events. Therefore, dietary and pharmacological cholesterol lowering provides an alternative approach to the treatment of coronary atherosclerosis that substantially reduces the necessity for balloon angioplasty or bypass surgery.

    Several methods for lowering cholesterol demonstrate these benefits, including very low fat, low cholesterol diet alone (less than 10% of calories as fat), moderate low fat diet combined with cholesterol-lowering drugs, and ileal bypass surgery. Those studies with more vigorous cholesterol lowering of 35% or more or very low fat diets tend to show greater benefit on regression or prevention of events than studies with less vigorous intervention. Control groups in recent randomized trials on an American Heart Association diet of 20% of calories as fat show substantial progression of coronary artery disease and coronary events. In contrast, patients on diets of less than 10% of calories as fat showed regression or no progression. With a large number of food products made with no fat or low fat content, adhering to a very low fat diet is readily achievable with only moderate effort, even for tightly scheduled working individuals as subsequently discussed.

    The combination of low fat diet of less than 10% fat as calories combined with cholesterol-lowering drugs has a more profound cholesterol-lowering effect than either of these treatment approaches alone and readily decreases cholesterol to 140 mg/dL or below in most patients, even with modest doses of an HMG CoA reductase inhibitor (statin) as the only drug. For individuals with low high-density lipoproteins (HDL), the addition of smoking cessation, adequate dietary protein, exercise and/or gemfibrozil or niacin usually normalizes HDL.

    In patients with coronary artery disease and relatively normal levels of cholesterol at baseline, lowering cholesterol to well below normal ranges has substantial benefit, probably more than in patients with very high cholesterol levels. In the correlation of coronary-related deaths to cholesterol levels in the 10-year follow-up of 361,662 men screened for the MRFIT program, mortality decreased continuously and was directly related to decreasing cholesterol down to levels of 140 mg/dL. Based on these reports and the author's personal experience, achieving lean body mass and a total cholesterol of 140 mg/dL or below with an HDL of 45 mg/dL or greater using a very low fat diet and lipid-altering drugs increases to over 90% the probability of partial regression or no progression of disease and absence of clinical events. Partial reversal of coronary artery stenosis and protection from clinical events occurs even in patients with initially normal cholesterol levels if these targets are reached.

    The essential major advance derived from these multiple cholesterol-lowering trials is the demonstration of partial regression or no progression by vigorous cholesterol-lowering with an associated major decrease in clinical events proportionately larger than might be expected on the basis of the modest anatomic regression observed. These new approaches to the treatment of coronary atherosclerosis provide a relatively low-cost alternative to traditional invasive approaches that markedly decreases myocardial infarction, death, balloon angioplasty, or bypass surgery in patients with moderate or severe coronary artery stenoses. Finally, healthcare costs are substantially reduced with optimal outcomes.

    Although used as a measure of changing stenosis severity in lipid-lowering trials, percent diameter narrowing by coronary arteriography does not account for the complex shape changes of stenoses, is poorly related to flow capacity or coronary flow reserve, and fails to account for diffuse disease present in most patients with or without localized coronary artery narrowing. The degree of improvement of percent stenosis in regression trials is quite modest, ranging up to 5% diameter stenosis units for all stenoses and up to 10% diameter stenosis units for more severe stenoses. Based on automated, objective, quantitative analysis of PET images before and after vigorous cholesterol lowering, the size and severity of myocardial perfusion abnormalities by PET after dipyridamole stress decrease or improve in patients undergoing intense dietary changes and being treated with cholesterol-lowering drugs in comparison to an increase or worsening in patients treated with standard antianginal therapy alone. The improvement in perfusion abnormalities on PET images after vigorous cholesterol lowering demonstrates the functional changes in the atherosclerotic coronary arterial tree associated with the modest extent of anatomic regression by arteriography after cholesterol lowering. We have also demonstrated that vigorous cholesterol lowering by extreme dietary restriction or cholesterol-lowering drugs over a relatively short time of 90 days improves myocardial perfusion in patients with coronary artery disease before anatomic regression occurs, thereby suggesting improved vasomotor function.

