Heart Disease: America's leading Cause of Death – An "Equal Opportunity" Illness by Lawrence Broxmeyer MD

Inflammation plays a crucial role in the pathogenesis of arteriosclerosis, especially in acute coronary syndromes such as happen with a heart attack. And it was the very inability of ‘established’ risk factors such as high blood cholesterol (hypercholesterolemia), high blood pressure (hypertension) and smoking to fully explain the incidence of cardiovascular disease that has resulted in historically repeated calls to search out an infectious cause and the specific microbe behind it. Today, half of US heart victims have acceptable cholesterol levels, including HDL and LDL fractions, and 25% or more have none of the “risk factors” associated with heart disease, including smoking, high blood pressure or obesity, most of which are not inconsistent with being caused by infection to begin with. [1,2] Cholesterol itself was on the rise in Japanese blood during the very decade (1980-1989) when its incidence in coronary heart disease was on its way down. [22] So Nieto stressed the need to continue to look for an infectious disease behind heart disease. [3}

Which Disease?

Ever since a 1988 report of raised antibodies against Chlamydia pneumoniae in patients with heart disease, it was hoped that this microbe might be behind heart disease and atherosclerosis [28] Hurting this was the low incidence of atherosclerosis in the tropics despite Chlamydia’s high frequency there. [29]. Also Loehe, Bittman and other groups concluded that although Chlamydia, on occasion, might be present, it was not a causative factor in heart disease [30], because there was no correlation between the severity or extent of atherosclerosis and the involvement of chlamydial infection. Recently the Chlamydial hypothesis has been subject to a flurry of antibiotic trials, with mixed results, leaving some investigators to conclude that possibly Chlamydia doesn’t even play a role in atherosclerosis. [42] Certainly this was born out in two sizeable trials, one of which [47] had 1,187 participant. In neither trial [48] could any of the commonly thought of bacterial causes of heart problems – Chlamydia pneumonia and Helobacter pylori be correlated with cardiovascular disease. Nor could a virus. Also, in those trials which did show benefit antibiotics used (Azithromycin, Clarithromycin) are first line agents against certain forms of tuberculosis (fowl tuberculosis or Mycobacterium avium). Contrary to common belief, TB infections occur as a mixed infection with “atypical” TB in up to 11% of cases, even in HIV free individuals. [41] Today the antibiotic Rapamycin is used to coat coronary stents. [45] Rapamycin enhances the killing of mycobacteria like tuberculosis by human white blood cells called macrophages. [46]

Historical Associations

The association between active pulmonary tuberculosis and Acute Myocardial Infarction or heart attack has been reported and stubbornly ignored for around four and a half decades. Certainly, TB shares a more striking connection to heart disease than its nearest competitor, Chlamydia pneumonia. CDC maps for cardiovascular disease case rates bear a striking resemblance to comparable state and regional tuberculosis maps. [4,5]

Long before there was such a thing as a ‘heart specialist’ The National Tuberculosis Association created an offshoot called the American Heart Association (AHA). In one of its first bulletins, the American Heart Association came up with a long list of similarities between tuberculosis and heart disease. [17] And Ellis’s 1977 New England Journal of Medicine article [6], confirmed that the mortality rate for TB and heart disease were curiously about the same: 200 to 300 persons per 100,000.

By 1965, Rutgers investigators Livingston and Alexander-Jackson, working with sterile, post-catastrophic coronary artery and muscle specimens, established low-grade tubercular infection, staining ‘acid-fast’ (stains which did not decolorize when acid-alcohol was added) occuring in all ischemic heart specimens. [11] In that same year Russian investigators began generating their own proof that tuberculosis was causative in both atherosclerotic heart disease [18,19,20,21] and acute myocardial infarction (a heart attack) itself. [13,14,15].

Measuring Heart Trouble With Cardiac Enzymes In The Blood

Cases were soon on record of individuals with no cardiac risk factors, presenting with acute onset chest pain, ST elevation on their electrocardiogram (EKG), and elevated cardiac enzymes – all indicative of a heart attack with no other involvement than pulmonary tuberculosis [37]. As with its predecessor creatine kinase (CK-MB), today’s new enzymatic gold standard for detecting a heart attack, the troponins, are elevated in disseminated tuberculosis, an example of which can be found in TB’s role in acute pericarditis. [43]. Acute pericarditis, often not detected either until death was historically linked most commonly to Mycobacterium tuberculosis. In 1951, Christian [44] suggested that viral infection was more responsible for “idiopathic” (of unknown cause) or “benign” pericarditis. Such a viral cause, however, was never substantiated in many cases. Also, when it was found that the fatty substance (phospolipid) phosphatidylinositol  was not only housed itself inside TB’s cell wall, but was a potent coagulant and thrombin former as well – it further raised the question as to whether M. tuberculosis, by its very nature, lays down the conditions for the vessel clogging atherosclerosis behind heart disease and myocardial infarctions or heart attacks. [31]

Livingston and Alexander-Jackson [11] were far from the first ones to document lab evidence that TB can cause heart disease. Hektoen [7], Osler [8], and Schwartz [11], all documented lab and animal evidence to this effect. MacCallum [9] claimed that of all the infectious causes of heart disease, one one, tuberculosis, caused arteriosclerosis. At autopsy MacCallum cited 101 cases of advance tuberculous arteriosclerosis. In separate studies, Kossowsky [13], Tarakanova [14] and Ferrari-Sacco [15] all directly linked heart attacks with pulmonary tuberculosis.

