http://news.bbc.co.uk/2/hi/health/8051800.stm

Miller VM, Rodgers G, Charlesworth JA, Kirkland B, Severson SR, Rasmussen TE, Yagubyan M, Rodgers JC, Cockerill FR 3rd, Folk RL, Rzewuska-Lech E, Kumar V, Farell-Baril G, Lieske JC.

Department of Surgery, Mayo Clinic, Rochester, Minnesota 55905, USA. miller.virginia@mayo.edu

Mechanisms mediating vascular calcification remain incompletely understood. Nanometer scale objects hypothesized to be a type of bacteria (nanobacteria) are associated with calcified geological specimens, human kidney stones, and psammona bodies in ovarian cancer.

Experiments were designed to evaluate human vascular tissue for the presence of similar nanometer-scale objects. Calcified human aneurysms (n = 8), carotid plaques (n = 2), femoral arterial plaques (n = 2), and cardiac valves (n = 2) and noncalcified aneurysms from patients with bicuspid aortic valve disease (n = 2) were collected as surgical waste from the Heart Hospital of Austin, Austin, Texas, and Mayo Clinic, Rochester, Minnesota.

Whole mounts or adjacent sections from each specimen were examined by electron microscopy, stained for calcium phosphate, or stained with a commercially available antibody (8D10). Filtered (0.2 microm) homogenates of aneurysms were cultured and costained with 8D10 antibody followed by PicoGreen to detect DNA or incubated with [3H]uridine.

Staining for calcium phosphate was heterogeneously distributed within all calcified tissues. Immunological staining with 8D10 was also heterogeneously distributed in areas with and without calcium phosphate. Analysis of areas with positive immunostaining identified spheres ranging in size from 30 to 100 nm with a spectral pattern of calcium and phosphorus (high-energy dispersive spectroscopy).

Nanosized particles cultured from calcified but not from noncalcified aneurysms were recognized by a DNA-specific dye and incorporated radiolabeled uridine, and, after decalcification, they appeared via electron microscopy to contain cell walls.

Therefore, nanometer-scale particles similar to those described as nanobacteria isolated from geological specimens and human kidney stones can be visualized in and cultured from calcified human cardiovascular tissue.

PMID: 15142839

Sample PubMed cite¹⁾

33. Ewald PW, Cochran GM. Chlamydia pneumoniae and cardiovascular disease: an evolutionary per- spective on infectious causation and antibiotic treatment. J Infect Dis. 2000;181(suppl 3):S394-S401.

34. Ellis RW. Infection and coronary heart disease. J Med Microbiol. 1997;46:535-539.

35. Gupta S, Leatham EW. The relation between Chlamydia pneumoniae and atherosclerosis. Heart. 1997;77:7-8.

36. Juvonen J, Juvonen T, Laurila A, et al. Demonstra- tion of Chlamydia pneumoniae in the walls of ab- dominal aortic aneurysms. J Vasc Surg. 1997;25:499-505.

37. Cook PJ, Lip GY. Infectious agents and atheroscle- rotic vascular disease. Quart J Med. 1996;89:727-735.

38. Muhlestein JB, Hammond EH, Carlquist JF, et al. In- creased incidence of Chlamydia species within the coronary arteries of patients with symptomatic ath- erosclerotic versus other forms of cardiovascular disease. J Am Coll Cardiol. 1996;27:1555-1561.

39. Ramirez JA. Isolation of Chlamydia pneumoniae from the coronary artery of a patient with coronary atherosclerosis. Ann Intern Med. 1996;125:979-982.

40. Wimmer ML, Sandmann-Strupp R, Saikku P, Haberl RL. Association of chlamydial infection with cere- brovascular disease. Stroke. 1996;27:2207-2210.

25. Nieto FJ. Infections and atherosclerosis: new clues from an old hypothesis? Am J Epidemiol. 1998;148:937-948.

“I doubt that “breaking old habits” and “improving your lifestyle” will do anything much to slow the decline of your heart health. Still, I wish you the best, and you know where to find us when you come to realize that the answers in cardiology are just about as elusive as they are in immunology, if not more so.

You may be interested in a Letter to the Editor of the BMJ I wrote a few days ago about atherosclerosis http://bmj.bmjjournals.com/cgi/eletters/331/7513/361

Yes, there is an emerging school of thought in mainstream Cardiology that atherosclerosis is caused by microbes, IMO the same microbes which we have found to be behind the Th1 diseases.”