    The improvement in size and severity of myocardial perfusion abnormalities after dipyridamole stress in patients undergoing cholesterol lowering in comparison to worsening in control subjects most likely involves two mechanisms. The first, occurring over one or more years, is partial anatomic regression of localized coronary artery stenosis, as previously demonstrated by quantitative coronary arteriography. A second mechanism for decreased size and severity of perfusion abnormalities by dipyridamole PET is improved endothelium-mediated coronary artery and arteriolar vasodilation in response to high flows after initial direct arteriolar vasodilation induced by dipyridamole. In primates with coronary atherosclerosis, this improvement in endothelium- mediated vasomotor function of the coronary vasculature after cholesterol lowering precedes anatomic regression. Our observations of improved perfusion and smaller abnormalities by PET imaging after dipyridamole stress in humans relatively rapidly after cholesterol lowering are consistent with experimental studies in animals showing restoration of endothelium-dependent vasodilation by dietary fat restriction and/or cholesterol lowering.

    With the modest changes in anatomic severity of coronary artery stenoses after lipid lowering, the commonly used terms regression and reversal might be questioned. The process of atherosclerosis in the coronary arterial wall consists of a complex mix of cholesterol deposition, cellular proliferation, inflammation, and calcification. With vigorous cholesterol lowering, lipid content and inflammatory cells in the wall decrease, but cellular and fibrotic elements remain with calcification. The lumen becomes somewhat larger, due in part to diminution of lipids and inflammation and in part due to structural remolding of the artery , which remains scarred and smaller than normal. With diminution of lipids and inflammation, plaque stabilization occurs with a decrease in unstable coronary syndromes or coronary events. These pathological correlates with coronary events or lack of events parallel the clinical observation that progression of stenosis severity on arteriograms is associated with subsequent coronary events, whereas stabilization or partial regression by arteriography is associated with low risk of coronary events. Thus, the terms reversal and regression as used clinically incorporate the spectrum of beneficial changes in plaque composition and pathology, compensatory arterial structural changes, arteriographic severity, vasomotor function, flow capacity, symptoms and prognosis. Certainly, regression back to normal in all of these processes does not occur. However, these terms appropriately characterize the cumulative benefits seen clinically as a symptom-free individual at low risk of coronary events with continuing lifelong risk factor modification.

    Comprehensive Noninvasive Management of Coronary Artery Disease
    In clinical application, treatment regimens to partially reverse or stop progression of coronary atherosclerosis predictably with high probability of success involve substantial commitment to a very low fat diet, moderate exercise, smoking cessation and cholesterol-lowering drugs, in addition to good control of hypertension, if present. Of patients with risk factors for coronary artery disease, approximately two thirds may not develop the disease, while the remainder do. Consequently, a firm diagnosis of coronary artery disease is essential as the basis for undertaking a vigorous, lifelong reversal regimen, as for example documentation by prior myocardial infarction, coronary arteriography, previous PTCA, or coronary artery bypass surgery. Most such patients should be on a reversal regimen due to the benefits of decreasing symptoms and coronary events.

    For individuals without an established diagnosis of coronary artery disease, standard noninvasive testing does not appear to provide adequate diagnostic certainty for identifying the presence and severity of coronary artery disease as the basis for lifelong reversal treatment. For example, as shown in Table 1, in eight publications since 1983 involving over 4,000 patients, the diagnostic sensitivity and specificity of thallium stress testing averaged 86% and 54%, respectively. If corrected for referral bias, the specificity increases to 68% and the sensitivity falls to 70%. In asymptomatic subjects with risk factors, where exercise testing is commonly used, the diagnostic specificity of standard perfusion stress imaging is less than in these clinical populations, falling to 40% or less.



    In cholesterol-lowering trials to date, coronary artery disease documented by quantitative coronary arteriography has been the basis for both diagnosis and follow-up of changes in severity of disease. However, reliance on an invasive diagnostic test for noninvasive reversal treatment precludes consideration of a principally noninvasive alternative approach to managing coronary artery disease. Although the data are less extensive than for single-photon imaging, cardiac PET detects coronary artery disease and assesses its severity with a diagnostic sensitivity and specificity of 95%, as shown in Table 2, thereby providing a noninvasive, reliable diagnosis of coronary artery disease as the basis for reversal treatment. PET identifies which coronary arteries are involved and the qualitative severity of disease, is as accurate in asymptomatic as in symptomatic subjects in one study, and is as good or better than arteriography for following changes in stenosis severity in our experience. Since myocardial perfusion reflects the integrated effects of single or multiple stenoses, diffuse atherosclerosis, and vasomotor dysfunction on coronary flow, quantitative PET imaging indicates severity of coronary artery disease beyond a single-dimension percent stenosis of a single localized coronary arterial narrowing by arteriography. In addition, since perfusion is related to lumen radius raised to the fourth power, small changes in arteriographic lumen diameter that are difficult to see or measure on an arteriogram produce proportionately greater changes in perfusion that are visually obvious and easily quantified on a PET scan.

