Carotid artery intima-media thickness (CIMT) measured by ultrasound has been shown to be correlated with the presence of cardiovascular disease and is now accepted and used as a surrogate marker for atherosclerotic disease. I like to use it in my practice because I can do follow measurements to see if treatment is working to reverse plaque. I also like it because I can identify subclinical atherosclerosis before it becomes a problem. Remember that it starts in the late teens. In the Cardiovascular Health Study, increases in the CIMT of the carotid artery were associated with an increased risk of heart attack and stroke in older adults without a history of cardiovascular disease. Common carotid IMT greater than 0.87 mm and Internal Carotid IMT greater than 0.90 mm were associated with a progressively increased risk of cardiovascular events. For each 0.20 mm increase in CCA IMT, the risk increased by almost 30%. IMTs above 1.18 mm were associated with more than a 2-fold increase in the risk of a cardiovascular event over 6 years.

Also, several studies evaluated the effect of statins on the progression of atherosclerosis using imaging of CIMT as an outcome measure. In these studies carotid IMT was used a surrogate marker for coronary atherosclerosis. The LIPID trial randomized 522 subjects to receive pravastatin 40 mg/day or placebo in addition to a low-fat diet. Total cholesterol, triglycerides, HDL, and LDL cholesterol were measured at randomization repeatedly during follow-up. Ultrasound scans of the common carotid artery were performed before randomization, and after 2 and 4 years using B-mode ultrasonography. The study showed a regression of the common carotid artery IMT following pravastatin therapy.

According to recent evidence from the ARBITER 6-HALTS trial, treatment with extended-release niacin, in combination with statin therapy, significantly increases HDL-cholesterol levels and causes a small, but significant, reduction in carotid intima-media thickness. Niacin alone also reduces CIMT.

Ten patients were supplemented with pomegranate for 1 year and five of them continued for up to 3 years. Blood samples were collected before treatment and during PJ consumption. In the control group that did not consume pomegranate, CIMT increased by 9% during 1 year, whereas, pomegranate  consumption resulted in a significant IMT reduction, by up to 30%, after 1 year.

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50 y/o F with hx of DVT X 3 without PE who requests workup for cause of thrombosis and help getting off Coumadin. She has adverse reactions to Coumadin including fatigue, brain fog, and muscle pain. Extensive hemotology workup for thrombosis done at my office only demonstrated elevated Lip (a). Lip (a) was never done by previous doctors despite a hx of three DVTs, Pt is on Coumadin until recently. 

1. 146 (H) 12/11 (Start red yeast rice, niacin, CoQ10 nattokinase)
2. 179 (H) 1/12 (Carnitine started 1,500 mg tablet, Prorite started 4/day)
3. 183 (H) 3/12 (Carnitine form changed to Acetyl L-Carnitine and increased to 3,000 mg liquid, Prorite stopped)
4. 120 (H) 4/25 (result of higher dose Acetyl L-Carnitine)

Despite three months of Carnitine at 1,500 mg her Lip (a) went up! “That’s not supposed to happen", I said,…."there are good human studies on this treatment”. Lipids were stable the whole time. As a last ditch effort I switched her to Acetyl L-Carnitine which is more bioavailable and increased the dose. It worked, and I’ll check her Lip (a) again later this month. Stay posted.

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New data posted last month in The Annals of Pharmacotherapy have emerged shedding more light on and easing concerns about statins and cognitive decline/impairment. Several reports have documented cognitive impairment associated with the use of statins. One randomized controlled trial demonstrated that simvastatin impaired some measures of cognition compared to placebo. Most studies have not shown this, however. In fact, in many trials statins were found to have a neutral or modestly beneficial effect on cognitive performance; thus, the bulk of the evidence suggests that statins do not have a clinically meaningful effect on cognition, at least for most people.

Potential mechanisms for cognitive impairment include:

·         The brain contains high concentrations of cholesterol; unlike other areas of the body, cholesterol in the brain is produced locally. Some cholesterol drugs pass through the blood brain barrier.

·         Cholesterol is a key component of myelin, which is integral in regulating myelin membrane permeability and fluidity. Treatment with statins may reduce cholesterol synthesis in the brain and interfere with myelin formation and function.

·         Animal models have demonstrated that following chemical demyelination, treatment with simvastatin may impair the remyelination process. Impaired myelination may lead to damage to the nerves and subsequent cognitive impairment.

·         Another potential toxic mechanism relates to the impact of statins on oxidative stress and mitochondrial function through the well-known depletion of CoQ10. CoQ10is an essential component for proper mitochondrial function and cellular adenosine triphosphate production and also exhibits antioxidant properties. Statins reduce CoQ10levels, which may lead to impaired mitochondrial functioning and increased oxidative stress.

We must remind ourselves that the cardiovascular benefits of statins have been well established and provide clear reduction in cardiovascular events. Conversely, the cognitive benefits of statins are far less well established, but data from animal models and limited human data suggest these drugs may even possess cognitive benefits. This is probably because atherosclerosis can affect the arteries in the brain too, thus restricting blood flow and oxygenation.

