Panaceia or Hygeia

immunize yourself against the pandemic of lifestyle diseases

Archive for the ‘coronary artery disease’ Category

The cause of angina, heart attacks and most cases of sudden death.

“Low risk” nurse with normal cholesterol but self-destructive lifestyle ends up with heart transplant after CCTA

Posted by Colin Rose on December 20, 2010

Here in a nutshell is a demonstration of the problem with expecting technology to substitute for good clinical medicine and save us from our self-destructive addictions. If anyone is puzzled about the dichotomy between the exorbitant cost of the US medical system and its relative lack of effect on any measure of health here is the reason.

Below is a story from theheart.org followed by the actual paper in the Archives of Internal Medicine minus the references.

In the absence of any symptoms attributable to coronary artery disease there was no reason to do any more testing but the temptation to use high tech tools without good indication is irresistible to many doctors. CCTA is the latest expensive test to detect coronary atherosclerosis. Patients think that they will never have a heart attack and live longer if the disease is detected and some surgical procedure, like an angioplasty or bypass is done and doctors making $millions from doing them are not about to discourage them and point out the total lack of evidence for any significant benefit from angiography or the surgical procedures in patients with chronic coronary disease.

The authors have labelled this patient “low risk” because her “cholesterol” was normal but clearly she was at high risk based on her obesity and hypertension, both indices generally of  junk food addiction, in spite of her being a nurse.  When she started new exercises she probably got muscle pain from weight lifting. With an obvious self-destructive lifestyle, she should not have been “simply reassured” as recommended by the editors. But instead of encouraging her to make meaningful lifestyle change her doctors ordered tests with no clinical indication.

Framingham scores, lipid profiles and CRPs can be very deceptive because they do not assess LDL modification in the arterial wall, essential to the formation of atherosclerotic plaque. In spite of having “normal” numbers for all the usual “risk factors” she had advanced atherosclerosis in her coronary arteries. Apparently no dietary history was taken and no attempt was made to encourage her to change her lifestyle, an example of gross diagnostic and therapeutic incompetence, all too common in an era of absolute faith in the power of technology to protect us from our self-destructive addictions. Doctors abdicate professionalism by ordering tests instead of dealing with the real problems, like junk food addiction, which take much time for which they are not compensated and risk alienating patients who demand a high-tech fix or reassurance so that they can continue their risky behaviour.

——————————————————————

Case study shows how “just-in-case” CCTA in a low-risk patient may spectacularly backfire

DECEMBER 17, 2010 | Reed Miller

San Francisco, CA – Coronary computed tomographic angiography (CCTA) in patients with a low pretest risk of coronary disease wastes resources and can even lead to horrendous outcomes, a case study published December 13, 2010 in the Archives of Internal Medicine shows. The report tells the story of a 52-year-old white female who initially presented with chest pain and had a CCTA; this was followed by an unfortunate chain of events in which she suffered an aortic dissection during cardiac catheterization and that culminated in her having a heart transplant.

Part of its ongoing “Less is More” series begun last April, the latest case, reviewed by Dr Matthew Becker (St Vincent’s Heart and Vascular Institute, Erie, PA), Dr John Galla (Providence Hospital, Mobile, AL), and Dr Steven Nissen (Cleveland Clinic, OH), describes how the well-meaning attempt to reassure a patient with a low risk of coronary disease backfired spectacularly.

“Perhaps the most important point to be learned from the case described by Becker and colleagues is that there are safer ways to reassure patients,” say journal editors Drs Rita RedbergMitchell Katz, and Deborah Grady (University of California, San Francisco) in an accompanying editorial. “Patients value our advice. Talking with our patients should be our first choice for reassurance.” They add that “applying the ‘less-is-more’ principles prospectively could have avoided this unfortunate case.”

From diagnostic uncertainty to disaster
The 52-year-old nurse had hypertension and mild obesity and had recently begun an exercise and diet regimen to control her weight and blood pressure. She presented to her primary physician with chest pain, but no other symptoms: she had a normal ECG with a normal lipid profile and normal C-reactive-protein level. Her doctor attributed the chest pain to a musculoskeletal cause but performed a CCTA to reassure her that she was not at risk for a coronary event.

The CCTA showed discrete, noncalcified, nonobstructive plaque in the mid and distal segments of the left circumflex and dominant right coronary arteries and diffuse, complex calcification in the proximal left anterior descending (LAD) coronary artery. Because that calcification was difficult to quantify, the physician recommended that she undergo cardiac catheterization to get a clearer look at the LAD.

This exam, performed at the local community hospital, revealed only a mild irregularity in the LAD, but during the procedure, the patient complained of chest pressure, which prompted an aortogram that revealed an aortic root dissection that was compromising the left main coronary artery.

So the patient underwent urgent coronary artery bypass graft (CABG) surgery and stayed in the hospital for two weeks with a residual left ventricular ejection fraction of 35%. The bypass graft soon failed and was treated with multiple drug-eluting stents, but despite her compliance with dual antiplatelet medical therapy, a stent in the vein graft supplying the circumflex artery developed a thrombosis, causing an ST-segment-elevation MI complicated by cardiogenic shock. The thrombosis was successfully treated, but the patient remained in refractory cardiogenic shock and ultimately underwent orthotopic heart transplantation.

Unnecessary testing happening every day
“With few cardiac risk factors and an atypical chest pain presentation, this patient had a low pretest probability for coronary artery disease and should have been reassured and not undergone any further risk stratification,” say the authors. “Lacking randomized data suggesting improvement in clinical outcomes and with clear risks, including contrast load, radiation exposure, and suboptimal diagnostic specificity, CCTA should have a very limited role in the evaluation of patients who present with chest pain.”

They acknowledge the risk of complications associated with cardiac catheterization is low, but catastrophic events are always a possibility. They believe the physicians in this case overestimated the stenosis in this patient’s coronaries because they did not fully appreciate the CCTA’s potential for false-positive findings. Complete visualization of all segments of the coronary tree with CCTA is often hindered by cardiac motion, which can lead to the appearance of “blooming artifacts” of coronary calcification that may cause the observer to overestimate the extent of stenosis.

Becker et al point out that previous studies comparing CCTA with conventional coronary angiography in diverse patient populations show CCTA’s sensitivity is between 79% and 100% for the detection of obstructive coronary disease, but its specificity is only 64% to 85%, corresponding to “an unacceptably high false-positive rate” of up to 81% in some populations.

As reported by heartwire, the recently released professional guidelines on Appropriate Use Criteria for Cardiac Computed Tomography list CCTA as “inappropriate” for detection of CAD patients with a low risk of heart disease, ability to exercise, nonacute symptoms that may be an “ischemic equivalent,” and an interpretable ECG.

Patient could have been simply reassured
“If a test is not sufficiently accurate to change clinical management in a particular setting, it should not be done,” but according to Redberg et al, often these tests are done anyway—sometimes even before the patient sees a physician—because nobody has assessed the patient’s pretest probability of the disease or properly considered how the test result will change the clinical management of the patient.

“There are cases where [the test presents] more risks than benefits, and you really need to consider the risks and benefits and not [assume that] just because you can do the test, you should do the test. And this case highlights that,” Redberg told heartwire.

Cases like this where an inappropriate test leads to many complications and near catastrophe are rare, “but to have a CT or another test that was just done for reassurance, when you could have just told the patient ‘You’re fine,’—I think that’s done every day lots of times.

“You don’t know which [tests] are going to lead to that kind of problem, but you do know which of those is not going to give you any benefit, so if there is no benefit, it’s better not to be taking any risk, even a small one.”