    With currently commercially available generator sources of radionuclides that do not require a cyclotron, the total component costs of a cardiac PET scan at $2200 per study (including amortization for equipment costs and interpretation) are the same as or less than standard perfusion imaging stress tests at $2500 (all costs per study in some large American cities); for these similar costs per study, PET has an accuracy of 95% compared to 50% to 60% for the standard tests. Individuals definitely identified as having coronary artery disease by noninvasive PET may then undergo a vigorous reversal program, with changes in severity of disease followed by dipyridamole PET. Therefore, although they are separate, independent tools in our diagnostic-therapeutic armamentarium, the combination of PET and reversal treatment applied together are powerful as the basis for noninvasive management of patients with symptomatic or asymptomatic coronary artery disease.


    As examples, Fig. 1 shows the orientation of three-dimensional PET images of the heart in relation to coronary anatomy. Fig. 2 illustrates an example of the baseline, control, resting PET (upper row), and dipyridamole PET images (lower row) in right (septal), anterior, left lateral, and inferior views (left to right, respectively) of a patient with a moderate inferior resting defect that was larger and more severe after dipyridamole.

    Fig. 3 illustrates the dipyridamole PET image before treatment (upper row) and the dipyridamole PET image of this same patient (lower row) after two years of intense lipid-lowering treatment on a very low fat diet and on statin without mechanical revascularization. The PET image shows a markedly smaller, less severe inferior perfusion abnormality at the end of the two year treatment period compared with the larger, more severe abnormality at baseline. Perfusion was improved and more uniform throughout the heart, particularly in border-zone areas of defects, thereby making them smaller. Completely automated computerized measurements of size and severity of the perfusion abnormalities on dipyridamole PET of the above studies were made without operator interpretation or drawing regions of interest. Percent of the left ventricle outside of 2.5 standard deviations of normal was 26% at baseline and 15% on the follow-up dipyridamole image after two years of reversal treatment. The changes in quantitative severity paralleled the visual appearance. By comparison Fig. 4 shows the dipyridamole PET image at baseline (upper row) and the dipyridamole PET image 13 months later (lower row) of another patient showing progression of atherosclerosis in all three coronary arteries in the absence of adequate reversal treatment.

    Fig. 5 illustrates a clinical pathway or algorithm relying principally on noninvasive PET and reversal treatment for the comprehensive management of coronary artery disease other than acute unstable syndromes. For patients who do not choose reversal treatment or prefer the immediate results of PTCA or coronary artery bypass surgery, or if the reversal program is not successful, these invasive procedures are backup alternatives in this clinical algorithm. This approach parallels conclusions of the CASS study demonstrating the appropriateness and safety of antianginal medical treatment with deferral of invasive revascularization. However, in this algorithm, the principally antianginal treatments used in the CASS study are augmented by reversal regimens that stabilize plaque, partially reverse stenoses, and prevent myocardial infarction, sudden death, and unstable coronary syndromes requiring bypass surgery or PTCA even for patients with severe stenoses. Consequently, even for severe perfusion abnormalities by dipyridamole PET, reversal treatment is indicated with PTCA or bypass surgery being options.

    Since cardiovascular disease is a major cause of mortality and disability, for highest probability of successful outcome as an alternative to invasive procedures, a coronary disease reversal program requires a vigorous approach combining concurrently all the major therapeutic steps available, including very low fat food, cholesterol-lowering drugs, (and/or HDL-increasing drugs) smoking cessation, exercise, antianginal drugs, and vitamin antioxidants in order to optimize regression or stop progression and to minimize the risk of future clinical events. As an alternative approach competitive with elective bypass surgery or PTCA, how much should cholesterol be reduced? Is the percent decrease in cholesterol or the absolute lowest level of cholesterol more important? The literature supports both points of view. Most recent arteriographic trials have involved secondary intervention in patients with established coronary artery disease and hypercholesterolemia in whom cholesterol was significantly lowered but remained above normal levels. Several of these studies included subsets of patients with coronary artery disease and mild hypercholesterolemia or with normal cholesterol levels and reported significant benefit of further lowering of cholesterol to lower than normal levels. Relatively greater lowering of cholesterol confers relatively greater benefit, and the lowest absolute levels of cholesterol and lowest incidence of coronary events are associated with the lowest mortality at cholesterol levels of 140 mg/dL or below. In the recent SCRIPT trial, there was a modest decrease in coronary events but no regression - only slowed progression of arteriographic disease. However, the extent of cholesterol lowering was also modest, with cholesterol levels in the treated group not decreasing to the levels of even 160 mg/dL recommended by the NCEP guidelines. Therefore, although incomplete, existing data suggests that lowering cholesterol as much as possible by diet and drugs to levels below normal or below consensus levels recommended by the American Heart Association may be beneficial, particularly in patients with coronary artery disease and relatively normal cholesterol levels.

