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Heart Disease - Beyond The Stent & Bypass
Cardiac Coverup

Dr. Lawrence Broxmeyer, MD
©Copyright 2009
Once upon a time, by the turn of the last century, flying in the face of over a hundred years of research and clinical observation to the contrary, medicine abandoned the link between infection and atherosclerotic heart disease; not because it was ever proven wrong, but because it did not fit in with the trends of a medical establishment convinced that chronic disease such as heart disease must be multifactorial, degenerative and non-infectious.
Yet it was the very inability of 'established' risk factors such as hypercholesterolemia, hypertension and smoking to fully explain the incidence and trends in cardiovascular disease that resulted in historically repeated calls to search out an infectious cause, a search that began more than a century ago.
Today, half of US heart attack victims have acceptable cholesterol levels 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 [7,56].
Even the traditionalist's 2003 assault in JAMA (Journal of the American Medical Association) to 'debunk' what they call the "50% risk factor myth" [20] fell woefully short under scrutiny. In one group 30% died of heart disease with a cholesterol of at least 240 mg/dl, a condition which also existed in 21% who did not die during the same period. And the overlap was obvious throughout the so-called risk categories. Under such scrutiny, lead author Greenland conceded that if obesity, inactivity and elevated cholesterol in the elderly are included, just about everyone has a risk factor and he likened the dilemma of people who do or do not wind up with heart disease akin to the susceptibility of people who are exposed and at one time contract tuberculosis, but do not presently have active disease.
In Infections and Atherosclerosis: New Clues from an old Hypothesis? Nieto stressed the need to extend the possible role of infectious agents beyond the three infections which have in recent years been the focus of research: Cytomegalovirus (CMV), Chlamydia pneumonia, and Helicobactor pylori [39].
Mycobacterial disease shares interesting connections to heart disease. Not only is tuberculosis the only microorganism to depend on cholesterol for its pathogenesis but CDC maps for cardiovascular disease bear a striking match to those of State and regional TB case rates. Why should this be?
Ellis, Hektoen, Osler, McCallum, Swartz, Livingston and Alexander- Jackson all saw clinical and laboratory evidence of a causative relationship between the TB, its related mycobacteria and heart disease. And Xu showed that proteins of mycobacterial origin actually led to experimental atherosclerosis in laboratory animals. Furthermore present day markers suggested as indicators for heart disease susceptibility such as C-Reactive Protein (CRP), interleukin-6 and homocysteine are all similarly elevated in tuberculosis.
Although more than 120 years have passed since its discovery, Mycobacterium tuberculosis is still the leading cause of death globally due to a single infectious agent (Dye et al. 1999). This high mortality rate exists in spite of the fact that for over 50 years tuberculosis has been a preventable, diagnosable, and treatable disease.
It therefore behooves us to explore the historical, clinical, and pathological link between heart disease, typical, and atypical tuberculosis.
Attached at the hip, the American Heart Association (AHA), first to push towards medical heart specialization, was actually an offshoot of The National Tuberculosis Association, without whose money and help it would never have survived. In one of its first Bulletins, the AHA (American Heart Association) came up with a long list of the similarities between tuberculosis and heart disease [2], a view supported by Ellis in The New England Journal of Medicine half a century later [15]. In a 'name that disease' Ellis fleshes-out a medical condition who's mortality rate was 200 to 300 per 100,000, was widespread, and by whom many in their prime were struck down. Treatment was only partially effective. Doctors recommended diet and exercise. Special hospitals were built for it. In a tough decision, Ellis's readers only recognized the disease as TB when he said it struck 75 years ago, the white plague of the 20th century, for the mortality rate for ischemic heart disease (IHD) at the time of Ellis's writing was also 200 to 300 persons per 100,000.
Yet it was not until after WWII that the subject was pursued in earnest, and by two women, one of them the first female medical resident in New York. Sometime in 1965, Rutger's investigators Virginia Livingston, M.D. and Eleanor Alexander-Jackson PhD, fueled by Fleet and Kerr Grants, working with sterile, post catastrophic heart attack coronary artery specimens, established low-grade tubercular infection, staining 'acid-fast' (not decolorized with acid-alcohol) in all ischemic heart disease specimens [32].
Even in stained slides of the heart muscle itself, Livingston documented small, acid-fast globoidal tubercular bodies which soon appeared to enter into a gradual state of digestion (Ibid).
In 1986, Hektoen, studying how tuberculosis attacked blood vessels of the cardiovascular system, saw the blood born microbes implanting themselves in cardiovascular walls. Eventually these microbes would penetrate all layers of the arterial wall, including its muscular coat. The offshoot led, often, to the degeneration of whole arterial segments.[23]. Since tubercular attack came from the inside of the vascular wall outwards, Hektoen often spotted the initial attack as involving the intimal or adventitial layers.