There is insufficient evidence to confidently conclude that statins can cause or contribute to cognitive impairment. The current evidence demonstrating an association between statins and cognitive impairment is flawed in several ways including: failure to establish a cause-effect relationship, inability to account for all confounders, lack of controls and inconsistent assessments of cognition. When balanced with the established vascular benefits of statins and the evidence demonstrating either neutral or possibly beneficial effects on cognition, the risk of cognitive impairment is low and the benefits outweigh the risks.

Actions steps to ensure that there is no cognitive impairment include:

·         Taking CoQ10 100-300 mg/day

·         Exercise regularly 6-7 days a week

·         Switch to a less fat soluble statin such as pravastatin and rosuvastatin

·         Use niacin with statin so that a lower dose in needed

·         Use a low cholesterol, low saturated fat diet so that a lower dose is needed

·         Other supplements that lower bad cholesterol include green tea, sterols, tocotrienols, berberine, bergomont, myoinostitol and fiber.

Source: Is Statin-associated Cognitive Impairment Clinically Relevant? A Narrative Review and Clinical Recommendations Carlos H Rojas-Fernandez PharmD; Jean-Christy F Cameron BSc(Pharm)

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Cardiologists, dentists, and infectious disease specialists reviewed more than 500 studies addressing the connection between the two diseases. The results were published Wednesday in a statement by the AHA.

The connection was made years ago when studies showed that people with gum disease tended to have more heart attacks and strokes than people with better dental hygiene. It was postulated that the bacteria causing the infection in the gums got into the blood stream and traveled to the fatty plaques in blood vessels where they attached and increased vascular inflammation. Vascular inflammation can lead to plaque accumulation which then increases risk of a heart attack or stroke.

People who do not pay much attention to their oral health are not likely to be the healthiest folks and I do feel that there is a higher incidence of poor oral hygiene in the high risk population but this study important t because it found NO DECREASE IN CADIOVASCULAR EVENTS WHEN PERIODONTAL DISEASE WAS TREATED.

So, see your dentist to save your teeth just don’t expect a miracle if you have a lot of plaque in your arteries.

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Testosterone protects against heart attacks and may even help reverse atherosclerosis in men.  Low testosterone is associated with and contributes to metabolic syndrome, atherosclerosis, heart attack and stroke. Metabolic syndrome and diabetes are bad things to have if you're trying to avoid a heart attack. If “your gut is larger than your butt” you probably have metabolic syndrome.

The benefits of healthy levels of testosterone in men include improved ejection fraction (a measure of the heart's ability to pump blood to the rest of the body), increased muscle mass, decreased fat mass, improved sex drive, improved mood and improved bone density. High naturally occurring levels of testosterone in men are associated with low mortality from all causes, cardiovascular disease, and cancer.

Low testosterone is strongly associated with atherosclerosis but exactly how testosterone replacement therapy can slow down or reverse atherosclerosis is not completely understood yet. Lower levels of testosterone are associated with increased CIMT particularly in men with type II diabetes . Remember that CIMT is a measure of carotid artery wall thickness and is a imaging toll that can detect the earliest stages of atherosclerosis.

Just how may correcting low testosterone play a role in reversing heart disease? 

1) Testosterone may be beneficial as a treatment for CAD because testosterone can improve conditions at contribute to heart disease such as diabetes, obesity, hypercholesterolemia and hypertriglyceridemia. 

2) Testosterone has been shown to dilate the arteries, improve circulation, and lower blood pressure in most studies.  Because some people get an increase in blood pressure on testosterone therapy it is very important to monitor blood pressure.

3) Testosterone receptors have been found within human arteries, including aortic, coronary, pulmonary, and carotid arteries, providing evidence that it can affect the arterial wall.

4) Testosterone can lower LDL, triglycerides and lip (a)

5) Testosterone activates nitric oxide synthase and thus increases nitric oxide dependent vasodilatation.

6) Testosterone gets converted into estrogen via the aromatase enzyme and normal levels of estrogen may have a beneficial impact on the arterial wall in men.

Prostate cancer and testosterone: Concern about the risk of prostate cancer is still the primary reason many practitioners get nervous about prescribing testosterone. Though existing prostate cancer is clearly a contraindication for testosterone therapy recent studies indicate no increased risk of prostate cancer with higher levels of testosterone. The problem with taking testosterone when you have prostate cancer may be due to the fact that testosterone converts to estrogen and estrogen is known to stimulate cancer growth. Testosterone replacement therapy may also stimulate your body's production of growth hormone.  According to Dr. Mark A. Rubin, professor of pathology and laboratory medicine and vice chair for experimental pathology at Weill Cornell Medical College estrogen is a key player in about half of all prostate cancers, especially aggressive types.

A leading Urologist at Harvard Medical School, Dr. Abraham Morgentaler, also published a paper debunking the myth that testosterone causes prostate cancer. He has even found that low levels of testosterone can be a risk factor for getting prostate cancer.