    Due to the association of low HDL with future coronary events, substantial efforts are appropriate for normalizing HDL by smoking cessation, increasing exercise, and use of HDL-raising drugs such as niacin, gemfibrozil, and estrogens in women. Because of the direct relation between body mass and mortality, with the lowest mortality in lean individuals, and the effect of achieving lean body mass on lowering cholesterol, another important part of a reversal program is reducing weight to approximate lean body mass by appropriate carbohydrate restriction in addition to fat restriction. Thus, for optimal probability of partial reversal and preventing coronary events with a certainty comparable to or better than invasive alternatives, a reversal regimen should achieve lean body mass, total cholesterol of 140 mg/dL or below, LDL below 80 to 90 mg/dL, HDL 45 mg/dL or above, and absence of smoking. At these goals, coronary events are simply uncommon.

    For consistent patient acceptance, these components of our program are individually planned for each patient, depending on his or her time constraints, work demands, prior lifestyle, and personal preferences, thereby increasing compliance. They are adapted for each patient with emphasis on developing knowledge, motivation, and active self-maintenance of reversal treatment for coronary artery disease. The principles of reversing coronary heart disease are emphasized and adapted for each individual's application with follow-up reinforcement, motivation, and monitoring by a variable mix of outpatient clinic visits, home lifestyle rehabilitation, intensive telephone, fax or written follow-up locally or at long distance and/or exchange with the private physician. Individuals are carefully informed about all aspects of their lipid-altering drugs, particularly how to check their own lipid and liver profiles along with the physician as an active participant in their own care. There is no single fixed or rigid regimen, diet, or method to which all individuals must conform because the needs and preferences of individuals are highly varied. Multiple subspecialty consultations, special equipment or facilities, group interaction, classroom meetings, excessive clinic visits, time demands, or disruption of busy schedules are avoided in this program in favor of integrating essential lifestyle changes and medical management into the individual's daily life at home and at work.

    Table 3. Essentials of CAD Reversal Regimen


    Personal physician patient time
    Review images and CAD with patient
    Emphasize diffuseness of CAD, progression on standard treatment
    Alternate treatment, risks, failures of PTCA, CABG, medical treatment
    Personal food review, each meal adapted for patient's habits
    Review lipid-lowering drugs, lab tests
    Personal review of exercise routine
    Reinforcement by clinic visits, phone, lab tests
    CAD indicates coronary artery disease; PTCA, percutaneous transluminal coronary angioplasty; and CABG, coronary artery bypass grafting.


    Table 3 outlines the essential components of a program aimed at reversing or stopping progression of coronary artery disease. For optimal results as an alternative to PTCA or coronary artery bypass surgery, a reversal program does require the strong input of a physician or cardiologist comparable to time spent performing an invasive procedure. The influence of a committed, interested physician is an essential part of developing patient self-motivation that becomes subsequently internalized with successful achievement of goals and/or relief of symptoms. In initially stable patients with coronary artery disease who adhere to the program, balloon dilation or bypass surgery is usually not necessary because the response to this treatment regimen is so consistent and effective. The abnormal endothelial function caused by elevated cholesterol and/or coronary artery disease starts to heal within three months after undertaking vigorous cholesterol lowering, usually with decreased symptoms, increased exercise capacity and increased sense of well-being within weeks followed by marked, sustained improvement in myocardial perfusion by two to four years, as shown in the above example (Fig. 3). On a combined regimen of very low fat diet (less than 10% of calories as fat) and cholesterol-lowering drugs together, reversal or cessation of progression and decrease of clinical events exceeds 90% in the author's current practice. However, a small percentage of patients may still develop unstable coronary syndromes despite very low cholesterol and smoking abstinence and may require PTCA or bypass surgery. In the author's experience, such patients usually have persisting low HDL with low total cholesterol and often have ongoing work stress imposed by job circumstances.

