A CDC press release tells us seven cases of "cardiac adverse events [three myocardial infarctions, two cases of angina, and two cases of myopericarditis] have been reported among civilian vaccinees since the beginning of the smallpox vaccination program." And another 10 cases of myopericarditis (inflammation of the heart muscle and outer lining of the heart) were reported among those in the military who received the vaccine.

The CDC noted that "a causal association between vaccination and adverse cardiac events in the civilian population is unproven," but that it nonetheless recommends (as a precautionary measure) "that persons with physician-diagnosed cardiac disease with or without symptoms (e.g. previous myocardial infarction, angina, congestive heart failure, or cardiomyopathy) be excluded from vaccination during this smallpox preparedness program."

Because the civilian casualties of the vaccination program ranged in age from 43 to 55 years and all were found to have had cardiac problems in their medical histories--including hypertension and angina--the possible link between the smallpox vaccine and the deaths that have occurred appears to have been down-played. However, recently published research in reputable medical literature suggests that the connection between the smallpox vaccine and death from cardiovascular disease may be more than mere conjecture.(i)

The presence of viruses in the blood stream has been scientifically shown to induce a physiological state called "hypercoagulability." The "hypercoagulable state" is a condition in which a person has the increased potential to develop a thrombosis, commonly called a "blood clot." Thus, the possibility that vaccinia, injected into the blood stream at the time of vaccination, caused the blood to clot. And that could have led to the sudden cardiac deaths.

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.(ii)

The physiology of the hypercoagulable state is complex. The cascade of events begins when an irregularity develops on the inside lining of a blood vessel called the endothelial wall. As the blood flows over the turbulent surface, platelet cells are disrupted, causing the release of an enzyme called thrombin. Thrombin catalyzes the conversion of proteins called fibrinogen into molecules called soluble fibrin monomers (SFM), generally referred to as fibrin. Strands of this "sticky," insoluble protein forms 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 during the creation of fibrin, more and more fibrinogen is released into the blood stream from the liver. The combination of the additional quantities of both fibrinogen and free, non-polymerized fibrin fragments in the blood increases its viscosity, meaning the blood becomes "thicker and stickier." Over time, the excessive amounts of circulating "sticky" fibrin adhere to the walls of capillaries in the microcirculation, resulting in narrowed blood vessels. Tissues that are dependent on blood squeezing through the narrowed vessels become compromised, as the supply of both oxygen and essential nutrients is reduced. If this is occurring in the vessels delivering oxygen to the heart, the result is ischemic heart disease and heart attacks. If it is occurring in the brain, strokes can result.

Cardiologists understand the phenomenon of hypercoagulability and routinely recommend a daily aspirin or other "blood thinning" drugs to reduce the risks of clot development. However, these medications are only treating the symptom, and do nothing to address the underlying cause of the hypercoagulation.

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 tissues that are deprived of oxygen. Fibrin-narrowed vessels delivering less oxygen to tissues allow the pathogens to become embedded, creating tiny tissue "abscesses" that fester and cause inflammation.(iii) This theory provides a possible explanation for the muscle aches seen in fibromyalgia, and why aerobic exercise--which serves to deliver more oxygen to the problem areas--seems to decrease pain. (iv)

Viruses create a self-perpetuating, hypercoagulable state by adhering directly to blood vessel walls. When this occurs, circulating fibrin is deposited directly onto the virus creating a protective "coating" in an attempt to isolate the virus from the rest of the body. The result is the formation of visible "bumps" along the inside wall of the blood vessels, increasing the blood flow turbulence, releasing more thrombin, creating a perpetual thrombin-fibrin-deposition cycle, leading to hypercoagulabilty and clot formation. (v)

Conventional medicine primarily blames the narrowing of blood vessels and subsequent clot formation on elevated cholesterol and fat deposits.