If either free or total testosterone is low I believe there is much more benefit to than risk when it comes to taking testosterone.  Testosterone is helpful in women for improving sex drive, for treating severe osteoporosis and for increasing muscle mass.  Testosterone should be kept in physiologic range. I recommend dosing testosterone to achieve levels in the upper third of the reference range for age.  If a weekly shot is used such as testosterone cypionate I like to check levels at 7 days which is the half -life. Typically 400-600 indicates adequate dosage. Other labs that should be monitored include DHT, estradiol, CBC, PSA and lipids.

Negative cardiovascular side effects may occur however and include decreased HDL, increased blood pressure (increased fluid volume), and polycythemia.

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New results from studies following more than 120,000 health care professionals link red meat consumption to higher mortality, cardiovascular disease, and cancer. An Pan and colleagues report findings from up to 22 years of observation among 37,698 men enrolled in the Health Professionals Follow-up Study and up to 28 years of observation among 83,644 women enrolled in the Nurses’ Health Study.

Here are the hazard ratios for a 1-serving-per-day increase in unprocessed and processed red meat, respectively:

·         Total mortality: 1.13 (CI 1.07-1.20) and 1.20 (CI 1.15-1.24)

·         CVD mortality: 1.18 (CI 1.13-1.23) and 1.21 (CI 1.13-1.31)

·         Cancer mortality: 1.10 (CI 1.06-1.14) and 1.16 (CI 1.09-1.23)

Not: any number greater than 1 means there is more risk of death. 

The authors calculated that replacing one serving per day of red meat with other foods like fish, poultry, nuts, legumes, low-fat dairy, and whole grains would result in a 7% to 19% reduction in mortality over the follow-up period.

Reference: Red Meat Consumption and Mortality Results From 2 Prospective Cohort Studies,  Arch Intern Med. 

 Dose-response relationship between red meat intake and risk of all-cause mortality in the Health Professionals Follow-up Study (A) and the Nurses' Health Study (B). The results were adjusted for age (continuous); body mass index (calculated as weight in kilograms divided by height in meters squared) category (<23.0, 23.0-24.9, 25.0-29.9, 30.0-34.9, or 35); alcohol consumption (0, 0.1-4.9, 5.0-29.9, 30.0 g/d in men; 0, 0.1-4.9, 5.0-14.9, or 15.0 g/d in women); physical activity level (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, or 27.0 hours of metabolic equivalent tasks per week); smoking status (never, past, or current [1-14, 15-24, or 25 cigarettes per day]); race (white or nonwhite); menopausal status and hormone use in women (premenopausal, postmenopausal never users, postmenopausal past users, or postmenopausal current users); family history of diabetes mellitus, myocardial infarction, or cancer; history of diabetes mellitus, hypertension, or hypercholesterolemia; and intakes of total energy, whole grains, fruits, and vegetables, all in quintiles. Broken lines represent 95% CI.

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Part of my job as a specialist in preventive cardiology is to stay abreast of all the latest developments and share them with patients. Key developments in preventive cardiology in recent years have been:

- The stratification of risk using blood markers such as high sensitivity C reactive protein, fibrinogen, homocysteine, Lipoprotein (a), Apo b, plasminogen activator inhibitor 1 and so forth

- Measuring lipoprotein particle size, number and density (NMR, VAP)

- Using electron beam computed tomography to measure plaque. This is also known as the “heart scan.”

A new test has emerged over the last few years that may rival all other medical tests for heart disease risk. This new test measures the thickness of the blood, technically called blood viscosity.[1] This new test gives two numbers, one for blood moving very slowly (called low shear viscosity) and the other for blood that is moving fast (called high shear viscosity). Whole blood is a fluid that behaves in a non-linear fashion similar to catsup or motor oil. It is thicker at rest and thinner when it is moving- much like catsup leaving the mouth of a bottle.

I have written previously on the role of blood viscosity in exercise performance and how blood viscosity may be related to heart disease in athletes. Accumulating evidence suggests that increased blood viscosity is an independent risk factor for atherosclerotic heart disease and its complications. [2] In this article I will discuss the entire topic as it relates to the work the heart must do and how elevated blood viscosity may be the real cause of atherosclerosis.

Atherosclerosis is an inflammatory response the body mounts to injurious insults at the artery wall. Think of it like a callus you might get on your skin in response to friction. A callus of this type is not detrimental, in fact it improves function. However, the body adapts to stress in various ways, not all of them are beneficial in the long term. Forming a callus in your artery is a good example of an adaptation that may protect the artery in the short term but decrease functionality in the long term.

After an artery wall becomes injured, it forms a scar and the scar can grow forming more extensive plaque over time. Plaque grows in size and shape over time depending on genetic, environmental and biochemical factors. Plaque can do two bad things. It can occlude (block) the artery and cause limitations to blood flow or it can rupture and cause a heart attack. The main cause of heart attacks is a plaque rupture. Gradually occluding coronary arteries limit blood flow to the heart and often the patient will have symptoms such as chest pain or shortness of breath, but not always.

