But the vaccination has never been associated with heart problems before. 

Do not believe this statement. A quick search turned up contrary information.
P.M.

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=977376&form=6&db=m&Dopt=b
1: Helv Paediatr Acta 1976 OCT;31(3):257-60
Cardiac complications after vaccination for smallpox


http://www.vaccinationnews.com/Scandals/Feb_8_02/SmallVaxReactionsLS.htm
      Ann Clin Res 1978 Oct;10(5):280-7
     Related Articles, Books, LinkOut 
     
Myocardial complications of immunisations.

Helle EP, Koskenvuo K, Heikkila J, Pikkarainen J, Weckstrom P.

Immunisation may induce myocardial complications. In this pilot study clinical, electrocardiographic, chemical and immunological findings have been studied during a six weeks' follow-up after routine immunisation (mumps, polio, tetanus, smallpox, diphtheria and type A meningococcal disease) among 234 Finnish conscripts at the beginning of their military service. Serial pattern of ECG changes suggestive of myocarditis was recorded in eight of the 234 conscripts one to two weeks after vaccination against smallpox and diphtheria. Changes were mainly minor ST segment elevations and T wave inversions and usually they disappeared in a few weeks. The ECG positives more often had a history of atopy, and their mean body temperatures and heart rates after the vaccinations were higher than among the other subjects (p less than 0.01). However, clinical myocarditis was never noted, nor were immunological or enzymological changes different among the ECG positives. Thus in 3% of the study population, evidence of postvaccinal myocarditis was noted, based on serial ECG patterns, but without any other evidence of cardiac disease.

PMID: 736507 [PubMed - indexed for MEDLINE] 
 



washingtonpost.com
Cardiac Cases Raise New Vaccination Questions
By Ceci Connolly
Washington Post Staff Writer
Thursday, March 27, 2003; Page A12

As federal health officials raced to investigate a possible link between smallpox immunizations and heart problems, the federal vaccination campaign faced fresh skepticism yesterday from physicians, health care groups and Democratic lawmakers. On Capitol Hill, House Republican leaders retreated from plans to vote on a compensation package for people harmed by the vaccine, further clouding the future of the Bush administration's efforts to inoculate millions of health care workers and emergency responders.

At least 17 people recently immunized against smallpox have experienced cardiac-related problems, including a Maryland nurse who died of a heart attack Sunday. Although heart problems have not been traced to the smallpox vaccine, the surprising number of recent incidents has raised alarm. Yesterday, the Centers for Disease Control and Prevention issued an alert to state health commissioners recommending that people with heart disease not get the vaccine. The agency called the move temporary and precautionary, but it summoned a team of cardiologists and its vaccine advisory committee to review the developments.

"My gut feeling is they are probably coincidental," said Walter Orenstein, director of CDC's National Immunization Program. "We want to err on the side of caution and investigate further." Ten members of the armed services -- out of 350,000 immunized -- have been treated for inflammation in and around the heart, a condition known as pericarditis or myocarditis, said Col. John Grabenstein, who runs the military vaccination program. Every case was treated with pain relievers, and long-term damage is not expected, he said.

On Sunday, Andrea Deerhart Cornitcher, 56, became the first civilian death potentially tied to the immunization program. The nurse, who lived in Princess Anne, was inoculated five days before her death. Another woman, whose whereabouts have not been disclosed, suffered a heart attack after inoculation and is on life support; a Florida health care worker is recovering from a heart attack. Two people experienced angina, and two had myocarditis. Nearly all of them had a history of heart trouble or a risk factor such as obesity, smoking or high blood pressure, Orenstein said. It is possible, he said, that the heart problems would have occurred even without exposure to the smallpox vaccine.

CDC planned to rush new information packets and consent forms to local health officials last night describing the concerns and recommending that anyone who has suffered a heart attack or has a history of coronary artery disease not be immunized. Other health experts said that recommendation fell short. "That's nice if you know you have heart disease," said Richard Wenzel, chief of internal medicine at the Virginia Commonwealth University
Medical Center in Richmond. "It doesn't help if you don't know."

Eric J. Topol, chairman of cardiovascular medicine at the Cleveland Clinic, said the safer course would be to halt vaccinations in anyone over 50 or do thorough medical exams first. "A simple question about prior heart disease is not going to be enough," he said. As the vaccination program passes the two-month mark, only 24,000 health care workers have responded to the call for volunteers to be inoculated in preparedness for a possible biological attack. News of the cardiac cases -- even if they turn out to be coincidence -- was certain to add another layer of hesitation, some experts said.

"I think many doctors will be just as conservative as the CDC," said William Schaffner, chairman of preventive medicine at Vanderbilt University. "They'll say, 'Why don't you wait till this sorts itself out? There's no rush; the president said there's no immediate threat. You can be vaccinated later.' " Schaffner, who praised the CDC for its swift response to the new information, said the recent cases highlight the challenges in administering a risky vaccine to an adult population. Between illness and risky behavior, "adults come to vaccination with many more risk factors than children," he said.

In a letter to President Bush, Andrew Stern, president of the Service Employees International Union, said, "The grave dangers associated with the smallpox vaccine may no longer be a remote possibility for seven American civilians. . . . We expect full disclosure of the conclusive evidence before another frontline worker is put at unnecessary risk, before another family faces indescribable grief."

On Capitol Hill, lawmakers squabbled over the compensation bill. Democrats have said the White House offer to pay $262,000 in death or disability benefits and up to $50,000 in lost wages is insufficient. "I am deeply disappointed that the compensation scheme the administration has proposed is so inadequate and unfair that it may not jump-start this faltering program," Sen. Edward M. Kennedy (D-Mass.) said. Republicans, describing the benefits as "generous," said the White House is pressing for broader participation.

"We can't delay it any more because the administration clearly identifies it as a must-do emergency measure," said Energy and Commerce Committee Chairman W.J. "Billy" Tauzin (R-La.). "It's fifty-fifty right now."

Staff writers Juliet Eilperin, Anita Huslin and Michael D. Shear contributed to this report.
© 2003 The Washington Post Company
 



Comment by Dr. Sherri Tenpenny:

(Sherri J. Tenpenny, D.O. is a nationally renowned and respected vaccine expert. In August 2002, I hosted a timely and important teleconference featuring Dr. Tenpenny to discuss the real dangers of vaccines and how you can legally avoid them. "The Danger of Vaccines, and How You Can Legally Avoid Them" audio tape, a professionally recorded 90-minute cassette available in my "Recommended Products" section, presents that full
conference.)

Because the civilian casualties of the vaccination program ranged in age from 43 to 55 years and all patients had some form of cardiac problem in their medical histories--including hypertension and angina--the oft repeated vaccination industry mantra, “temporal association does not prove causality,” is once again being used to diminish the link between the smallpox vaccine and the deaths it has caused. Why is it that a vaccine is never the cause of a health problem? 

What is truly sad is that these deaths never should have happened, and not just because the vaccination is unnecessary. If the CDC were to do its homework, it would discover that the connection between the smallpox vaccine and death from cardiovascular disease is not conjecture. Nor is it something that needs “further study.” The mechanism of action has already been proven. 

The smallpox vaccine is capable of causing death because it is a live virus vaccine that induces a physiological state in the body called “hypercoagulability.”  A “hypercoagulable state” is a condition in which a person has an increased potential to develop a thrombosis, commonly known as a blood clot. There are many causes of hypercoagulability, ranging from rare genetic conditions and a variety of blood disorders, to surgical interventions, birth control pills and cancer. 

In addition, there is a long list of cardiovascular diseases, including valvular defects, bypass surgery and hypertension, that can lead to hypercoagulability.[1]  The physiology of the hypercoagulable state is complex. The cascade of events begins when an irregularity develops on the endothelial wall, or inside lining of a blood vessel. As the blood flows past this turbulent surface, platelet cells are disrupted, causing the release of thrombin. 

Thrombin is an enzyme that converts fibrinogen into molecules called soluble fibrin monomers (SFM), generally referred to as fibrin. Strands of this “sticky,” insoluble protein form a mesh that collects the other types of blood cells involved in the formation of blood clots and scars. However, the release of fibrin doesn’t necessarily result in the formation of blood clots. As the body depletes its supply of circulating fibrinogen to create fibrin, more and more fibrinogen is released into the circulatory system. The combination of the additional fibrinogen and free, non-polymerized fibrin fragments increases blood viscosity, meaning the blood becomes “thicker and stickier.” 

Over time, the excess “sticky” fibrin adheres to the walls of capillaries in the microcirculation, resulting in narrowed blood vessels. Tissues become compromised as oxygen and nutrients are blocked from entering the cells. In the heart, this leads to ischemic heart disease and heart attacks. In the brain, it can lead to strokes. 

Cardiologists understand the phenomenon of hypercoagulability and routinely recommend an aspirin a day and other drugs to “thin the blood.” However, these medications are only treating the symptom and do nothing to address what is causing the hypercoagulation in the first place. Pathogens that can activate the fibrin-forming cascade include a long list of bacteria, fungi, mycoplasma and viruses. Because these pathogens are primarily anaerobes, they thrive in cells that are deprived of oxygen. Fibrin-narrowed vessels deliver less oxygen, allowing the pathogens to become embedded in tissue and to propagate at the local level, creating tiny tissue “abscesses” that fester and cause inflammation.[2] 

This process is thought to be one of the causes of the muscle aches seen in fibromyalgia, and why aerobic exercise seems to decrease pain.[3] In addition, viruses create a self-perpetuating hypercoagulable state by adhering to the blood vessel wall. When this occurs, fibrin covers the virus to isolate it from the rest of the body. The result is the formation of additional “bumps” on the inside of the blood vessels, increasing the blood flow turbulence and continuing the thrombin-fibrin-deposition cycle. [4] 

The primary blame for narrowed blood vessels and clot formation is placed on elevated cholesterol levels. But it is the adherence of microbes to the endothelial lining of the blood vessels and subsequent fibrin deposition that is the underlying mechanism of action for cardiovascular disease.[5] In a word: heart disease is an infection. In fact, a recent edition of Critical Care Medicine describes in detail the number of different types of viruses that can cause hypercoagulability: “Direct interaction between microorganisms and endothelial cells can also occur, especially in the case of viral infections. Endothelial cell perturbation [disturbance] is a common feature of viral infection and can alter hemostasis in both a direct and indirect manner. Endothelial cells can be directly infected by a number of viruses (e.g., herpes simplex virus, adenovirus, parainfluenzavirus, poliovirus, echovirus, measles virus, mumps virus, cytomegalovirus, human T-cell lymphoma virus type I, and HIV. In particular, viral infection of endothelial cells has been demonstrated in hemorrhagic fevers (e.g., Dengue virus, Marburg virus, Ebola virus, Hantaan virus, and Lassa virus).”[6] 

Even though vaccinia, the virus that is the active component of the smallpox vaccine, is not specifically mentioned in this list, it should be. The link between vaccinia and hypercoagulability is the reason why cardiologists admit that the connection between the vaccine and cardiovascular side effects is “biologically plausible.” Smallpox vaccination causes a low-grade infection and initiates the hypercoagulability cascade.[7] Researchers have documented that a similar type of hypercoagulability is induced by the anthrax vaccine.[8] 

It took many years for conventional medicine to identify the bacteria, H.pyoli as the culprit in gastric ulcer disease. I wonder how many years it will be before viral infections are routinely considered the cause of cardiovascular disease. Even if conclusive evidence existed that viruses were responsible, the lack of a pharmaceutical answer to the problem would diminish their role. Some investigators have been studying the connection between Chlamydia and cardiovascular disease, but this hypothesis is being discarded.  In fact, a very recent study concluded that treating two groups of patients with the antibiotic azithromycin (Zithromax) for two weeks and three months respectively had “no effect” on the brachial artery response to nitroglycerin.[9] It is difficult to imagine how an antibiotic could affect a microbe buried beneath a layer of fibrin.  