————————————————————————–

Left Main Trunk Coronary Artery Dissection as a Consequence of Inaccurate Coronary Computed Tomographic Angiography

Matthew C. Becker, MD; John M. Galla, MD; Steven E. Nissen, MD

Arch Intern Med. Published online December 13, 2010. doi:10.1001/archinternmed.2010.464

ABSTRACT


A 52-year-old woman presented to a community hospital with atypical chest pain. Her low-density lipoprotein cholesterol and high-sensitivity C-reactive protein levels were not elevated. She underwent cardiac computed tomography angiography, which showed both calcified and noncalcified coronary plaques in several locations. Her physicians subsequently performed coronary angiography, which was complicated by dissection of the left main coronary artery, requiring emergency coronary artery bypass graft surgery. Her subsequent clinical course was complicated, but eventually she required orthotropic heart transplantation for refractory heart failure. This case illustrates the hazards of the inappropriate use of cardiac computed tomography angiography in low-risk patients and emphasizes the need for restraint in applying this new technology to the evaluation of patients with atypical chest pain.

REPORT OF A CASE

A 52-year-old white female nurse with a medical history that was notable for hypertension and mild obesity presented to her local primary care physician with the recent onset of chest pain. Further investigation revealed that in an effort to lose weight and assist in the control of her hypertension, she had adopted a new diet and exercise program several weeks earlier. At her initial presentation, she described 48 hours of nonexertional, sharp chest pain that was aggravated by elevation of her right arm and deep inspiration. She denied associated symptoms of shortness of breath, nausea, vomiting, or diaphoresis, and her office electrocardiogram showed no abnormalities.Other than mild hypertension (blood pressure, 142/85 mm Hg), the results of her physical examination were unremarkable except that elevation of her right arm and palpation of the right chest wall reproduced the symptoms with which she presented. With a normal lipid profile and an ultrasensitive C-reactive protein level, she was diagnosed as having atypical chest pain most likely of musculoskeletal origin. Hydrochlorothiazide was used to treat her hypertension, and cardiac computed tomography angiography (CCTA) was performed to exclude the possibility of coronary artery stenosis and to reassure her. Interpretation of the CCTA findings suggested that both the left circumflex and the dominant right coronary arteries had discrete areas of mild, noncalcified, nonobstructive plaque in their mid and distal segments. The large-caliber left anterior descending coronary artery (LAD) was reported to have diffuse and complex calcification of the proximal segment, which made accurate quantification of the luminal stenosis challenging.

Subsequently, the patient’s physician recommended cardiac catheterization to enable more precise assessment of the LAD luminal stenosis. Selective coronary angiography was performed at the local community hospital and revealed only a mild luminal irregularity of the LAD. Shortly after the second injection of contrast, the patient complained of intense chest pressure and was noted to be hypotensive and tachycardic (blood pressure, 78/45 mm Hg; heart rate, 110/min). Mild “staining” of contrast was noted in the left coronary cusp of the aorta, and an ascending aortogram revealed a dissection of the aortic root extending into, and resulting in compromise of, the left main coronary artery. An intra-aortic balloon pump was placed, and the patient underwent urgent coronary arterybypass with saphenous vein grafting of both the LAD and the left circumflex coronary artery.

Following a prolonged, 14-day hospital course and a residual left ventricular ejection fraction of 35%, the patient was discharged home with intensive cardiac rehabilitation. Unfortunately, within 6 months of the bypass, she presented again with escalating chest pain and was noted have premature graft failure that was treated with percutaneous coronary intervention with multiple drug-eluting coronary stents. Despite her compliance with dual antiplatelet medical therapy (aspirin and clopidogrel daily), she presented 8 weeks later with an ST-segment elevation myocardial infarction complicated by cardiogenic shock. Emergent catheterization revealed thrombosis of the stent in the vein graft supplying the circumflex artery that was successfully treated with a catheter-based intervention. However, the patient remained in refractory cardiogenic shock and ultimately required urgent orthotopic heart transplantation.

COMMENT


Emergency department visits for chest pain syndromes represent a large and growing health care burden. Because patients with chest pain require urgent triage and timely management, there are great incentives for developing a new generation of novel, complementary diagnostic strategies. A recent addition to the diagnostic armamentarium, multidetector CCTA, can noninvasively generate reconstructed images of the coronary circulation. However, the brisk expansion and rapid adoption of CCTA over the past decade has outpaced supportive clinical data and has led to the referral of a much larger, and often lower-risk, segment of the population for coronary artery catheterization. We believe that in this case the unwarranted use of advanced diagnostic imaging (false-positive CCTA findings) directly contributed to unnecessary cardiac catheterization that resulted in a tragic complication and significant morbidity.Advanced diagnostic imaging technologies or the latest biomarker cannot, and should not, replace a thorough history and physical examination with subsequent decision making guided by the bestevidence-based practice. The need for testing in patients with chest pain is based on the clinician’s estimation of the pretest probability of coronary disease. In a patient with a low pretest probability (<10%) of having significant coronary disease, the preferred course is to reassure the individual and to focus the treatment plan on primary or secondary prevention strategies. Additional diagnostic testing rarely garners useful information and exposes the patient to unnecessary risk—both from the diagnostic test itself and from subsequent invasive testing because of false-positive results. While the risk of complications associated with cardiac catheterization is low, catastrophic events can occur. As opposed to CCTA, in appropriately selected patients coronary angiography allows the presence, location, and, most importantly, the functional significance (eg, fractional flow reserve, intravascular ultrasonography) of lesions to be determined. Because there is often discordance between luminal stenosis and the physiologic significance of lesions, functional testing has assumed critical importance in the assessment of patients with a moderate pretest probability (10%-90%) of coronary disease.

Therefore, given the possible adverse consequences of the overuse of diagnostic imaging in a broad and uncensored population of patients with chest pain, recent joint professional guidelines emphasize that ” . . . an appropriate imaging study is one in which the expected incremental information, combined with clinical judgment, exceeds the expected negative consequences by a sufficiently wide margin for a specific indication that the procedure is generally considered acceptable care and a reasonable approach for the indication. . . . “Furthermore, because of differences in body habitus, coronary physiology, exercise physiology, symptom presentation, and disease prevalence, the diagnostic accuracy of stress testing may be affected by the female sex. In addition to having a markedly different ST-segment response to exercise from a young age, data suggest that ST-segment depression tends to be less sensitive and specific for coronary artery disease in women. With normal electrocardiographic findings, negative cardiac biomarkers, and a classically atypical presentation, our patient had an age-specific risk level that was below average. She had a low pretest probability of coronary disease (<10% risk of myocardial infarction or death per 10 year interval), making further testing inappropriate and the chance of false-positive study results unacceptably high. However, in an era of rapid advancement in diagnostic imaging strategies, the savvy clinician must not forget the basic tenets of data-driven medicine, patient selection, and risk tolerance and ultimately realize when less may be more. Such is precisely the case with CCTA.

