Is it possible to consciously increase or decrease your own heart beat?

Is it possible to consciously increase or decrease your own heart beat?

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By doing yoga, can we manipulate our own heart beat? Is that possible for humans?

Yes, you can decrease your own heart rate very simply by stimulating the vagus nerve in what are called 'vagal maneuvers'. If you stick your thumb in your mouth, wrap your lips tightly around your thumb, and blow on your thumb like you are blowing up a balloon, you will stimulate the vagus nerve and decrease HR. This technique is often used clinically, and is termed the 'valsalva maneuver'. The vagus nerve runs posterior to the oropharynx. Blowing on the thumb increases pressure in the chest cavity and stimulates a parasympathetic response. Another technique is carotid sinus massage, which works in a similar way, by modulating vagal tone. Many other techniques exist. Another is the result of the 'mammalian diving reflex', which slows heart rate in response to immersing the face in cold water.

Vagal maneuvers

Carotid sinus

Carotid sinus massage

Vagus nerve

Valsalva maneuver (see section on heart, where tachycardia means high heart rate)

WebMD on decreasing HR

Foods That Are Bad for Your Heart

Over time, high amounts of salt, sugar, saturated fat, and refined carbs raise your risk for a heart attack or stroke. If you’re worried about your heart, you’ll want to keep these out of regular rotation.

But rather than fixate on any one bad food, it’s wise to focus on your overall diet. You can still have these things if you mostly eat heart-healthy fruits and vegetables, whole grains, lean protein, and low-fat dairy.

Why is your heart pumping slowly?

Sometimes our heart rates can be slower than 60 bpm, and although your first instinct may be to feel alarmed, a slow heart rate doesn&rsquot necessarily indicate a problem with your heart. Beta blocker medications, for starters, could promote a slower heart rate. Additionally, athletes or those who are physically fit may have a slower resting heart rate simply because their heart is strong and is utilizing oxygen more effectively.

If you want to improve the strength and performance of your heart, the secret is to get your heart pumping.

Is Herceptin right for you?

Herceptin is used to treat breast cancers that are HER2-positive.

There are several tests used to find out if breast cancer is HER2-positive. Two of the most common tests are:

IHC (ImmunoHistoChemistry)

The IHC test uses a chemical dye to stain the HER2 proteins. The IHC gives a score of 0 to 3+ that measures the amount of HER2 proteins on the surface of cells in a breast cancer tissue sample. If the score is 0 to 1+, it’s considered HER2-negative. If the score is 2+, it's considered borderline. A score of 3+ is considered HER2-positive.

If the IHC test results are borderline, it’s likely that a FISH test will be done on a sample of the cancer tissue to determine if the cancer is HER2-positive.

FISH (Fluorescence In Situ Hybridization)

The FISH test uses special labels that attach to the HER2 proteins. The special labels have chemicals added to them so they change color and glow in the dark when they attach to the HER2 proteins. This test is the most accurate, but it is more expensive and takes longer to return results. This is why an IHC test is usually the first test done to see if a cancer is HER2-positive. With the FISH test, you get a score of either positive or negative (some hospitals call a negative test result “zero”).

Symptoms of Hyperventilation

Hyperventilation is not dangerous. But it causes symptoms that mimic severe disorders. Hyperventilation causes carbon dioxide levels in your bloodstream to drop. This imbalance causes your blood vessels to constrict. All of this leads to a host of problems that those with anxiety attacks will find very familiar, including:

  • Rapid heartbeat.
  • Chest pains.
  • Lightheadedness/feelings of faint.
  • Difficulty concentrating.
  • Shortness of breath
  • Weak or tingling limbs.

On their own, these symptoms would already cause significant discomfort. When combined with anxiety, these symptoms often lead to severe anxiety attacks, health fears, and more.

How to Reverse Heart Disease with the Coronary Calcium Score

The AHA (American Heart Association) has denied for years that Coronary Calcium Scoring is a valid marker for heart disease risk. Well guess what? They have recanted, and finally admitted the coronary calcium score reliably predicts heart attack risk.(1) UCLA cardiologist, Dr. Matt Budoff, a long-time champion of the Coronary Calcium Scan, and author of the AHA paper says:

“The total amount of coronary calcium (Agatston score) predicts coronary disease events beyond standard risk factors.”(1)

Dr. Detrano, in a recent article in NEJM (New England of Medicine), says:

The coronary calcium score is a strong predictor of incident coronary heart disease and provides predictive information beyond that provided by standard risk factors”. (31)

The Coronary Calcium Score is a precise quantitative tool for measuring and tracking heart disease risk, and is more valuable and accurate than other traditional markers, such as total cholesterol, which is practically worthless as a predictor of heart disease risk. Image upper left, courtesy of Wikipedia Rembrandt, The Anatomy Lesson

What is Coronary Artery Disease? It’s Plaque Formation. Coronary Arteries in Cross Section

Age 20-30 years Age 50-70 years
In youth, at left, there is minimal plaque formation. However, at right with passage of time the plaque grows larger. About 20% of this plaque volume contains calcium which is measurable on CAT scan, providing a marker for the total plaque burden. Calcium score and by inference, plaque volume typically increases 30-35% per year in untreated patients.

Note that even though the right vessel has a larger plaque, the lumen has remodeled so that the inner diameter remains freely open. Eventually, as we age, the enlarging plaque eventually obstructs blood flow causing a heart attack. Another common scenario is plaque rupture which exposes the inflammatory debris of the plaque to the circulating blood. This quickly results in clot formation (thrombosis) resulting in a heart attack and possibly sudden death.

Repeat: The calcified portion of the plaque is consistently 20% of the total plaque volume, allowing use of the calcium score as a marker for total plaque volume.

Arterial Calcification – Why Does it Happen? Below image: Microscopic view of arterial calcification (yellow arrows outline blue calcifications)

Calcification in the soft tissues (connective tissue, ligaments, muscles, arteries) is found in many disease states, and commonly identified on pathology slides of tissues. Whenever there is cell death or tissue necrosis (death of cells), the body invokes a process of calcification which can be regarded as part of the healing process. Arterial calcification is actually a form of bone formation in the wall of the artery triggered by an inflammatory process. Pathology studies have shown that coronary artery calcium forms in areas of healed plaque ruptures. (21) Calcification and plaque formation increases with age, with calcium score typically increasing 30-35% per year in untreated patients (William Davis MD).

Chart below shows increasing heart attack rate as coronary calcium goes up Chart Above shows that Calcium Score is Highly Predictive of Heart Attack Risk A heart attack is cell death of heart muscle caused by lack of blood flow with oxygen deprivation. AS previously mentioned, this is caused by a arterial blockage by enlarging plaque formation which occludes the lumen, or plaque rupture which causes clot formation which occludes blood flow. If a small area of heart muscle is involved, the heart attack may be silent with no symptoms. If a large area is involved, there may be severe chest pain radiating to the left arm or jaw, or other symptoms such as shortness of breath. If the conduction system is involved, there may be irregular heart rhythm called ventricular tachycardia which can cause sudden death. Some people have chronic chest pain from diseased arteries and this is called angina pectoris, treated with medicines to dilate the arteries such as nitroglycerine. Left image chart of calcium score years to event courtesy of Detrano Mesa NEJM 2008 MESA Study MESA_NEJM_Detrano_Robert_2008.

Common Sites of Plaque Formation -Bifurcations and Mechanical Stress

Left image shows xray angiogram of typical ulcerated plaque with stenosis at carotid bifurcation, Right Image shows gross pathology of inside of the vessel with darkened plaque (arrow).

In this example, we have an artery in the neck that feeds blood flow to the brain. Plaque rupture and occlusion of the artery in this case caused a stroke, however, the same process occurring in the heart causes a heart attack.

Ask any interventional radiologist or invasive cardiologist where they find the plaque formation and obstructions in the arterial tree, and they will say its the same few places over and over again. These places are the carotid bifurcation, the distal aorta at the bifurcation, the femoral bifurcation, the exit from the adductor canal. And of course, the proximal coronary arteries, and bifurcations of the coronary arteries. A birfurcation is where the vessel branches into two vessels, making a Y pattern. The bifurcations have maximal turbulance and mechanical stress on the vessel wall. Remember the blood is flowing under pulsatile pressure, and this mechanical pressure and turbulence, over time, causes little stress cracks in the vessel. The cracks appear at sites of maximal stress. The coronary arteries are a special case because of the extra motion of the cardiac muscle which moves and stretches the coronary arteries every heart beat, especially as the arteries branch off from the aorta which is relatively stationary, while lower down over the surface of the heart, the vessels move vigorously with each heart beat. Atherosclerosis is essentially the net result of the healing process for these little cracks in the arterial wall resulting from mechanical stress.