But it is highly possible that the actual underlying mechanism has been overlooked. It may be the adherence of microbes--specifically viruses--to endothelial lining of the blood vessels is the underlying culprit. (vi) In a word: are heart attacks really caused by an unrecognized, underlying 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 infections 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 (HTLV) 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).(vii)

Even though vaccinia, the virus that is in the smallpox vaccine, is not specifically mentioned on this list, it could be because the vaccine virus, vaccinia, can cause inflammation, possibly involving the heart, and increase the risk of blood clots, which may result in a heart attack. (viii)

The "inflammation" is the connection between viremia and hypercoagulability. (As an aside, researchers have documented that a similar type of hypercoagulabitliy is induced by the anthrax vaccine.) (ix)

It took many years for conventional medicine to identify bacteria known as "H.pylori," as the offender in gastric ulcer disease. I wonder how many years it will be before viral infections and other microbes are routinely considered to play a major role in cardiovascular disease? Some investigators have been studying the connection between Chlamydia and cardiovascular disease, but this hypothesis is being minimized, possibly for no good reason. 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 brachial artery response to nitroglycerin.(x) It is difficult to imagine how an antibiotic could affect a microbe buried beneath a layer of fibrin.

Comments by the CDC suggest that officials are disturbed over the highly publicized anxiety the general public has surrounding the use of the smallpox vaccine. Once the complications of this vaccine are fully appreciated, it is only one, small, precarious step to begin questioning what impact other live-virus vaccines--specifically measles, mumps, rubella, chickenpox and oral polio--may be having on health.

The impact on the body caused by live-virus vaccines may well be completely underestimated because hypercoagulability can occur in people of all ages. The virus-hypercoagulability connection may eventually prove to be a critically important "missing link" between the myriad of health problems we are facing due to our one-size-fits-all mass vaccination policies. The effects of this connection deserve more attention and serious research.

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.(xi) There are 184,000 organ recipients,(xii) 850,000 individuals with diagnosed and undiagnosed HIV infection or AIDS,(xiii) and 8.5 million people with cancer.(xiv) The presence of these health conditions constitutes a reason for avoiding the vaccine.

An even more extensive list of people at risk are the untold millions who are taking immunosuppressive drugs such as the corticosteroids Prednisone® and Medrol®. These medications, 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 rheumatic arthritis and autoimmune diseases.

Newly added to the "exclusion" list will be all those who have a history of cardiovascular disease. Nearly 61 million Americans (almost one-fourth of the population) live with cardiovascular disease and coronary artery disease, a condition thought to be the leading cause of premature, permanent disability in the U.S. workforce.(xv) All of these patients would be at risk for serious complications from contact with individuals who have received the smallpox vaccine. When adding up the number of Americans who should not receive this vaccine, it comes to more than 98.5 million people. Who will be left?

However, the plan for mass vaccination with the smallpox vaccine is not likely to go away anytime soon. A document published by the Government Accounting Office (GAO) on reports that the CDC and HHS are having severe difficulties in fulfilling President Bush’s orders to vaccinate 500,000 workers. Nonetheless, the plan is proceeding and ways are being sought to address the program’s major challenges: the extraordinarily high costs of implementation and the hesitancy of participants.(xvi)

To address the concerns for resources, Congress enacted legislation to appropriate an additional $100 million to the Public Health and Social Services Emergency Fund to support implementation of the smallpox vaccination program.(xvii) However, because CDC still has not finalized the complete cost of the program, it is unclear whether even this amount of funding will be sufficient in the long run.

In addition, Congress has taken steps to address volunteers’ concerns regarding compensation for the very real possibility of vaccine injury. The House voted 414-12 and the Senate voted 93-0 to approve separate supplemental appropriations bills that included funding for a smallpox vaccine compensation program. Legislation referred to as "The Smallpox Personnel Protection Act of 2003," was presented to the President for his signature. The vaccination protection program will provide benefits to public health personnel and health care response team who are injured as a result of receiving the smallpox vaccine. The nearly $80 billion Senate plan (S.762) includes $200 million for first responders in large cities, and $105 million to help states administer smallpox vaccines to emergency workers.(xviii)

The Senate bill sets aside $35 million for a smallpox vaccine compensation program but does not endorse a specific plan. The new legislation agrees to pay a $262,100 lump sum payment to survivors of people who die or to people who become disabled from receiving the smallpox vaccine. It also would compensate people with less severe injures for up to $50,000 in lost wages after they miss more than five days of work and pay for medical treatment.(xix)

With this amount of newly available funding, the quest for a feasible implementation plan for a mass smallpox vaccination program will continue to be pursued in earnest, and therefore we can expect the very real possibility of more reported deaths and injuries due to the virus-hypercoagulability connection.