Because CCTA is rapid and noninvasive and has wide availability, it has increasingly been used to detect coronary atherosclerosis in a broad array of patient populations. However, the lack of randomized data suggesting clinical benefit, as well as technical and anatomical limitations, restricts its application in many patients. Studies comparing CCTA with conventional coronary angiography in diverse patient populations suggest that CCTA is highly sensitive (79%-100%) for the detection of obstructive coronary disease, with a positive predictive value ranging from 86% to 91%. However, these same studies report suboptimal specificity (64%-85%) and negative predictive values of 83% to 90% that correspond to an unacceptably high false-positive rate of up to 81% in selected subpopulations. Further limiting the diagnostic accuracy of CCTA is the fact that complete visualization of all segments of the coronary tree is hindered by cardiac motion (heart rate, >70/min), smaller vessel caliber (<2 mm), and tortuousity that may result in portions of a vessel moving in and out of an imaging plane. Furthermore, given its high attenuation coefficient, the presence of coronary calcification commonly produces a “blooming artifact” that makes accurate assessment of adjacent arterial luminal challenging and may result in overestimation of the degree of luminal stenosis, which is likely the case in the patient described herein. Therefore, CCTA often overestimates the presence and severity of coronary atherosclerosis to a degree that is dependent on the study population, the equipment used, and the experience of the interpreting physician, which may lead to unnecessary, higher-risk, and costly invasive procedures.

Nevertheless, the use of CCTA has increased dramatically over the past decade, with some estimates suggesting up to 26% per year. In an era in which comparative efficacy of therapies has assumed critical importance, the unchecked growth of CCTA seems not only unfounded but also irresponsible and unsustainable. Aside from its cost implications, CCTA also exposes the patient to substantial amounts of ionizing radiation. It is estimated that the collective dose received from medical radiation increased by more than 700% between 1980 and 2006, with increases in computed tomography accounting for more than 50%. Furthermore, 64-slice CCTA (without tube current modulation) exposes the patient to an average effective dose of 15 mSv of radiation compared with only 7 mSv for diagnostic coronary angiography. With recent data suggesting that 1.5% to 2.0% of all reported cancers in the United States may be linked to ionizing radiation from computed tomography, there is reason for pause.

In conclusion, our patient suffered a rare but devastating complication from an cardiac catheterization that was the direct result of unnecessary CCTA and false-positive findings. With few cardiac risk factors and an atypical chest pain presentation, this patient had a low pretest probability for coronary artery disease and should have been reassured and not undergone any further risk stratification. Lacking randomized data suggesting improvement in clinical outcomes and with clear risks including contrast load, radiation exposure, and suboptimal diagnostic specificity, CCTA should have a very limited role in the evaluation of patients who present with chest pain.

Posted in atherosclerosis, cardiology, CCTA, cholesterol, coronary artery disease, coronary computed tomographic angiography, diet, ethics, heart transplant, junk food, lifestyle, obesity, professionalism, surgery, technology, waist circumference | 1 Comment »

MY FAITH IN SWEET SCIENCE IS DOUBLE-BLIND

Posted by Colin Rose on August 16, 2009

Those chiropractors certainly look like willfully ignorant charlatans but some medical doctors are also guilty of the same unwillingness to perform or abide by the results of randomized trials. For example angioplasty of coronary arteries for “treating” stable angina (chest pain caused by inadequate blood flow to the heart during exercise) has been shown in multiple randomized trials to cause more heart attacks than treating with drugs only. But these procedures are still done at great expense to our medical system. As an example of unwillingness to perform randomized trials, consider “bariatric” surgery. Even our Minister of Health and Social Services, Yves Bolduc, a neurosurgeon, believes various forms of gastric surgery is a cure for obesity but there has never been a single randomized, sham-operated controlled study showing surgery is any better than treatment for junk-food addiction alone without the operation. Bariatric surgeons refuse to do a randomized trial and are not compelled to. And yet $billions are being spent on these operations. Like the chiropractors, if you ask these doctors why they are ignoring or not doing randomized trials they will answer that they know what is right for the patient, no need to do trials.


MY FAITH IN SWEET SCIENCE IS DOUBLE-BLIND
SCHWARCZ
The Gazette
16 Aug 2009

“Awhite crystalline substance is known to be either glucose or fructose. How would you identify it?” That’s been a standard question asked on organic chemistry exams for over a hundred years. Glucose and fructose are both simple sugars with exactly…read more…


Posted in bariatric surgery, coronary artery disease, ethics, obesity, professionalism, randomized trial, surgery | Tagged: , | Leave a Comment »

Cardiac disease threatens diabetics

Posted by Colin Rose on November 26, 2008

Dr. Terrence Ruddy, chief of cardiology at the University of Ottawa Heart Institute, says the increasing number of people with diabetes is a major concern across the medical profession.

“The increasing number with diabetes is directly related to the increasing number with obesity,” he says. “We have an epidemic of obesity in young and older people. In older people, that is giving them diabetes now. In younger people, it will give them diabetes in the next 20 to 40 years.” It’s vital to reduce obesity, “not just for 40- to 50-year-olds but in 10 to 20-year-olds,” he says. “We need more money flowing into educational programs focused on lifestyle changes — increased activity, appropriate diet and weight loss in young people. Decrease obesity to decrease diabetes.”

Yet at least 500 cardiologists around the world were paid by AstraZeneca to take part in JUPITER, a clinical “trial” of Crestor in which most subjects were overweight or obese and NO attempt was made to reduce their weights. 1.5% per year became diabetic due to their inflamed excess visceral fat. Probably at least US$500 million flowed into this “trial” with NO “educational programs focused on lifestyle changes”.

Doctors pay lip service to the need to fight obesity but money talks. Those cardiologists probably received at least $1000 per subject to enroll them in the JUPITER “trial”. Why would they dare to insist upon lifestyle change first before enrolling the subject and forgo this income? Members of the “JUPITER Study Group” presumably overseeing the “trial” for AstraZeneca were probably paid $100,000 each for their “consultation”. Why would they insist on lifestyle change first before agreeing to participate?

 


Cardiac disease threatens diabetics
IRIS WINSTON CANWEST NEWS SERVICE
The Gazette
26 Nov 2008

Just one year after Dale Frayling was diagnosed with type 2 diabetes, he suffered his first heart attack. Four months later, he had a second, more severe attack followed by bypass surgery. That was 11 years ago. The Saskatoon resident, now 57, has…read more…

 

Also blogged here: 1, 2


————————————————-

Here is the list of the cardiologists paid to participate in the JUPITER study who care more about money than advising patients on the best way to prevent atherosclerosis and diabetes.

Paul M Ridker, M.D., Eleanor Danielson, M.I.A., Francisco A.H. Fonseca, M.D., Jacques Genest, M.D., Antonio M. Gotto, Jr., M.D., John J.P. Kastelein, M.D., Wolfgang Koenig, M.D., Peter Libby, M.D., Alberto J. Lorenzatti, M.D., Jean G. MacFadyen, B.A., Børge G. Nordestgaard, M.D., James Shepherd, M.D., James T. Willerson, M.D., Robert J. Glynn, Sc.D., for the JUPITER Study Group

