Viruses and Infections Cause Heart Attacks

The publishers of Dr. Blaylock's newsletter always send out notices which are advertisements of enticements to subscribe. They give little health clips from his newsletters.

Here's the latest. This isn't the first we've heard of 'bugs' causing heart problems. I have another interview that I intend to post here eventually by a doctor who was interviewed on this same topic. This goes to the silent inflammation issue we discuss and also to the blood viscosity issue as inflammation increases viscosity.

Jackie

Quote:

Viruses and Infections Cause Heart Attacks

A considerable amount of evidence indicates that atherosclerosis is caused by chronic inflammation, which often begins very early in life.

The dispute among experts is what causes the inflammation. One theory holds that bacteria and viruses may cause this inflammation. In addition, several studies have found a strong relationship between a common bacterium causing gum disease and atherosclerosis. In fact, the same bacterium has been cultured from the crud, or plaque, seen in arteries.

It is the battle between the bacteria/viruses and the immune system, which is in perpetual action to destroy the invaders, that begins the process of atherosclerosis.

When a bacterium or virus invades the body, the immune system sends in its special cells to kill the invaders. One team of special cells, macrophages, does this by releasing a burst of free radicals that destroy the germs long before cholesterol makes its appearance.

As with any infection, especially one that continues for decades, the body tries to seal off the infection. It does this by building a fibrous wall around the battle zone. Over time, this wall can also contain calcium deposits, and as this battle progresses, LDL cholesterol enters the injured blood vessel wall and oxidizes.

The oxidized LDL cholesterol becomes a very irritating substance, causing inflammation.

White blood cells attempt to rid the body of the cholesterol by gobbling it up like a Pac-Man, but some of these cells become so stuffed with the oxidized cholesterol that they burst, adding to the inflammation.

Immune cells then secrete a number of caustic chemicals that cause intense inflammation. Because the immune cells cannot rid the area of the microorganisms, the immune attack continues over decades.

Lead, mercury, monosodium glutamate (MSG) and fluoride can also cause the same set of inflammatory reactions in blood vessels.

Unquote

Source: NewsMax.com

There is no consensus yet on whether viruses and/or bacteria cause atherosclerosis and its sequalae; there are conflicting results from the studies testing the hypothesis. Various studies have used antibiotics specific to bacteria suspected of causing arterial dysfunction, these trials have failed to prove cause and effect, cure or substantial improvement in cardiovascular endpoints.

There are some intriguing recent studies though that suggest an apparent link between treating infection and an improvement in arterial function. Extracts of two are below.

Also see the abtract below about helicobacter pylori possibly causing afib. (Helicobacter causes ulcers and stomach cancers). Interesting though this study is, I still have not seen a followup study which shows that when helicobacter is eradicated in patients with afib that their afib is cured or improved. Maybe nobody has attempted such a study yet.

For some people the cause of their afib might be found in a mutation of their genes. See article below.
_____________________

[www.medicalnewstoday.com]

'Treatment of Periodontitis and Endothelial Function' is published in the March issue 2007 of the New England Journal of Medicine.

Scientists at University College London (UCL) have conducted the first clinical trial to demonstrate that an intensive treatment for periodontitis (infectious gum disease) directly improves the health of blood vessels.

The study enrolled 120 otherwise healthy patients with a severe form of periodontitis in a six-month trial and compared the effects of regular tooth cleaning with those of intensive periodontal treatment (scaling and root planing, locally administered antibiotics and tooth extraction, when necessary). The intensive treatment group showed important and statistically significant improvements in blood flow (as measured by brachial arterial dilation) within two months of treatment. The improvement was greater six months after treatment.