Dr. Trevor Marshall, PhD f14 http://www.marshallprotocol.com/view_topic.php?id=1263&forum_id=32&jump_to=91814#p91814

New Science.com (Article Preview)

http://www.newscientist.com/article.ns?id=mg15020334.100

Can you catch a heart attack?

08 June 1996 Phyllida Brown Magazine issue 2033

Ten years ago, most people scoffed at the idea that a bacterium caused stomach ulcers. But linking chlamydia to coronary heart disease is seen as an even bigger heresy, says Phyllida Brown

IT'S spread by coughs and sneezes. And by the time you're 20, there's a fifty-fifty chance that you're carrying the infection. But could Chlamydia pneumoniae really trigger coronary heart disease, that narrowing of the arteries which suffocates the heart muscle and kills more adults worldwide than any other disease. The theory is fuelling one of the fiercest controversies ever seen in the multimillion-dollar industry of cardiovascular research.

The bacterium—often called TWAR after the original laboratory strain—is the prime suspect because its fingerprints keep appearing at the scene of the crime. People with coronary heart disease are likely to have high levels of antibodies to TWAR, suggesting that they have been persistently or repeatedly infected with it. TWAR's DNA and proteins keep showing up in atheroma, the fatty, diseased tissue that blocks the coronary arteries. And now, in as yet unpublished research, the bacterium itself has turned up alive and kicking, …

……………………………………..

Isn't it scary that it is 10 years since this publication (almost) and yet they still haven't solved the problem?

Koch's dogma (the determination to find one single species at the root of one specific disease) is the primary reason for this failure, IMO.

..Trevor..

See also 'More Evidence That Infections Cause Heart Disease' and 'A Host with Infectious Ideas' http://www.rainbowminerals.net/infections_cause_heart_disease.htm

s74 http://www.marshallprotocol.com/view_topic.php?id=4304&forum_id=37&jump_to=40285#p40285

See When should I be concerned about cardiac symptoms? http://www.marshallprotocol.com/forum32/1420.html

Members' experiences

Mitral Valve Prolapse http://www.marshallprotocol.com/view_topic.php?id=5690&forum_id=11&jump_to=54763#p54763

-When I was diagnosed with MVP, I was told I might also have dysautonomia, an imbalance of the central nervous system. This is part of something called MVP Syndrome, and the imbalance can cause jittery anxiety, irritable bowel syndrome, headaches, physical sensations that mimic low blood sugar, etc. So I decided that I must have this syndrome, because I had all these symptoms. Now I realize it probably all goes back to the sarcoidosis.

If you look at the symptoms list, you'll be amazed at how many of them are Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. disease symptoms. There's also a link to anxiety/depression. When I found this site 10 years ago I was relieved to find that I wasn't the only MVP person suffering with odd things–at different times I've suffered from about 90% of the MVP Syndrome symptoms listed–but then I found the MP site and it all began to click. ~Jen Hicks

-I hope what I have shared will give you some confidence to go forth. My heart inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. over the past year has diminished considerably and so I no longer have the pain levels that I once suffered. That to me verifies that I am improving and I am on the right track. I still get heart herxes but they are controllable and the pressure and arrythmias although are very irritating no longer cause me such concern. I have been through the cycles enough times to have a good feel for what is going on and I can regulate them without too much distress. ~CelticLadee

-Cardiac symptoms greatly reduced with the MP. Without treating the infection/TH1 disease, my cardiac issues became more severe, the angina worsened, the EKG's more abnormal, with an increase in arythmia, and less blood perfusion to areas of the heart. Why? because treatment was aimed at the cardiac symptoms only, and the disease/infections were receiving no treatment, were progressing and affecting my heart more and more.

I am happy to report that on the MP– My cardiac sxes have been reduced at this point to almost nil. Why? Because the Benicar is protecting that organ, and with the adjustment of Benicar dosing encouraged and manipulation of abx dosing, I can keep cardiac herxing at bay. (No more ambulance rides, ER visits, and cardiac care units.)

Even with a good size dose of Verapamil daily and nitroglycerine, pre-MP, I was experiencing cardiac sxes and events. Once I started the Benicar—they stopped. :) I haven't had to pop sub ling. nitroglycerine tabs—since starting! (Prior to starting the Benicar, I was taking 3 nitro tabs during an event, and then sometimes that wasn't enough).