    Is reversal treatment suitable only for patients with mild to moderate severity or extent of coronary artery disease? Most lipid-lowering trials report that the most severe stenoses show the greatest regression. Since coronary atherosclerosis is a diffuse process subjecting the entire epicardial coronary tree to plaque rupture, reversal treatment is beneficial for preventing future sudden death, myocardial infarction, or unstable coronary syndromes requiring PTCA or bypass surgery. Based on the author's anecdotal experience with individual patients who have severe coronary artery disease, particularly unstable coronary syndromes, but have refused PTCA or bypass surgery, very aggressive lipid-lowering and antianginal treatment usually controls or eliminates angina and allows long-term noninvasive reversal treatment. However, in the absence of systematic data for unstable syndromes, revascularization by PTCA or bypass surgery may be necessary or preferable.

    Economics of Reversal Treatment for Coronary Artery Disease
    Although medical care in the United States is considered optimal for those with access to it, the cost for achieving optimal outcomes is high. This inefficiency of high-cost for good outcomes involves not only high-cost procedures but excessive diagnostic tests that are not definitive, unnecessary interventional procedures, and the practice pattern of "doing everything to all patients," so that overall costs are high to produce good outcomes in some individuals. Current reimbursement policies and insurance coverage provide definite economic incentives for such inefficient practice patterns. The field of healthcare is therefore focusing on containment of costs, effectiveness of outcomes, elimination of unnecessary tests or procedures, alternative less-expensive but effective treatment modalities, and alternative less-costly clinical pathways. These issues in healthcare reflect a fundamental problem long familiar to industry and business, i.e., the problem of cost versus quality of product: in this case, healthcare.

    Most current approaches to this problem in healthcare have utilized potentially counter-productive strategies of discounted fees, restricted access, second-opinion requirements, preapproval programs for many services, precertification for diagnostic testing and hospital admission, omission of services (particularly new services or new technology), and coercive forces for early discharge from hospital care. These "clamp-down" approaches may ultimately hinder optimal solutions to the problem because they disallow innovation, flexibility of developing basic, new clinical practice strategies, protocols, and technologies that provide better answers with high quality at lower cost than heavily discounted traditional practices. It is therefore important to consider reversal treatment as an alternative to the current standard practice of PTCA or bypass surgery in the management of stable coronary artery disease. However, currently only 15% to 25% of patients who have established coronary artery disease documented by PTCA or coronary bypass surgery undergo intensive cholesterol-lowering and risk management programs despite the benefits of decreased cardiac events and partial regression of disease. Analyzing why regression treatment is not more widely used requires consideration of broad practice patterns in cardiovascular medicine now being scrutinized in an environment of cost and outcome consciousness.

    Table 4. Published Problems of Standard Technology for CAD


    Error in standard exercise tests 46%
    Coronary arteriograms without significant CAD 25%
    Visual overestimates of severity 30%
    Overestimates of improved severity by PTCA 180%
    Recurrence of narrowing after PTCA 30%
    Potential overutilization of CABG, PTCA 44%
    Patients after CABG/PTCA on reversal treatment 17%
    CAD indicates coronary artery disease; PTCA, percutaneous transluminal coronary angioplasty; and CABG, coronary artery bypass grafting.



    The most common algorithm or pathway for evaluation and treatment of coronary artery disease currently includes (1) exercise treadmill testing, (2) stress perfusion imaging, (3) coronary arteriography, (4) antianginal drugs and, (5) PTCA or coronary artery bypass surgery. Table 4 lists some of the documented limitations of this approach when applied broadly. These limitations arise from multiple complex causes including inherent biological limitations and complexity of pathophysiology, past practice traditions, clinical approaches ingrained during training, and strong economic incentives for procedures in the current reimbursement system.

    Table 5. Five-Year Costs per Patient of Reversal Vs Standard Treatment


    Positron emission tomography + reversal treatment: diet, drugs $14,000
    Standard exercise test, arteriogram, dilation $35,000
    Standard exercise test, arteriogram, surgery $60,000

    Since cost is an important issue currently, Table 5 lists the total cost of a reversal program over a 5-year period as follows: all costs of a diagnostic PET scan including interpretation, $2200; costs for cholesterol-lowering drugs, $1200 per year for 5 years; clinic visits, laboratory monitoring of lipid and liver profiles, and all costs associated with noninvasive medical management, $1160 per year for 5 years, giving a total cost of $14,000 over a 5-year period. Based on published cost data, the total component costs of PTCA and bypass surgery are also shown for comparison calculated as follows: all costs for standard stress perfusion imaging including interpretation, $2200; coronary arteriography including professional fee, $9000; PTCA including professional fee, $15,000 plus a times 1.3 factor for 30% restenosis (actually 40%), plus another times 1.3 factor for 30% repeat restenosis gives a total cost of $35,000 over a five year period without clinic fees. Total costs for diagnostic studies and bypass surgery including professional fee were calculated as follows: standard stress perfusion imaging, $2200; coronary arteriography, $9,000; bypass surgery, all costs, $41,000 plus a times 1.15 factor for 15% graft failures requiring repeat surgery over 5 years, for a total of $60,000. Thus, the comprehensive noninvasive management of coronary artery disease by PET and reversal treatment provides substantial reductions in costs of cardiac care compared with traditional invasive approaches but with comparable optimal outcomes for stable coronary artery disease as reported in lipid-lowering trials.