Appendix. JUPITER Clinical Sites

Argentina 253: Altamirano J, Berrizbeitia M, Boskis P, Colombo H, Cuadrado J, Cuneo
C, Diaz M, Esper R, Fernandez A, Foye R, Hershson A, Kuschnir E, La Greca R,
Lorenzatti A, Lozada A, Luciardi H, Luquez H, Maffei L, Majul C, Marin M, Muntaner
J, Nul D, Paolasso E, Rey R, Rodenas P, Rodriguez P, Rojas C, Telsolin P, Vita N,
Belgium 487: Adrianes G, Argento O, Bacart P, Baeck L, Baguet J, Balthazar Y, Battello
G, Behets J, Beke P, Bemden S, Berwouts P, Boermans P, Bolly F, Borms J, Boulad M,
Boulanger L, Bous J, Boxstael R, Brands Y, Buyse L, Calozet Y, Camps K, Capiau L,
Celis H, Coucke F, D’Argent F, De Beeck G, De Meulemeester M, De Praeter K, De
Rouck S, Delcourt A, Delvaux J, Demanet E, Derijcke M, Deruyck C, Devaux J, Dupont
C, Duyse J, Erpicum L, Gilio C, Gillet A, Grosjean J, Heeren J, Henry G, Heyvaert F,
Hollanders G, Hutsebaut A, Janssens P, Lannoy H, Ledoux C, Legros P, Leliaert R,
Martens R, Maury O, Mehuys G, Michaux J, Migeotte A, Mortelmans J, Mulders N,
Parijs P, Peer W, Pieters E, Reynders P, Riet D, Robert P, Stee J, Teheux J, Teuwen J,
Timmermans B, Tshinkulu M, Vantroyen D, Veevaete M, Vercruysse K, Vereecken G,
Vermeersch L, Vernijns J, Verspecht E, Vinck G, Vrancken F, Watte G, Weymans J,
Windmolders S, Ziekenhuis J, Ziekenhuis P, Brazil 327: Albuquerque D, Barbosa E,
Bertolami M, Blacher C, Brasileiro A, Eliaschewitz F, Esteves J, Feitosa G, Filho H,
Filho R, Fonseca F, Forti A, Francischetti E, Franco R, Gomes M, Gross J, Jardim P,
Kohlmann O, Loures-Vale A, Magalhaes M, Maia L, Moriguchi E, Nogueira P, Oigman W,
Repetto G, Saraiva J, Xavier H, Bulgaria 197: Balanescu S, Benov H, Chompalova B,
Donova T, Gocheva N, Goudev A, Grigorov M, Gruev T, Hergeldjieva V, Marchev S,
Mihov A, Pasheva V, Penev A, Popov A, Raev D, Sirakova V, Slavcheva A, Stoikov A,
Stoilov R, Tisheva S, Todorov G, Torbova S, Uzunangelov J, Canada 2020: Achyutna G,
Akhras R, Arun N, Barriere G, Bartlett J, Behiels S, Bell A, Bergeron J, Berlingieri J,
Bhamjee H, Bodok-Nutzati R, Booth W, Boyd C, Brault S, Bruckswaiger D, Bukovy B,
Campbell G, Carlson B, Cha J, Chehayeb R, Cheng W, Chilvers M, Chouinard G,
Chow W, Conter H, Conway J, Craig D, Dattani I, Del Grande R, Dharamshi S,
Dickson M, Dion D, Dowell A, Drexler J, Dube S, Dupont A, Dworkin B, Fields L,
Filteau P, Gardiner E, Gervais B, Gillis G, Girard R, Goldman H, Gorfinkel I, Goulet S,
Greenspoon A, Gritter R, Gupta A, Gupta M, Habib R, Harding R, Hart R, Henein S,
Henry D, Hirsch A, Ho K, Hoag G, Houde D, Howlett E, Ing G, Jadd J, Janes J, Jardine F,
Johnston T, Kanani S, Kazimirski M, Kelly A, Klajner F, Kooy J, Lalani A, Lam S,
Laranjeiro J, Larose D, Leiter L, Leung W, Li J, Lowe D, Luces K, Ma P, MacKinnon R,
Martinho V, Matangi M, McCrossin M, McIsaac J, McMullen W, Mehta P, Meunier M,
Misik K, Ng A, Nigro F, Noronha L, O’Mahony W, Pandey S, Papp E, Patel V , Patrick L,
Peddle C, Pinsky N, Poirier P, Powell C, Price J, Rolfe A, Saliba N, Sawkiw R, Senior R,
Shu D, Smith R, Somani R, Soowamber M, Stakiw K, Talbot P, Taliano J, Tan K,
Teitelbaum I, Threoux P, Tremblay G, Turcotte C, Tytus R, Walsh P, Webb G,
Willoughby P, Woo V, Woodland R, Yee G, Chile 83: Blanco M, Cardenas N,
Dominguez J, Gutierrez M, Jalaf M, Olivares P, Rodriguez B, Saelezer C, Stockins B,
Colombia 345: Ardila W, Aschner P, Botero J, Botero R, Calderon C, Casas L,
Castellanos R, Chaves A, Cure C, Escobar I, Fortich A, Garcia L, Hernandez E, Isaza D,
Jaramillo N, Kattah W, Marin M, Matiz C, Quintero A, Rizcala A, Rodriguez N, Ruiz A,
Urina M, Valenzuela A, Costa Rica 270: Cob-Sanchez A, Gutreiman-Golberg M,
Lainez-Ventosilla A, Ramirez-Zamoraa L, Slon-Hitti C, Vinocour-Fornieri M, Denmark
336: Hansen H, Nordestgaard B, Steffensen R, Stender S, El Salvador 162: Abrego H,
Renderos J, Rivera-Ochoa L, Estonia 85: Eha J, Jaanson E, Kaasik U, Keba E, Maetos E,
Petersen M, Reinmets S, Roostalu U, Vahula V, Veidrik K, Germany 222: Bellmann R,
Hanefeld M, Horacek T, Klein C, Knels R, Koenig W, Laus S, Meibner G, Mondorf C,
Schell E, Schuster H, Sehnert W, Stahl H, Szelazek G, Winkelmann B, Witczak E, Israel
143: Avishay E, Gavish A, Grossman E, Haratz D, Hussein O, Keider S, Levy Y, Shapiro
I, Shveydel E, Wolfovitz E, Yogev R, Zeltser D, Mexico 741: Escarcega J, Galvez G,
Gonzalez J, Guajardo S, Gutierrez-Fajardo P, Ibara M, Leon J, Lozano F, Munoz E, Pina
J, Romero-Zazueta A, Sanchez R, Takahashi H, Villalpando C, Villegas E, Netherlands
987: Agous I, Bak A, Bartels G, Basart D, Cornel J, De Schipper L, Holwerda N, Kose
V, Koster Y, Lok D, Lokhorst B, Mosterd A, Nierop P, Oude Ophuis A, Somer S, Tiebesl
J, Trip M, Van Hessen M, Van Kempen W, Wassenaar M, Norway 204: Andresen M,
Berz A, Bjurstrom M, Bo P, Brunstad O, Daae-Johansen T, Elle S, Fauske J, Fossdal B,
Gjefsen O, Hallaraker A, Haugen J, Helberg S, Holm-Johnsen S, Istad H, Jacobsen T,
Johansen R, Jorstad T, Jorum I, Kjorlaug K, Kontny F, Langaker K, Larsen B, Lonning