Benicar puts up a wonderful blockade. But here's the point, if you have cardiac infections and are symptomatic, and are not treating, they WILL worsen. If you treat them, you will fix the problem. So the treatment is designed to prevent the inevitable progression—which is harmful—not the protocol. ~Hrts

s80 http://www.marshallprotocol.com/view_topic.php?id=4304&forum_id=37&jump_to=80072#p80072

Elevated CRP

First Link Found Between Obesity, Inflammation and Vascular Disease

Key points:

Researchers at The University of Texas M.D. Anderson Cancer Center and The University of Texas Health Science Center at Houston have found that human fat cells produce a protein that is linked to both inflammation and an increased risk of heart disease and stroke.

They say the discovery, reported in Journal of the American College of Cardiology, goes a long way to explain why people who are overweight generally have higher levels of the molecule, known as C-reactive protein (CRP), which is now used diagnostically to predict future cardiovascular events.

Even as the CRP picture becomes clearer, there is still much that is not known, the researchers say, including the reason why fat tissue produces an inflammatory response, and just precisely how CRP participates in that process.

Dr. Marshall's comment:

They are so near and yet so far. CRP is part of the body's reaction to bacterial infection.

S73 http://www.marshallprotocol.com/view_topic.php?id=4304&forum_id=37&jump_to=38563#p38563

When we are ill with unusual diseases, our case can be challenging for medical professionals. Sometimes we just have to decide whether we think they are evaluating us correctly or they have been thrown off by how confusing the disease is.

Here is a simple overview of congestive heart failure. Many of the symptoms of CHF are non-specific. The presenting clinical symptoms of CHF and sarcoidosis overlap (SOB, fatigue, weakness, cold extremities, cyanosis of lips and nail beds, mental confusion). Notice that the first consideration in treating CHF is “removing the precipitating cause.”

It is possible for sarcoidosis to result in congestive heart failure, either due to uncontrolled arrhythmia or due to sarcoid thickening of the myocardium, which results in restrictive cardiomyopathy, a very rare condition. We caution all patients on the MP to assume they may have hidden cardiac involvement. Anyway, diagnosing heart failure can be fairly complicated.

Angiotensin II causes some real problems for people who do have congestive heart failure. - It causes blood vessels to constrict, which raises blood pressure. - It causes the kidneys to retain sodium and fluid, which can lead to edema. - It increases our thirst and desire for salt, which can cause more edema.

You can see then why angiotensin receptor blockers, which block Angiotensin II, are used in treating congestive heart failure. It makes little sense, in my opinion, that ARBs would in any way cause this problem. Olmesartan is known to have cardio-protective effects.

Belinda f7 http://www.marshallprotocol.com/view_topic.php?id=1420&forum_id=32&jump_to=100007#p100007

Heart failure

Angiotensin II in the failing heart. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16534230&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Explains how elevated levels of Angiotensin II are related to clinical signs of heart failure. Angiotensin receptor blockers block production of Angiotensin II and can improve mortality rates in heart failure patients.

Do all angiotensin II type 1 receptor blockers have the same beneficial effects? http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17572701&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Notes that ARBs have been used to block various bad effects of Angiotensin II, including heart failure and discusses how ARBs have differing molecular characteristics.

See Congestive Heart Failure http://www.marshallprotocol.com/view_topic.php?id=1420&forum_id=32&jump_to=100007#p100007

s75 http://www.marshallprotocol.com/view_topic.php?id=4304&forum_id=37&jump_to=40550#p40550

The connection between bacteria and calcification in heart disease has already been noted. Researchers at the Hospital Das Clinicas in Brazil found significantly higher concentrations of Chlamydia pneumoniae and Mycoplasma pneumoniae in calcified nodes of blood vessels throughout the body, including the heart and the aorta - causing them to suggest that “these bacteria may be associated with the development of calcification and inflammation.”[5][6] 16007307 16983590

1. —

Atherosclerois (coronary artery disease)

There is an emerging school of thought in mainstream cardiology that atherosclerosis is caused by microbes; IMO the same microbes which we have found to be behind the Th1 diseases.

One of the Th1 chemokines is called CAM (Cellular Adhesion Molecule) and it is a key component both of how the plaque macrophages adhere to the arterial wall in atherosclerosis and protect themselves from the immune system. More papers are coming out on both these things every month, but mainstream medicine has still to tie CAM to occult Th1 inflammation. It will take a decade for that to happen, IMO.