    Limitations to Reversal Treatment
    Potential limitations to reversal treatment for coronary atherosclerosis include inadequate long-term adherence to risk factor modification, the risk of interim coronary events, the side effects and expense of cholesterol-lowering drugs, and poor clinical recognition of the benefits of reversal treatment, particularly the decreased need for PTCA and coronary artery bypass grafting and associated costs. To some extent or in some individuals, these limitations are valid. However, in comparison to the documented limitations of current practice patterns of cardiovascular medicine outlined in Table 4, the limitations of reversal treatment are greater in perception than in fact and are readily managed in daily practice. In the author's experience, there is a large number of patients who are able and want to undergo reversal treatment including the lifestyle changes but are not able to obtain appropriate guidance and medical management from the cardiology profession oriented toward principally invasive alternatives.

    Strict dietary reduction of fat to 10% or less of calories is commonly regarded as not attainable by most patients with coronary artery disease. However, a diet of less than 10% of calories as fat has been previously reported in the Life Style Heart Trial. In the author's reversal clinic, diets of 10% of calories as fat and high in protein are routinely achieved in patients with coronary artery disease by an individualized approach, particularly with the large number of no-fat food products now available commercially, particularly nonfat protein sources. Strong motivation is generated by the patient's reviewing his own PET scan with a physician and by the knowledge that a low fat diet combined with lipid-lowering drugs is associated with relief of angina, partial reversal or stopping progression of stenoses, and prevention of clinical events such as death, myocardial infarction, bypass surgery, or balloon angioplasty in most patients. This approach nearly always combines both very low fat diet and cholesterol-lowering drugs to achieve optimal results. When it is presented appropriately and adapted to individual needs, the majority of patients will succeed in maintaining a reversal program.

    While the risk of coronary events is always a concern, cholesterol-lowering trials have shown a remarkable decrease in coronary events. Moreover, in patients with new-onset angina, in asymptomatic or mildly symptomatic patients, or even in patients with severe exercise-induced ischemia, ischemic episodes during daily life or with exercise do not predict future coronary events. If restenosis is considered a coronary event after PTCA and graft closure after bypass surgery, coronary events after these procedures are quite common in up to 40% of patients - more than events after a reversal program. These observations in parallel with the CASS study suggest that it is appropriate and safe to pursue a medical regimen, such as antianginal and reversal treatment with deferral of revascularization in most patients having stable coronary artery disease, where revascularization is an option if reversal treatment is not successful. It is therefore appropriate to treat such patients initially with reversal regimens using diet, cholesterol-lowering and antianginal drugs, antioxidants and exercise as an alternative to PTCA or bypass surgery.

    Use of cholesterol-lowering drugs requires that liver enzymes be checked monthly for 3 months after starting or changing dose of an HMG CoA reductase inhibitor (statin) every 3-4 months thereafter. It is thereafter occasionally necessary to discontinue drugs because of side effects, but such instances are not common and substantially less than the 40% restenosis rate documented after PTCA. The expense of cholesterol-lowering drugs is also a valid limitation but is substantially less than the cost of PTCA, more so if the cost of repeat procedures due to restenosis is accounted for.

    Regarding adequacy of evidence documenting benefits of reversal treatment, further studies and more data would always be of interest. However, publications since 1990 consistently show benefits of vigorous lipid management. The benefits of these more recent trials compared with less convincing results in trials before 1990 are probably due to more vigorous cholesterol-lowering measures and/or lower fat diets in studies published since that time. In comparison, despite the current widespread use of PTCA, there are no randomized trials of elective PTCA in stable coronary artery disease compared to medical antianginal or reversal treatment. Furthermore, in long-term follow-up, coronary bypass surgery does not appear to decrease incidence of myocardial infarction or death. Therefore, on balance in the literature, there are more trials showing decreased coronary events by reversal treatment than reports on decreased coronary events by elective PTCA or bypass surgery in stable coronary artery disease.