Related Articles:

Everything You Ever Wanted to Know About Smallpox Bioterrorism

Smallpox Myths, Revisited

Reactions to Smallpox Vaccine Alarm Experts

Smallpox Vaccine Risky for Eczema Patients

Details of Plan to Administer Smallpox Vaccine

References

i Whiteman, T. Hypercoagulable States. Hematol. Oncol. Clin. North Am. - 01-Apr-2000; 14(2): 355-77

ii ibid.

iii Marshall, John C. MD, FRCSC. Inflammation, coagulopathy and the pathogenesis of multiple organ dysfunction syndrome. Crit Care Med. Vol. 29; No. 7. July, 2001

iv Berg, David. Berg D, Berg LH, Couvaras J, Harrison H. Chronic fatigue syndrome &/or fibromyalgia as a variation of antiphospholipid antibody syndrome (APS): An explanatory model and approach to laboratory diagnosis. Blood Coagulation and Fibrinolysis 1999: 10 435-438.

v Arid, William C., MD Endothelial cell dynamics and complexity theory. Crit Care Med Vol. 30; No.5; May, 2002

vi Friedman, H.M. Virus infection of endothelial cells. J Infect Dis. February 1, 1981; 143(2): 266-73

vii Marcel Levi, MD. Endothelium: Interface between coagulation and inflammation. Crit Care Med. Vol. 30, No. 5. May, 2002.

viii The New York Times, March 28, 2003. A NATION AT WAR: BIOLOGICAL DEFENSES; Second Death Follows Smallpox Vaccination by Denise Grady.

ix Hannan KL. et al. Activation of the coagulation system in Gulf War Illness: a potential pathophysiologic link with chronic fatigue syndrome. Blood Coagulation and Fibrinolysis, 11(7);2000:673-678.

x Jeffrey T. Kuvin, MD et al. Effect of short-term antibiotic treatment on chlamydia pneumoniae and peripheral endothelial function. The American Journal of Cardiology. Vol. 91; No. 6 • March 15, 2003

xi Diepgen TL. Is the prevalence of atopic dermatitis increasing? In: Williams HC, ed. Atopic Dermatitis: The Epidemiology, Causes and Prevention of Atopic Eczema. New York: Cambridge Univ Pr; 2000:96-112.

xii United Network for Organ Sharing (UNOS). All Recipients: Age at Time of Transplant. www.unos.org

xiii Joint United Nations Programme on HIV/AIDS. Epidemiological Fact Sheets on HIV and Sexually Transmitted Infections: United States. http://www.unaids.org/fact_sheets /index.html

xiv National Cancer Institute. CanQues. http://srab.cancer.gov/Prevalence/canques.html

xv CDC. Preventing Heart Disease and Stroke: Addressing the Nation’s Leading Killers http://www.cdc.gov/nccdphp/aag/aag_cvd.htm

xvi GAO Report 03-578. Smallpox Vaccination: Implementation of National Program Faces Challenges. April, 2003. pg. 24.

xvii Emergency Wartime Supplemental Appropriations Act, 2003, Pub. L. No. 108-11, 117 Stat. 559, 586 (2003). The Conference Committee Report states that this amount is to assist state and local health authorities with costs associated with the smallpox vaccination program. H.R. Conf. Rep. No. 108-76, at 86 (2003).

xviii Smallpox Emergency Personnel Protection Act of 2003, H.R. 1770, 108th Cong. (2003). (enrolled).

xix Ibid.