In atherosclerosis it is known that hemodynamic forces (pushing and shoving) of the monocytes which eventually form plaque are what cause the plaque to build up at junctions in the arteries. This may be due to mechanical disruption of the protective L-formDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria. cytoskeletons.

“I doubt that “breaking old habits” and “improving your lifestyle” will do anything much to slow the decline of your heart health. Still, I wish you the best, and you know where to find us when you come to realize that the answers in cardiology are just about as elusive as they are in immunology, if not more so.

You may be interested in a Letter to the Editor of the BMJ I wrote a few days ago about atherosclerosis http://bmj.bmjjournals.com/cgi/eletters/331/7513/361

An article, from the medical news section of the Saint Lewis Washington University publication, talks about how inflammatory processes are associated with disease.

“Many years ago, atherosclerosis was thought to be related to lipids and to the excessive deposit of cholesterol in the arteries,” Fontana says. “Nowadays, it's clear that atherosclerosis is an inflammatory disease. There also is evidence that inflammation plays a role in cancer, and there is even evidence that it plays a role in aging. Someday we may learn that visceral fat is involved in those things, too.”

The above quote is by Luigi Fontana, M.D., Ph.D., assistant professor of medicine at Washington University in St. Louis and an investigator at the Istituto Superiore di Sanita, Rome, Italy

Dr. Trevor Marshall, PhD

The following scientific studies verify the efficacy of ARBs in treating CAD: Angiotensin receptor blockers don't seem to increase risk of MI

Severity of Hyperlipidemia Does Not Affect Antiatherosclerotic Effect of an Angiotensin II Receptor Antagonist in Apolipoprotein E-deficient Mice.

The following articles discuss the relationship of atherosclerosis and inflammation: MEDICAL BIOLOGY: INFLAMMATION AND CORONARY ARTERY DISEASE

Inflammation and CAD

Inflammation markers signal rapidly advancing coronary disease

The Role of Infection in the Pathogenesis of Cardiovascular Disease

Is CAD caused by atherosclerosis, inflammation or both?

Healing from cardiovascular disease: bacteria, fat, cholesterol, and more

Olmetec(R) Is First Angiotensin Receptor Blocker (ARB) To Suggest Atherosclerosis Regression (In Hypertensives With Cardiovascular Risk), UK

s72 http://www.marshallprotocol.com/forum37/4304.html#p38531

Olmetec(R) Is First Angiotensin Receptor Blocker (ARB) To Suggest Atherosclerosis Regression (In Hypertensives With Cardiovascular Risk), UK

11 Dec 2007 - 1:00 PST

Olmetec(R) (olmesartan medoxomil), licensed in the UK for essential hypertension, is the first ARB to suggest a regression of atherosclerosis (plaque volume (PV)) , a major risk factor for cardiovascular disease (CVD)1, according to a new study published in the inaugural issue of Therapeutic Advances in Cardiovascular Disease.

Regression of PV is a compelling clinical goal, with potential to prevent cardiovascular and cerebrovascular events. In the Multicentre Olmesartan Atherosclerosis Regression Evaluation (MORE)2 study the primary end point, common carotid - intima media thickness (CC-IMT), a surrogate risk factor for CVD, decreased after 2 years treatment with olmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. .

A post hoc analysis in patients with larger plaques demonstrated a significant reduction in PV compared to atenolol the active comparator, although change in PV for the whole study population only showed trend towards significance for olmesartan. This is a promising finding which provides a focus for further evaluation in future clinical studies.

In the MORE study, olmesartan did not significantly reduce plaque volume (PV) compared with the beta-blocker atenolol in the overall population. However a post hoc analysis of patients with above average plaques (≥33µl) at baseline (those at greater risk of cardiovascular events) olmesartan showed a significant reduction in PV by -8.9%, compared with a 2.4% increase with atenolol.

In very large plaques the beneficial effect of olmesartan was even greater - PV declined by -12.8% and increased by 2.1% respectively in the olmesartan and atenolol groups. Both olmesartan and atenolol patients showed a similar reduction in blood pressure2. The observed decrease in plaque volume may thus occur independently of blood pressure lowering and offers a further potential benefit of olmesartan.

The MORE findings add to Olmesartan's growing portfolio of vascular protective studies.3-8 “The MORE study is a landmark because it is the first study to show an anti-atherosclerotic effect using an ARB.