Heart disease is a term the media likes to use to describe coronary artery disease (CAD)[3] but this is a general term that includes many disorders. To discuss all these is beyond the scope of this paper and includes prolapsed (leaky) valves, irregular heart beat, and heart failure.  The topic I am concerned with is preventing heart attacks, the main cause of death for Americans. To do this we must reverse or stabilize plaque.

Now that we know that plaque is the problem lets discuss how and why plaque forms.

Arteries have three layers starting from the inside out with the intima, then the media and finally the adventitia (Fig 1). The intima is composed of a single layer of endothelial cells. Endothelial cells are similar to skin cells. The intima is the one most involved in atherosclerosis, specifically a dysfunctional intima. Endothelial dysfunction is the term that describes an intima that is not functioning well. Endothielial dysfunction has been described as the cause of atherosclerosis.

When the intima is injured platelets adhere the injured area and release growth factors that lead to the growth of endothelial cells. These cells try to cover up the injured area. As a result, muscle cells move to the intima and the intima becomes thicker. This process is an adaptive response to injury that improves function in the short at the expense of long term function. In the end stage of atherosclerosis the plaque is so large that the center outgrows the blood supply and it becomes more susceptible to rupture.

Additionally, there are three basic types of plaque, soft, and hard plaque. These are also referred to as vulnerable and stable plaque, respectively. Mixed plaque is a combination of the two.  Researchers are still trying to determine the exact characteristics that make a plaque unstable. Plaque generally starts with a thin fibrous cap and progresses as more calcium is deposited and a stronger cap is formed. Two features of plaque that make it more vulnerable are spotty calcium deposits and a lipid (fatty) core. Estimating one’s degree of vulnerable plaque subject to rupture is an inexact science. How much calcification occurs in an individual is variable and depends on certain factors. Vitamin K and D imbalances, coumadin therapy and existing kidney disease are a few factors that increase calcification.

Endothelial dysfunction

The endothelium controls constriction and expansion of the artery (think blood pressure), coagulation (clotting), and inflammatory responses. The endothelium is the layer of cells right next to where the blood flows.  When healthy, the endothelial layer keeps plaque from forming, maintains good blood flow, and controls blood pressure. Endothelial dysfunction leads to hypertension and plaque. Many researchers think that endothelial dysfunction is the final common pathway in heart disease. Through proper treatment, endothelial function can be restored.

Endothelial dysfunction precedes plaque formation in the artery wall and often gets worse as the plaque becomes more extensive. An improvement in endothelial function is associated with a decreased risk of future cardiovascular events.

But what causes endothelial dysfunction? Causes include smoking, diabetes, high blood pressure, LDL cholesterol, homocysteine, oxidative stress and shear stress. Interesting, all these factors also cause elevated blood viscosity. Elevated blood viscosity is the reason why plaque is often site specific.

In exploring how and where plaque forms we can see why cholesterol alone can not be the main cause of atherosclerosis and here why:

1.    Premenopausal women have less risk of heart disease than men because they have lower blood viscosity. Estrogen may play a role but the monthly menstrual cycle is more important. Menstruation causes a monthly loss of blood which keeps viscosity down and also lowers iron levels. Iron is a potent but necessary free radical promoting metallic ion but the reason women have less atherosclerosis is not due to lower iron alone. Studies have been done comparing heart attack incidence in groups of men who do and do not donate blood that support my argument.

2.    When veins are used in bypass surgery they form plaque and “arterialize” because they are subject to more shear stress and mechanical stress. The shear stress is a function of velocity and viscosity. Mechanical stress is determined by how forcefully the heart beats and how high the peak systolic and pulse pressures are.

3.    Veins do not form plaque because the blood pressure, pulse pressure, and shear stress are low. If cholesterol alone were the main determinant of atherosclerosis we would see in veins.

4.    Arteries subject to the highest mechanical stress and shear stress have the most plaque.

5.    Healthy adults with normal blood pressure and normal cholesterol can have sudden heart attacks. How can this be? It’s Because of blood viscosity.

6.    Heart attacks occur more frequently in the morning because blood viscosity and clot formation is at its highest.

Why lowering your blood viscosity through therapeutic phlebotomy is a very good idea:

1.    Therapeutic phlebotomy is the medical term for removing blood. In practical terms you just donate blood. Sometimes your blood may not be eligible for donation and in that case we will do it for you. The blood is then discarded and picked up by a medical waste company. Your body makes new red blood cells to replace of the ones lost. Think of this as “blood rejuvenation.” Old cells are stiff and don’t deform well when they need to get through a vessel that is narrower then the width of the cell. New cells deform much better and are able to deliver oxygen to tissues more efficiently. The net effect is improved cardiovascular efficiency because the work of the heart is reduced and oxygen delivery improves.

2.    Donating blood decreased the number of old rigid cells. Because old rigid cells can not deform well, they cause frictional damage to the artery wall at high velocities. The callus of atherosclerosis is an adaptive response to this frictional damage.