Even William Osler, arguably the greatest physician since Hippocrates, and to this day an icon for accurate clinical judgment, made clear that arteriosclerosis was frequently associated with tuberculosis [42].
MacCallum's investigation [34] recognized that of all the infectious causes of heart disease, only one, tuberculosis, caused arteriosclerosis. At autopsy, he cited 101 cases of advanced tuberculosis. Of these cases, there were 49 cases in children in the first decade of life - none of which showed arterial changes. Even in the second, third and fourth decades there were only 11 autopsies who died of TB with moderate cardiovascular sclerosis; while 13 showed nothing. But by the fifth, sixth, seventh and eighth decades, true to current coronary timetables, there were only 2 autopsies with normal arteries and 26 with TB arteriosclerosis (Ibid).
By 1972, pathologist Phillip Schwartz, once a student of Loffler, became aware that the 'lardaceous', waxy degeneration misnamed by Virchow as starch-like "amyloid" (starch was called amylum), showed that amyloid (starch-like) degeneration occurred more frequently in elderly cardiovascular systems than hardening and atheromatous lesions of their arteries. But along with this, he noticed that such amyloid degeneration, upon autopsy, usually revealed signs of lingering pulmonary and lymph node tuberculosis [59].
Classic thought regarding atherosclerosis never was terribly convincing. It supposedly begins with the appearance of cholesterol and fat-laden macrophages (white blood cells) called "foam cells". The fact that some of these macrophages died, just added to the debris. Macrophages died, tradition dictated, because they could not eliminate cholesterol the way they got rid of bacteria. They simply stuffed themselves compulsively with more and more cholesterol, converting into the large 'foam cells' that filled the plaques of advanced atherosclerosis. Macrophages, then, said orthodoxy, literally ate themselves to death at our cardiac blood vessels expense.
But there were obvious flaws to such thinking. First, unlike with other microbes, human macrophages were not that good at eliminating germs like tuberculosis, which in turn kills many of them. Second cholesterol by itself, normally the most abundant steroid in man, was on the rise in Japanese blood during the very decade (1980­1989) when the incidence of coronary heart disease was on its way down [40]. In the meantime, in the US, half the people who had a heart attack had acceptable cholesterol levels, including its HDL and LDL fractions.
Although cholesterol thus seemed an imperfect criterion for determining coronary heart disease, its intimate interaction with TB and the mycobacteria presented extremely interesting coincidental findings. Not only were virulent tuberculosis and the mycobacteria the only pathogens that actually relied upon cholesterol to enter the body's white blood cells or macrophages [17], but, it was the Mycobacteria that in addition were able to produce [31], esterify [29], take up, modify, accumulate [4], and promote the deposition of and release [26] of cholesterol.
Orthodox thought then pronounced that smooth muscle cells of the cardiovascular system somehow responded to fat proliferation under the influence of certain platelet factors, which are otherwise supposed to function exclusively in clotting, to eventually cause inflammation. But, to many, it seemed fuzzy logic that inflammation should occur from fat proliferation to begin with. Livingston and Alexander- Jackson's meticulous work clarified this, finding in all specimens, an infectious agent behind that inflammation and fat propagation [32]. But unfortunately, they worked as "outsiders" at a time when women doctors and scientists weren't fully accepted.
Others Notice
A 1973 watershed study by Benditt and Benditt reported that cells found in artherogenic plague had a monoclonal origin, that is, they were derived from a single cell population [6]. Confirmatory studies [43,44] prompted the revival and legitimization of a search for an infectious cause. But by concluding that such monoclonal origins were caused by "Chemical mutagens or viruses or both" Benditt and Benditt's agenda blindsided a third major possibility- tuberculosis and the mycobacteria, each capable of churning out its own monoclonal enzymes, once systemic [13,45].
It was in no small part as a result of Benditt's study, much of the world's scientific and medical community focused on an extremely limited role for tuberculosis and the mycobacteria in heart disease, and at the same time seemed to purposefully marginalize studies that kept seeping into the Index Medicus. For example, in the same year Livingston pursued her heart work at Rutgers, the Russians, unhindered by the American brand of politicized medicine, began proving the link between tuberculosis, atherosclerosis and heart disease [8,25,27,28].
Which Infection?
Since a 1988 report of raised antibodies against Chlamydia pneumoniae in patients with heart disease appeared, it was hoped that the microbe might be behind atherosclerosis [21,41,50]. Hurting this hypothesis was the low incidence of atherosclerosis in the tropics despite chlamydia's high frequency there [52].