The mechanism by which periodontitis affects endothelial function in the body is still uncertain. The gum disease involves a bacterial infection that invades the tissue around the teeth. One possibility is that the bacteria disturb endothelial function directly, since some bacteria can enter the bloodstream. Alternatively, the periodontitis might trigger a low grade inflammatory response throughout the body that has a detrimental effect on the vascular wall.'
_______________________

J Am Dent Assoc, Vol 137, No suppl_2, 14S-20S. [2006]

Periodontal infections and cardiovascular disease

The heart of the matter

ABSTRACT

Background. Oral infection models have emerged as useful tools to study the hypothesis that infection is a cardiovascular disease (CVD) risk factor. Periodontal infections are a leading culprit, with studies reporting associations between periodontal disease and CVD. The results, however, have varied, and it often is unclear what conclusions can be drawn from these data.

Summary. An association exists between periodontal disease and CVD. It is unknown, however, whether this relationship is causal or coincidental. Early studies predominantly used nonspecific clinical and radiographic definitions of periodontal disease as surrogates for infectious exposure. While most studies demonstrated positive associations between periodontal disease and CVD, not all studies were positive, and substantial variations in results were evident. More recent studies have enhanced the specificity of infectious exposure definitions by measuring systemic antibodies to selected periodontal pathogens or by directly measuring and quantifying oral microbiota from subgingival dental plaque. Results from these studies have shown positive associations between periodontal disease and CVD.

Conclusions. Evidence continues to support an association among periodontal infections, atherosclerosis and vascular disease. Ongoing observational and focused pilot intervention studies may inform the design of large-scale clinical intervention studies. Recommending periodontal treatment for the prevention of atherosclerotic CVD is not warranted based on scientific evidence. Periodontal treatment must be recommended on the basis of the value of its benefits for the oral health of patients, recognizing that patients are not healthy without good oral health. However, the emergence of periodontal infections as a potential risk factor for CVD is leading to a convergence in oral and medical care that can only benefit the patients and public health.

After two decades of research, it has been firmly established that an association exists between periodontal disease and cardiovascular disease (CVD). The pertinent question, however, is about the nature and relevance of this association. Specifically, does the infectious and inflammatory periodontal disease process contribute causally to heart attacks and strokes, or are these two conditions coincidentally associated?

Although the evidence of a potentially contributory role of periodontal infections in the natural history of CVD continues to mount, there are well-founded reasons for skepticism. With this in mind, we provide a state-of-the-science article regarding the association between periodontal disease and CVD.
_______________________

[www.nelm.nhs.uk]

Helicobacter pylori infection linked to atrial fibrillation?

Date Published 16 June 2005

Abstract According to a report published in the July issue of the journal Heart, patients with atrial fibrillation (AF) are nearly 20 times more likely to be infected with the common gastric microbe Helicobacter pylori than are healthy controls, with the association strongest in patients with persistent rather than paroxysmal atrial fibrillation. AF patients also had higher levels of C-reactive protein (CRP) than did controls, suggesting that H. pylori's effects on this arrhythmia may be mediated through an inflammatory pathway. The researchers carried out a study investigating H. pylori positivity and CRP levels in 59 patients with AF and 45 healthy controls. The AF group was further divided into 29 patients with persistent disease and 30 with paroxysmal disease. In the overall analysis, 97.2% of AF patients were seropositive for H. pylori compared with just 5.3% of controls. As noted, CRP levels were significantly higher among AF patients as well (p < 0.001). Further analysis showed that persistent AF was tied to a higher rate of H. pylori seropositivity (p = 0.027) and to higher CRP levels than was paroxysmal disease (p = 0.041).

Although the exact mechanism is unknown, the researchers hypothesise that it may relate to autoantibodies that develop in some H. pylori-infected patients. These antibodies, which normally attack a proton pump found on gastric cells, may instead attack a similarly appearing pump on cardiac cells, ultimately triggering AF. The researchers conclude that their findings show a significant link between H. pylori seropositivity and AF. However they add, "More data will be necessary from controlled studies to further identify how H. pylori can influence the pathogenesis of AF".