3.    Lowering you blood viscosity reduces the wear and tear on your arteries. Also known as shear stress, this slow continuous damage accelerates atherosclerosis.

4.    Lowering your blood viscosity through donating blood makes your heart more efficient. Decreasing your blood viscosity lowers peripheral resistance to flow and lowers the “contractility” of the heart’s left ventricle. This, in turn, lowers the pulse pressure and peak systolic pressure. Less pressure = less damage to the artery wall and less work for the heart.

5.    In the human body, blood viscosity dictates how hard the heart must work to pump blood. Any increase in the work of the heart absorbed by the arterial system either by stretching or by friction on the inner artery wall (the endothelium).

What are some other factors that affect blood viscosity?

Red blood cell volume also known as hematocrit is the largest determinant of blood viscosity.  The following affect blood viscosity:

1.    HDL: Low HDL increases blood viscosity high HDL decreases it

2.    LDL cholesterol: LDL is inversely related to blood viscosity.

3.    Triglycerides: Triglycerides are a type of fat in the blood that can raise viscosity.

4.    Smoking

5.    Diabetes and elevated blood sugar

6.    Exercise: Exercise reduces blood viscosity, a sedentary lifestyle increases it.

7.    Obesity increases blood viscosity

8.    Sex: Premenopausal women have lower blood viscosity than men of the same age

9.    Elevated plasma proteins (IgA, IgG, IgM). This can be seen with a special blood test.

10.                       Fibrinogen: Fibrinogen forms fibrin a component of blood clots. Fibrinogen increases blood viscosity and increases risk of heart attack.

11.                       Loss of red blood cell deformability as seen in sickle cell anemia and diabetes. Red blood cell size is about 7.5 um while the inside diameter is most capillary vessels is 4 to 9 um. Thus, red blood cells must alter their shape or deform to get through these tiny vessels. Fish oil help improve red blood cell deformability.

What evidence is there that lowering whole blood viscosity (WBV) helps prevent heart attacks and stroke?

1.    Koenig et al. conducted a study on the relationship between blood viscosity and heart attacks in 1998. He examined 933 males between the ages of 45 and 64 years of age. The researchers reported that subjects with viscosity in the highest quintile were three times more likely to have fatal and non fatal cardiac events compared with those subjects in the lowest quintile (A quintile is one fifth or 20% of a given amount).

2.    Junker et al. compared the degree of vessel occlusion in 1142 male patients who had survived a heart attack in 1998. Patients were divided into two groups without any, and with one to three stenosed vessels. They found a positive relationship between plasma viscosity and the severity of coronary heart disease, even after adjusting groups for age, fibrinogen, and use of diuretics. Differences between the groups were significant.

3.    Yarnell et a. compared plasma viscosity, fibrinogen, and white blood cell counts in 4,860 middle aged men. The chances of dying or having a heart attack for men with viscosity measurements in the highest quintile (20%) were almost five times than for the men in the lowest tertile (20%).

4.    Ranier et al. measured blood viscosity in 17 patients with chest pain (angina). Compared to patients without chest pain the patients with chest pain all had elevated blood viscosity, hematocrit and red blood cell aggregation.

5.    Resch et al. looked at the association of blood viscosity and future cardiovascular events in stroke survivors. His team followed 625 stroke survivors for an average of two years. A total of 85 patients (13.6%) had a second stroke or heart attack. Whole blood viscosity and fibrinogen were higher in the patients who had cardiovascular events than in those who did not. Fibrinogen is a major contributor to elevated WBV. Others have found the same association. Di Perri et al. examined 106 patients with cerebrovascular disease and noted that symptoms were associated with increases in WBV, fibrinogen and red blood cell deformability. Acute symptoms regressed when the WBV was lowered. Other researchers including Fong and Chia, Coull et al., Grotta et al and Ernst et al support these findings.

High Blood pressure

Blood viscosity also affects blood pressure. Elevated blood pressure is a major risk factor for developing atherosclerosis and becomes a stronger risk factor after age 45. Remember that blood pressure depends on two factors; cardiac output and total peripheral resistance. Elevated blood viscosity increases peripheral resistance. Blood pressure must increase to maintain cardiac output when there increased resistance due to hyper-viscous blood (Stoltz et al.) Increased blood pressure then damages arteries further.

Koenig et al. found that plasma viscosity was more strongly associated with hypertension than smoking, cholesterol and alcohol. Fossum et al. reported that WBV was directly related to systolic blood pressure, total cholesterol triglycerides, body mass index. Subjects with blood pressure over 130 all had higher blood viscosity.

In summary, blood viscosity may be the final common pathway to atherosclerosis. Elevated WBV increases arterial mechanical stress due to increased pulsitile forces and increased stretching of the vessel wall. Shear stress is damage caused by the frictional forces of thick blood on the arterial wall, causing endothelial dysfunction. I believe that treating elevated WBV can result in regression of plaque and a lower overall risk of stroke and heart attack. I recommend blood viscosity testing for all patients 35 and over with a positive family history of heart disease, anyone with atherosclerosis (or a positive heart scan) and for all patients with high blood pressure.