The CDC is deeply disturbed over highly publicized anxiety surrounding the smallpox vaccine. Once the complications from this vaccine are exposed, we are only one, small precarious step away from questioning the unspoken impact that all vaccines have on health.  After all, the vast majority of vaccines are viral vaccines--including measles, mumps, rubella, chicken pox and oral polio. Even more, they are “live virus” vaccines, just like the smallpox vaccine. It is my personal opinion that the impact of the viral load caused by vaccines has been overwhelmingly underestimated and is creating hypercoagulability problems in people of all ages. The virus-hypercoagulability connection will eventually prove to be the “missing link” in connecting a myriad of health problems to our one-size-fits-all mass vaccination policies.  

It is good that the CDC is taking a cautionary stance regarding the smallpox vaccine and those with a history of cardiovascular disease. Many others have already been medically exempted from the vaccine.  It is estimated that at least 10 percent, or more than 28 million people in the United States, have eczema.[10] There are 184,000 organ recipients,[11] 850,000 individuals with diagnosed and undiagnosed HIV infection or AIDS,[12] and 8.5 million people with cancer.[13] The presence of these health conditions constitutes a reason for avoiding the vaccine. An even more extensive list of people at risk is the untold millions who are taking immunosuppressive drugs such as corticosteroids. Prednisone and Medrol, given to both adults and children, are prescribed for dozens of conditions including but not limited to: asthma, emphysema, allergies, Crohn's disease, multiple sclerosis, herniated spinal discs, acute muscular pain syndromes, and all types of rheumatoid arthritis and autoimmune diseases. All of these patients would be at risk for serious complications from contact with a smallpox vaccinated individual.

And now those with a history of cardiovascular disease are being excluded from receiving the smallpox vaccine. Nearly 61 million Americans (almost one-fourth of the population) live with cardiovascular disease, and coronary heart disease is a leading cause of premature, permanent disability in the U.S. workforce.[14]  When adding up the number of Americans who should not receive this vaccine, it comes to more than 98.5 million people. Who is left? Perhaps the rush to spend $780 million to develop this vaccine will turn out to be the
industry’s ultimate boondoggle. 



http://www.nature.com/cgi-taf/DynaPage.taf?file=/nrn/journal/v4/n5/full/nrn1111_fs.html

Nature Reviews Neuroscience 4, 333 (2003); doi:10.1038/nrn1111 

[423K] NEURODEGENERATIVE DISORDERS
Fighting fire with fire 

Heather Wood Since the pioneering work of Edward Jenner in the late 1700s, the idea of creating immunity to disease by challenging the immune system with a pathogenic agent has formed the basis for numerous successful immunization programmes. Research in mice has indicated that Alzheimer's disease (AD) might be amenable to this approach, although clinical trials were halted because of potentially serious side effects. However, despite this setback, some encouraging findings have emerged, as Nicoll and colleagues now report in Nature Medicine. 

Their paper describes the case of a 72-year-old woman with a five-year history of AD. The woman was immunized with amyloid- (A) peptide — one of the main constituents of the plaques that accumulate in the brains of patients with AD. Previous studies in mice had shown that immunization with A caused animals to mount an immune response against the endogenous peptide, leading to breakdown of many of the plaques. The mice also showed evidence of cognitive improvement — one of the principal goals of any AD therapy.

As the new paper illustrates, the human trials seemed to be considerably less successful than their animal counterparts. The woman described by Nicoll et al. showed no obvious signs of improvement in her AD symptoms, and several months into the trial, her overall condition deteriorated rapidly. Like several other patients that received the vaccine, she showed signs of brain inflammation. Twenty months after the start of the treatment — and twelve months after she received her last injection — she died from a pulmonary embolism. The trial was terminated at the beginning of 2002.

The prospects for the vaccine looked bleak at this stage. However, a post mortem examination has now shown that the woman's brain contained significantly fewer plaques than would be expected for a person at this stage of the disease. Moreover, some of the remaining A was associated with microglia — the cells that are believed to be important for clearing A from the brain — implying that removal of A might still have been taking place at the time of her death.

So, what does the future hold for the Alzheimer's vaccine? These new findings seem to indicate that it is worth pursuing, but the side effects will clearly need to be resolved. One problem with the A vaccine is that it seems to provoke a T-cell-mediated immune response, which results in a harmful encephalitis. The T-cell response might be bypassed by immunizing with antibodies against A, rather than with the peptide itself. Alternatively, as the A epitope that elicits the strongest immune response is in the amino terminus, it might be preferable to immunize with a fragment of A instead of the full peptide. Assuming that the problems can be ironed out, it will be necessary to show that the vaccine can actually relieve the symptoms of AD in humans, or even prevent them if administered before the disease process starts. This is important both from a clinical and a research perspective —it is widely believed that amyloid plaques are at least partly responsible for the cognitive decline in AD, and the vaccine has the potential to allow the further exploration of this idea.

References 
ORIGINAL RESEARCH PAPER
Nicoll, J. A. et al. Neuropathology of human Alzheimer disease after immunization with amyloid- peptide: a case report. Nature Med. 17 March 2003 (doi: 10.1038/nm847) | Article

FURTHER READING
Schenk, D. Amyloid- immunotherapy for Alzheimer's disease: the end of the beginning. Nature Rev. Neurosci. 3, 824-828 (2002)

Bard, F. et al. Epitope and isotype specificities of antibodies to -amyloid peptide for protection against Alzheimer's disease-like neuropathology. Proc. Natl Acad. Sci. USA 100, 2023-2028 (2003)
 




"Smallpox Vaccine, Heart Inflammations May Be Linked"
Atlanta Journal-Constitution (www.accessatlanta.com/ajc) (05/23/03) P. 7A;
Wahlberg, David

The Centers for Disease Control and Prevention (CDC) has uncovered a possible link between the smallpox vaccine and heart inflammations.  The CDC said Thursday that about 24 civilians have developed inflammation around the heart or surrounding membranes after receiving the smallpox vaccine, and the Defense Department reported similar symptoms in 27 members of the military who had received the vaccine.  During the 1950s and 60s, when smallpox vaccination was routine, the number of cardiac events were rare; however, the number has gone up since the government reactivated smallpox vaccinations in case of a possible bioterrorism attack.  Many of the individuals vaccinated back then were children, and the primary tests used today to identify heart disease had not yet been developed.  Dr. J. Michael Lane, former head of the CDC's smallpox eradication program, also noted that some of the heart problems may be unrelated to the vaccine. Earlier this year, the CDC recommended against smallpox vaccination for people with heart disease or at least three risk factors, such as high blood pressure, high cholesterol, or diabetes.

 

http://www.eurekalert.org/pub_releases/2003-11/aha-sdh102203.php

Public release date: 10-Nov-2003
Contact: Carole Bullock
carole.bullock@heart.org
214-706-1279
American Heart Association

Studies describe heart disease following smallpox vaccination American Heart Association meeting report Orlando, Fla., Nov. 10 –

Heart-related complications can occur after the smallpox vaccine, but symptoms are usually mild, according to three studies presented at the American Heart Association's Scientific Sessions 2003. The rate of adverse cardiac events was about 58 per 100,000 vaccinations in data collected between January and May 2003, said Richard Schieber, M.D., of the Smallpox Vaccine Adverse Events Monitoring and Response Activity, National Immunization Program at the Centers for Disease Control and Prevention (CDC) in Atlanta, Ga.

Twenty-four cases of pericarditis, myocarditis, dilated cardiomyopathy or acute coronary syndromes (heart attack or chest pain known as angina) were identified among 37,876 U.S. civilian healthcare workers vaccinated as part of the nation's bioterrorism readiness program. Twenty-two patients had pericarditis or myocarditis.

Pericarditis is inflammation of the pericardium, the thin sac (membrane) that surrounds the heart and the roots of the great blood vessels. Chest pain is one of the first signs. Myocarditis is inflammation of the heart muscle caused by conditions such as infection, rheumatic fever, diphtheria, tuberculosis or toxic drug poisoning.

The average interval from vaccination to illness was about 12 days. Most patients with myocarditis had a mild form of the disease, but two of eight patients with acute coronary syndromes died suddenly within three weeks after vaccination. Five of the eight had three or more risk factors for, or a history of, coronary artery disease before vaccination. In a large population in the same age range, some acute coronary events will occur over several weeks even in the absence of any identifiable cause, Schieber said.

Public health officials expected some adverse reactions associated with the smallpox program, but didn't anticipate heart complications, he said. "As the civilian vaccination program unfolded, we received reports about cardiac complications among the military personnel in December, in addition to some apparent cases of myocarditis and pericarditis," he said. "Since the deaths occurred soon after the vaccinations, the CDC convened an emergency meeting to review the data and determine if changes were needed in the vaccine program."

"While we couldn't determine a direct causal link between the vaccine and the acute coronary syndrome, the CDC did recommend that anyone who has three of these five known heart disease risk factors -- high blood pressure, high cholesterol, diabetes, a family history of heart disease or cigarette smoking -- should not be vaccinated."