William Davis MD, Advocate of the Coronary Calcium Score

William Davis MD recommends screening CAT heart scans in males over 40 and females over 50. He would start at younger ages if high-risk features are present, such as strong family history of early heart disease, cigarette smoker, diabetes mellitus, or severe lipid or lipoprotein genetic disorders. (2)(3) The Coronary Calcium Score test is currently covered by Medicare and many health insurances. (32)

Credit and Thanks is given to William Davis MD at the Track Your Plaque Web site for much of the information in this article. I have added a few items, though.

What does Calcium Look Like? Calcium looks White on the CAT scan (red arrows at right).
(Above) CAT scans of the Coronary Arteries.
The left image shows a normal coronary artery (red arrows), while the right image shows a heavily calcified coronary artery (white line outlined by red arrows) indicating high risk for coronary artery disease and heart attack.

All About Coronary Calcium Scoring

1) Calcium scoring may be superior to angiography as a means to track plaque. That’s because the vast majority of heart attacks are due to plaque rupture and thrombosis at areas of thickened plaque with minimal lumen narrowing. Over time, the body’s healing process automatically remodels the areas of thickened plaque, and increases lumen size to compensate for the reduced blood flow.

2) Calcium scoring gives a precise number which correlates with the amount of plaque volume. Although only the hard plaque, or calcium in the artery is actually measured, this is useful because it consistently occupies 20% of plaque volume (Total hard and soft plaque).

3) The new 64-slice CAT scanners provide reliable calcium scoring just like any other scanner, both multi-slice and EBT(Electron Beam Cat).

The Track Your Plaque Program, by William Davis MD

1) Quantify plaque with Coronary Calcium Score with CAT scan (or with Electron Beam CT). Obtain your CAT Scan serially, every 12 months to assess response to treatment and lifestyle modification (track your plaque).

2) Use Sophisticated Lipoprotein Panel (Quest-Cardio-IQ, LabCorp-NMR) (7)(8) to uncover hidden causes of plaque progression. LDL particle size and number, Lipoprotein (a). Repeat every 6 months.

3) The Main Treatment Goal is the reduction in Coronary Artery Calcium Score, and by inference, reduction in plaque volume and reduction in cardiovascular mortality. The cardiology community still awaits the hard data on these results (CHD mortality and CHD events, treatment arm vs no treatment arm). These numbers have not been published as far as I know.

How to Measure Success in Halting or Reversing Heart Disease Plaque

According to Dr. Davis, calcium score typically increases at an astonishing rate of 30-35% per year without treatment. Therefore, Dr. Davis considers treatment success to be reduction in this rate from 30 to perhaps only a 5-10 per cent increase in calcium score per year. An absolute reduction in calcium score on follow up scanning is the optimal outcome, which is difficult to achieve even with strict adherence to the Track Your Plaque program, in Dr Davis’s experience.

Track Your Plaque Program Details – Attain the Following Targets:

a) Reduction of LDL to 60 mg/dl (LDL should be measured directly, not calculated)
b) Reduction of triglycerides to 60 mg/dl.
c) Raising HDL to 60 mg/dl.

(Note: Although reduction in cholesterol was part of the original protocol, this has changed. New studies prove that LDL-Cholesterol does not cause cardiovascular disease . See this 2018 article by Ravnskov (63) However cholesterol is a useful marker for metabolic syndrome and diabetes which are strong risk factors for heart disease. Expect cholesterol levels and LDL size and particle numbers to improve with improvement in blood sugar and A1C. for more on this see: LDL particle Size, What gives?)

d) Correction of hidden causes of plaque on Lipoprotein profile such as total number of small LDL particles, IDL, and Lp(a).

e) Achieving normal blood pressure (<130/80) Even a small elevation of blood pressure in diseased arteries can cause increased mortality. Diseased arteries are fragile and plaque rupture can occur easily.

f) Achieving normal blood sugar (≤100 mg/dl). Diabetes is a high risk factor for heart disease.

g) Reduction of C-reactive protein to <1 mg/l

Dietary Modification and Supplements to Attain Above Targets:


a) Niacin vitamin B3 Slo-Niacin Upsher-Smith (44) or Niaspan Kos Pharmaceuticals 500-1500mg. per day (avoid the no-flush niacin which contains inositol).(6)(44) (Note: Since the original protocol was devised, we are no longer using Niacin, which is considered optional.)

Omega 3 Fish Oil

b) Fish oil (Omega 3 oils) 4000 mg per day (providing 1200 mg omega-3 fatty acids). (molecular distilled pharmaceutical grade).(36)

Vitamin D

Vitamin D3 level restored to above 50 ng/ml (Vitamin D3 – 5,000 u/day), Vitamin K2 (MK-7) is also used. Low vitamin D is associated with increasing arterial calcification and increased heart disease risk. (26) Consumption of calcium tablets by women increases arterial calcification and heart attack risk, and is no longer advised.(5) Read my previous article on vitamin D which can be found here. (60)

d) Low Glycemic Diet (avoid Fructose Corn Syrup, avoid wheat products), and eliminate wheat products like Shredded Wheat cereal, Raisin Bran, and whole wheat bagels.

e) Consume foods such as raw almonds, walnuts, pecans olive oil and canola oil. Beneficial for lipoprotein profile.

f) Increasing protein intake, our major building block for body tissues. Added benefit of protein intake is that it doesn’t increase blood sugar. This is low glycemic nutrition.

g) Wine—Red wines contain resveratrol, (don’t exceed two glasses/ day). Bioflavonoids and anti-oxidants have a strong anti-inflammatory effect.

h) Fiber – Gound flaxseed (2 tbsp/day)-Extra fiber aids in detoxifying liver and the entire body by interrupting the enterohepatic circulation. Psyllium (metamucil). Regulates bowel movements and has favorable effect on lipoprotein profile.

Vitamin C (buffered 1000–3000 mg/day), is a key player, as it is the vitamin for strong collagen formation, strengthening the arterial wall. See Linus Pauling’s patented protocol which includes Vitamin C and amino acids Proline and Lysine, the two amino acids that act as receptors for Lp(a). By consuming additional Lysine and Proline, the receptor sites on the Lp(a) and other lipoproteins are covered up and made less sticky, resulting in less deposition in the artery wall. The vitamin C is important not only for strong collagen formation, a major component of the arterial wall, but also for all other structural elements of the body, for that matter. (37)(52)(53)(54)(55)(56)(57)

Humans have a genetic deficiency in Gulano-Lactone-Oxidase (GLO), the final enzyme step in the manufacture of Vitamin C, and therefore unlike all the other animals who make their own Vitamin C, we cannot make this necessary vitamin. We share with all other primates this genetic disease, the inability to manufacture vitamin C, producing a vitamin C deficiency state in all humans.(58)

Also see Thomas Levy’s two books on Vitamin C. (49)(50)(51)

j) Exercise and weight loss- improves insulin sensitivity, reduces inflammatory markers, reduces blood pressure, improves lipoprotein profile.


k) Magnesium supplementation is inexpensive and safe. Magnesium deficiency due to dietary deficiency or thiazide diuretics for hypertension is common, and is associated increased heart disease risk. Magnesium reduces blood pressure, relaxes smooth muscle in arteries, and is needed for normal endothelial function.(41)(42)(43)

L-Arginine is converted to nitric oxide, an important substance for arterial health. Research by Furchgott and other showed that nitric oxide (NO) relaxes arterial smooth muscle, dilating coronary arteries by up to 50%.(35) However, Nitric Oxide (NO) is gone after a few seconds, so it must be replenished at a constant rate to keep the arteries relaxed and open. Lack of NO is associated with constricted arteries, damage to the arterial lining, and accelerated plaque growth. L-arginine shrinks coronary plaque, corrects “endothelial dysfunction”, improves insulin sensitivity, is anti-inflammatory and shrinks plaque. Dosage: l-arginine 6000 mg twice a day, best taken on an empty stomach.