Also Loehe and Bittman concluded that although Chlamydia, on occasions, might be present, it was not a causative factor [33] because there was no correlation between the severity or extent of atherosclerosis and the involvement of chlamydial infection at the same site. This report was in concert with Thomas [57] and Gibbs [19]. Combined, these studies seemed to ask: What if Chlamydia pneumoniae was just a passenger bacteria, a friendly bystander? And when, in 1995, MC Sutter's editorial Lessons For Atherosclerotic Research From Tuberculosis And Peptic Ulcer, warned we might be overlooking the role of a microorganism in atherosclerosis, he did not have chlamydia specifically in mind [53]. Nevertheless, statistics showed that people who used a lot of antibiotics had less 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, heart attacks, angioplasty or after by-pass surgery.
And certain antibiotics did seem to work, but the question was their efficacy based upon their anti-Chlamydial activity? Azithromycin, for example has a documented, if moderate activity against certain mycobacteria as well.
Something More conclusive
As the millennium approached, something much more irrefutable was happening. Xu had previously been found that injecting rabbits with normal cholesterol with protein from TB resulted in atherosclerotic changes [61]. Now George and Shoenfeld were implicating these very same proteins in not only the origin of the atherosclerosis in cardiovascular blood vessels but of fatty streak formation there as well [18]. In the meantime, Mukherjee and De Benedictis showed that an increase in antibodies against such tubercular proteins somehow already in the body was actually associated with re-stenosis or future closure of coronary vessels [37]. By 2000, it became obvious to Afek that mice injected with high doses of such tuberculoproteins developed significantly larger areas of atherosclerosis despite the fact that their diet was devoid of high fat content [1]. Revisiting this subject, Xu, also using the same tubercular protein (HSP-65), proved the same thing in New Zealand white rabbits [62]. In Xu's study, such rabbits with normal serum cholesterol injected with the TB preparation led to the formation of all the classic features of arteriosclerosis in humans - the inflammatory cell accumulation and the smooth cell proliferation (Ibid) that Livingston and Alexander-Jackson had decades ago attributed to tuberculosis.
In fact, the only finding missing from Xu's study using normal cholesterolemic animals were "foam cells": tissue macrophages in which tuberculosis not only lived but thrived in, capable of ingesting material that dissolved during tissue preparation, especially lipids. However, this missing piece of the puzzle was soon remedied when in addition to tuberculous proteins his animals were given a cholesterol rich diet, at which point Xu saw all the lesions found in classic human heart disease, including foam cells. Obviously, tuberculoproteins were overwhelming the systems macrophages, not allowing them to get rid of ingested fat.
When Man Thinks - Heaven Laughs
There was also incriminating epidemiologic evidence. The higher incidence of coronary heart disease in young males had a remarkable parallel in bacterial diseases such as TB [52]. And the association between low socioeconomic status and coronary disease found common ground with the incidence of tuberculosis.
The Centers for Disease Control and Prevention (CDC) maps for the total cardiovascular disease and death rates across the country [10] bore a conspicuous similarity to state and regional incidence for CDC TB case rates maps in the United States [9]. In addition, the statins, among the most popular drugs in America (Lipitor, Lescol), though inhibitors of Coenzyme-A compound (HMG-CoA or 3-hydroxy-3-methylglutaryl CoA reductase) and as such lowered serum cholesterol levels, did much more.
Specifically, when macrophages were depleted of cholesterol by such pharmacological treatment, mycobacteria such as tuberculosis could not enter the macrophage TB liked to house in, thrive in and depend upon [17]. Furthermore, this block of macrophage uptake with cholesterol depletion was specific only for tuberculosis and the mycobacteria and no other pathogen. In other words, cholesterol played a crucial role in tuberculosis's establishment of intracellular infection leading both to the long term survival of the germ and the death of 1.9 million people a year.
The large British heart protection study took many by surprise when they learned that even lowering "normal" cholesterol levels lowered heart disease risk [12]. This led again to speculation that there must be some other risk factor involved besides cholesterol itself. Lead- author Collins countered that the reason for his study's finding was that even what we call "normal" cholesterol values are too high, but it is just as easily posited that the lower the blood cholesterol the less likely there is to be chronic mycobacterial infection which would also be of benefit derived from lower than normal cholesterol levels.