    Whether marked cholesterol lowering causes increased deaths due to suicide or trauma has been a concern. For example, in the LRC-CPPT and Helsinki trials involving several thousand patients, there were 12 accidental or suicidal deaths in the treated group and 8 in the control group; of those individuals in the treated group dying of accidental deaths or suicide, four were not taking the cholesterol-lowering drug but were included in the treatment group based on the intent-to-treat principle in the study design. Therefore, in these trials, there is no evidence for increased accidental or suicidal deaths associated with cholesterol-lowering treatment. In large population studies, there may be an association between low cholesterol and accidental death, suicide or cancer. This association can be explained by the likelihood that psychiatrically depressed individuals prone to accidental or suicidal death are often anorexic and therefore have low cholesterol. Similarly, individuals with undiagnosed cancer may have low cholesterol, with a subsequent diagnosis of cancer thereby making an association. However, prospective trials of low fat or low calorie diets do not show these associations. In the Multiple Risk Factor Intervention Trial, no excessive traumatic deaths were observed. In the Family Heart Study, the group on the low fat diet of a cholesterol-lowering program showed a reduction in depression and aggressive hostility paralleling lowered cholesterol as compared to the control group on a standard high fat "American diet." Even very low calorie diets in addition to low fat diets are not associated with adverse violent events. Therefore, in prospective trials there is no identifiable risk of increased suicide, traumatic deaths, or cancer.

    Other Non-invasive Technologies For Identifying Coronary Artery Disease
    Other noninvasive technologies have been tested for identifying coronary artery disease. Magnetic resonance imaging holds promise for measuring myocardial perfusion and imaging coronary arteries. However, imaging or measuring myocardial perfusion has not been clinically satisfactory to date. Imaging the coronary artery lumen has been accomplished by magnetic resonance techniques for identifying flowing blood in the lumen. However, the apparent lumen size imaged depends on the characteristics of the flow profile. Small, localized areas of turbulence or disordered flow appear as the inner lumen border and therefore as apparent stenosis or as apparent worse stenosis than is anatomically present. The reliability of this approach, particularly for quantifying severity of narrowing or for following changes in severity, remains to be developed.

    Fast computed tomography has been used to identify coronary calcification as reflecting the presence of coronary artery disease. However, the specificity of this approach for coronary artery narrowing is low because many individuals over 50 years old have coronary calcification without coronary artery narrowing. A recent publication suggest that the sensitivity of fast computed tomography for identifying coronary artery disease is also limited.

    Stress echo and stress gated blood imaging have been used to indirectly identify coronary artery disease by monitoring abnormal left ventricular function under stress conditions. The diagnostic accuracy of these indirect methods is not sufficient or direct enough to provide the basis for lifelong drug treatment and risk factor alterations essential for reversing coronary atherosclerosis. These technologies also do not provide measures of severity of stenoses or changes in severity for following regression or progression.

    Role of Coronary Arteriography, Intracoronary Doppler/Echo, PTCA, and Bypass Surgery In The Noninvasive Management of Coronary Artery Disease Based on Reversal Treatment
    Current invasive diagnostic technology of arteriography, intracoronary Doppler and intracoronary echo provides powerful insights into coronary anatomy and function not previously possible except experimentally. Analysis of the pressure gradient-flow characteristics of coronary artery stenoses that was first done only in experimental animals is now routinely feasible in humans. Coronary flow reserve initially described in animals as an integrated measure of stenosis severity is now routinely measured by intracoronary Doppler for absolute coronary flow reserve and from intracoronary pressure measurements for relative coronary flow reserve. Structure of the arterial wall visualized by intracoronary echo, with or without coronary artery stenoses, may show atherosclerosis in vivo, previously identifiable only in pathologic specimens. Functional responses of coronary blood flow and/or lumen diameter after intracoronary vasoactive drugs provide insights into regional endothelial function for clinical purposes. Finally, coronary arteriography has evolved to a quantitative integrated analysis of the entire coronary arterial tree for multiple segmental stenoses or diffuse coronary artery disease, reflecting the interrelations and integration of anatomy and function. Thus, invasive evaluation of the coronary arteries has progressed far beyond visual interpretation of regional narrowing on an arteriogram.