Reverse Cholesterol Transport and Essential Phospholipid – Phosphatidyl Choline (PC) (38)(39)

James C. Roberts MD FACC, a practicing invasive cardiologist, lectures extensively on his clinical success with Phosphatidylcholine (IV or in Liposomal Oral Format with EDTA): Reverse Cholesterol Transport and Metal Detoxification. A DVD of his lectures is available which describes considerable clinical success with oral EDTA and phosphytidylcholine. This page contains his DVD lecture material complete with clinical case histories.(61)

Essential Phospholipid is available under trade name Phoschol which increases Lecithin Cholesterol Acyl Transferase activity (LCAT) (Dobiasova M 1988).(40)(40b) Activating LCAT is beneficial because LCAT is the crucial substance which transports cholesterol from the arterial plaque back to the liver for metabolic breakdown into bile. This process reverses atherosclerotic plaque formation. Dosage: 3 softgels Phoschol a day each containing 900 mg PC.(38)(39)

Thyroid Function

Normalize thyroid function. Broda Barnes MD showed that low thyroid function was a significant risk factor for heart disease. This conclusion was based on autopsy data from Graz Austria and detailed in his book, Hypothyroidism the Unsuspected Illness, and his other book, Solved the Riddle of Heart Attacks. Barnes felt that the thyroid lab tests were frequently unreliable, and he used clinical judgement instead. (59)

LipoProtein (a)All About Reducing Lipoprotein (a)(2)(3)

Lipoprotein little A, also written as Lp(a) is a genetic variant lipoprotein which is associated with a high risk of heart disease, and therefore identification and reduction is essential. The problem is that the conventional Lipid panels done in your doctor’s office do not include Lp(a). Only the more sophisticated lipoprotein panels such as the Cardio-IQ or NMR panels provide Lp(a) data.

Lp(a) and Lipoproteins:

1) Lp(a) is best to measured in (nmol/l), and target below 75 nmol/l .
2) Lp(a) measured in mg/dl (weight may not be accurate), then target below 30 mg/dl .
3) Measured (not calculated) LDL target 50–60 mg/dl.
4) LDL particle number target (NMR) of 600–700 nmol/l or apoprotein B of 50–60 mg/dl. Reduce small LDL to <10% of total LDL.

Treating Lp(a) with Niacin

Use Niaspan® (Kos Pharmaceuticals) or over-the-counter Slo-Niacin® (Upsher-Smith).
Both are better tolerated than OTC plain niacin, which may cause the hot flushes. Reduce hot flushed by drinking a full glass of water with each gelcap, and some find adding an aspirin tablet to the routine helps to reduce flushing.

Lp(a) and BioIdentical Hormones

Bio-Identical hormones are beneficial for reducing heart disease. In menopausal females, estrogen preparations such as Bi-Est are used. Estrogens have been shown to reduce coronary artery calcium score.(46)

In males over 50, bio-identical testosterone cream may lowers Lp(a) by as much as 25% (William Davis MD). Medical studies show that optimizing Testosterone levels in aging males can reduce risk of coronary artery disease by 60%. (47)(48)

DHEA can promote weight loss, and improve insulin sensitivity.(45)

Lp(a) and L-Carnitine

The supplement L-carnitine can be a useful adjunct 2000–4000 mg per day (1000 mg twice a day) can reduce Lp(a) 7–8%, and occasionally will reduce it up to 20%.

Remember, reduction in calcium score on follow up calcium scan is the goal.

What about Statin-Cholesterol Lowering drugs?

Dr Davis admits that the total cholesterol and the LDL cholesterol numbers are of little value in predicting heart disease risk. And, he says that the statin drug side effects, ie. muscle pain and weakness, are more common in actual practice than the drug advertising would suggest, making statin drugs difficult to take for the long term. In my opinion, statin drugs are not recommended for women as explained in my previous article on Statin Drugs for Women (33). Also see article on Lipitor and the Dracula of Medical Technology. (34)

What about Calcium Supplements for women to prevent osteoporosis?

Dr Davis points out that women who take calcium tablets have double the risk of heart attacks than those on placebo.(5)Credit and Thanks is given to William Davis MD at the Track Your Plaque Web Site and Blog for the above information.(2)(3)

For more on this, see my new book on Amazon: Heart Book (see cover – left image)

Update 4/20/15 : Supplements for Coronary Artery Disease by By Donald W. Miller, Jr., MD April 25, 2015

Update Nov 2017: How to Reduce Your Heart Scan Score November 15, 2017 By Dr. William Davis

This article is Part One of a series.
For Part Two click here.
For Part Three click here.

Jeffrey Dach MD
7450 Griffin Road Suite 180/190
Davie, Florida 33314

Articles with Related Interest:


(1) cgi/content/full/114/16/1761
(Circulation. 2006114:1761-1791.) AHA Scientific Statement
Assessment of Coronary Artery Disease by Cardiac Computed Tomography
A Scientific Statement From the American Heart Association Committee on Cardiovascular Imaging and Intervention, Council on Cardiovascular Radiology and Intervention, and Committee on Cardiac Imaging, Council on Clinical Cardiology. Matthew J. Budoff, MD, FAHA Stephan Achenbach, MD Roger S. Blumenthal, MD, FAHA J. Jeffrey Carr, MD, MSCE Jonathan G. Goldin, MD, PhD Philip Greenland, MD, FAHA Alan D. Guerci, MD Joao A.C. Lima, MD, FAHA Daniel J. Rader, MD, FAHA Geoffrey D. Rubin, MD Leslee J. Shaw, PhD Susan E. Wiegers, MD

(2) William R. Davis, MD, FACC Heart Disease Reversal Expert Web: Dr. Davis is author of UnDoctored, Wheat Belly and Track Your Plaque and founder of website communities devoted to the concept of early detection of heart disease using CT heart scans. He is a vocal advocate of self-empowering strategies to reduce risk of heart disease. He is Medical Director of Milwaukee Heart Scan and practices cardiology in the Milwaukee area. He is a graduate of St. Louis University School of Medicine and obtained his training in medicine and cardiology at the Ohio State University Hospitals and Case-Western Reserve/ MetroHealth Medical Centers.

(3) How to Reduce Your Calcium Score Wheat Belly Blog.
William Davis MD

(4) cgi/content/full/19/5/1250
Arteriosclerosis, Thrombosis, and Vascular Biology. 199919:1250-1256.)
Fish Intake, Independent of Apo(a) Size, Accounts for Lower Plasma Lipoprotein(a) Levels in Bantu Fishermen of Tanzania The Lugalawa Study Santica M. Marcovina Hal Kennedy Gabriele Bittolo Bon Giuseppe Cazzolato Claudio Galli Edoardo Casiglia Massimo Puato Paolo Pauletto

(5) content/full/bmj.39440.525752. BEv1
(Bolland MJ, Barber PA, Doughty RN et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Brit Med J BMJ, doi:10.1136/bmj.39440.525752. BE published 15 January 2008)

Over 5 years, women taking calcium had twice the risk of having a heart attack compared with women taking the placebo women taking calcium had a 47 percent higher risk of having any one of three “events” (heart attack, stroke or sudden death) than women in the placebo group.

LipoScience NMR Lipiprotein Analysis through LabCorp

(9) clinical_consensus_coronary_ artery_calcium_scoring.pdf
ACCF/AHA 2007 Clinical Expert Consensus Document on Coronary Artery Calcium Scoring By Computed
Tomography in Global Cardiovascular Risk Assessment and in Evaluation of Patients With Chest Pain
A Report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus
Document on Electron Beam Computed Tomography) Developed in Collaboration With the Society of Atherosclerosis Imaging and Prevention and the Society of Cardiovascular Computed Tomography Journal of the American College of Cardiology Vol. 49, No. 3, 2007

(10) cgi/content/full/164/12/1285
Using the Coronary Artery Calcium Score to Predict Coronary Heart Disease Events. A Systematic Review and Meta-analysis Mark J. Pletcher, MD, MPH Jeffrey A. Tice, MD Michael Pignone, MD, MPH Warren S. Browner, MD, MPH. Arch Intern Med. 2004164:1285-1292. Vol. 164 No. 12, June 28, 2004

Conclusion The coronary artery calcium score is an independent predictor of coronary heart disease events.