John Murphy, M.D., a cardiologist at the Mayo Clinic in Rochester, Minn.,studied 18 cases of myocarditis or pericarditis among 230,000 military personnel. "That's an incidence of about one case per 12,700 vaccinees," Murphy said. In the third study, Gregory K. Bruce, M.D., reported biopsy results from one of those 18 cases. The 29-year-old soldier was admitted to the hospital with shortness of breath two weeks after he received his smallpox vaccination. He also had elevated cardiac troponin levels, which indicates heart muscle damage, and high C-reactive protein levels, which indicates inflammation.

Myocarditis was confirmed with a biopsy. After he was diagnosed, further tests suggested that his heart muscle injury was caused by an immune system response to the initial vaccination. "The smallpox vaccine appears to be associated with myocarditis and pericarditis, but so far disease has been mild in civilians who received the vaccine," Schieber said. The relationship between the vaccine and acute coronary syndromes or heart attacks is still not clear, he said.

In a statement regarding the first ischemic heart disease complications that occurred after vaccinations began, the American Heart Association said, "In the past, cardiac complications after smallpox vaccination have been rare, but the majority of individuals undergoing vaccination in previous programs were children or young adults at low risk for underlying heart disease. Now that a large number of adults are receiving the vaccine, especially those in middle age who may have underlying heart disease, it will be important to carefully and continuously monitor the situation."

The American Heart Association urges people who have been vaccinated for smallpox to be aware of the symptoms of pericarditis, myocarditis and acute coronary syndromes and to contact their healthcare provider with any concern about their heart health. These symptoms may include chest pain or discomfort, palpitations, shortness of breath, ankle swelling, and/or unusual fatigue. 


Schieber's co-authors are Juliett Morgan; Martha H. Roper; Linda Neff; Louisa Chapman; John Iskander; Gina Mootry; Laurence Sperling; Rose Marie Robertson and David Swerdlow. Murphy and Bruce's co-authors are Scott Wright; Keith Bruce; James Riddle; William D. Edwards; Larry M. Baddour and Leslie T. Cooper.

NR03 – 1145 (SS03/Schieber/Smallpox)

Abstracts
P3391 (11/11/03 9:30 a.m.) Schieber
1825 (11/10/03 9:15 a.m.) Bruce
2358 (11/11/03 8:30 a.m.) Murphy
This news release contains updated data from the abstracts.

 



http://www.upi.com/view.cfm?StoryID=20031006-113325-5591r


Mystery blood clots felling U.S. troops
By Mark Benjamin
Investigations Editor
Published 10/6/2003 12:41 PM
View printer-friendly version

WASHINGTON, Oct. 6 (UPI) -- Unexplained blood clots are among the reasons a number of U.S. soldiers in Operation Iraqi Freedom have died from sudden illnesses, an investigation by United Press International has found. In addition to NBC News Correspondent David Bloom, who died in April of a blood clot in his lung after collapsing south of Baghdad, the Pentagon has told families that blood clots caused two soldiers to collapse and die. At least eight other soldiers have also collapsed and died from what the military has described as non-combat-related causes.

A disturbing parallel has also surfaced: soldiers becoming ill or dying from similar ailments in the United States. In some cases, the soldiers, their families and civilian doctors blame vaccines given to them by the military, particularly the anthrax or smallpox shots. Some of the soldiers who died suddenly had complained about symptoms suffered by Bloom -- including pain in the legs that could indicate problems with blood clots.

"If there is a significant number of deaths of this type, it would make you wonder what was going on," said Rose Hobby, whose brother-in-law, Army Spc. William Jeffries, died of a massive lung blood clot and swelling of his pancreas on March 31 after being evacuated from Kuwait. "How many others are out there?"

"I would say that that number of cases among young healthy troops would seem to be unusual," Dr. Jeffrey Sartin, an infectious diseases doctor at the Gundersen Clinic in La Crosse, Wis., said about blood clot deaths. Sartin, a former Air Force doctor, last spring treated a soldier who might have died from anthrax or smallpox side effects. "I am not aware that there were this many cases" during the first Gulf War, Sartin said.

The Pentagon has been investigating cases of a mysterious pneumonia that has killed two soldiers and put 17 more on ventilators. Besides the pneumonia, there do not seem to be any unexpected health trends given the number of troops in the region, said Army Surgeon General spokeswoman Virginia Stephanakis.

"We are not seeing larger numbers of most illnesses than we could have expected," Stephanakis said. "We have not seen any red flags. As far as I know, there has not been a huge red flag other than the pneumonia." UPI's investigation found 17 soldiers who died of sudden illnesses. Families say they are bewildered by the deaths. "Bill just dropped. They thought he had been shot. That is how suddenly it happened," said Rose Hobby, the woman whose 39-year-old brother-in-law William Jeffries collapsed in Kuwait.

After being evacuated from Kuwait to Rota, Spain, he was in intensive care for a week before dying, Hobby said in a telephone interview from Evansville, Ind. A doctor in Spain said Jeffries had "the largest pulmonary embolism he had ever seen," Hobby said. Jeffries also had a swelling of the pancreas, often caused by heavy drinking or some drugs. Jeffries was not a drinker, Hobby said.

Jeffries was back in the United States just days before his death to attend his own father's funeral. He had a scab on his arm from his recent smallpox vaccination. Hobby said she does not know if he got anthrax shots also, like most soldiers in the region. Patrick Ivory arrived in Germany Aug. 16 to see his 26-year-old son, Army Spc. Craig S. Ivory, before he died. By then, Craig Ivory was already brain dead from a blood clot that hit his brain on Aug. 11. "I had to make a decision to turn off life support, which was the most difficult thing I have ever done in my life," Patrick Ivory said in a telephone interview from his home in Port Matilda, Pa.

In other cases of apparently healthy soldiers who died suddenly in Operation Iraqi Freedom, families told UPI they have gotten few answers from the military. Local media reports have quoted military officials saying some of the deaths were apparent heart attacks; they have occurred from the beginning of the conflict through last week. "If anybody has a right to know what my husband died of, it is me," said Lisa Ann Sherman, whose husband, Lt. Col. Anthony Sherman, suddenly clutched his chest and died Aug. 27 in Camp Arifjan, Kuwait. "The only thing they (the military) had to tell me was severe myocardial infarction," or a heart attack.

Anthony Sherman, 43, was a marathon runner and a triathlete. Sherman said her husband complained of pain in his legs after getting anthrax shots. She said she has since learned that he went to sick call complaining of pain in his legs on the day he died. NBC's Bloom, who also got the anthrax and smallpox vaccines, complained of pain in his legs, presumably from a blood clot that has been attributed to cramped quarters in his armored vehicle.

"I am very suspicious about the true reason behind my husband's death," Sherman said. The Pentagon said side effects from the anthrax vaccine are generally mild and rare. In one case, however, the military said the anthrax vaccine did cause a soldier's chronic blood-clot condition.

Capt. Jason M. Nietupksi says he has suffered severe reactions to three anthrax shots given to him in the Army Reserves in February 2000, when he was 29 years old. Nietupski said the vaccine caused chronic fatigue, a skin reaction and a blood clot condition called Deep Vein Thrombosis. Nietupski described intense pain in his legs caused by the clots from that condition. Nietupski is on blood thinners for the rest of his life. His records from the military state his blood clot condition was caused by the anthrax shots.

"CPT Nietupski had multiple adverse medical problems associated with three anthrax vaccinations he received while assigned to the 8th United States Army," read the results of a military line-of-duty inquiry report. "A condition described as Deep Vein Thrombosis, chronic fatigue and Steven Johnson's Syndrome all are adverse reactions that developed in this previously healthy individual from the anthrax vaccine. Evaluation by Walter Reed Physicians state (sic) that his symptoms are related to the anthrax vaccine." The anthrax vaccine label warns of infrequent reports of heart attacks or strokes among people who have taken that vaccine. Both heart attacks and strokes can be caused by blood clots.

With smallpox shots, top Pentagon health officials released a study in June that said 37 soldiers have had a swelling of the tissue around the heart probably caused by the vaccine and eight other "cardiac events" occurred within a fortnight of getting the vaccine, including heart attacks. The Pentagon said they had seen no deaths that might have been caused by the smallpox vaccine. Civilian officials have disagreed, at least in one case.

In the April 4 death of Army Spc. Rachael Lacy of Lynwood, Ill., a civilian doctor who treated her and the civilian coroner who performed her autopsy said the smallpox and anthrax vaccines the Army gave her March 2 in preparation for her deployment for Operation Iraqi Freedom might have caused her death. Lacy had pneumonia and a swelling of the tissue surrounding the heart, among other things.

The Deputy Director of the Military Vaccine Agency, Col. John D. Grabenstein told UPI in August that Lacy's death has not been classified by the military as related to either vaccine. "Rachael Lacy is still in the unexplained death program" at the Centers for Disease Control and Prevention, Grabenstein said. After two health care workers died of heart attacks after getting smallpox shots, in March the Centers for Disease Control and Prevention recommended that people with a risk of heart disease not take the vaccine.

Copyright (c) 2001-2003 United Press International

 



J Am Coll Cardiol. 2000 Mar 1;35(3):819-20.

Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction.

Frustaci A, Magnavita N, Chimenti C, Caldarulo M, Sabbioni E, Pietra R,
Cellini C, Possati GF, Maseri A.

Department of Cardiology, Catholic University, Rome, Italy.

OBJECTIVES: We sought to investigate the possible pathogenetic role of myocardial trace elements (TE) in patients with various forms of cardiac failure. BACKGROUND: Both myocardial TE accumulation and deficiency have been associated with the development of heart failure indistinguishable from an idiopathic dilated cardiomyopathy. METHODS: Myocardial and muscular content of 32 TE has been assessed in biopsy samples of 13 patients (pts) with clinical, hemodynamic and histologic diagnosis of idiopathic dilated cardiomyopathy (IDCM), all without past or current exposure to TE. One muscular and one left ventricular (LV) endomyocardial specimen from each patient, drawn with metal contamination-free technique, were analyzed by neutron activation analysis and compared with 1) similar surgical samples from patients with valvular (12 pts) and ischemic (13 pts) heart disease comparable for age and degree of LV dysfunction; 2) papillary and skeletal muscle surgical biopsies from 10 pts with mitral stenosis and normal LV function, and 3) LV endomyocardial biopsies from four normal subjects. RESULTS: A large increase (>10,000 times for mercury and antimony) of TE concentration has been observed in myocardial but not in muscular samples in all pts with IDCM. Patients with secondary cardiac dysfunction had mild increase (< or = 5 times) of myocardial TE and normal muscular TE. In particular, in pts with IDCM mean mercury concentration was 22,000 times (178,400 ng/g vs. 8 ng/g), antimony 12,000 times (19,260 ng/g vs. 1.5 ng/g), gold 11 times (26 ng/g vs. 2.3 ng/g), chromium 13 times (2,300 ng/g vs. 177 ng/g) and cobalt 4 times (86,5 ng/g vs. 20 ng/g) higher than in control subjects. CONCLUSIONS: A large, significant increase of myocardial TE is present in IDCM but not in secondary cardiac dysfunction. The increased concentration of TE in pts with IDCM may adversely affect mitochondrial activity and myocardial metabolism and worsen cellular function.