This suggests that in patients with hypertension, in addition to effective blood pressure lowering, olmesartan may potentially protect against cardiovascular and organ damage, benefits that should be considered seriously when prescribing an anti-hypertensive agent in patients who already have atherosclerotic disease” said Dr Lina Izzat, Associate Specialist in Cardiology, Prince Phillip Hospital, Llanelli.

s89 http://www.marshallprotocol.com/view_topic.php?id=4304&forum_id=37&jump_to=141643#p141643

Beneficial effects of olmesartan, a novel angiotensin II receptor type 1 antagonist, upon acute autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body myocarditis. http://tinyurl.com/8yzx2

1: Mol Cell Biochem. 2004 Apr;259(1-2):217-22. Beneficial effects of olmesartan, a novel angiotensin II receptor type 1 antagonist, upon acute autoimmune myocarditis.

Nimata M, Kishimoto C, Yuan Z, Shioji K.

Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Excess amount of cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. produced by inflammatory stimuli contributes to the progression of myocardial damage in myocarditis. Some angiotensin II receptor type 1 antagonists are reported to inhibit proinflammatory cytokine production in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory. and in vivoA type of scientific study that analyzes an organism in its natural living environment.. We tested the hypothesis that olmesartan, a novel angiotensin II receptor type 1 antagonist, ameliorated experimental autoimmune myocarditis (EAM) in rats attributing to the suppression of inflammatory cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. in the heart. We orally administered olmesartan 1, 3, and 10 mg/kg/day to rats with EAM for 3 weeks. The results showed that olmesartan decreased blood pressure significantly compared with the untreated group, but markedly reduced the severity of myocarditis by comparing the heart weight/body weight ratio, pericardial effusion scores, macroscopic scores and microscopic scores. Myocardial interleukin (IL)-1beta expression by western blotting and IL-1beta-positive staining cells by immunohistochemistry were significantly lower in rats with EAM given olmesartan treatment compared with those of rats given vehicle. We conclude that Olmesartan ameliorates acute EAM in rats. The cardioprotection of olmesartan may be due to suppression of inflammatory cytokines dependent of the hemodynamic modifications.

PMID: 15124927 [PubMed - indexed for MEDLINE]

s77 http://www.marshallprotocol.com/view_topic.php?id=4304&forum_id=37&jump_to=47792#p47792

Anti-theft devices might cause implanted heart devices to malfunction

“Dr. J. Rod Gimbel of East Tennessee Heart Consultants and Dr. James Cox of the University of Tennessee Medical Center in Knoxville described two cases in which anti-theft devices apparently caused implanted heart devices to malfunction.

One of the patients had a pacemaker and she collapsed after pausing in a store doorway. Another had an implantable cardiac defibrillator that shocked him after he stood near an anti-theft unit.

The devices are called electronic article surveillance or EAS systems and use an electromagnetic field.

More than 1 million EAS systems are installed worldwide,” Gimbel and Cox wrote.

Store employees need to know of the danger, they cautioned.

Simply moving the person away from the anti-theft device may save their life,” Gimbel said in a statement.”

TENS units used for pain control may also interfere with a pacemaker…..check with your doctor before using one.

Any MP patient on diurectics (such as Lasix) or cardiac medications to strengthen the heart should be evaluated by his or her physician if breathing gets suddenly worse, they experience a sudden weight gain and/or increased swelling in the legs. An exacerbation in congestive heart failure symptoms may require an adjustment in palliative medications.

Congestive heart failure symptoms develop more slowly and most folks know if they have this problem. Ask your doctor what symptoms you should report. For example, when does s/he want to know if you gain weight, experience swelling or increased shortness of breath.

If you experience significantly increased or sudden:

• exercise intolerance
• severe shortness of breath
• fluid retention or swelling
• weight gain (3 lbs overnight or 5 lbs in 3 days)

Do not take your next dose of antibiotic/s and increase Benicar to 40mg every four hours until symptoms are gone or minimized.

        GETCONTENT

Jane Taylor-Aoki

neurosarcoidosis, systemic sarcoidosis; spasticity, myasthenia, CNS dysfunction, joint pain, pulmonary, splenic and cardiac involvement

Read the interview

Freddie Ash

sarcoidosis of the heart, coronary artery disease, atrial fibrillation

Read the interview

Interviews of patients with other diseases are also available.