Dr. John Rumberger. Heart Scan 2161 Ygnacio Valley Road Suite #100 Walnut Creek, CA 94598

(13) Clinton Heart Disease Reveals Misconceptions about Testing Colorado Heart & Body Imaging says “Clinton Syndrome” reveals limitations of stress tests and promise of EBT heart scans

(14) content/abstract/95/3/667
American Journal of Roentgenology, Vol 95, 667-672, 1965 by American Roentgen Ray Society. THE SIGNIFICANCE OF CORONARY CALCIFICATION JOSEPH JORGENS M.D., PH.D.1, WILLIAM J. BOARDMAN M.D.2, SHELDON W. DAMBERG M.D.2, WILLIAM N. KINNEY M.D.2, and ROBERT R. KUNDEL M.D.2

(15) content/full/187/1/73
AJR 2006 187:73-80 American Roentgen Ray Society
How Predictive Is Breast Arterial Calcification of Cardiovascular Disease and Risk Factors When Found at Screening Mammography?

(16) cgi/content/full/94/5/1175
(Circulation. 199694:1175-1192.)© 1996 American Heart Association, Inc. Coronary Artery Calcification: Pathophysiology, Epidemiology, Imaging Methods, and Clinical Implications

(17) Sangiorgi, Giuseppe, et al. “Arterial calcification and not lumen stenosis is highly correlated with atherosclerotic plaque burden in humans: a histologic study of 723 coronary artery segments using nondecalcifying methodology.” Journal of the American College of Cardiology 31.1 (1998): 126-133. Sangiorgi Giuseppe Arterial calcification highly correlated with atherosclerotic plaque burden Amer Coll CArdiology Jan 1998

Conclusions. Coronary calcium quantification is an excellent method of assessing atherosclerotic plaque presence at individual artery sites. Moreover, the amount of calcium correlates with the overall magnitude of atherosclerotic plaque burden. This study suggests that the remodeling phenomenon is the likely explanation for the lack of a good predictive value between lumen narrowing and quantification of mural calcification.

(18) cgi/content/abstract/27/2/285
J Am Coll Cardiol, 1996 27:285-290 Prognostic value of coronary calcification and angiographic stenoses in patients undergoing coronary angiography R Detrano, T Hsiai, S Wang, G Puentes, J Fallavollita, P Shields, W Stanford, C Wolfkiel, D Georgiou, M Budoff, and J Reed Saint John’s Cardiovascular Research Center, Los Angeles, California, USA.

CONCLUSIONS. Electron beam computed tomographic calcium scores correlate moderately well with angiographic findings. These scores predict coronary heart disease-related events in patients undergoing angiography as well as do the number of angiographically affected arteries.

(19) cgi/content/full/162/5/421
Coronary Artery Calcium Score and Coronary Heart Disease Events in a Large Cohort of Asymptomatic Men and Women Michael J. LaMonte1, Shannon J. FitzGerald1, Timothy S. Church1, Carolyn E. Barlow1, Nina B. Radford2, Benjamin D. Levine3,4, John J. Pippin2, Larry W. Gibbons2, Steven N. Blair1 and Milton Z. Nichaman1

Long-Term Prognosis Associated With Coronary Calcification Observations From a Registry of 25,253 Patients. Matthew J. Budoff, MD*,*,1, Leslee J. Shaw, PhD, Sandy T. Liu*, Steven R. Weinstein*, Tristen P. Mosler, Philip H. Tseng*, Ferdinand R. Flores*, Tracy Q. Callister, MD, Paolo Raggi, MD and Daniel S. Berman, MD * Harbor-UCLA Los Angeles Biomedical Research Institute, Torrance, California Cedars-Sinai Medical Center, Los Angeles, California EBT Research Foundation, Nashville, Tennessee. Division of Cardiology and Department of Radiology, Emory University, Atlanta, Georgia.

Objectives: The purpose of this study was to develop risk-adjusted multivariable models that include risk factors and coronary artery calcium (CAC) scores measured with electron-beam tomography in asymptomatic patients for the prediction of all-cause mortality.

Background: Several smaller studies have documented the efficacy of CAC testing for assessment of cardiovascular risk. Larger studies with longer follow-up will lend strength to the hypothesis that CAC testing will improve outcomes, cost-effectiveness, and safety of primary prevention efforts.

Methods: We used an observational outcome study of a cohort of 25,253 consecutive, asymptomatic individuals referred by their primary physician for CAC scanning to assess cardiovascular risk. Multivariable Cox proportional hazards models were developed to predict all-cause mortality. Risk-adjusted models incorporated traditional risk factors for coronary disease and CAC scores.

Results: The frequency of CAC scores was 44%, 14%, 20%, 13%, 6%, and 4% for scores of 0, 1 to 10, 11 to 100, 101 to 400, 401 to 1,000, and >1,000, respectively. During a mean follow-up of 6.8 ± 3 years, the death rate was 2% (510 deaths). The CAC was an independent predictor of mortality in a multivariable model controlling for age, gender, ethnicity, and cardiac risk factors (model chi-square = 2,017, p < 0.0001). The addition of CAC to traditional risk factors increased the concordance index significantly (0.61 for risk factors vs. 0.81 for the CAC score, p < 0.0001). Risk-adjusted relative risk ratios for CAC were 2.2-, 4.5-, 6.4-, 9.2-, 10.4-, and 12.5-fold for scores of 11 to 100, 101 to 299, 300 to 399, 400 to 699, 700 to 999, and >1,000, respectively (p < 0.0001), when compared with a score of 0. Ten-year survival (after adjustment for risk factors, including age) was 99.4% for a CAC score of 0 and worsened to 87.8% for a score of >1,000 (p < 0.0001).

Serial noninvasive monitoring of calcified atherosclerosis using CAC measurement has been proposed as a means of monitoring medical treatment for CAD as well as assessing change in CVD prognosis (58).

The validity of serial coronary calcium measurements as a method to monitor progression of atherosclerosis requires:

1) that progression of coronary calcium has biologic relevance to atherosclerosis activity
2) that progression of coronary calcium can be detected relative to inter-test variability
3) that changes in coronary calcium severity have prognostic relevance and 4) that modification of cardiovascular risk factors modulates the progression of coronary calcium. Each of these points is subsequently discussed.

Biologic Relevance of Coronary Atherosclerosis Progression.

The extent of coronary calcium found on fast CT is broadly related to plaque burden, but there is a high degree of site-to-site variability in the presence and extent of calcium within any single atherosclerotic plaque. Pathology studies have shown that the extent of coronary calcium within plaques tends to be related to the presence of healed plaque ruptures (59).

Moreover, vulnerable plaques tend to be those with less extensive calcium deposits frequently seen in a spotty distribution (59), a finding supported by intravascular ultrasound studies of patients with acute coronary syndromes (60).

Opposed to Calcium Score

(22) cgi/content/full/114/5/e83
Circulation. 2006114:e83.) Correspondence Response to Letter Regarding Article, “Coronary Artery Calcium: Should We Rely on This Surrogate Marker?” Rita F. Redberg, MD, MSc
Division of Cardiology, University of California, San Francisco, San Francisco, Calif

Drs Schmermund and Erbel take issue with my assertion1 that coronary artery calcium (CAC) scores, as of now, are not reliable predictors of cardiac events. However, they offer no data to refute this statement. First, they correctly note that CAC is related to coronary atherosclerosis. This relation, however, does not mean CAC is a predictor of cardiac events. Indeed, as coronary atherosclerosis is so prevalent, “only a small proportion of persons with atherosclerosis and detectable coronary calcium will eventually develop clinical coronary events.𔄤 Therefore, although levels of coronary calcium and atherosclerosis are associated with increased cardiac events on a population level, the relationship in any individual person is weak. Indeed, calcification may stabilize atherosclerotic lesions and make them less likely to rupture and cause an acute cardiac event.