PMID: 10334427 [PubMed - indexed for MEDLINE]
 



http://www.apria.com/resources/1,2725,494-129554,00.html

Acute Myocarditis Associated with Tetanus Vaccination 
  Dilber, Embiya; Karagoz, Tevfik; Aytemir, Kudret; Ozer, Sema; Et al 
  
  Originally Published:20031101. 

To the Editor: Millions of people undergo vaccination each year; thus, it is perhaps not surprising that a fraction develop adverse effects because of immunologic responses to the target antigen and to other nonspecific antigens contained within the vaccine. These immunologic reactions can result in aberrations in systemic physiology or direct injury to tissues and organs. Hypersensitivity myocarditis is an inflammatory disease of the myocardium, usually related to drug allergy. Many drugs have been reported as possible etiologic agents.1,2 We report a case of hypersensitivity myocarditis apparently related to a tetanus vaccination. 

Report of a Case.-A previously healthy 14-year-old boy presented with fever and intermittent (lasting a few minutes) chest pain. The symptoms developed 3 days after he had received a vaccination for tetanus (Tetavax, Aventis Pasteur SA, Lyon, France). His medical history was unremarkable except for a severe skin eruption that occurred after trimethoprim-sulfamethoxazole treatment when he was 8 years of age. He had no history of adverse  reactions to tetanus or other vaccinations. Findings on physical examination were normal except for fever (38.3[degrees]C) that was recorded on 4 occasions. Heart sounds were normal, and no precordial friction rub was detected. On admission, laboratory investigations yielded the following results (reference ranges shown parenthetically): white blood cell count, 10.6 x 10^sup 9^/L with 3% eosinophils; erythrocyte sedimentation rate, 42 mm/h; IgE, 72 kU/L (&lt;10 kU/L); troponin T, 1.04 ng/mL (&lt;0.1 ng/mL); myoglobin, 83 [mu]g/L (&lt;72 [mu]g/L); creatine kinase, 1218 U/L (&lt;190 U/L); CK-MB fraction, 80.86 ng/mL (&lt;5 ng/mL); alanine aminotranserase, 28 U/L; and aspartate aminotransferase, 117 U/L (Table 1). Chest radiography revealed normal findings, and echocardiography showed normal left ventricular function and no pericardial effusion. The initial electrocardiogram (ECG) showed mild ST-segment elevation in the inferior leads and a notable ST-segment elevation in precordial leads V^sub 4^, V^sub 5^, and V^sub 6^. The patient's intermittent chest pain persisted throughout the day. On the second day of hospitalization, repeated ECG revealed diffuse ST-segment elevation, especially in leads V^sub 4^, V^sub 5^, and V^sub 6^, and inverted T waves in the left precordial leads (Figure 1). Findings on repeated echocardiography were again normal. Urgent angiography showed normal coronary arteries. On the third hospital day, ECG
disclosed slight ST-segment elevation and inverted T waves in the left precordial leads. The patient's course was uneventful, and he was discharged on hospital day 4. Three days later, the patient was symptom-free, and his ECG was completely normal. Cardiac enzyme levels had decreased to nearly normal levels. 14#vety=11;enum=1;<ECAP> Table 1. Serial Laboratory Measurements in Patient With Hypersensitivity Myocarditis </ECAP>13#vety=7;enum=2;<ECAP> Figure 1. Electrocardiographic tracings recorded on hospital day 1 (I), 2 (II), and 3 (III) and 7 days (VII) after hospitalization, showing ST-segment and T-wave changes in left precordial leads. bpm = beats per minute. </ECAP> Discussion.-The clinical features of hypersensitivity myocarditis include nonspecific findings such as rash and fever as well as cardiac manifestations.3 Cardiac involvement can manifest within hours or months after the initial exposure to the drag. Sinus tachycardia, mild cardiomegaly, conduction delays, and nonspecific ST-T changes are common, whereas pseudoinfarction patterns are seen less frequently.1,2 Cardiac enzyme levels are usually mildly elevated, rarely more than twice the normal value.3 The mechanism of action has been postulated to be a delayed hypersensitivity reaction.2 Our patient's symptoms, ECG, and laboratory findings were consistent with myocardial involvement. 

Although hypersensitivity myocarditis has been reported in association with a variety of drugs,1,2 cardiovascular complications due to vaccination are rare,4-6 and only a few cases of myocarditis after vaccination have been reported. One recent report5 described a case of myopericarditis after
triple vaccination against diphtheria, tetanus, and poliovirus. The patient had symptoms similar to our patient's, with slightly elevated cardiac enzymes and normal findings on echocardiography and coronary angiography. The vaccination was the suspected cause in view of the chronology of the symptoms. Performing a provocative test that would confirm the causal relationship between the vaccination and the cardiac anomalies would be unethical. 

Our patient's illness had a pseudoinfarction pattern that is seen infrequently in hypersensitivity myocarditis.7,8 The acute chest pain, ST-segment elevation and T-wave inversion on ECG, and slight increase in cardiac enzyme levels were consistent with myocardial involvement. However, echocardiography revealed normal left ventricular function, and angiography showed normal coronary arteries, findings that suggest the ECG abnormalities were due to myocarditis and not to ischemia. 

Hypersensitivity myocarditis should be considered when new ECG changes occur in association with acute-onset chest pain, mildly elevated cardiac enzyme levels, and eosinophilia due to drugs and vaccination. 13#vety=5;enum=0;<ETXT> 1. Fenoglio JJ Jr, McAllister HA Jr, Mullick FG. Drug related myocarditis, I: hypersensitivity myocarditis. Hum Pathol. 1981; 12:900-907. 

2. Taliercio CP, Olney BA, Lie JT. Myocarditis related to drug
hypersensitivity. Mayo Clin Proc. 1985;60:463-468. 

3. Kounis NG, Zavras GM, Soufras GD, Kitrou MP. Hypersensitivity
myocarditis. Ann Allergy. 1989;62:71-74. 

4. Amsel SG, Hanukoglu A, Fried D, Wolyvovics M. Myocarditis after triple
immunisation. Arch Dis Child. 1986;61:403-405. 

5. Boccara F, Benhaiem-Sigaux N, Cohen A. Acute myopericarditis after
diphtheria, tetanus, and polio vaccination. Chest. 2001;120:671-672. 

6. Helle EP, Koskenvuo K, Heikkila J, Pikkarainen J, Weckstrom P.
Myocardial complication of immunisations. Ann Clin Res. 1978; 10:280-287. 

7. Galiuto L, Enriquez-Sarano M, Reeder GS, et al. Eosinophilic myocarditis
manifesting as myocardial infarction: early diagnosis and successful
treatment. Mayo Clin Proc. 1997;72:603-610. 

8. Hirakawa Y, Koyanagi S, Matsumoto T, Takeshita A, Nakamura M. A case of
variant angina associated with eosinophilia. Am J Med. 1989;87:472-474.
</ETXT>14#vety=16;enum=0;<ETXT> Embiya Dilber, MD 

Tevfik Karagoz, MD ,Kudret Aytemir, MD ,Sema Ozer, MD, Dursun Alehan, MD , Ali Oto, MD, Alpay Celiker, MD 

Hacettepe University Faculty of Medicine 

Ankara, Turkey </ETXT> 
  
  (C) 2003 Mayo Clinic Proceedings. via ProQuest Information and Learning
Company; All Rights Reserved 
 




http://www.timesonline.co.uk/article/0,,8122-1250768,00.html

1 in 5 children shows signs of heart disease
By Mark Henderson and Nigel Hawkes


DAMAGE to microscopic blood vessels that is linked to heart disease and strokes can be detected in children as young as 11, scientists have discovered. A study of Scottish children aged between 11 and 14 has revealed that 20 per cent have already developed flaws in their capillaries and arteries that can contribute to cardiovascular disease later in life.

The findings, from the University of Dundee, suggest that poor diet and a lack of exercise are having a serious impact on long-term cardiovascular health at a much earlier stage than has generally been thought: the changes were most pronounced in children with elevated blood sugar and above-average body fat.

The research also raises the prospect of screening children for potential problems long before they are likely to show any symptoms of heart or circulatory disorders, allowing those most at risk to change their diet and lifestyle while any damage is still reversible. “This shows us that changes are occurring at a very early stage of our lives,” Faisal Khan, who led the study, told the British Association Festival of Science at the University of Exeter.

“These can perhaps give us predictions of those people who might be candidates for later cardiovascular diseases such as stroke and heart disease. “By implementing lifestyle changes we may be able to reverse the damage at a stage where this is still possible. If you leave it to the 40s these factors become much more difficult to control.” In the study, Dr Khan’s team examined the blood vessel function of 158 Dundee children aged between 11 and 14. The researchers concentrated on the smallest vessels in the body – capillaries and arterioles thinner than a human hair at less than 100 microns in diameter.

All blood vessels are lined with a layer of cells known as the endothelium,which controls their ability to contract and dilate, as well as limiting blood clots, inflammation and unwanted blood vessel growth. Disruption of the endothelium’s functions can induce the hardening process known as atherosclerosis — one of the key drivers of cardiovascular disease. Such damage is at least as strongly linked to these conditions as an unhealthy cholesterol balance. “My guess is that it’s probably an even stronger predictor because endothelial cells are so fundamental to how blood vessels work,” Dr Khan said. To test the children’s endothelial function, the researchers applied to the skin a drug that promotes the dilation of microscopic blood vessels, and then measured blood flow using lasers. These tests showed impaired endothelial function in 20 per cent of the children.