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Aspirin is used for a wide variety of indications, and an analysis of randomized trials by Rothwell and colleagues, which was published in the January 1, 2011, issue of the Lancet, found that aspirin was effective in reducing the overall risk for death from cancer. Aspirin was particularly effective in reducing the risk for death from gastrointestinal tract cancer, and longer duration of aspirin therapy was associated with greater reductions in cancer mortality risks. However, the dose of aspirin did not appear to affect this outcome.

Nonetheless, many reviews have failed to provide a balance between the risks and benefits of aspirin as primary preventive therapy. A new meta-analysis said to provide "the largest evidence to date regarding the wider effects of aspirin treatment in primary prevention" has shown that cardiovascular benefits are offset by an elevated risk of bleeding [1].

Senior author Dr Kausik Ray (St George's University of London, UK) commented: "On a routine basis I would not recommend aspirin use in primary prevention”.

The new analysis included nine randomized placebo-controlled trials with a total of 100 000 participants. Results showed that during a mean follow-up of six years, aspirin treatment reduced total cardiovascular events by 10%, driven primarily by a reduction in nonfatal myocardial infarction (MI), but there was a 30% increased risk of nontrivial bleeding events. The number needed to treat to prevent one cardiovascular event was 120, compared with 73 for causing a nontrivial bleed.

Effect of Aspirin on Vascular and Nonvascular Outcomes or Death (below I = benefit)

Possible Benefit in Those at High Risk

The authors conclude that the "rather modest benefits" and the significant increase in risk of bleeding do not justify routine use of aspirin in the primary-prevention population. They say that further study is needed to identify subsets that may have a favorable risk/benefit ratio. They note that their results suggest an increased risk of nontrivial bleeding in individuals receiving daily (vs alternate-day) aspirin treatment and a particularly unfavorable risk/benefit ratio for individuals at lower baseline cardiovascular risk.

1.    Seshasai SRK, Wijesuriya S, Sivakumaran R, et al. Effect of aspirin on vascular and nonvascular outcomes: meta-analysis of randomized controlled trials. Arch Intern Med 2012; DOI:10.1001/archinternmed.2011.628. Available at: http://archinte.ama-assn.org/cgi/content/short/archinternmed.2011.628.

My Comments:

1.    I only advise aspirin for patients at high risk for heart attack and stroke (as demostrated by high CIMT, high calcium score or previous history of MI or stroke).

2.    I never use it in patients with high blood pressure as it may cause a hemorrhagic stroke.

3.    I do like to use 81 mg in people with a strong family history of GI cancer.

4.    I use it when there is elevated blood viscosity along with natto and phosphatidylcholine.

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Tocotrienols are effective in lowering serum total and LDL-cholesterol levels by inhibiting the hepatic enzymic activity of beta-hydroxy-beta-methylglutaryl coenzymeA (HMG-CoA) reductase through the post-transcriptional mechanism. alpha-Tocopherol, however, has an opposite effect (induces) on this enzyme activity. Since tocotrienols are also converted to tocopherols in vivo, it is necessary not to exceed a certain dose, as this would be counter-productive. The present study demonstrates the effects of various doses of a tocotrienol-rich fraction (TRF25) of stabilized and heated rice bran in hypercholesterolemic human subjects on serum lipid parameters. Ninety (18/group) hypercholesterolemic human subjects participated in this study, which comprised three phases of 35 days each. The subjects were initially placed on the American Heart Association (AHA) Step-1 diet and the effects noted. They were then administered 25, 50, 100, and 200 mg/day of TRF25 while on the restricted (AHA) diet. The results show that a dose of 100 mg/day of TRF25 produce maximum decreases of 20% (total cholesterol), 25% (LDL-cholesterol), 14% (apolipoprotein B)  and 12% (triglycerides), respectively, suggesting that a dose of 100 mg/day TRF25 plus AHA Step-1 diet may be the optimal dose for controlling the risk of coronary heart disease in hypercholesterolemic human subjects.

TRF25 works in similar way to a statin but withmuch fewer if any side effects. Also, there is no inhibition of CoQ10 synthesis. 

Atherosclerosis. 2002 Mar;161(1):199-207. Dose-dependent suppression of serum cholesterol by tocotrienol-rich fraction (TRF25) of rice bran in hypercholesterolemic humans. Qureshi AA, Sami SA, Salser WA, Khan FA.

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Background  

Exhausting exercise induces muscle damage associated with high production of free radicals and pro-inflammatory mediators.

Aim  

The objective of this study was to determine for the first time and simultaneously whether oral coenzyme Q₁₀ (CoQ₁₀) supplementation can prevent over-expression of inflammatory mediators and oxidative stress associated with strenuous exercise.

Methods  

The participants were classified in two groups: CoQ₁₀ group (CG) and placebo group (PG). The physical test consisted in a constant run (50 km) that combined several degrees of high effort (mountain run and ultra-endurance), in permanent climbing.