Secondly, Schmermund and Erbel argue that CAC scores add prognostic information “over and above” cardiovascular risk factors. I respectfully disagree. The great majority of cardiac events that CAC predicts3–5 are soft events—revascularizations and unstable angina. Use of such soft events as end points may be misleading. As stated in the 2000 American College of Cardiology/American Heart Association Expert Consensus document, the test result itself often determines who undergoes these procedures, and it is improper to include them as events predicted by the test.6 In addition, the high rate of revascularization after CAC testing is of concern, because no data show any benefit of revascularization in asymptomatic patients.7

Thirdly, the studies cited include no data regarding the best proof of incremental predictive value, an increase in area under the receiver operator characteristic curve for risk prediction from CAC testing that is incremental to Framingham Risk Scoring (FRS).

Finally, they seem to suggest that calcification does not correlate with cardiac events in people taking statins, but that calcification does correlate in others. Although this hypothesis is interesting, it remains untested.

We are fairly skilled at cardiac risk prediction. FRS remains the reference standard, and no test, CAC included, has been shown to significantly increase the accuracy of FRS. More importantly, additional tests such as evaluation of CAC levels have not been shown to lead to better patient outcomes. Risk factors in FRS, including high blood pressure and cholesterol levels, indisputably may be lowered to reduce cardiovascular risk. CAC cannot be treated, even if lowering CAC were shown to reduce cardiovascular risk. On one point, we are in agreement: We clearly need more epidemiological and clinical trial data on the use of CAC.

(23) http://www.pubmedcentral.nih. gov/pagerender.fcgi?artid= 458849&pageindex=1
Br Heart J. 1974 May 36(5): 499–506. PMCID: PMC458849
Incidence and significance of coronary artery calcification. J H McCarthy and F J Palmer
Circulation. 2001104:412.) Clinical Investigation and Reports

Long-Term Prognostic Value of Coronary Calcification Detected by Electron-Beam Computed Tomography in Patients Undergoing Coronary Angiography. Paul C. Keelan, MB Lawrence F. Bielak, DDS, MPH Khalid Ashai, MD Lama S. Jamjoum, PhD, MPH Ali E. Denktas, MD John A. Rumberger, MD, PhD Patrick F. Sheedy, II, MD Patricia A. Peyser, PhD Robert S. Schwartz, MD From the Division of Cardiovascular Diseases (P.C.K., K.A., A.E.D., J.A.R., R.S.S.) and Diagnostic Radiology (P.F.S.), Mayo Clinic, Rochester, Minn, and Department of Epidemiology (L.F.B., L.S.J., P.A.P.), University of Michigan, Ann Arbor, Mich. Dr Rumberger is currently Professor of Medicine in the Department of Cardiology, Ohio State University, Columbus.

(24) cgi/content/abstract/104/4/412
Correspondence to Robert S. Schwartz, MD, FACC, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905.

Conclusions— In patients undergoing angiography, CAC extent on EBCT is highly predictive of future hard cardiac events and adds valuable prognostic information.

(25) cgi/content/full/36/1/18
Journal of Nuclear Medicine Technology Volume 36, Number 1, 2008 18-24
Cardiac CT: Indications and Limitations*Susanna Prat-Gonzalez, Javier Sanz and Mario J. Garcia The Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of Medicine, New York, New York

Calcium Scoring The most widely used measure of calcium burden is the calcium score (often known as the Agatston score), which is based on the radiographic density–weighted volume of plaques with attenuation values of greater than 130 HUs. The presence of coronary calcification is a robust predictor (for a calcium score of >100, the risk ratio = 1.88) of adverse cardiovascular events, and the prognostic value of coronary calcium burden has been clearly established (7).

Although the utility of screening asymptomatic individuals remains controversial, several studies have indicated that the calcium score provides prognostic information independent of conventional risk factors. In a recently published study, a calcium score of greater than 300 was associated with a significant increase in cardiac events compared with that determined by a clinical score alone (8), supporting the notion that a high calcium score can modify predicted risk this is especially true for patients in the intermediate-risk category, for whom clinical decision making is most difficult. Patients determined to be at low risk by clinical criteria, however, appear to derive minimal additional prognostic benefit from calcium scoring. These conclusions are represented in a clinical consensus document recently issued by the American College of Cardiology and the American Heart Association (9).

Active Serum Vitamin D Levels Are Inversely Correlated With Coronary Calcification

Karol E. Watson, MD Marla L. Abrolat, MD Lonzetta L. Malone, BS Jeffrey M. Hoeg, MD Terry Doherty, BA Robert Detrano, MD, PhD Linda L. Demer, MD, PhD
Circulation. 2008117:503-511.)

Vitamin D Deficiency and Risk of Cardiovascular Disease. Thomas J. Wang, MD Michael J. Pencina, PhD Sarah L. Booth, PhD Paul F. Jacques, DSc Erik Ingelsson, MD, PhD Katherine

Background— Vitamin D receptors have a broad tissue distribution that includes vascular smooth muscle, endothelium, and cardiomyocytes. A growing body of evidence suggests that vitamin D deficiency may adversely affect the cardiovascular system, but data from longitudinal studies are lacking.

Methods and Results— We studied 1739 Framingham Offspring Study participants (mean age 59 years 55% women all white) without prior cardiovascular disease. Vitamin D status was assessed by measuring 25-dihydroxyvitamin D (25-OH D) levels. Prespecified thresholds were used to characterize varying degrees of 25-OH D deficiency (<15 ng/mL, <10 ng/mL). Multivariable Cox regression models were adjusted for conventional risk factors. Overall, 28% of individuals had levels <15 ng/mL, and 9% had levels <10 ng/mL. During a mean follow-up of 5.4 years, 120 individuals developed a first cardiovascular event. Individuals with 25-OH D <15 ng/mL had a multivariable-adjusted hazard ratio of 1.62 (95% confidence interval 1.11 to 2.36, P=0.01) for incident cardiovascular events compared with those with 25-OH D 15 ng/mL. This effect was evident in participants with hypertension (hazard ratio 2.13, 95% confidence interval 1.30 to 3.48) but not in those without hypertension (hazard ratio 1.04, 95% confidence interval 0.55 to 1.96). There was a graded increase in cardiovascular risk across categories of 25-OH D, with multivariable-adjusted hazard ratios of 1.53 (95% confidence interval 1.00 to 2.36) for levels 10 to <15 ng/mL and 1.80 (95% confidence interval 1.05 to 3.08) for levels <10 ng/mL (P for linear trend=0.01). Further adjustment for C-reactive protein, physical activity, or vitamin use did not affect the findings.

Conclusions— Vitamin D deficiency is associated with incident cardiovascular disease. Further clinical and experimental studies may be warranted to determine whether correction of vitamin D deficiency could contribute to the prevention of cardiovascular disease.

(27) cgi/content/abstract/19/6/1167
J Am Coll Cardiol, 1992 19:1167-1172
Fluoroscopic coronary artery calcification and associated coronary disease in asymptomatic young men
TH Loecker, RS Schwartz, CW Cotta, and JR Hickman Jr

Clinical Sciences Division, U.S. Air Force School of Aerospace Medicine, Brooks Air Force Base, San Antonio, Texas.

Little is known about the diagnostic significance of coronary artery calcification detected fluoroscopically in apparently healthy young men. This study compared the presence of fluoroscopically detected coronary artery calcification with angiographic coronary artery disease in asymptomatic male military aircrew undergoing noninvasive cardiac screening tests and coronary arteriography for occupational indications. Of 1,466 men screened with coronary fluoroscopy, 613 underwent coronary arteriography because of one or more abnormal noninvasive test results. The mean age (+/- SD) of all subjects screened was 40.2 +/- 5 years (range 26 to 65). Significant coronary artery disease (greater than or equal to 50% diameter stenosis) was found in 104 of the 613 subjects with arteriograms (16.9% disease prevalence). Overall sensitivity and specificity for coronary artery calcification detection of significant disease, based only on those subjects undergoing arteriography, were 66.3% and 77.6%, respectively. For measurable disease (mild plus significant), sensitivity was 60.6% and specificity 85.9%. Positive and negative predictive values were 37.7% and 91.9%, respectively, for significant disease. For measurable disease, positive and negative predictive values were 68.9% and 80.9%, respectively.

In these asymptomatic young men, a fluoroscopic examination negative for coronary artery calcification indicated a low risk of significant coronary artery disease, whereas a positive test result (calcification present) substantially increased the likelihood of angiographically significant coronary artery disease.