Ref. Heart 2005; 91:960-961
__________________________


Irregular Heartbeat Linked To Genetic Mutation, Mayo Clinic Study Shows

24 Feb 2007

Every day for 10 years, a seemingly heart-healthy 53-year-old woman experienced rapid and irregular heartbeats. She had no personal or family history of hypertension or hyperthyroidism. She did not suffer from myocardial or coronary artery disease, or any abnormalities of the heart as best doctors and medical science could determine. Yet, she complained of heart palpitations and dizziness nearly to the point of fainting.

For the patient in this case study, her symptoms first appeared 10 years ago and they persisted through the years. The symptoms peaked in the morning and occurred more frequently as time went on. Doctors prescribed medication, but it proved to be ineffective.

As a next step, Mayo Clinic physician researchers explored and confirmed the presence of a genetic mutation that clearly established an inherited predisposition to atrial fibrillation.

Their study findings appear in the February issue of Nature Clinical Practice Cardiovascular Medicine (http://www.nature.com/clinicalpractice/cardio).

"Why certain patients develop atrial fibrillation while others do not, despite comparable environmental stress exposure, might ultimately depend on their genetic makeup," the authors write.

Atrial fibrillation is recognized more often in the elderly who have underlying structural heart disease. But in this study, Mayo Clinic researchers address the gene-based form of atrial fibrillation that affects younger people who do not otherwise harbor risk factors for the disease. The case was compared to 2,000 individuals who did not carry the mutation or suffer from atrial fibrillation.

The Mayo Clinic study is the first to identify an atrial fibrillation- associated genetic mutation of the ATP-sensitive potassium (KATP) channel. Researchers uncovered its role as a safeguard against atrial arrhythmia under stress conditions. The fail-safe mechanism present in most people to provide electrical stability to the heart under stress was defective in this patient. The sequencing of KATP channel genes, using genomic DNA extracted from the patient's peripheral white blood cells, revealed a genetic mutation.

The discovery of the genetic mutation's role in contributing to atrial fibrillation may ultimately improve physicians' ability to identify patients who have a hereditary predisposition to atrial fibrillation, which is often complicated by increased risk for stroke and heart failure.

"Our findings support the emerging understanding of atrial fibrillation in younger patients as an inherited disease of ion channels, the building blocks of electrical pathways," says Timothy Olson, M.D., a pediatric cardiologist and lead author of the study.

Because medications were ineffective in this case, the Mayo Clinic team treated the woman's atrial fibrillation by targeting high-energy radio waves to an area of the atrium -- an upper heart chamber -- most vulnerable to stress-induced electrical instability. This approach highlights the capacity to successfully treat patients who have genetic forms of atrial fibrillation.

"This case is a fine example of individualized medicine in practice, highlighting the benefit of translating molecular technology into an understanding of disease processes in the clinical setting," says Andre Terzic, M.D., Ph.D., a cardiologist and senior author of the study.

Hi Mako,
interesting post. Also interesting that we have the same internet provider.
If you put the link you refer to within <> without any spaces it will be "clickable"

When I get the chance to dig out my notes on this topic, I'll quote some findings from a doctor who has examined plaques and isolated a variety of 'bugs' in them. The names and number are surprising. I can't remember if he has published studies to back it up, but I do recall that his talk was very convincing as well as enlightening.

The theory of viral or bacterial involvement has been around a long time. It's felt that the body walls off the microbes with the calcified plaques which is one of the reasons treating with antibiotics doesn't work.

The inflammation involved is at the root of what some think is contributory to the cardiovascular diseases and some feel also to afib.

It's a fascinating topic. Well over 10 years ago - probably more like 15, it was found that there was a genetic tendency for those who had periodontal disease. It was very experimental at the time; but I did see families - like elderly mother with period disease and then her children tested and they all tested positive. Cardiologist, Stephen Sinatra wrote about the perio connection and cardiovascular issues many years ago.

Has anyone ever posted these studies before here about genetics or this H pylore bug causing afib? If not perhapos they should be reposted under their own titles. I almost missed them.

CR 42 was a discussion of afib and helicobacter pylori. See:

[www.afibbers.org]

George