Further evidence

There can no longer be any doubt that tubercular protein HSP-65 is involved in atherosclerosis. Xu [12] used it to cause experimental atherosclerosis in laboratory animals with normal cholesterol. George and Shoenfeld found it not only in atherosclerosis but fatty streak formation in cardiovascular blood vessels. [32] Mukherjee and De Benedictis showed also that the higher the antibodies against such tubercular protein in the body, the higher the possibility of “restenosis” or future closure of heart vessels. Also Afek proved that the higher the amount of tuberculoprotein (HSP-65) administered, the larger the area of vessel clogging atherosclerosis, even despite a low-fat diet. [34] Xu saw similar changes in New Zealand White Rabbits. [35] Xu’s rabbits had normal serum cholesterol, but when injected with tubercular protein, their arteries soon developed the classic features of arteriosclerosis in humans – both with regards to inflammatory cell accumulation and smooth cell proliferation. [IBID]. The only finding missing from Xu’s animals were “foam cells” – fat laden tissue white blood cells called macrophages in which tuberculosis lives and thrives. Xu remedied this by subjecting his animals to a cholesterol rich diet in addition to tubercular protein. this combination produced classic human heart disease, with foam cells. Xu continued to find sustained antibodies to HSP-65 in human subjects with the severe atherosclerosis predictive of mortality. [49] By 2004 Mandal and Xu even confirmed a positive association between high levels of antibodies to HSP-65, which are cytotoxic, and the vexing atrial fibrillation that often accompanies cardiac surgery. [50]

Present day heart disease “markers” have been suggest as indicators of possible heart disease, even in the 25 million US patients who have none of its “risk factors”. These include blood test for C-Reactive Protein (CRP), interleukin-6 and homocysteine [39] – all of which are similarly elevated in tuberculosis. [32,33,34,40,36].

Although blood cholesterol seems an imperfect criterion by itself for determining coronary heart disease, its intimate interaction with TB is unique. Tuberculosis is the only microorganism to depend on cholesterol for its destructive pathogenesis, and it relies upon cholesterol to enter the body’s white blood cell macrophages. [23] The tuberculous bacilli alone is able to produce [24], esterify [25], take up, modify, accumulate [26], and promote the deposition of, and release [27] of cholesterol. The statins, among the most popular drugs in America (Lipitor), inhibit Coenzyme-A compounds, and as such lower serum cholesterol levels. But they do more. Specifically, when macrophages were depleted of cholesterol by these agents, it hinders tuberculosis’s entrance into the body’s macrophages that TB likes to house in, thrive in, and depends upon. [23]

Nieto concludes that the introduction of antibiotic therapies in the 1940’s and 1950’s could have contributed to the decline of heart disease and heart attacks, and so, by 2000, the CDC found that 14% of the cardiologists in Alaska and West Virginia treated heart patients with antibiotics for angina, heat attacks, angioplasty or after by-pass surgery.


In Tuberculosis in Disguise, Rab and Rahman report cases of congestive heart failure and ischemic heart disease (IHD) with chest pain, raised erythrocyte sedimentation rate, leukocytosis (elevated white cell count) and inverted T-waves across the chest leads in an Electrocardiogram – otherwise indistinguishable from a heart attack, which turned out to be miliary (systemic) tuberculosis. [38]

Though more than 120 years have passed since its discovery Mycobacterium tuberculosis is still the leading cause of infectious death globally due to a single infectious agent. At least a staggering 1.7 million around the globe die of tuberculosis each year, while another 1.9 million are infected and at risk for active tubercular disease. [16] The World Health Organization [WHO] estimates that 1/3 of the planet has contracted TB. It would take such a disease of such magnitude to adequately explain the scope of cardiovascular disease, which affects, according to the CDC (Centers for Disease Control) about 61 million people, or almost one-fourth of the population of the US alone. Almost 6 million US hospitalizations each year are due to cardiovascular disease, which has become an equal opportunity disease that is now both the leading cause of death among women as well as the general US population.

There is at least as much, and probably much more evidence that Mycobacteria, particularly Mycobacterium tuberculosis causes cardiovascular disease than there is regarding Chlamydia Pneumoniae. Yet oddly, to this point Chlamydia has been pursued in therapeutic antibiotic trial after trial…………with not one such trial directed towards tuberculosis.


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© 2010

Source by Jack Kelly

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