Lipoprotein Subclasses and Particle Sizes and Their Relationship With Coronary Artery Calcification in Men and Women With and Without Type 1 Diabetes. Helen M. Colhoun1, James D. Otvos2, Mike B. Rubens3, M. R. Taskinen4, S. Richard Underwood3, and John H. Fuller1 1 Royal Free and University College

Low-Density Lipoprotein Size and Cardiovascular Disease: A Reappraisal, CLINICAL REVIEW 163: CARDIOVASCULAR ENDOCRINOLOGY 4 Frank M. Sacks and Hannia Campos
Harvard School of Public Health, Department of Nutrition, Boston, Massachusetts 02115

Because the classical lipid risk factors by no means perfectly predict CHD in patients, lipoprotein subfractionation has the potential to improve risk prediction.

(30) Sacks, Frank M., and Hannia Campos. “Low-density lipoprotein size and cardiovascular disease: a reappraisal.” The Journal of Clinical Endocrinology & Metabolism 88.10 (2003): 4525-4532.

In summary, the picture that is emerging from epidemiology is that small LDL does not have a special relationship to CHD beyond its contribution to LDL concentration.

The burden of proof for any newly proposed risk factor is that it must add significantly to risk assessment by existing measurements, or that it is equivalent but more economical. LDL subtyping does not meet either of these expectations.

The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects.

Lamarche B, Lemieux I, Després JP. Department of Food Sciences and Nutrition, Laval University, Ste-Foy, Québec, Canada.

More than decade ago, several cross-sectional studies have reported differences in LDL particle size, density and composition between coronary heart disease (CHD) patients and healthy controls.

Three recent prospective, nested case-control studies have since confirmed that the presence of small, dense LDL particles was associated with more than a three-fold increase in the risk of CHD. The small, dense LDL phenotype rarely occurs as an isolated disorder. It is most frequently accompanied by hypertriglyceridemia, reduced HDL cholesterol levels, abdominal obesity, insulin resistance and by a series of other metabolic alterations predictive of an impaired endothelial function and increased susceptibility to thrombosis. Whether or not the small, dense LDL phenotype should be considered an independent CHD risk factor remains to be clearly established. The cluster of metabolic abnormalities associated with small, dense LDL particles has been referred to as the insulin resistance-dyslipidemic phenotype of abdominal obesity.

Results from the Québec Cardiovascular Study have indicated that individuals displaying three of the numerous features of insulin resistance (elevated plasma insulin and apolipoprotein B concentrations and small, dense LDL particles) showed a remarkable increase in CHD risk. Our data suggest that the increased risk of CHD associated with having small, dense LDL particles may be modulated to a significant extent by the presence/absence of insulin resistance, abdominal obesity and increased LDL particle concentration.

We suggest that the complex interactions among the metabolic alterations of the insulin resistance syndrome should be considered when evaluating the risk of CHD associated with the small, dense LDL phenotype. From a therapeutic standpoint, the treatment of this condition should not only aim at reducing plasma triglyceride levels, but also at improving all features of the insulin resistance syndrome, for which body weight loss and mobilization of abdominal fat appear as key elements.

Finally, interventions leading to reduction in fasting triglyceride levels will increase LDL particle size and contribute to reduce CHD risk, particularly if plasma apolipoprotein B concentration (as a surrogate of the number of atherogenic particles) is also reduced.

Coronary Calcium as a Predictor of Coronary Events in Four Racial or Ethnic Groups. Robert Detrano, M.D., Ph.D., Alan D. Guerci, M.D., J. Jeffrey Carr, M.D., M.S.C.E., Diane E. Bild, M.D., M.P.H., Gregory Burke, M.D., Ph.D., Aaron R. Folsom, M.D., Kiang Liu, Ph.D., Steven Shea, M.D., Moyses Szklo, M.D., Dr.P.H., David A. Bluemke, M.D., Ph.D., Daniel H. O’Leary, M.D., Russell Tracy, Ph.D., Karol Watson, M.D., Ph.D., Nathan D. Wong, Ph.D., and Richard A. Kronmal, Ph.D.

ABSTRACT Background In white populations, computed tomographic measurements of coronary-artery calcium predict coronary heart disease independently of traditional coronary risk factors. However, it is not known whether coronary-artery calcium predicts coronary heart disease in other racial or ethnic groups.

Methods We collected data on risk factors and performed scanning for coronary calcium in a population-based sample of 6722 men and women, of whom 38.6% were white, 27.6% were black, 21.9% were Hispanic, and 11.9% were Chinese. The study subjects had no clinical cardiovascular disease at entry and were followed for a median of 3.8 years.

Results There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%. The areas under the receiver-operating- characteristic curves for the prediction of both major coronary events and any coronary event were higher when the calcium score was added to the standard risk factors.

Conclusions The coronary calcium score is a strong predictor of incident coronary heart disease and provides predictive information beyond that provided by standard risk factors in four major racial and ethnic groups in the United States. No major differences among racial and ethnic groups in the predictive value of calcium scores were detected.

(33) Cholesterol Lowering Statin Drugs for Women Just Say No to Statin Drugs

(34) Lipitor and The Dracula of Modern Technology by Jeffrey Dach MD

(35) prizes/medicine/laureates/ 1998/press.html
Nobel Prize in Physiology or Medicine for 1998 jointly to Robert F. Furchgott, Louis J. Ignarro and Ferid Murad for their discoveries concerning “nitric oxide as a signalling molecule in the cardiovascular system”. L-Arginine is converted to Nitric Oxide.

(36) EPA/DHA Essentials is an ultra-pure, molecularly distilled fish oil concentrate that has been tested for environmental contaminants (heavy metals, PCBs, dioxins and furans), microbial contaminants, and oxidation and rancidity. It contains well below the strict limits for these criteria as established by the Council for Responsible Nutrition (CRN), Europea Pharmacoepeia (EP) and U.S. Pharmacoepeia (USP).

Linus Pauling Protocol Vitamin C

(37) pauling/short.html
Linus Pauling Protocol SHort Version for prevention, reversal of heart disease

Essential Phospholipid

(38) Essential Phospholipid, PhosChol® is 100 percent pure polyenylphosphatidylcholine (PPC), with up to 52% DLPC. In fact, PhosChol delivers the highest available concentrated source of ilinoleoylphosphatidylcholine (DLPC).

(39) Source for PPC, 3 PhosChol capsules delivers 2700mgs of purified PPC.

(40) content/full/270/10/5151
Effect of the Cholesterol Content of Reconstituted LpA-I on Lecithin:Cholesterol Acyltransferase Activity Daniel L. Sparks G. M. Anantharamaiah Jere P. Segrest Michael C. Phillips

The major HDL protein is apoA1, or Lipoprotein A1, or LpA-I

(40b) Dobasiova M, Stribrna J, Matousovic K. Effect of polyenoic phospholipid therapy on lecithin cholesterol acyltransferase activity in the human serum. Physiol-Bohemoslov. 198837(2):165–172.

(41) http://www.pubmedcentral.nih. gov/pagerender.fcgi?artid= 1345822&pageindex=1#page
Can Med Assoc J. 1985 February 15 132(4): 360–368. PMCID: PMC1345822
A clinical approach to common electrolyte problems: 4. Hypomagnesemia.
C Berkelhammer and R A Bear

(42) http://www.pubmedcentral.nih. gov/articlerender.fcgi?tool= pmcentrez&artid=2146789
Can Fam Physician. 1996 July 42: 1348–1351. PMCID: PMC2146789
Muscle cramps and magnesium deficiency: case reports.
D. L. Bilbey and V. M. Prabhakaran

(43) pubmed/3282851
Magnesium metabolism in health and disease.Elin RJ.Clinical Pathology Department, National Institutes of Health, Bethesda, Maryland. A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders.

Slo Niacin


(45) content/full/292/18/2243
Effect of DHEA on Abdominal Fat and Insulin Action in Elderly Women and Men
A Randomized Controlled Trial Dennis T. Villareal, MD John O. Holloszy, MD
JAMA. 2004292:2243-2248.