Children were particularly likely to show this sort of damage if they had raised concentrations of glucose in the blood, which may lead to diabetes later in adulthood, or had larger than normal deposits of fat around the midriff, even if they were not clinically obese. This “central adiposity” or “apple shape” fat is recognised as a risk factor for heart disease. These links suggest that the damage to the endothelium may be influenced by the effects of poor diet or a lack of exercise, though other factors such as genetics, birth weight and the environment in the mother’s womb are also likely to be involved.

Asked whether the study worried him, Dr Khan said: “It does. If you look at the incidence of heart disease in Scotland and the diet in parts of Scotland, I think these are early signs that we need to be taking some action. “From a public health perspective, it is clear that endothelial dysfunction is related to lifestyle factors, such as smoking, obesity and lack of exercise. Given the rise in obesity in the general public, and of more concern in children, incorporating regular exercise into everyday life and healthier eating is of more importance than ever.”

The researchers are now seeking to establish more precisely the extent to which endothelium damage in childhood can predict heart disease risk, and whether changes in lifestyle lead to any long-term improvements.
 



 http://www.pittsburghlive.com/x/tribune-review/health/s_272498.html
Smallpox vaccine linked to heart inflammation
By The Associated Press

Saturday, November 13, 2004 

WASHINGTON (AP) -- Wyeth Pharmaceuticals Inc. will add black-box warnings linking its smallpox vaccine to heart inflammation, the government announced Friday. Healthy adults given Dryvax vaccine suffered acute myopericarditis -- inflammation of the heart and its surrounding sac -- says the warning approved by the Food and Drug Administration. Wyeth spokesman Doug Petkus said the company no longer manufactures or markets the smallpox vaccine. The vaccine had remained in storage since the 1980s. After the Sept. 11, 2001, terrorist attacks, the government asked Wyeth to test the smallpox vaccine to ensure it was potent. 

The black-box warnings apply to those vaccines repackaged by Wyeth for immediate use by firefighters, medical personnel and other first responders. The company had provided nearly 15 million doses for government use, enough to vaccinate up to 8 million people. Government health agencies vaccinated 36,217 civilians. The military has inoculated nearly 680,000 personnel since December 2002. Roughly 13 million smallpox vaccine doses remain in the Centers for Disease Control and Prevention's stockpile. 

Because of life-threatening complications associated with existing smallpox vaccines, the government has sought safer new-generation smallpox vaccines to prepare for another terror attack. In a recent clinical trial comparing Dryvax to an investigational smallpox vaccine, eight confirmed or suspected cases of myopericarditis were detected among 1,162 patients. That means people had a 1 in 145 chance of developing the heart condition after vaccination with Dryvax.  The conclusion followed concerns raised during a 2002-03 Department of Defense vaccination program. Of 540,824 military personnel who received Dryvax, 67 developed myopericarditis -- or 1.2 per 10,000 vaccinations. The heart problems developed quickly, in three to 25 days. 

Among vaccinated civilians, 21 cases of myopericarditis were reported as of May 9, 2003, according to the FDA. Col. John Grabenstein, deputy director for military vaccine at the Army Surgeon General's Office, said the Department of Defense has warned about the heart problem since April 2003. "This is not a new finding. This is paperwork catching up with an old finding," Grabenstein said. While the heart condition is alarming -- sending otherwise healthy people to the emergency room with chest pains mistaken for heart attacks -- he said it remains uncommon. 

People stricken with the heart ailment get better, according to follow-up blood tests, heart exams and exercise stress tests. "Their recovery is very good," he said. This summer, tens of thousands of troops stationed in the Pacific and the Middle East received mandatory anthrax and smallpox vaccines to protect against biological warfare. In response to a federal judge's order in late October, the Pentagon halted the mandatory anthrax vaccinations for the military -- six shots spaced over 18 months. 

Mandatory smallpox vaccinations, not yet challenged in the courts, continue for personnel headed to Afghanistan, Iraq and Korea. In addition, a team of smallpox-vaccinated staffers are assigned to nearly 100 military hospitals and large clinics around the world, Grabenstein said. 

The Associated Press can be reached at or . 


Images and text copyright © 2004 by The Tribune-Review Publishing Co.
Reproduction or reuse prohibited without written consent from PittsburghLIVE.

 



December 2004 • Volume 145 • Number 6 

Clinical and Laboratory Observation
Stroke after varicella vaccination

Elaine Wirrell, MD, FRCPC * Michael D. Hill, MD, MSc, FRCPC  Taj Jadavji, MD, FRCPC, FAAP [MEDLINE LOOKUP] Adam Kirton, MD [MEDLINE LOOKUP] Karen Barlow, MB, ChB, MRCP [MEDLINE LOOKUP] • Previous article in Issue 
•
Two children presented with acute hemiparesis 5 days and 3 weeks following varicella vaccination. Both showed unilateral infarction of the basal ganglia and internal capsule, a distribution consistent with varicella angiopathy. Both children had small patent foramen ovale (PFO), and one child also had severe iron-deficiency anemia, which may have predisposed the patient to this adverse effect.

 



Volume 351:2611-2618 December 16, 2004 Number 25 

Risk of Myocardial Infarction and Stroke after Acute Infection or Vaccination

Liam Smeeth, Ph.D., Sara L. Thomas, Ph.D., Andrew J. Hall, Ph.D., Richard Hubbard, D.M., Paddy Farrington, Ph.D., and Patrick Vallance, M.D. 
ABSTRACT

Background There is evidence that chronic inflammation may promote atherosclerotic disease. We tested the hypothesis that acute infection and vaccination increase the short-term risk of vascular events. 

Methods We undertook within-person comparisons, using the case-series method, to study the risks of myocardial infarction and stroke after common vaccinations and naturally occurring infections. The study was based on the United Kingdom General Practice Research Database, which contains computerized medical records of more than 5 million patients. 

Results A total of 20,486 persons with a first myocardial infarction and 19,063 persons with a first stroke who received influenza vaccine were included in the analysis. There was no increase in the risk of myocardial infarction or stroke in the period after influenza, tetanus, or pneumococcal vaccination. However, the risks of both events were substantially higher after a diagnosis of systemic respiratory tract infection and were highest during the first three days (incidence ratio for myocardial infarction, 4.95; 95 percent confidence interval, 4.43 to 5.53; incidence ratio for stroke, 3.19; 95 percent confidence interval, 2.81 to 3.62). The risks then gradually fell during the following weeks. The risks were raised significantly but to a lesser degree after a diagnosis of urinary tract infection. The findings for recurrent myocardial infarctions and stroke were similar to those for first events. 

Conclusions Our findings provide support for the concept that acute infections are associated with a transient increase in the risk of vascular events. By contrast, influenza, tetanus, and pneumococcal vaccinations do not produce a detectable increase in the risk of vascular events. 

Source Information

From the Departments of Epidemiology and Population Health (L.S.) and Infectious and Tropical Diseases (S.L.T., A.J.H.), London School of Hygiene and Tropical Medicine, London; the Division of Respiratory Medicine, University of Nottingham, Nottingham (R.H.); the Division of Statistics, Open University, Milton Keynes (P.F.); and the Centre for Clinical Pharmacology, British Heart Foundation Laboratories, Division of Medicine, University College London (P.V.) — all in the United Kingdom. 

Address reprint requests to Dr. Smeeth at the Department of Epidemiology and Population Health

 



http://www.tkb.org/NewsStory.jsp?storyID=45827

Long lines for flu shots, but no shortage of smallpox vaccine 

As of Oct. 31, the federal Centers for Disease Control andPrevention reported 59 cases of adverse events associated with thevaccine, including 21 cases of myocarditis or pericarditis and one caseof encephalitis, a potentially fatal inflammation of the brain orcentral nervous system. 

The CDC reported another 107 serious adverseevents that may or may not have been caused by the vaccine.Meanwhile,Defense Department officials reported 82 cases of myocarditis andpericarditis since December 2002, when the military began mandatorysmallpox vaccinations for selected personnel. 

Military officials alsoreviewed seven deaths among the more than 700,000 personnel who havereceived the vaccine and say three people have received vaccinia immuneglobulin, which is injected or given intravenously to treat seriousadverse reactions.As in the military, some civilians have diedafter receiving the smallpox vaccine, including Deerheart Cornitcher,55, a nurse at Peninsula Regional Medical Center in Salisbury, Md."I don't think that helped us," Prue Albright, director of public health nursing in Delaware, said of Cornitcher's death.

Health officials knew that the vaccine, made with a live virus,carried a small risk of life-threatening complications, but they weresurprised by reports of heart attacks and cases of myocarditis andpericarditis, inflammations of the heart and surrounding membrane,after people were vaccinated."

 



http://72.14.207.104/search?q=cache:mVgtYdxF88MJ:www.altcorp.com/
DentalInformation/heartdis.htm+idiopathic+dilated
+cardiomyopathy++dr.+haley&hl=en&

Marked Elevation of Myocardial Trace Elements in Idiopathic
Dilated Cardiomyopathy Compared With Secondary Dysfunction

1Frustaci, A., 2Magnavita, N., 1Chimenti, C., 2Caldarulo, M., 3Sabbioni, E., 3Pietra, R., 4Cellini, C., 4Possati, G.F. and 1Maseri, A.

1Department of Cardiology, 2Department of Occupational Medicine, and 3Department of Cardiac Surgery, Catholic University, Rome Italy and CEC 4Environmental Institute Joint Research Center Ispra, Rome, Italy

Journal of the American College of Cardiology

Vol. 33, No. 6, 1999, pp. 1578-1583

Objectives:    We sought to investigate the possible pathogenic role of myocardial trace elements (TE) in patients with various forms of cardiac failure.

Background:    Both myocardial TE accumulation and deficiency have been associated with the development of heart failure indistinguishable from an idiopathic dilated cardiomyopathy.

Methods:    Myocardial and muscular content of 32 TE has been assessed in biopsy samples of 13 patients (pts) with clinical, hemodynamic and histologic diagnosis of idiopathic dilated cardiomyopathy (IDCM), all without past or current exposure to TE.  One muscular and one left ventricular (LV) endomyocardial specimen from each patient, drawn with metal contamination-free technique, were analyzed by neutron activation analysis and compared with 1) similar surgical samples from patients with valvular (12 pts) and ischemic (13 pts) heart disease comparable for age and degree of LV dysfunction; 2) papillary and skeletal muscle surgical biopsies from 10 pts with mitral stenosis and normal LV function, and 3) LV endomyocardial biopsies from four normal subjects.