    For noninvasive management, the identification of stable coronary artery disease and qualitative assessment of its severity provided by visual interpretation of a coronary arteriogram can now be provided by PET (Table 2). For following changes in disease severity, either progression or regression, PET is as good or perhaps better than coronary arteriography because the changes in perfusion reflect flow effects that depend on the fourth power of lumen diameter. Small changes in arteriographic lumen size that are difficult to measure reliably even by quantitative coronary arteriography are quite apparent by PET imaging of myocardial perfusion after dipyridamole. As important, the PET perfusion images show the cumulative effects on flow of diffuse disease and endothelial function of the macrocirculation as well as recently demonstrated abnormalities of the microcirculation in the presence of epicardial coronary artery disease. Whereas percent diameter fails to account for other stenosis geometry, diffuse disease, or functional pressure-flow characteristics of coronary artery stenoses, these newer invasive diagnostic modalities provide a wide range of sophisticated anatomic and function measurements that completely characterize the coronary arterial tree for both research investigation and as the basis for procedures such as PTCA, atherectomy, lasers, and coronary bypass surgery.

    In this scheme of principally noninvasive management of coronary atherosclerosis, the complete characterization of the arterial wall, pressure gradient-flow characteristics, flow reserve, and integrated analysis of the entire arteriographic coronary tree have become the raison d'ętre for carrying out invasive diagnostic studies. In essence, these new diagnostic procedures provide the basis of new knowledge. As noninvasive diagnostic imaging such as PET advances to the accuracy and clinical utility of a visually interpreted arteriogram for noninvasive treatment, the invasive diagnostic procedures need to advance to a quantitative accuracy and clinical utility of characterizing the functional and anatomic characteristics of the entire coronary artery tree, including the arterial wall.

    In this algorithm for the principally noninvasive management of coronary artery disease, reversal treatment is not antithetical to invasive treatment. Rather, reversal treatment is a valid, safe, effective alternative that requires patient and physician preference. In the author's experience, the majority of patients will pursue an effective reversal regimen when it is presented and managed appropriately. However, a minority will not alter risk factors despite predictable future events, morbidity and mortality. For such patients, catheter procedures or coronary bypass surgery are appropriate. Many patients and physicians may choose both invasive procedures and reversal treatment for a complex variety of reasons, depending on personal preference of the patient and clinical judgment reflecting the training, skills, personal preference, community standards, and economic incentives influencing the physician.

    CONCLUSION
    Current knowledge and practical experience demonstrate that the comprehensive noninvasive management of coronary artery disease based on PET and reversal treatment is a valid, safe, and effective alternative to traditional invasive approaches for diagnosing and treating coronary heart disease at potential cost reductions of 20% to 50% compared to standard cardiology practice emphasizing coronary arteriography, balloon dilation, and bypass surgery.


    The pictures and figures do not transfer well.

     
    Old 09-23-2002, 09:35 AM   #26
    capnez
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    How about the homocysteine theory of athersclerosis (plaque build up in the arteries)? Are there any new studies that relate the two???

     
    Old 09-25-2002, 05:13 AM   #27
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    Kico166:

    I'm sorry things didn't work out well for your father. You also may be correct in stating that when your time is up, your time is up. Life is really a crap-shoot. There simply is no one single treatment that will prove effective for everyone, including angioplasty and bypass surgery. Many people who go into the hospital for angioplasties, catherizations, and bypass surgeries don't leave the hospital alive. So, whatever form of treatment a patient may opt for, the truth is he or she is simply rolling the dice and hoping for the best. That's really all we can do in life.
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    Old 09-25-2002, 06:08 AM   #28
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    I first have to give you my sincerest condolences.Your loss is very heart wrenching.
    I do have to ask a couple of things.
    He had a heart attack in June,what did the cardiac catherization show in June? How much heart damage was there? What was his ejection fraction?
    What problems was he experiencing after he was released to prompt an angioplasty 2 months later? What tests did they do?
    What tests and problems did he have after the angioplasty? Who did, and what tests were given that said he had his arteries 90-100% open?
    What medications was he on? Was restenosis present at his angio site?
    His heart attack was unfortunate but,the subsequent events seem questionable however unfortunate they are.If,after his third chelation treatment they did not do at least a nuclear stress test,then somone missed the call.Ideally another cardiac catherization would be called for,but if they had went in and found the blockages they would have opened them up.

     
    Old 09-25-2002, 02:24 PM   #29
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    kico.....sorry about your dad. did your dad smoke,or is there a family history?

     
    Old 09-25-2002, 03:48 PM   #30
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    It appears to me that somebody made a serious blunder regarding those test results. Kico166's father was told his arteries were 90-100% open after only 3 chelation treatments? I don't see how that's possible. A typical course of treatment involves 25 to 50 visits over a six to twelve month time span, so even if the patient does experience a reduction in the degree of blockage, the improvement is likely to occur over a much longer period of time and many more treatments. But 90-100% open? I doubt it.
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