Results  

Exercise was associated with an increase in TNF-α, IL-6, 8-hydroxy-2′-deoxyguanosine (8-OHdG), and isoprostane levels, revealing the degree of inflammation and oxidative stress induced. Oral supplementation of CoQ₁₀ during exercise was efficient reducing oxidative stress (decreased membrane hydroperoxides, 8-OHdG and isoprostanes generation, increased catalase, and total antioxidant status), which would lead to the maintenance of the cell integrity. Data obtained also indicate that CoQ₁₀prevents over-expression of TNF-α after exercise, together with an increase in sTNF-RII that limits the pro-inflammatory actions of TNF. Moreover, CoQ₁₀ supplementation reduced creatinine production.

Conclusions  

CoQ₁₀ supplementation before strenuous exercise decreases the oxidative stress and modulates the inflammatory signaling, reducing the subsequent muscle damage.

Study: Coenzyme Q₁₀ supplementation ameliorates inflammatory signaling and oxidative stress associated with strenuous exercise. EUROPEAN JOURNAL OF NUTRITION DOI: 10.1007/s00394-011-0257-

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A new analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) shows that changes in coronary artery calcium (CAC) (as measured by the heart scan) may lag behind changes in coronary disease risk factors. 

CAC is a common measure of subclinical coronary disease, but the association between changes in coronary disease risk factors and progression of CAC is not clear. So Arguelles and colleagues analyzed data from 6800 participants of the MESA study. All participants underwent a CAC imaging test with computed tomography at baseline and either 1.6 or 3.2 years later. A quarter of the study subjects also underwent a third CAC test at an average of 4.9 years after baseline.

Reason: Individuals who come in with a very high risk-factor profile and are the most likely to be placed on medications already have a very high underlying level of pathology that could be driving that calcification process independent of declines in risk factors, including blood pressure, lipid levels, and blood glucose. 

The authors analyzed if the changes in CAC over time were associated with changes in blood pressure and lipid levels. The analysis was adjusted for age, ethnicity, smoking status, family history of cardiovascular disease, total income as a marker of socioeconomic status, and previous use of hypertension, lipid, and glucose-lowering drugs.

Among men who had detectable CAC at baseline, CAC increased an average of 57 Agatston units/year. In women, CAC progressed by 39 Agatston units/year. In all patients, the risk-factor measures went up or down depending on whether they were taking antihypertensivse, statins, or other medications. 

The researchers said that CAC "occurs in a time-lagged fashion" such that a longer study would have eventually seen CAC progression stop or reverse many years after the reversal in risk factors in patients taking medication. Whether risk factors such as high blood pressure and hyperlipidemia are more important to the initiation of calcification--or if they have more of a role in the progression of existing disease--is not clear yet.

I like to use CAC for a baseline before treatment or to monitor progress. I aslo require all chelation patients to get one. I have seen this time lag in my practice many times now but it took me about three years to notice it. It typically takes two to three years to see a reversal of plaque after initiating aggressive treatment. This is a very important thing to explain to patients. I typically see less calcium deposition per year the above numbers because I use combination therapy.  A moderate to high risk patient in my office would typically be on some or all of the following: fish oil, Coenzyme Q10, statins, vitamin K2, vitamin D, blood pressure meds, antioxidants, superoxide dismutase, pomegranate, phosphatidylcholine, lipoic acid, vitamin C, niacin and tocotrienols. After all, the goal is to reverse plaque or stop its progression. Sometimes patients do intravenous treatments as well.

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Vitamin D deficiency is traditionally associated with bone and muscle weakness, but in recent years a number of studies have shown that low levels of the vitamin may predispose the body to high blood pressure, congestive heart failure, and chronic blood vessel inflammation leading the increased risk of heart attack.. It also alters hormone levels to increase insulin resistance, which raises the risk of diabetes. Several large studies have shown that people with low vitamin D levels were twice as likely to have a heart attack, stroke, or other heart-related event during follow-up, compared with those with higher vitamin D levels.

In a review article published in the Journal of the American College of Cardiology, researchers surveyed recent studies on the link between vitamin D deficiency and heart disease to come up with practical advice on screening and treatment. 

They concluded that vitamin D deficiency is much more common than previously thought, affecting up to half of adults and apparently healthy children in the U.S. 

Researchers say higher rates of vitamin D deficiency may be due in part to people spending more time indoors and efforts to minimize sun exposure through the use of sunscreens. Sunscreen with a sun protection factor (SPF) of 15 blocks approximately 99% of vitamin D synthesis by the skin. An hour in the sun without sunblock at the beach in mid summer will cause the skin to produce about 10,000 iu of vitamin D. 

We are outside less than we used to be, and older adults and people who are overweight or obese are less efficient at making vitamin D in response to sunlight. A little bit of sunshine is a good thing, but the use of sunscreen to guard against skin cancer is still a good idea for prolonged sun exposure.