S, Loraas A, Mansilla-Tinoco R, Medhus R, Meyer I, Nasrala S, Ofjord E, Ose L, Palmas
J, Risberg K, Sandberg A, Sirnes P, Skjegstad E, Skjelvan G, Solnor L, Storm-Larsen A,
Tandberg A, Tomala T, Torkelsen A, Ursin A, Valnes K, Walaas K, Panama 202: Binns
R, Delgado A, Lombana B, Noriega L, Trujillo R, Poland 804: Artemiuk E, Asankowicz-
Bargiel B, Banas I, Baranska E, Baranski M, Bijata-Bronisz R, Sikorska A, Blasszczyk B,
Bolanowski J, Brokl-Stolarczyk B, Brzecki K, Buczkowski K, Chmielewski T, Chojnowska-
Jezierska J, Chwist-Nowak A, Cygan W, Czajkowska-Kaczmarek E, Dargiewicz A,
Dluzniewski M, Dudka C, Fares I, Flasinska J, Gadzinski W, Gaszczyk G, Golebiowski G,
Gozdur W, Grudzien K, Kalamarz J, Kalinowska A, Kornacewicz-Jach Z, Korol M,
Korycka W, Kostka T, Kostrzewska A, Kot A, Kowalczyk-Kram M, Kowalska-Werbowy B,
Krupinska G, Lotocka E, Luberda-Heynar Z, Lukas W, Lysek R, Machyna-Dybala A,
Mlynarczyk-Jeremicz K, Mocarska-Gorna B, Niedbal-Yahfouf I, Pasternak D, Potakowska I,
Ramian U, Roleder M, Rosinska-Migda J, Sidorowicz-Bialynicka A, Skierkowska J,
Skorinko I, Slaboszewska J, Sleziak-Barglik K, Sobieska E, Stachlewski P, Superson-Byra E,
Tissler-Nahorska G, Turbak R, Uzunow A, Wasowicz D, Wodniecki J, Wojnowski L,
Wrzol A, Zdrojewska J, Zurakowska-Krzywonos A, Zurowska-Gebala M, Romania 32:
Ablachim T, Abobului M, Bobescu E, Bojinca M, Cristea M, Gaita D, Stoicovici R, Tataru R,
Tudose A, Russia 273: Ardashev V, Arutyunov G, Azarin O, Barbarash O, Bondarev S,
Borisov M, Boyarkin M, Burova N, Chazova I, Dovgalevsky P, Duplyakov D, Egorova L,
Goloshchekin B, Gratsianskiy N, Ivleva A, Karpov R, Karpov Y, Khokhlov A, Khokhlov R,
Khrustalev O, Konyakhin A, Kostenko V, Libov I, Lukyanov Y, Mezentseva N, Panov A,
Repin M, Shabalin A, Shalaev S, Shilkina N, Shulman V, Sidorenko B, Smolenskaya O,
Starodubtsev A, Talibov O, Titkov Y, Tsyba L, Uspenskil Y, Vishnevsky A, Yarokhno N,
South Africa 2497: Ahmed S, Ashtiker H, Bester A, Bhorat Q, Biermann E, Boyd W, Burgess L,
Dindar F, Dulabh R, Engelbrecht I, Erasmus E, Fouche L, Furman S, Govind U, Herbst
L, Jacovides A, Kahanovitz C, Kruger C, Lakha D, Lombaard J, MacLeod A, Makan H,
Manuel E, McDonald M, Mitha E, Mitha I, Moola S, Nell H, Nieuwoudt G, Olivier P,
Padayachee T, Pillai P, Pillay S, Ranjith N, Reyneke S, Routier R, Sandell P, Sebastian P,
Skriker M, Smit J, van Rensburg D, van Zyl L, Vawda Z, Wellman H, Switzerland 15:
Stahl M, United Kindom 2873: Adbulhakim E, Angus M, Balmer F, Balmer J, Barrat R,
Blair D, Blyth A, Brodie R, Brydie D, Campbell C, Campbell I, Church M, Clark C,
Clements R, Donnachie H, Fitpatrick P, Godley C, Hill J, Jarvie F, Kieran W, Langridge S,
Leslie R, Liddell A, MacKenzie J, MacKintosh C, Mair R, Marshall G, Martin R,
McCann C, McKibbin C, McLachlan B, McLean F, Murray S, Norris A, Pawa R, Pexton
N, Ramage A, Reid S, Robertson A, Rourke E, Sarmiento R, Shaw H, Shaw R, Sheil L,
Spence G, Stewart E, Thomas H, Thomson J, Thomson W, Travers J, Ward R, Williams
L, Wooff D, Young W, Uruguay 14: Belzarena C, Huarte A, Kuster F, Lluberas R,
Speranza-Sanchez M, United States 4021: Abarikwu C, Abate L, Abbott R, Ackley C,
Adams G, Adkins S, Albakri E, Albarracin C, Allison J, Alvarado O, Alwine L, Amin K,
Amin M, Anderson J, Anderson M, Anderson W, Andrawis N, Andrews C, Angles L,
Aquino N, Ariani M, Armstrong C, Aronoff S, Arora N, Atri P, Baker J, Baker K, Balli
E, Banish D, Bardenheier J, Barnett G, Bartkowiak A, Basista M, Beliveau W, Bell G,
Benchimol G, Bennett B, Bennett N, Bermudez Y, Bernstein J, Berroya A, Bhargava M,
Biaggioni I, Bimson S, Bittar N, Bleser S, Blumberg M, Bobson C, Boeren J, Bogan R,
Boling E, Booras C, Borge A, Brady J, Brandon D, Bredlau C, Brideau D, Brobyn T,
Brodowski M, Broker R, Broussard C, Brown C, Browning D, Brusco O, Bryant J,
Buchanan P, Bueso G, Burgess G, Burke B, Buynak R, Byrd L, Camilo-Vazquez E,
Campbell J, Cannon L, Capo J, Carmouche D, Castaldo R, Castilleja J, Caudill T, Caulin-
Glaser T, Champlin J, Chardon-Feliciano D, Cheng T, Cherlin R, Cheung D, Chodock A,
Christensen J, Christian D, Christiansen L, Ciemiega R, Clark J, Coble S, Cohen K,
Colan D, Cole F, Cole R, Colleran K, Collins G, Conard S, Cook J, Cooperman M,
Cooze D, Copeland T, Corder C, Courtney D, Cox W, Crump W, Cruz L, Cuellar J,
Cunningham T, Daboul N, Dailey R, Dallas A, Dansinger M, Dao L, Darwin C, Dauber
I, Davidson M, Davis P, Degarmo R, Degoma R, Dempsey M, Denny D, Denyer G,
Desai V, Despot J, Dewan M, Dickert J, Diederich C, Doben S, Dobratz D, Douglas B,
Drehobl M, Dresner J, Dreyfus J, Drummond W, Dunbar W, Dunlap J, Dunmyer S,
Eaton C, Ecker A, Edris M, Egbujiobi L, Elkind A, Ellis J, Ellison H, Engeron E, Erdy G,
Ervin W, Eshowsky S, Estock D, Fang C, Fanning J, Feinberg B, Feld L, Fenton I,
Fernandez E, Ferrera R, Fiacco P, Fierer R, Finneran M, Fintel D, Fischer M, Flippo G,