Results:    A large increase (>10,000 times for mercury and antimony) of TE concentration has been observed in myocardial but not in muscular samples in all pts with IDCM.  Patients with secondary cardiac dysfunction had mild increase (<5 times) of myocardial TE and normal muscular TE.  In particular, in pts with IDCM mean mercury concentration was 22,000 times (178,400 ng/g vs. 8 ng/g), antimony 12,000 times (19,260 ng/g vs. 1.5 ng/g), gold 11 times (26 ng/g vs. 2.3 ng/g), chromium 13 times (2,300 ng/g vs. 177 ng/g) and cobalt 4 times (86.5 ng/g vs. 20 ng/g) higher than in control subjects.

Conclusions:    A large, significant increase of myocardial TE is present in IDCM but not in secondary cardiac dysfunction.  The increased concentration of TE in pts with IDCM may adversely affect mitochondrial activity and myocardial metabolism and worsen cellular function.

To order a copy of this abstract or a complete copy of this study from the National Library of Medicine see the following:

Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction. Frustaci et al., (1999). J. Am. Coll. Cardiol. 33:1578-83. (10334427)



Source: American Heart Association (http://www.americanheart.org/)Date: Posted 4/29/2002Mercury Ups Heart Disease Risk

Science Daily Magazine

http://www.sciencedaily.com/releases/2002/04/020429073754.htm

HONOLULU, April 24 – Finnish men with the highest concentrations of mercury in their hair also had the highest death rates from cardiovascular disease, congestive heart failure and stroke, according to a study presented today at the American Heart Association’s Asia Pacific Scientific Forum.

Mercury content in the hair is a marker for the amount of methyl mercury, a toxic form of the element, accumulated in the body by eating contaminated fish. Some scientists believe that the amalgam in dental fillings may also be a significant source of mercury, but questions remain about whether the mercury in dental fillings, which is inorganic, is absorbed into the body.

“Although consumption of fish may be healthy in general, some fish may contain methyl mercury in amounts harmful for humans,” says study author Jukka T. Salonen, M.D., Ph.D, MScP.H., professor of epidemiology at the Research Institute of Public Health at the University of Kuopio in Finland.

In the Kuopio Ischemic Heart Disease Risk Factor (KIHD) study, a total of 2,005 men without heart disease, between 42 and 60 years old were divided into four groups based on the mercury content of their hair, and tracked for an average of 12 years. 

Heart disease was defined as a history of an acute coronary event, like a heart attack, or angina pectoris, stroke or other cardiovascular event. The researchers controlled for other risk factors that could have affected their results, including age, levels of high-density lipoprotein (HDL, “good” cholesterol), low-density lipoprotein (LDL, “bad” cholesterol), triglycerides, family history of coronary heart disease, systolic blood pressure, weight and intake of fatty acids and antioxidants. 

The men who scored in the top 25 percent for hair mercury content had a 60 percent increased risk of death from CVD compared to the men in the lower mercury content. Those same men had a 70 percent increased risk of coronary heart disease alone, says Salonen. The amount of mercury in the hair was determined by flow injection analysis-cold vapor atomic absorption spectrometry and amalgamation, one of several tests available to determine mercury content. 

“Men who consumed 30 grams or more of fish daily – had 56 percent higher average hair mercury than those whose daily consumption was less than 30 grams. Those same men also tended to consume certain types of ‘predatory’ fish,” says Salonen. Fish higher in the food chain – i.e., those who eat smaller contaminated fish – tend to have the highest levels of methyl mercury. 

“The results also showed that men whose hair mercury levels were in the top 20 percent had a 32 percent faster increase in the thickness of the inner walls of their arteries, a measure of atherosclerosis, compared to men in the rest of the group. 

Atherosclerosis is the build-up of fatty plaque in arteries and is the underlying process that causes cardiovascular disease. Previous studies have shown that increasing dietary levels of fish containing omega-3 fatty acids benefits people with cardiovascular disease, as well as healthy people. 

The American Heart Association currently recommends that individuals consume two servings of fish weekly, both for the benefits of omega-3 fatty acids, and because fish tends to be low in saturated fats, which contribute to elevated cholesterol levels. 

“These results from Kuopio are intriguing, but preliminary, and should be viewed in the context of many other studies that have shown a clear cardiovascular benefit to consuming fish on a regular basis,” says Barbara V. Howard, Ph.D., chair of the American Heart Association’s Nutrition Committee and president of MedStar Research Institute in Washington, D.C.

“It is important to note that this is an observational study, and the conclusions do not prove a direct relationship between the amount of mercury in the hair and heart attacks. There may be factors such as the socio-economic status of the men or other dietary factors that are hard to measure, that account for the higher risk,” says Howard. 

Researchers became interested in looking at an association between mercury and cardiovascular disease because mercury has been shown to promote the oxidation of low-density lipoproteins in the arteries. Oxidation is a major component in the development of atherosclerosis. In addition, mercury can interfere with the antioxidant effects of selenium, an essential trace element found mainly in plant foods, and in the U.S., in grains and meat.

The KIHD study is an ongoing, population-based study designed to investigate risk factors for cardiovascular diseases and their outcomes among men in Eastern Finland. Previous studies with shorter follow-up periods from the same research group found a strong association between high hair mercury content and an increased risk of death. Researchers wanted to retest these results over a longer follow-up period. 

“It should be noted that we are not against eating fish per se,” adds Salonen. “What these results mainly say is that one should avoid regular consumption of old, large predatory fish, in which mercury levels are high, especially when caught from sources that are known to have a high mercury content. Our best advice is to consume a variety of fish, preferably young and small, from different lakes and seas in order to avoid possible high local levels of mercury.” 

The American Heart Association suggests consuming fish such as mackerel, lake trout, herring, sardines, albacore tuna and salmon twice a week. 

Co-authors include Jyrki K.Virtanen M.S.c., R.D.; Sari Voutilainen Ph.D., R.D.; Tiina H. Rissanen, M.Sc, R.D.; Jaakko Mursu, M.Sc, R.D.; Meri Vanharanta, M.Sc, R.D.; Kari Seppanen; and Jari Laukkanen, M.D. 



Mercury ups heart disease risk

Co-authors include Jyrki K.Virtanen M.S.c., R.D.; Sari Voutilainen Ph.D., R.D.; Tiina H. Rissanen, M.Sc, R.D.; Jaakko Mursu, M.Sc, R.D.; Meri Vanharanta, M.Sc, R.D.; Kari Seppanen; and Jari Laukkanen, M.D.

American Heart Association Meeting Report 04/24/2002

http://216.185.112.5/presenter.jhtml?identifier=3002342

HONOLULU, April 24 - Finnish men with the highest concentrations of mercury in their hair also had the highest death rates from cardiovascular disease, congestive heart failure and stroke, according to a study presented today at the American Heart Association's Asia Pacific Scientific Forum.

Mercury content in the hair is a marker for the amount of methyl mercury, a toxic form of the element, accumulated in the body by eating contaminated fish. Some scientists believe that the amalgam in dental fillings may also be a significant source of mercury, but questions remain about whether the mercury in dental fillings, which is inorganic, is absorbed into the body.

"Although consumption of fish may be healthy in general, some fish may contain methyl mercury in amounts harmful for humans," says study author Jukka T. Salonen, M.D., Ph.D, MScP.H., professor of epidemiology at the Research Institute of Public Health at the University of Kuopio in Finland.

In the Kuopio Ischemic Heart Disease Risk Factor (KIHD) study, a total of 2,005 men without heart disease, between 42 and 60 years old were divided into four groups based on the mercury content of their hair, and tracked for an average of 12 years.

Heart disease was defined as a history of an acute coronary event, like a heart attack, or angina pectoris, stroke or other cardiovascular event. The researchers controlled for other risk factors that could have affected their results, including age, levels of high-density lipoprotein (HDL, "good" cholesterol), low-density lipoprotein (LDL, "bad" cholesterol), triglycerides, family history of coronary heart disease, systolic blood pressure, weight and intake of fatty acids and antioxidants.

The men who scored in the top 25 percent for hair mercury content had a 60 percent increased risk of death from CVD compared to the men in the lower mercury content. Those same men had a 70 percent increased risk of coronary heart disease alone, says Salonen. The amount of mercury in the hair was determined by flow injection analysis-cold vapor atomic absorption spectrometry and amalgamation, one of several tests available to determine mercury content.

"Men who consumed 30 grams or more of fish daily - had 56 percent higher average hair mercury than those whose daily consumption was less than 30 grams. Those same men also tended to consume certain types of 'predatory' fish," says Salonen. Fish higher in the food chain - i.e., those who eat smaller contaminated fish - tend to have the highest levels of methyl mercury.

"The results also showed that men whose hair mercury levels were in the top 20 percent had a 32 percent faster increase in the thickness of the inner walls of their arteries, a measure of atherosclerosis, compared to men in the rest of the group. Atherosclerosis is the build-up of fatty plaque in arteries and is the underlying process that causes cardiovascular disease.

Previous studies have shown that increasing dietary levels of fish containing omega-3 fatty acids benefits people with cardiovascular disease, as well as healthy people.

The American Heart Association currently recommends that individuals consume two servings of fish weekly, both for the benefits of omega-3 fatty acids, and because fish tends to be low in saturated fats, which contribute to elevated cholesterol levels.

"These results from Kuopio are intriguing, but preliminary, and should be viewed in the context of many other studies that have shown a clear cardiovascular benefit to consuming fish on a regular basis," says Barbara V. Howard, Ph.D., chair of the American Heart Association's Nutrition Committee and president of MedStar Research Institute in Washington, D.C.

"It is important to note that this is an observational study, and the conclusions do not prove a direct relationship between the amount of mercury in the hair and heart attacks. There may be factors such as the socio-economic status of the men or other dietary factors that are hard to measure, that account for the higher risk," says Howard.

Researchers became interested in looking at an association between mercury and cardiovascular disease because mercury has been shown to promote the oxidation of low-density lipoproteins in the arteries. Oxidation is a major component in the development of atherosclerosis. In addition, mercury can interfere with the antioxidant effects of selenium, an essential trace element found mainly in plant foods, and in the U.S., in grains and meat.

The KIHD study is an ongoing, population-based study designed to investigate risk factors for cardiovascular diseases and their outcomes among men in Eastern Finland. Previous studies with shorter follow-up periods from the same research group found a strong association between high hair mercury content and an increased risk of death. Researchers wanted to retest these results over a longer follow-up period.