(46) content/short/356/25/2591
Volume 356:2591-2602 June 21, 2007 Number 25 Estrogen Therapy and Coronary-Artery Calcification JoAnn E. Manson, M.D., Results: The mean coronary-artery calcium score was lower among women receiving estrogen (83.1) than among those receiving placebo (123.1) (P=0.02 by rank test).

(47) http://care.diabetesjournals. org/cgi/content/full/26/6/1929
Diabetes Care 26:1929-1931, 2003 Testosterone and Atherosclerosis Progression in Men
Shalender Bhasin, MD and Karen Herbst, MD, PHD Studies in LDL receptor-deficient mice provide compelling evidence that testosterone retards early atherogenesis, and that the effects of testosterone on atherogenesis are mediated through its conversion to estradiol in the vessel wall.

The Journal of Clinical Endocrinology & Metabolism. Aug 2002. Vol. 87, No. 8 3632-3639 Low Levels of Endogenous Androgens Increase the Risk of Atherosclerosis in Elderly Men: The Rotterdam Study A. Elisabeth Hak, Jacqueline C. M. Witteman, Frank H. de Jong, Mirjam I. Geerlings, Albert Hofman and Huibert A. P. Pols

Optimal testosterone levels in men have been shown to decrease the risk of coronary artery disease by 60%

Tom Levy MD and Vitamin C

(49) bin/htmlos.cgi/LV/apps/stop- americas-killer.html
STOP AMERICA’S #1 KILLER! Reversible Vitamin C deficiency found to be cause of heart disease.
A new book by Thomas E. Levy, MD JD, a Board Certified Cardiologist, What Initiates a Breakdown in Arterial Walls? Answer: an arterial Vitamin C deficiency — a condition that Dr.Levy calls “arterial scurvy.”

Tom Levy MD author of two books on Vitamin C

Linus Pauling and Vitamin C

Linus Pauling Protocol for prevention and reversal of heart disease

(53) http://www.newmediaexplorer. org/chris/5278189.pdf

(55) http://www.pubmedcentral.nih. gov/articlerender.fcgi?artid= 54501
Proc Natl Acad Sci U S A. 1990 August 87(16): 6204–6207. PMCID: PMC54501
Hypothesis: lipoprotein(a) is a surrogate for ascorbate. M Rath and L Pauling Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306.

(56) http://www.pubmedcentral.nih. gov/articlerender.fcgi?artid= 55170
Proc Natl Acad Sci U S A. 1990 December 87(23): 9388–9390. PMCID: PMC55170
Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. M Rath and L Pauling Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306-2025.

(57) Pauling L, Rath M. Solution to the puzzle of human cardiovascular disease: its primary cause is ascorbate deficiency leading to the deposition of lipoprotein(a) and fibrinogen/fibrin in the vascular wall. J Orthomol Med. 19926:125-133.

(61) James C. Roberts MD FACC. Web Page practicing invasive cardiologist, lectures extensively on his clinical success with Phosphatidylcholine(IV or in Liposomal Oral Format with EDTA): Reverse Cholesterol Transport and Metal Detoxification. A DVD of his lectures is available which describes considerable clinical success with oral EDTA. This page contains the lecture material also found on the DVD.

62) Detrano, Robert, et al. “Coronary calcium as a predictor of coronary events in four racial or ethnic groups.” New England Journal of Medicine 358.13 (2008): 1336-1345 Coronary_calcium_predictor_coronary_events_score_MESA_NEJM_Detrano_Robert_2008

63) Ravnskov, Uffe, et al. “LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature.” Expert review of clinical pharmacology 11.10 (2018): 959-970. LDL-C does not cause cardiovascular disease Ravnskov Uffe Expert rev clin pharm 2018

The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician. Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship. Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.

Copyright (c) 2016-2017 Jeffrey Dach MD All Rights Reserved. This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.

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Why Your Heart Might Beat Too Hard or Too Fast

A sudden change in heart rate can occur under virtually any circumstance—whether you’re working outside or sitting at a desk, or laughing or crying—which is one reason an unexpected pounding or racing heart is such an attention-grabber. While the episodes may seem to have nothing in common, it’s been my experience that most can be traced to two causes:

Hidden emotions

Whether we’re consciously aware of it or not, our heart rate reflects our emotions. A heart beating too fast or too hard can be a messenger telling us that we need to acknowledge and own stressful or negative emotions lurking just below the surface.

For example, say you’re out with friends to celebrate a big promotion or retirement. It’s a happy occasion still, your heart starts racing. Why? Perhaps beneath your excitement, you’re also fearful about what the future holds and how you’ll cope with it. Or maybe you’ve been struggling with one of your children. You brush aside the stress and tell yourself, “It’s their life.” But then out of nowhere, while you’re doing something completely unrelated, your heart starts pounding.

Despite what we tell ourselves about our lives, the heart never lies. Our brains rationalize our guilt, shame, fear, and anger, but the heart always knows our truth—and sometimes it will beat in unusual ways to bring our attention to those issues. So if you’ve been experiencing a racing or pounding heart, first ask yourself if you’re harboring untended emotions. An honest answer to that question often will begin to resolve the heart rate issue.

Environmental hazards, like EMF exposure

When spontaneous surges in the heart rate aren’t related to emotions, I look for environmental causes. Exposure to chemicals, poor air quality, specific foods and food additives, and EMF are all potential culprits.

EMF, especially, is high on my list. Though the studies are still producing mixed results on the degree to which EMF can affect heart rate, specifically, I hear anecdotal evidence in support of the fact that it does, just about everywhere I go. On my last trip to the west coast, I met a young mother who told me that her son frequently suffers from a rapid heartbeat while at school. Since the boy is fine while he’s at home, they think the problem is due to the fact that he’s exposed to wi-fi all day long.

Wi-fi isn’t the only source of trouble, of course. Cell phones and cell phone signaling towers, microwave ovens, baby monitors, and cordless phones all emit radiation that can potentially cause the heart to beat too hard or too fast. In fact, one study found that using a cordless phone caused a disturbance in heart rate variability in 40 percent of study participants, as well as a link between cordless phone use and both elevated heart rate and an increase in the number of irregular heartbeats.

Possible choices include:

Manufactured Mechanical Valve

These valves are made of strong, durable materials. They are the most long-lasting type of replacement valve. Most will last throughout a patient&rsquos life.

Patients who receive a manufactured valve will almost always require a blood-thinning medication for the rest of their lives. The blood thinner will keep clots from forming, which is critical because clots can lodge in the valve flaps or hinges and cause a malfunction. Clots can also break off and form into an embolism (traveling clot), which may move through the bloodstream and lodge into a vessel where it may lead to problems such as heart attack or stroke.

Donor Valve Implantation

Human donor valves are often used for someone suffering from a condition that affects the valve, such as infective endocarditis. A donor valve can be expected to last 10 to 20 years.

Tissue Valve

Tissue valves are created from animal donors&rsquo valves or animal tissue that's strong and flexible. Tissue valves can last 10 to 20 years, and usually don't require the long-term use of medication. For a young person with a tissue valve replacement, the need for additional surgery or another valve replacement later in life is highly likely.

For each surgery in which the valve must be replaced, careful considerations should be given to durability of the valve, medication options and risks. If you need a valve procedure, heart valve centers of excellence are recommended. The centers are located throughout the country and must meet very high standards of care.

You have options when choosing a heart valve. Survivor Robert Epps shares the factors that influenced his own heart valve choice:

Play without Auto-Play Play Video Text

Written by American Heart Association editorial staff and reviewed by science and medicine advisers. See our editorial policies and staff.

EBME & Clinical Engineering Articles

Your heart's electrical system controls all the events that occur when your heart pumps blood. The electrical system also is called the cardiac conduction system. The heart test called an ECG (electrocardiogram) is a graphical picture of the heart's electrical activity.

Your heart's electrical system is made up of three main parts:

  • The sinoatrial (SA) node, located in the right atrium of your heart.
  • The atrioventricular (AV) node, located on the interatrial septum close to the tricuspid valve.
  • The His-Purkinje system, located along the walls of your heart's ventricles.

A heartbeat is a complex cycle of electrical conductive events. These events take place inside and around your heart. A heartbeat is a single cycle in which your heart's chambers relax and contract to pump blood. This cycle includes the opening and closing of the inlet and outlet valves of the right and left ventricles of your heart. Each heartbeat has two basic parts: diastole and systole. During diastole, the atria and ventricles of your heart relax and begin to fill with blood.