Flores A, Folkerth S, Forbes R, Fowler R, Francis P, Franco M, Frank A, Fraser N,
Fuchs R, Gabriel J, Gaddam S, Gaffney M, Gamponia M, Gandhi D, Ganzman H, Gaona
R, Gaona R Jr, Garibian G, Garofalo J,, Gatewood R, Gazda S, Geiger R, Geller M,
Germino W, Gibbs R, Gifford C, Gilhooley N, Gill S, Gillespie E, Godwin D, Goldberg
M, Goldberg R, Goldstein M, Gonzalez-Ortiz E, Goodman D, Gordon G, Gordon M,
Goswami A, Gottlieb D, Gottschlich G, Graham D, Gray J, Gray W, Green S, Greenberg
R, Greenspan M, Greenwald M, Grover D, Gupta, R, Gupta-Bala S, Guthrie R, Gutmann
J, Gvora T, Habib G, Hack T, Haidar A, Hamdy O, Hansen M, Hanshaw C, Hargrove J,
Harris H, Harris H, Harrison B, Hart T, Heacock J, Head D, Headley D, Henderson D,
Herman L, Herrera C, Hershberger V, Hershon K, Heym H, Hill G, Hippert R, Hirsch A,
Hnatiuk G, Hoekstra J, Holt W, Homan J, Honsinger R, Howard J, Howard V, Howard
W, Huling R, Imburgia M, Isajiw G, Ison R, Iverson W, Jacks R, Jackson B, Jackson K,
Jacobs J, Jacobson E, James A, Jayanty V, Johary A, Johnson G, Jones P, Jones T, Joseph
J, Julien C, Kahn Z, Kalvaria I, Kang J, Kaplan I, Karns R, Kashi K, Kaster S, Kaufman
A, Kawley F, Keller R, Kenton D, Kerlin J, Kern J, Kerwin E, Kerzner B, Ketchum J,
Khan J, Khan S, Khawar M, Khera A, Kinstrey T, Klein B, Klein E, Klein S, Klein T,
Kleinsteuber K, Klementowicz P, Knopp R, Knutson T, Koch S, Kramer M, Krause R,
Krisciunas V, Krueger C, Kruszewski D, Kumar R, Kunst E, Kuo D, Kuritsky L,
Kushner P, Kutner M, Kwiterovich P, Kwong S, Lanese J, Lang B, Lary J, Lasalle J,
Lasater S, Lasser N, Laughlin D, Lawless J, Lawlor D, Ledbetter J, Ledesma G, Lee D,
Lemanski P, Levinson G, Levinson L, Lewis D, Lewis L, Lewis S, Linden D, Loh I,
Look M, Lopez D, Loskovitz L, Lubin B, Lucas M, MacAdams M, Madden B, Magee P,
Maggiacomo F, Magier D, Magnuson S, Mahaffey R, Makowski D, Maletz L, Mally A,
Maloney R, Mancha V, Manolukas P, Marple R, Martin R, Masri A, Masri B, Mattingly
G, Mayer N, McCain A, McCall Bundy J, Mccartney M, Mcclain D, McConn M,
Mccullum K, Mcdavid R, Mcgettigan J, McIvor M, Mcneff J, Mendolla M, Mercado A,
Mersey J, Milam J, Milko T, Miller M, Miller R, Miller S, Mobley D, Modi T, Modiano
M, Mollen M, Montgomery R, Moran J, Morelli J, Morin D, Moskow H, Moursi M,
Mueller N, Mullins M, Myers E, Nadar V, Naiser J, Nash S, Natarajan S, Neft M,
Neuman D, Nevins B, Newman J, Newman R, Newman S, Nolen T, Nwasuruba C,
Oberoi M, Odom A, Ong Y, Oppy J, Owen S, Pampe E, Pangtay D, Parker R, Patel B,
Patel J, Patel M, Patel R, Paul A, Pearlstein R, Penepent P, Peniston J, Perlman M,
Persson D, Peters P, Peterson G, Peterson J, Pettyjohn F, Phillips A, Phillips D, Piel M,
Pillai T, Pi-Sunyer F, Pollack A, Pond M, Pongonis J, Porras C, Portnoy E, Potos W,
Powers J, Prasad J, Pritchett K, Pudi K, Pullman J, Purdy A, Quinones Y, Raad G,
Radbill M, Radin D, Rai K, Raikhel M, Raine C, Ramanujan R, Ramirez G, Ramos-
Santana Z, Rapo S, Ravin S, Rawtani P, Reeves R, Reeves W, Reiter W, Rendell M,
Resnick H, Reynolds W, Rhudy J, Rice L, Rictor K, Ringrose R, Riser J, Rizvi M, Rizzo
W, Robinson J, Robison W, Rogers W, Rohlf J, Rosen R, Ross, E, Roth E, Rovner S,
Rucki P, Runde M, Ryan W, Rybicki J, Saleem T, Salvato P, Santram D, Scharf B,
Schear M, Schectman G, Schmidt J, Schneider A, Schneider P, Schneider R,
Schoenfelder S, Schussheim A, Schwartz R, Schwartz S, Schwarze M, Scott C, Segal S,
Settipane R, Shah M, Shamim T, Shanes J, Shapero P, Shapiro J, Shealy N, Shepard M,
Shepherd A, Sheta M, Shrivastava R, Shusman R, Siddiqi M, Sidney A, Silvers D,
Simek C, Simpson C, Sinatra L, Singh S, Singson D, Slabic S, Smith D, Smith K, Smith
S, Smith T, Snell P, Specter J, Speer J, Spees R, Sperling M, Spuhler W, Staab P,
Stafford J, Stanton D, Stein E, Stern S, Stocks T, Stone A, Strader W, Strout C, Strzinek
R, Subich D, Suen J, Sugimoto D, Sulman S, Suresh D, Sweeney G, Szatkowski A, Szeto
J, Szewczak S, Szulawski I, Taber L, Taghizadeh B, Tague R, Tambunan D, Tannoury G,
Tavarez Valle J, Thieneman A, Thigpen D, Thompson P, Tidman R, Tilton G, Tokatlian
E, Topkis R, Torelli M, Tortorice F, Toth P, Touger M, Treat S, Trevino M, Trupin S,
Turner A, Turner M, Tweel C, Ugarte J, Ulmer E, Urbach D, Vacker M, Vallecillo J, van
de Beek M, Vargas L, Vazquez Tanus J, Verma, A, Vijayaraghavan K, Wade P, Wade T,
Wagner S, Wahle J, Walker J, Walker M, Weinstein R, Weisbrot A, Weiss R, West P,
White A, Wickemeyer W, Wieskopf B, Wiggins M, Williams H, Wilson M, Wiseman J,
Yataco A, Yates S, Zamarra J, Zamora B, Zawada E, Zemel L, Zigrang W, Zusman R,
Venezuela 209: Aguiton M, Arroyo-Parejo M, Beaujon Sierralta J, Carrizales de Marlin
Y, Colan Parraga J, Fernandez C, Fuenmayor N, Giesen G, Gonzalez Gomez C, Guaipo
A, Herrera Rivera C, Lopez de Montoreano N, Lopez Nouel R, Marturet L, Marulanda
M, Mata L, Morr I, Nass A, Palmucci G, Ponte C, Rivas I, de Roa E, Figarella Salazar G,
Sanchez F, Sirit U, Viloria A.