"It should be noted that we are not against eating fish per se," adds Salonen. "What these results mainly say is that one should avoid regular consumption of old, large predatory fish, in which mercury levels are high, especially when caught from sources that are known to have a high mercury content. Our best advice is to consume a variety of fish, preferably young and small, from different lakes and seas in order to avoid possible high local levels of mercury."

The American Heart Association suggests consuming fish such as mackerel, lake trout, herring, sardines, albacore tuna and salmon twice a week.

Co-authors include Jyrki K.Virtanen M.S.c., R.D.; Sari Voutilainen Ph.D., R.D.; Tiina H. Rissanen, M.Sc, R.D.; Jaakko Mursu, M.Sc, R.D.; Meri Vanharanta, M.Sc, R.D.; Kari Seppanen; and Jari Laukkanen, M.D.

American Heart Association





Circulation. 1995;91:645-655.

Intake of Mercury From Fish, Lipid Peroxidation, and the Risk of Myocardial Infarction and Coronary, Cardiovascular, and Any Death in Eastern Finnish Men 

Jukka T. Salonen, MD, PhD, MScPH; Kari Seppänen, MSc; Kristiina Nyyssönen, MSc; Heikki Korpela, MD, PhD; Jussi Kauhanen, MD, PhD; Marjatta Kantola, MSc; Jaakko Tuomilehto, MD, PhD; Hermann Esterbauer, PhD; Franz Tatzber, PhD; Riitta Salonen, MD, PhD 

From the Research Institute of Public Health (J.T.S., K.S., K.N., J.K., R.S.) and Departments of Community Health and General Practice (H.K.) and Chemistry (M.K.), University of Kuopio, Finland; the Department of Epidemiology and Health Promotion (J.T.), the National Public Health Institute of Finland, Helsinki, Finland; and the Institute of Biochemistry (H.E., F.T.), University of Graz, Austria. 

Correspondence to Prof Jukka T. Salonen, University of Kuopio, PO Box 1627, 70211 Kuopio, Finland.

Background Even though previous studies have suggested an association between high fish intake and reduced coronary heart disease (CHD) mortality, men in Eastern Finland, who have a high fish intake, have an exceptionally high CHD mortality. We hypothesized that this paradox could be in part explained by high mercury content in fish. 

Methods and Results We studied the relation of the dietary intake of fish and mercury, as well as hair content and urinary excretion of mercury, to the risk of acute myocardial infarction (AMI) and death from CHD, cardiovascular disease (CVD), and any cause in 1833 men aged 42 to 60 years who were free of clinical CHD, stroke, claudication, and cancer. Of these, 73 experienced an AMI in 2 to 7 years. Of the 78 deceased men, 18 died of CHD and 24 died of CVD. Men who had consumed local nonfatty fish species had elevated hair mercury contents. In Cox models with the major cardiovascular risk factors as covariates, dietary intakes of fish and mercury were associated with significantly increased risk of AMI and death from CHD, CVD, and any death. Men in the highest tertile (2.0 µg/g) of hair mercury content had a 2.0-fold (95% confidence interval, 1.2 to 3.1; P=.005) age- and CHD-adjusted risk of AMI and a 2.9-fold (95% CI, 1.2 to 6.6; P=.014) adjusted risk of cardiovascular death compared with those with a lower hair mercury content. In a nested case-control subsample, the 24-hour urinary mercury excretion had a significant (P=.042) independent association with the risk of AMI. Both the hair and urinary mercury associated significantly with titers of immune complexes containing oxidized LDL. 

Conclusions These data suggest that a high intake of mercury from nonfatty freshwater fish and the consequent accumulation of mercury in the body are associated with an excess risk of AMI as well as death from CHD, CVD, and any cause in Eastern Finnish men and this increased risk may be due to the promotion of lipid peroxidation by mercury. 

http://circ.ahajournals.org/cgi/content/abstract/91/3/645id=988754535598_145

http://circ.ahajournals.org/cgi/content/full/91/3/645id=988754554551_3830



Mortality in mice infected with an amyocarditic coxsackievirus and given a subacute dose of mercuric chloride.

South PK, Morris VC, Levander OA, Smith AD.

Beltsville Human Nutrition Research Center, US Department of Agriculture, Agricultural Research Service, Maryland 20705-2350, USA.

J Toxicol Environ Health A (2001) Aug 10;63(7):511-23.

http://www.ncbi.nlm.nih.gov/entrez/PubMed&list_uids=11497332&dopt=Abstract

An amyocarditic strain of coxsackievirus B3 (CVB3/0) induces heart damage when inoculated into selenium (Se)-deficient mice. Mercury (Hg), an Se antagonist, is known to aggravate viral infections. The experiments reported here assessed the effect of prior Hg treatment in mice subsequently inoculated with an amyocarditic strain of coxsackievirus. A pilot study showed that under our conditions the maximum tolerated dose of HgCl2 in uninfected mice was 6 mg HgCl2/kg body weight. In the main study, doses of 0, 3 or 6 mg HgCl2/kg body weight were administered intraperitoneally (ip) to 7-wk-old male mice fed a standard chow diet. Two hours later, half the mice were inoculated ip with CVB3/0. Ten days postinoculation, no mortality was observed in mice given only virus. In mice not given virus, 10% injected with 6 mg HgCl2/kg body weight died. On the other hand, 64% of the mice given both virus and 6 mg HgCl2/kg body weight died. Fifteen percent of the hearts from virus-infected mice given 3 mg HgCl2/kg body weight and 33% of the hearts from virus-infected mice given 6 mg HgCl2/kg body weight exhibited a higher incidence of lesions than hearts from mice-given virus alone. Moreover, viral heart titers were elevated in infected mice injected with 6 mg HgCl2/kg body weight compared to infected mice receiving no Hg. Thus, an amyocarditic coxsackievirus given to mice after a nonlethal subacute dose of Hg results in mortality, increased incidence of heart lesions, and elevated viral heart titers. These results demonstrate the important role of toxic elements in determining the severity of viral infections.



Mercury's Link to Heart Disease Begins in Blood Vessel Walls

http://heartlung.osu.edu/article.cfm?ID=3248

COLUMBUS, Ohio – Heavy metals and other toxins have been linked to many human diseases, but determining exactly how they damage the body remains a mystery in many cases. New research focusing on a relatively obscure, misunderstood protein suggests mercury’s link to heart disease can be traced to activation of this enzyme, which triggers a process leading to plaque buildup in blood vessel walls. The study examined three forms of mercury, matching its characteristics in the environment. Each form of mercury caused changes in the behavior of cells that line the blood vessel walls and that can lead to cardiovascular diseases. 

The study also suggests that chelation therapy, a process that removes metals from the body, and antioxidants both show signs of suppressing this activity and might be key to reducing the damage caused by mercury, and possibly other heavy metals. 

The research was published in a recent issue of the International Journal of Toxicology. 

“Mercury has been implicated as a risk factor in cardiovascular disease because of environmental concerns both from contamination and the atmosphere. But no one has looked at heavy metal regulation of this enzyme,” said Narasimham Parinandi, director of the lipidomics and lipid signaling laboratory at Ohio State University Medical Center and senior author of the study. “If we understand this regulation and know how to block it, we can come up with proper ways to prevent the activity.” 

Parinandi and colleagues focused on activation of an enzyme called phospholipase D, or PLD, in cells that line arteries in the lung. They exposed the cells to the inorganic, environmental and pharmaceutical forms of mercury, and observed that all three forms activated the enzyme. 

The activation of the enzyme involves a complex sequence of events in the cell membranes that in turn releases phosphatidic acid, which can damage cells in the vessel lining – called endothelial cells – and is believed to contribute to vascular disorders. 

To further test the enzyme’s role in blood vessel lining damage, the scientists then showed that metal chelators and antioxidants lessen the mercury-induced activation of the enzyme in endothelial cells. This portion of the study showed that different types of mercury affect the cells in different ways. 

In the three forms of mercury – methylmercury chloride, (environmental form), thimerosal (pharmaceutical form) and mercuric chloride (inorganic form) – the enzyme activation was prevented by metal chelators, which are organic chemicals that bind with and remove free metal ions from substances. 

The power of methylmercury chloride to activate the enzyme was also affected by antioxidants, including vitamin C, suggesting that this form of the metal generates free radicals. This is the form of mercury most closely associated with the food supply. 

“Chelators overall did a better job than antioxidants at protecting against mercury activation of the enzyme,” said Thomas Hagele, first author of the study and an undergraduate researcher in Parinandi’s lab. “This shows that activation of the enzyme is not isolated to one location in the cell. Since we can protect against the enzyme activation with both chelators and antioxidants, that means a few different types of activation are likely to occur, depending on the toxin.” 

This research is not just about mercury, noted Parinandi, also an assistant professor of pulmonary, critical care and sleep medicine. Mercury in this case acts as a model for other toxins that have similar effects on blood vessel walls, pointing to what happens in the body when toxic substances are a factor in causing diseases. 

This research was supported by the National Institutes of Health. 

Other Ohio State coauthors of the study are students Jessica Mazerik, Anita Gregory and Bruce Kaufman; Drs. Ulysses Magalang and Clay Marsh of pulmonary, critical care and sleep medicine; and Periannan Kuppusamy and M. Lakshmi Kuppusamy of the Davis Heart and Lung Research Institute. 

DOROTHY M. DAVIS
HEART AND LUNG
RESEARCH INSTITUTE 
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Columbus, Ohio 43210
p: 614.247.7766
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e: hlri-webmaster@osumc.edu 

 



Monday, 17 October 2011 23:31 The Role of Mercury Toxicity in Hypertension, Cardiovascular Disease and Stroke 


Houston, M. C. (2011), Role of Mercury Toxicity in Hypertension, Cardiovascular Disease, and Stroke. The Journal of Clinical Hypertension, 13: 621–627

Mercury induces mitochondrial dysfunction with reduction in adenosine triphosphate, depletion of glutathione, and increased lipid peroxidation. Increased oxidative stress and reduced oxidative defense are common.

Selenium and fish containing omega-3 fatty acids antagonize mercury toxicity.

The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. 

The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, cardiac arrhythmias, reduced heart rate variability, increased carotid intima-media thickness and carotid artery obstruction, cerebrovascular accident, generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria.

Pathological, biochemical, and functional medicine correlations are significant and logical.

Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity.

Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed.