Vitamin D levels can be measured with a blood test that looks at a specific form of vitamin D called 25-hydroxy vitamin D (25(OH)D). Vitamin D deficiency is defined as a blood 25(OH)D level below 20 ng/dL. Normal levels are considered to be above 30 ng/dL. Optimal evels are between 50 and 80ng/dL.

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Low serum testosterone is associated with increased adiposity, an adverse metabolic risk profile, and atherosclerosis. However, few prospective studies have demonstrated a protective link between endogenous testosterone and CV events. Polymorphisms in the SHBG gene are associated with risk of type 2 diabetes, but few studies have addressed SHBG as a predictor of CV events.

Results

During a median 5-year follow-up, 485 CV events occurred. Both total testosterone and SHBG levels were inversely associated with the risk of CV events (trend over quartiles: p = 0.009 and p = 0.012, respectively). Men in the highest quartile of testosterone (≥550 ng/dl) had a lower risk of CV events compared with men in the 3 lower quartiles (hazard ratio: 0.70, 95% confidence interval: 0.56 to 0.88). This association remained after adjustment for traditional CV risk factors and was not materially changed in analyses excluding men with known CV disease at baseline (hazard ratio: 0.71, 95% confidence interval: 0.53 to 0.95). In models that included both testosterone and SHBG, testosterone but not SHBG predicted CV risk.

Conclusion

High serum testosterone predicted a reduced 5-year risk of CV events in elderly men.

Study: Journal of the American College of Cardiology, Volume 58, Issue 16, 11 October 2011, Pages 1674-1681

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http://www.medscape.com/viewarticle/751263?src=mpnews Absolute garbage study, seriously. Regression analysis studies are notoriously inaccurate and the supplement use was self-reported. Why would a postmenopausal woman need iron anyway? Of course, iron should not be taken unless needed otherwise it can increase oxidative stress and risk of heart attack and stroke. Also, associating vitamin use with overall mortality is a pretty poor endpoint. Quality of life should be the endpoint.

Zinc can be toxic at high doses and zinc deficiency is associated with macular degeneration, low SOD function and low metalloproteinase activity in adults. Zinc and iron can be measured in the blood to determine if supplemental use is needed. As far as the calcium is concerned I question any association at all with overall mortality. It helps bone density and prevents colon cancer but increases heart attack risk (maybe). Possibly the benefits and risks cancel each other out.

 

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Elevated plasma fibrinogen is implicated in cardiovascular disease. However, it is not clear whether fibrinogen levels predict the development of hypertension.  Elevated plasma fibrinogen level was positively associated with prevalent hypertension both among men and women and positively associated with 5-year incident hypertension among men, independent of several cardiovascular risk factors but less so in women. These data provide prospective epidemiological evidence of an essential link between plasma fibrinogen level and incident hypertension among men but not among women, a finding consistent with that observed in the Atherosclerosis Risk in Communities Study.

Higher fibrinogen levels increase blood viscosity and increased blood viscosity causes arterial damage. I have contracted with a lab that measures blood viscosity and fibrinogen and developed a natural supplement that works to lower both fibrinogen and blood viscosity.

 

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Why am I always pushing for heart scans and carotid ultrasound??  Its becasue calcification can also be an indicator of increased risk of dementia and stroke. Calcification of the carotid artery has already been shown to predict the risk for stroke. Calcification of the heart's blood vessels is already known to be a big predictor of risk of heart attack.

Arterial calcification in major vessel beds outside the brain, as shown with MRI, is also associated with vascular brain disease and may be linked to future risk for dementia and stroke, a new study shows.

Carotid calcification load predicts brain damage and risk of stroke independent of ultrasound carotid plaque score.

The relationship between calcium in atherosclerotic plaque and brain changes exists on top of the effect of classic cardiovascular risk factors such as high blood pressure, smoking and diabetes. 

The amount of calcified plaque outside the brain provided more information about the extent of brain changes than traditional ultrasound measures of plaque in the carotid artery, the authors add. This is the type of carotid ultrasound most patients get. A CT scan might be better.

The findings were published online August 25 in Arteriosclerosis, Thrombosis and Vascular Biology.

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Lp-PLA2 strongly predicts the chance of a second cardiovascular event in patients with pre-existing CHD as well. It is an emerging independent risk factor even after taking into account other markers of inflammation, kidney function, and blood viscosity. People with levels in the top 25% had twice the risk of an event as compared with those in the bottom 25%.

Get your Lp-PLA2 tested today.

Strategies to reduce PLA-2 include:

·         ashwaganda ( Withania somnifera)

·         fish oil (marine omega-3 fatty acids)

·         the plant derived antioxidants quercetin and naringenin, and resveratrol

·         address liver stressors such as alcohol, acetaminophen (Tylenol).

Learn about more strategies in my new book Dare to Live.

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The reason is due to the fact that the standard of care for preventing and treating coronary artery disease is inadequate. Cholesterol control only has about a 40% success rate in prevention. Also many doctors assume that if a patient is active, does not smoke and is not overweight they are not at risk. NOT true. Heart scans and advanced blood testing can provide the information needed to turn heart disease around.

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