Posted in atherosclerosis, cardiology, cholesterol, coronary artery disease, diabetes, diabetes, Type 2, diet, drugs, junk food, obesity, professionalism, statins | Tagged: , , , , , , , , , , , , | 2 Comments »

JUPITER is a gas giant

Posted by Colin Rose on November 21, 2008

An excellent article by André Picard in today’s Globe and Mail, the only story on JUPITER I have seen in the lay press that reveals the massive fraud behind the reporting of this “study”.

JUPITER is aptly named. It’s gigantic. Probably the largest, most expensive drug trial in history. When one looks below the surface of the publication in the NEJM, the results are about as exciting as the Jovian composition. A lot of gas. I would conservatively estimate that this “study” cost at least $500 million. But if you are AstraZeneca and stand to sell $many billions worth of Crestor because of this paper that’s small change. And junk food addicts, who comprise most of the subjects of JUPITER have one more excuse, however deceptive, to continue their self-destructive habits.

Here is my opinion posted in the NEJM blog on the paper.

nyt-jupiter-unethical

A more detailed analysis of the marketing driven deception and lack of professionalism in the paper by Sandy Szwarc.

Another perspective by John McDougall similar to mine on the big lie behind the claim that many “healthy” people need Crestor..

When all of these criticisms are considered it turns out that JUPITER is nothing more than a thinly disguised  infomercial for Crestor and should never have been published in a presumably high quality journal like the NEJM. But in being able to make this paper freely available on the web (and not wait 6 months like other papers) the NEJM must have received a large payment from AstraZeneca.

Non-blinded statin trials like JUPITER, have the potential for bias in subjective outcomes like the decision to do an angioplasty or coronary bypass, outcomes that constitute the vast majority of the combined endpoint. Also, it is quite likely that when the JUPITER subjects knew that their blood LDL was low because they were taking Crestor they had less incentive to change self-destructive lifestyles. That is probably why the group treated with Crestor had significantly more diabetes. In light of the JUPITER trial the Therapeutics Initiatives group at the University of British Columbia has updated their recommendations for use of statins in primary prevention, which would include people like those entered into the JUPITER trial, and concluded that “statins do not have a proven net health benefit in primary prevention populations and thus when used in that setting do not represent good use of scarce health care resources.

See a slide show on JUPITER and “dyslipidemia”.

—————————–

Lead “investigators” of JUPITER

Paul M Ridker, M.D., Eleanor Danielson, M.I.A., Francisco A.H. Fonseca, M.D., Jacques Genest, M.D., Antonio M. Gotto, Jr., M.D., John J.P. Kastelein, M.D., Wolfgang Koenig, M.D., Peter Libby, M.D., Alberto J. Lorenzatti, M.D., Jean G. MacFadyen, B.A., Børge G. Nordestgaard, M.D., James Shepherd, M.D., James T. Willerson, M.D., Robert J. Glynn, Sc.D., for the JUPITER Study Group

——————–

Dominican Republic

What typical JUPITER subjects would look like. These are "apparently healthy" people? Is it not unethical to prescribe drugs to these people to "treat" the symptoms of their self-destructive lifestyles?

Nowhere in the JUPITER paper will you see it mentioned that CRP can be markedly reduced with cost-free lifestyle change alone, no statins, as shown in this paper in the Journal of Applied Physiology in 2006, results of which are summarized below. The subjects in the JAP paper were just the same as in the JUPITER study, obese people, many with metabolic syndrome but the authors did not call them “apparently healthy”. They had nothing to sell.

jap-diet-crp

——————————————-

When it comes to statins, don’t believe the hype

November 20, 2008
The Globe and Mail
André Picard”Cholesterol drug causes risk of heart attack to plummet” – Fox News.

“Cholesterol-fighting drugs show wider benefit” – The New York Times.

“Cholesterol drug cuts heart risk in healthy patients” – The Wall Street Journal.

The New York Times article summarized the exciting news in a front-page story saying that “millions more people could benefit from taking the cholesterol-lowering drugs known as statins.”

That’s big medical/business news, because statins are already the bestselling drugs in the world, with sales in excess of $20-billion (U.S.).

Quoting some of the world’s top heart researchers, media reports touted the importance of a blood test for C-reactive protein. That’s because those benefiting from statins had high levels of CRP (a marker for inflammation) rather than high levels of LDL cholesterol, which is usually the criterion for statin prescription.

The news stories were based on research published last week in the prestigious New England Journal of Medicine and presented, with much fanfare, at the annual convention of the American Heart Association.

Like much reporting on medical research (and drug research in particular), however, there is more (or, more accurately, less) to these stories than meets the eye.

The principal finding in this study was that participants who took a statin pill recorded a 50-per-cent reduction in the risk of heart attack, stroke, surgery and death compared with those who took a placebo (a sugar pill).

Who wouldn’t be wowed by those numbers? Who wouldn’t want that miracle drug?

But the benefits are relative risk reductions.

When you look at the raw data in the study, they reveal that 0.9 per cent of statin users had cardiovascular problems. By comparison, 1.8 per cent of those taking a placebo had heart problems.

There were 17,802 participants in the study, yet there were only 83 cardiac events among statin users, compared with 157 in the placebo group. That’s 50 per cent fewer.

Are those really “dramatic” findings? Do statins really make heart attack risk “plummet”?

According to a cautionary editorial in the New England Journal of Medicine (which received virtually no mention in news reports), 120 people in this study needed to be treated with a statin for two years to see a benefit in one person.

That’s a lot of people taking a pricey drug ($3 Canadian a day) for no benefit – not to mention that there are risks.

While researchers (and journalists who report on studies) love to highlight benefits of drugs, they too often gloss over risks.

Like all drugs, statins have side effects. The drug used in the study, rosuvastatin (brand name Crestor), has been associated with muscle deterioration and kidney problems.

In the study, those taking statins had a higher risk of developing Type 2 diabetes – 3 per cent compared with 2.4 per cent of those taking a placebo. That’s a 25 per cent higher relative risk among people with very little heart disease to begin with.

As noted earlier, researchers (and news stories) suggested that, based on the findings, the number of patients taking statins could and should expand dramatically.

But is that really what the research tells us, even in its most optimistic interpretation?

The study involved exclusively men older than 50 and women older than 60 who did not have high cholesterol or histories of heart disease or inflammatory illness. All the people in the study needed to have low cholesterol and high CRP.

Initially, researchers recruited 90,000 people in those age groups, but more than 80 per cent of them were deemed ineligible. This is a very select population.

To say, by extrapolation, that these “dramatic” (read: modest) benefits apply to the general population is erroneous.

Similarly, while it is true that about half of all heart attacks and strokes occur in people whose cholesterol is not considered high, does that mean everyone should get a blood test to measure levels of C-reactive protein? Hardly.

Yes, there is more heart disease among people with high levels of CRP, but the jury is still out on what this means.

Some scientists believe that because CRP – secreted in response to inflammation – is present in plaque, it increases the risk that the plaque will burst, leading to blood clots that cause heart attacks. But other researchers think that CRP levels are, at best, a telltale sign of heart disease, a bit like grey hairs are a sign of aging – not its cause.

The CRP test is expensive at almost $50. And it’s worth noting that one of the principal authors of the new research holds the patent on the test and makes money every time it is used.

When you cut through all the hype and the self-interest, what we know is this: Statins reduce levels of [LDL] cholesterol. This is beneficial to people who have had a heart attack or other serious heart problems.

But for otherwise healthy people, high CRP levels or not, the potential benefits of taking statins are marginal, and the risks are not insignificant.

Hardly the stuff of dramatic newspaper headlines.

Posted in atherosclerosis, cardiology, cholesterol, coronary artery disease, death, diabetes, diabetes, Type 2, drugs, junk food, obesity, professionalism, statins, waist circumference | Tagged: , , , , , , , , , , , , , , , , , , | 2 Comments »

CRP is only a marker and does not cause disease

Posted by Colin Rose on October 29, 2008

Dr. Paul Ridker, the inventor of a method for sensitively measuring C-reactive protein, has made a career and much money flogging the notion that C-Reactive protein, produced in the liver in response to various physiological stresses like inflammation and abdominal obesity, is the cause of atherosclerosis and must be treated. Ridker’s web site promotes the wonderful benefits of measuring hsCRP and “treating” it with drugs, most notably statins. He has been successful in convincing most cardiologists and family doctors that hsCRP is and essential measurement in assessing “risk”. However, there was never any proof that doing so would prolong life or prevent any disease.