At the end of diastole, your heart's atria contract (atrial systole) and pump blood into the ventricles. The atria then begin to relax. Your heart's ventricles then contract (ventricular systole), pumping blood out of your heart.

Two different types of cells in your heart enable the electrical signal to control your heartbeat:
i. Conducting cells carry your heart's electrical signal.
ii. Muscle cells enable your heart's chambers to contract, an action triggered by your heart's electrical signal.

The electrical signal travels through the network of conducting cell "pathways," which stimulates your upper chambers (atria) and lower chambers (ventricles) to contract. The signal is able to travel along these pathways by means of a complex reaction that allows each cell to activate one next to it, stimulating it to "pass along" the electrical signal in an orderly manner. As cell after cell rapidly transmits the electrical charge, the entire heart contracts in one coordinated motion, creating a heartbeat.

Heartbeat Conduction Cycle

(1) The sinoatrial (SA) node and the remainder of the conduction system are at rest.

(2) The SA node initiates the Action potential , which sweeps across the atria.

(3) After reaching the atrioventricular node, there is a delay of approximately 100 ms that allows the atria to complete pumping blood before the impulse is transmitted to the atrioventricular bundle.

(4) Following the delay, the impulse travels through the atrioventricular bundle and bundle branches to the Purkinje fibers, and also reaches the right papillary muscle via the moderator band.

(5) The impulse spreads to the contractile fibers of the ventricle.

(6) Ventricular contraction begins.

• Action potential : This gradual rise in electrical potential is called the pacemaker, or pre-potential. The rate of rise of the pacemaker potential is the main determinant of heart rate and is increased by adrenaline (epinephrine) and sympathetic stimulation and decreased by vagal (causing a drop in blood pressure) stimulation and hypothermia. Pacemaker activity normally only occurs in the SA and AV nodes, but there are latent pacemakers in other parts of the conducting system which take over when firing from the SA or AV nodes is depressed. Atrial and ventricular muscle fibres do not have pacemaker activity and discharge spontaneously only when damaged or abnormal.

The specialised cardiac conducting system consists of conducting tissue that is made up of modified cardiac muscle cells which have the property of automaticity, that is they can generate their own intrinsic action potentials (nerve impulses) as well as responding to stimulation from adjacent cells. The conducting pathways within the heart are responsible for the organised spread of action potentials within the heart and the resulting co-ordinated contraction of both atria and ventricles. In pacemaker tissue, after repolarisation has occurred, the membrane potential gradually rises to the threshold level for channel opening, at which point sodium floods into the cell and initiates the next action potential (nerve impulse).

The cells of the SA node at the top of the heart are known as the pacemaker of the heart because the rate at which these cells send out electrical signals determines the rate at which the entire heart beats (heart rate). The normal heart rate at rest ranges between 60 and 100 beats per minute. Your heart rate can adjust higher or lower to meet your body's needs. Your brain and other parts of your body send signals to stimulate your heart to beat either at a faster or a slower rate. Although the way all of the chemical signals interact to affect your heart rate is complex, the net result is that these signals tell the SA node to fire charges at either a faster or slower pace, resulting in a faster or a slower heart rate.

For example, during periods of exercise, when the body requires more oxygen to function, signals from your body cause your heart rate to increase significantly to deliver more blood (and therefore more oxygen) to the body. Your heart rate can increase beyond 100 beats per minute to meet your body's increased needs during physical exertion.

Similarly, during periods of rest or sleep, when the body needs less oxygen, the heart rate decreases. Some athletes actually may have normal heart rates well below 60 because their hearts are very efficient and don't need to beat as fast. Changes in your heart rate, therefore, are a normal part of your heart's effort to meet the needs of your body.

Catecholamines - During stress or a need for increased cardiac output, the adrenal glands release a hormone called norepinephrine into the bloodstream at the same time that the sympathetic nervous system is also triggered to increase your heart rate. This hormone causes the heart to beat faster, and unlike the sympathetic nervous system that sends an instantaneous and short-lived signal, norepinephrine released into the bloodstream increases the heart rate for several minutes or more.

Graphical ECG recording on paper

The ECG is usually recorded on a time scale of 0.04 seconds/mm on the horizontal axis and a voltage sensitivity of 0.1mv/mm on the vertical axis.
Therefore, on standard ECG recording paper, 1 small square represents 0.04seconds and one large square 0.2 seconds.
In the normal ECG waveform the P wave represents atrial depolarisation, the QRS complex ventricular depolarisation and the T wave ventricular repolarisation.
The P - R Interval is taken from the start of the P wave to the start of the QRS complex. The Q - T interval is taken from the start of the QRS complex to the end of the T wave. This represents the time taken to depolarise and repolarise the ventricles. The S - T segment is the period between the end of the QRS complex and the start of the T wave. All cells are normally depolarised during this phase.

ECG Normal values

P - R interval 0.12 - 0.2 seconds (3-5 small squares of standard ECG paper)
QRS complex duration less than or equal to 0.1 seconds (2.5 small squares)
Q - T interval corrected for heart rate (QTc) QTc = QT/ RR interval less than or equal to 0.44 seconds

Lead positions

The ECG may be used in two ways. A 12 lead ECG may be performed which analyses the cardiac electrical activity from a number of electrodes positioned on the limbs and across the chest. A wide range of abnormalities may be detected.

During anaesthesia, however, the ECG is monitored using only 3 (or occasionally 5) electrodes which provide a more restricted analysis of the cardiac electrical activity and cannot provide the same amount of information that may be revealed by the 12 lead ECG.

The term 'lead' when applied to the ECG does not describe the electrical cables connected to the electrodes on the patient. Instead it refers to the positioning of the 2 electrodes being used to detect the electrical activity of the heart. A third electrode acts as a neutral.

During anaesthesia one of 3 possible 'leads' is generally used. These leads are called bipolar leads as they measure the potential difference (electrical difference) between two electrodes. Electrical activity travelling towards an electrode is displayed as a positive (upward) deflection on the screen, and electrical activity travelling away as a negative (downward) deflection. The leads are described by convention as follows:

Lead I - measures the potential difference between the right arm electrode and the left arm electrode. The third electrode (left leg) acts as neutral.
Lead II - measures the potential difference between the right arm and left leg electrode.
Lead III - measures the potential difference between the left arm and left leg electrode.

Most monitors can only show one lead at a time and therefore the lead that gives as much information as possible should be chosen. The most commonly used lead is lead II - a bipolar lead with electrodes on the right arm and left leg. This is the most useful lead for detecting cardiac arrhythmias as it lies close to the cardiac axis (the overall direction of electrical movement) and allows the best view of P and R waves.


The American Heart Association (AHA) and American College of Cardiology (ACC) defines five blood pressure categories:

Normal Range - Normal
Systolic (top) blood pressure below 120 mm Hg
Diastolic (bottom) blood pressure below 80 mm Hg

Caution Range - Elevated
Systolic (top) blood pressure 120 - 129 mm Hg
Diastolic (bottom) blood pressure below 80 mm Hg
Take action!

High Range - Stage 1 Hypertension
Systolic (top) blood pressure 130 - 139 mm Hg
Diastolic (bottom) blood pressure 80 - 89 mm Hg
If in this range you have hypertension (high blood pressure).

Very High Range - Stage 2 Hypertension
Systolic (top) blood pressure 140 mm Hg or higher
Diastolic (bottom) blood pressure 90 mm Hg or higher
If in this range you have hypertension (high blood pressure).

Extremely High Range – Hypertensive Crisis
Systolic (top) blood pressure 180 mm Hg or high
Diastolic (bottom) blood pressure 120 mm Hg or higher
Consult your doctor immediately!

Eating a diet that includes potassium rich foods will help promote a lower blood pressure. I also recommend you learn about the DASH diet. It's a very effective way to lower and manage high blood pressure.

From the information you shared I think "white coat hypertension" may be playing a role. That doesn't mean you don't need the medication, but it's something to be aware of.

You should know: The answer above provides general health information that is not intended to replace medical advice or treatment recommendations from a qualified healthcare professional.

Watch the video: GRATIS Hypnose: ANGST for kroppens signaler (November 2022).