IMPORTANT FACTS ABOUT MERCURY

Mercury is the most dangerous of all the heavy metals. It will modify the distribution and retention of other heavy metals. Mercury has no known physiologic role in human metabolism, and the human body has no mechanisms to actively excrete mercury. Mercury thus accumulates during life so that the average 165-lb person has a total body burden of about 13 mg of mercury.

Mercury has a high affinity for sulfhydryl groups, various enzymes and amino acids, N-acetyl cysteine (NAC), alpha lipoic acid (ALA), and glutathione (GSH), which provide about 10% to 50% of the plasma protein antioxidant capacity.8,12,13 Both NAC and ALA, as well as cysteine, are precursors for glutathione, which is the most potent intracellular antioxidant and protects against oxidative stress, inflammation, and cardiovascular disease.3,4,5,8,9,12

This mercury-induced reduction in oxidant defense and increase in oxidative stress increase the risk for CVD and CVA. Selenium antagonizes some of the adverse effects of mercury by forming a seleno-mercury complex in tissue that is less toxic.9,14–20 Higher intake of selenium reduces mercury-related CVD and CVA.

PHYSIOLOGIC BASIS OF MERCURY TOXICITY

Mercury induces mitochondrial dysfunction and oxidative stress.

The primary three sources of mercury-induced lipid peroxidation include the Fenton reaction, affinity for sulfhydryl groups, and selenium deficiency.

TABLE II. Vascular Biologic Effects of Mercury

1. Increased free radical production and increase in oxidative stress

2. Inactivation of antioxidant defenses

3. Mitochondrial dysfunction

4. Binds to thiol-containing molecules (sulfhydryl groups)

5. Binds to SE forming Se-Hg complex-mercury selenide, which decreases Se available for cofactor with glutathione peroxidase

6. Inactivates glutathione, catalase, superoxide dismutase

7. Increases lipid peroxidation in all organs

8. Increases oxidation of low-density lipoprotein and oxidation of low-density lipoprotein immune complexes

9. Increased platelet aggregation and thrombosis

10. Increased coagulation and thrombosis: increases Factor VIII, platelet factor 4, and thrombin and reduces protein C

11. Inhibit endothelial cell formation and migration and decreases endothelial repair

12. Decreases nitric oxide bioavailability

13. Endothelial dysfunction

14. Increase apoptosis

15. Reduced monocyte function and phagocytosis

16. Immune function is impaired

17. Increased vascular inflammation with increase tumor necrosis factor a and interleukin 6

18. Stimulation of vascular smooth muscle cells

19. Inactivation of paroxonase and other high-density lipoprotein proteins and enzymes

20. Translocaion of membrane phosphytidyl serine

21. Activates phospholipase A2

22. Activates phospholipase D

TABLE III. Summary of the Overall Vascular Biologic Effects of Mercury

1. Oxidative stress

2. Inflammation

3. Thrombosis

4. Vascular smooth muscle proliferation and migration

5. Endothelial dysfunction

6. Dyslipidemia (oxidation of high-density lipoprotein and paraxonase)

7. Immune dysfunction

8. Mitochondrial dysfunction

In summary, the overall vascular effects of mercury include oxidative stress–decreased oxidative defense, inflammation, thrombosis, VSM proliferation and migration, endothelial dysfunction, reduced NO bioavailability, dyslipidemia, immune dysfunction, and mitochondrial dysfunction (Table III). All of these abnormalities have the potential to increase the risk for hypertension, CVD, and CVA.

CLINICAL VASCULAR CONSEQUENCES OF MERCURY TOXICITY

The clinical consequences of mercury toxicity include hypertension, CHD, MI, reduction in heart rate variability, increase in carotid intima-media thickness (IMT) and carotid obstruction, CVA, generalized atherosclerosis, renal dysfunction, and proteinuria, and an overall increase in total and cardiovascular mortality.

Evidence from these and other epidemiologic and clinical studies suggest that people with high levels of urine, hair, blood, and toenail mercury have an increased risk of cardiovascular diseases.

CORONARY HEART DISEASE AND MYOCARDIAL INFARCTION

This important study concluded that there exists a positive monotonic increase in the risk of MI with mercury toenail content above the 0.25 lg ⁄ g level, which was even steeper when adjusted for the DHA adipose tissue content.

SUMMARY

Mercury has a high affinity for sulfydryl groups, which inactivate numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (NAC, ALA, GSH) with decreased oxidant defense and increased oxidative stress.

Mercury binds to metallothionein and substitute for zinc, copper, and other trace metals, reducing the effectiveness of metalloenzymes.

Mercury also induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation. Oxidative stress and decreased oxidative defense are common (especially with mercury).

Selenium and fish high in omega-3 fatty acid content antagonize mercury toxicity.

The overall vascular effects of mercury include increases in oxidative stress and inflammation, reduction in oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction.

The clinical consequences of mercury toxicity include hypertension, CHD, MI, cardiac arrhythmias, sudden death, reduced heart rate variability, increased carotid IMT and carotid artery obstruction, CVA, generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria. Pathological, biochemical and functional medicine correlations are significant and logical.

Mercury diminishes the protective effect of fish and omega-3 fatty acids. 

Mercury inactivates catecholamine-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase BP and may be a clinical clue to mercury toxicity.

Mercury toxicity should be evaluated in any patient with hypertension, CVD, CHD, CVA, or other vascular disease and who have a clinical history of exposure or clinical evidence on examination of mercury overload.

Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed. The 24-hour urine measurements should be done with baseline and provoked samples.

Houston, M. C. (2011), Role of Mercury Toxicity in Hypertension, Cardiovascular Disease, and Stroke. The Journal of Clinical Hypertension, 13: 621–627

http://www.mercuryexposure.info/science/heart/item/738-the-role-of-mercury-toxicity-in-hypertension-cardiovascular-disease-and-stroke
New FDA-approved Hepatitis B vaccine found to increase heart attack risk by 700%Friday, August 11, 2017 by: Mike Adams
Tags: adverse events, Aluminum, cardiovascular health, Dangerous Medicine, formaldehyde, heart attack risk, heart damage, hepatitus B, neurotoxins, vaccine, vaccine ingredients

(Natural News) A new FDA-approved Hepatitis B vaccine has been found to increase the risk of heart attacks by 700%, yet Facebook, Google, YouTube and Twitter ban any talk of vaccine dangers. There is a complete blackout of medical and scientific facts if they show vaccines to be anything less than magical, risk-less, medical utopian gifts to humanity.
This new analysis comes from Dr. Jack Wolfson, a well-informed cardiologist practicing in Arizona who dares to speak out on the truth about vaccine risks. Here’s his report:
Hepatitis B vaccine linked to 700% increase in heart attacksThe FDA has approved a new vaccine for Hepatitis B. This is good news for the pharmaceutical company that makes the vaccine, but bad news for consumers.
You see, in the latest trial to examine effectiveness of the drug, heart attack risk was higher in the vaccine group. How much higher? Try 700% higher (1).
Vaccination and heart attack risk may not come as a surprise to you. The stated purpose of a vaccine is to invoke an immune response. The immune response is linked to inflammation, oxidative stress, and immune cell activation. All three are linked to heart attack risk.
Sadly, there a very few studies on vaccination and heart attack risk. Ironically, some studies demonstrate a beneficial effect of the influenza vaccine on heart attack risk. But researchers have identified flaws in study design and question the findings of flu vaccine benefits on heart attack risk (2). Other studies showed no difference between the vaccinated and the control group regarding the pneumonia vaccine(3).
Sponsored solution from CWC Labs: This heavy metals test kit allows you to test almost anything for 20+ heavy metals and nutritive minerals, including lead, mercury, arsenic, cadmium, aluminum and more. You can test your own hair, vitamins, well water, garden soil, superfoods, pet hair, beverages and other samples (no blood or urine). ISO accredited laboratory using ICP-MS (mass spec) analysis with parts per billion sensitivity. Learn more here.


Again, most of the vaccine schedule has not been studied for heart attack or stroke risk. In other words, we do not know if the DPT, MMR, shingles, polio, HPV or chicken pox vaccines increase heart attacks.
What is Hep B?Hepatitis B is a viral infection contracted from blood to blood contact. This makes IV drug abusers and people who have sex with multiple partners most vulnerable. HBV is not spread through food or water, sharing eating utensils, breastfeeding, hugging, kissing, hand holding, coughing, or sneezing.
95% of people infected with the Hepatitis B virus do NOT become chronic carriers of the virus. They do not suffer from long-term liver complications, according to the CDC (4). A small percentage develop cirrhosis and/or liver cancer.
Vaccine toxinsThe most popular Hepatitis B vaccine is nothing short of a witch’s brew including aluminum, formaldehyde, yeast, amino acids, and soy. Aluminum is a known neurotoxin that destroys cellular metabolism and function. Hundreds of studies link to the ravaging effects of aluminum. The other proteins and formaldehyde serve to activate the immune system and open up the blood-brain barrier. This is NOT a good thing.
An Ounce of PreventionHealth will never be found at the tip of a needle. We want to build the body up, not tear it down. Millions of years of evolution have provided us with the perfect immune system to protect us. Give the body what it needs and take away what it doesn’t. It is pretty simple.
Please follow these recommendations to extraordinary health.
1)    Eat organic. Can we all agree that organic feed with limited pesticide exposure and GMO-free is the best diet to follow. The Drs. Wolfson follow our genetic programming and stick with hunter-gatherer Paleo foods. Works for our patients and will work for you. Sugar kills immune function.
2)    Get sunshine. Before there was life on earth, there was the sun. Embrace its power to boost your immune system.
3)    Sleep with the sundown and awake with the sunrise. Artificial light is a killer.
4)    Get active. Walk, run, garden, and play.
5)    Relax. Meditate and do yoga.
6)    Drink quality water and a lot of it.
7)    Get adjusted. Chiropractic care boosts immune function.
8)    Get away from environmental toxins and EMF exposure.
Visit Dr. Jack Wolfson’s website to learn more about health, wellness and prevention. Follow more news on vaccine injuries at VaccineInjuryNews.com.
Sources:
1)  https://www.medpagetoday.com/Blogs/RevolutionandRevelation/67019
2)  https://www.ncbi.nlm.nih.gov/pubmed/21529703
3)  https://www.ncbi.nlm.nih.gov/pubmed/20442385
4)  https://www.cdc.gov/hepatitis/hbv/hbvfaq.htm#overview

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