But a clever non-American group in Copenhagen, remembering the basic rule that correlation is not causation, refused to be intimidated by Ridker’s arrogant, industry-funded propaganda and showed that people with genetic abnormalities that raise blood hsCRP without inflammation do not have more atherosclerosis. Like blood cholesterol, CRP is just another marker of an atherogenic lifestyle and excess visceral fat. Both of these responses to nutritional stress may actually be protective.

As a corollary we can also conclude that “treating” blood hsCRP with statins is futile.

In case Ridker’s web site is taken down in embarrassment, here is what Ridker’s site looks like so that posterity can see an example of the destruction of another profitable medical myth.

Posted in atherosclerosis, cholesterol, coronary artery disease, diet, professionalism, statins | Tagged: , , , , | Leave a Comment »

Prudent diet staves off heart woes (The Gazette, 21 Oct 2008, Page A4)

Posted by Colin Rose on October 21, 2008

Not a surprising finding, Dr. Yusuf. Fifteen years ago Dean Ornish proved that atherosclerosis, the underlying cause of heart attacks, could be reversed with a version of the prudent diet.  So why isn`t everyone doing this? Maybe because the cholesterol myth promoted by drug dealers and doctors on their payrolls convinced the population that all they had to do was take a pill to lower blood cholesterol and they could eat anything. Curiously, there is no mention of cholesterol in the story. Close reading of the paper published in Circulation reveals that there was no correlation between the diet and blood cholesterol, “bad” of “good”. Diet has a powerful effect on atherosclerosis independent of blood cholesterol. Probably something about the prudent diet reduces modification of LDL, so called “bad” cholesterol, in the arterial wall. Another body blow to the cholesterol myth which is slowly dying. Even Pfizer which has spend many $billions promoting the myth has given up on it.


SHARON KIRKEY CANWEST NEWS SERVICE
The Gazette
21 Oct 2008

Hold the fries, samosas or fried won tons: People who eat diets high in fried foods and meat are 35 per cent more likely than ?prudent? eaters to suffer acute heart attacks, a global study led by Canadian researchers shows. And in a surprising…read more…

Posted in atherosclerosis, cardiology, cholesterol, coronary artery disease, diet | Tagged: , , , , , | Leave a Comment »

Out of their league?

Posted by Colin Rose on October 16, 2008

A Russian hockey league is blamed for 19 year old Alexei Cherepanov’s death from atherosclerosis, proven by autopsy. Since when has hockey playing been a risk factor for atherosclerosis? There are two causes: tobacco and an atherogenic diet. I assume he didn’t smoke.

The league is blamed for not detecting it sooner. How would they have detected it? How do you predict atherosclerotic plaque rupture? If there is no plaque there is nothing to rupture. Plaque can be prevented and regressed by lifestyle alone. Did the coach ask him about his lifestyle, what he ate?


Out of their league?
BY MATTHEW COUTTS National Post, with files from news services
National Post
16 Oct 2008

The shift just before 19-year-old elite hockey prospect Alexei Cherepanov collapsed and died during a game in Russia’s Continental Hockey League exemplified exactly what the league’s founders had in mind when they created an entity to rival North…read more…

Posted in atherosclerosis, coronary artery disease, diet | Tagged: , , , , , | Leave a Comment »

Heart Attack at Age 19

Posted by Colin Rose on October 15, 2008

Cherepanov is not the first young Russian athlete to die of atherosclerosis. Remember Sergei Grinkov? The Russian diet is highly atherogenic and Russia has one of the highest rates of death from coronary artery disease.

————————————————-

In 1994 Gordeeva & Grinkov returned to Olympic competition and captured their second gold medal at the 1994 Winter Olympics in Lillehammer, Oppland, Norway. After these Olympics, they returned once again to professional skating and took up residence in Simsbury, Connecticut. During the 1994-95 season, they toured, yet again, with Stars on Ice, this time as headliners. However, tragedy struck in November 1995, when Sergei Grinkov collapsed and died from a massive heart attack in Lake Placid, New York, while he and Ekaterina were practicing for their upcoming performance in the 1995-1996 Stars on Ice tour. Doctors found that Sergei had severely clogged coronary arteries (to the point where his arterial opening was reportedly the size of a pinhole), which caused the heart attack.

“In spite of the autopsy findings, he never sought medical attention for a cardiac problem,” said Pascal Goldschmidt associate professor of cardiology at Johns Hopkins. “His risk for premature coronary artery disease was very low; he was not a smoker, did not use drugs or medications, did not have high blood pressure or diabetes, had normal cholesterol and lipid levels and he trained several hours a day.”


NO AMBULANCE
BY MASON LEVINSON Bloomberg News, with files from Gennady Fyodorov and Natalia Sokhareva, Reuters
National Post
15 Oct 2008

Russian officials opened a probe into the death of New York Rangers? first-round pick Alexei Cherepanov, who collapsed on the bench during a Continental Hockey League game in Russia on Monday. Moscow regional investigator Yulia Zhukova said officials…read more…

Posted in atherosclerosis, cardiology, cholesterol, coronary artery disease, diet | Tagged: , , , , | Leave a Comment »

Pfizer abandons “cholesterol”

Posted by Colin Rose on October 1, 2008

After spending tens of $billions in DTC ads and bribes to doctors to terrorize the world into believing that blood “bad cholesterol” is the cause of atherosclerosis, the most common fatal disease, and selling hundreds of $billions worth of Lipitor to lower it, Pfizer has admitted there is no truth to and no more profit to be made from the myth of “dyslipidemia” that Pfizer and other peddlers of statin drugs created. Its much hyped drug, torceptripib, touted as the next Lipitor, which did all the “right” things to blood cholesterol actually worsened atherosclerosis in the ILLUSTRATE trial. Finally, the proof was in that high blood “bad cholesterol” is only a symptom of an atherogenic lifestyle, not the cause of atherosclerosis. But it will take a generation or two for the cholesterol myth to disappear.

So now Pfizer is directing more of its research toward Type 2 diabetes, a disease directly related to obesity, which is directly related to the moral hazard effect created by the cholesterol myth (I can eat anything as long as my cholesterol is low). Very clever marketing! Create diseases, real or imagined, then sell high profit drugs to to “treat” numbers associated with them.


PFIZER REFOCUSES ITS STRATEGY
BY SHANNON PETTYPIECE Bloomberg News
National Post
01 Oct 2008

Pfizer Inc. will abandon early-stage research on heart drugs as part of a strategy to sharpen its focus on ailments such as cancer, Alzheimer’s disease and diabetes where the chances of a bigger profit are greatest. The New York-based company, the…read more…

Posted in atherosclerosis, cholesterol, coronary artery disease, diabetes, Type 2, drugs, obesity, statins | Tagged: , , , , , | Leave a Comment »

Obesity weighs heavy on heart

Posted by Colin Rose on September 22, 2008

Bottom line: obese people have heart attacks at least ten years sooner and have much more diabetes than thin people, regardless of their blood cholesterol. So all those who say fat is OK as long as you are happy are wrong. And all those drug dealers say you are OK as long as you take a statin to lower your “bad” cholesterol are selling you a very expensive mirage.


Obesity weighs heavy on heart: study
SHARON KIRKEY CANWEST NEWS SERVICE
The Gazette
22 Sep 2008

Heart attacks are hitting the overweight more than a decade sooner than ?normal? weight people, researchers are reporting. A study of more than 111,000 people is one of the first to put real numbers to the risk of obesity and suggests ?excess…read more…

Posted in atherosclerosis, cholesterol, coronary artery disease, diet, obesity, waist circumference | Tagged: , , , , | Leave a Comment »