It is hardly a coincidence that studies have shown that statins, which indirectly decrease mycobacterial disease, also lower C-reactive protein (CRP). C-reactive protein is an age-old, non-specific protein, first identified in 1930, and then found in the serum of various persons with certain inflammatory and degenerative diseases [48]. Recently an elevated CRP has been touted as an excellent marker for the approximately 25 million US patients that have none of the risk factors associated with heart disease, yet are at risk for a heart attack. However CRP and elevated sedimentation rate have long been excellent markers of active tuberculosis [22], CRP being present at all times when erythrocyte sedimentation rate (ESR) is elevated but returning to normal faster than ESR as tuberculosis, once treated, becomes inactive. Indeed CRP is a sensitive indicator of the activity of tuberculosis [5].
Researchers have even tried to neatly tie in excessive weight and its fat cells to indirectly increasing C-reactive protein (CRP) by dumping interleukin-6 (IL-6) into the blood, which, in turn supposedly promotes an inflammatory response, key to signaling the liver, and perhaps the arterial walls themselves, to churn out more CRP. But again, and significantly, higher levels of interleukin-6 are consistently found in either the lung secretions [58] or serum [54] where TB resides. Russell noted sustained release of IL-6 repeatedly issued from human macrophages infected with TB [49], a defense strategy the microbe uses to possibly create anergic conditions (conditions with lowered immunity) that prevent macrophages from killing them.
Others look towards elevated serum levels of homocysteine, an amino acid also linked as an index of potential heart disease, as the marker of the future even though a homocysteine marker metaanalysis appeared in JAMA, concluding that elevated homocysteine was at most a modest independent predictor of Ischemic Heart Disease (IHD) in healthy populations [24]. Nevertheless homocysteine, it is claimed by some, although not deposited in blood vessel walls like cholesterol, can damage the inside lining of these vessels and make platelets more likely to clot, the scenario which supposedly leads to stroke or heart attacks.
Homocysteine is formed from another amino acid in our diets, methionine. But methionine is also the protein that M. tuberculosis brings systemically into its host to initiate its own protein synthesis [11]. Although Homocysteine can be turned back into methionine and its level lowered in the blood, this requires two essential cofactors: vitamin B12 and "folate" or folic acid, both of which can be lowered in tubercular infection, leading to elevated homocysteine levels [35,46].
Nieto's extensive review concludes that the introduction of antibiotic therapies in the 1940s and 1950s could have contributed to the decline of heart disease and heart attacks in the last few decades [39]. Although the tetracyclines appeared in the 1950s it was only after the introduction of the macrolides, in particular erythromycin in the 1960s that the cardiovascular disease mortality curve began to sink. Though it was hypothesized that such decline was the effect of tetracycline and the macrolides against Chlamydia pneumonae, many of the atypical mycobacteria were also sensitive to erythromycin and the tetracycline doxycycline [36]. Also, the antibiotic time-curve Nieto cites excludes the actual introduction of anti-tubercular antibiotics.
Although erythromycin is very effective against C. pneumoniae, the microorganism may persist in the respiratory tract despite adequate blood levels of the antibiotic [51]. There can be no doubt that the availability of antibiotics lowered the morbidity and mortality of cardiovascular disease. Netter mentions that tuberculosis, once often associated with cor pulmonale was less so linked in recent years, probably because of the widespread use of antibiotics and antimicrobial agents [38].
Conclusion - Runs Silent, Runs Deep
When Nieto stressed the need to extend the possible role of infectious agents beyond the 3 infections which have in recent years been the focus of research: namely, Cytomegalovirus (CMV) C. pneumonia and Helicobactor pylori [39], was he picking Sir William Osler's brain regarding that arteriosclerosis was frequently associated with tuberculosis? [42]. Still many ridicule the possibility that microbes might be the agents of arteriosclerosis. These were the same minds that in another, far gone era, would have jeered the possibility that syphilis in its late stages had a special preference for the arteries and could cause devastation of major cardiovascular vessels. Eventually though, these minds were proven wrong. But the lessons of syphilis are far-gone or are they?
When by 1982, keynote speaker and then Harvard infectious disease guru Louis Weinstein addressed the annual session of the American College of Physicians he mentioned: "We thought initially that the disease (tuberculosis) was disappearing, but we are now seeing up to 27 different syndromes and extapulmonary forms, etc. It is today's great mimic, a greater mimic than syphilis ever was"[60].
In Atherosclerosis and Tuberculosis: Are They Both Chronic Diseases?, after going over the many similarities between tuberculosis and Chlamydia pneumoniae, Anestad focuses on Norwegian 20th century statistics in which two things become obvious. First, that until 1945 tuberculosis was easily the leading cause of infectious death in Norway, surpassing cardiovascular death at the time. Second, that as the diagnosed cases of tuberculosis fell from his statistics, cardiovascular disease increased dramatically until 1975, when its stats too somewhat tapered [3]. At first glance, these statistics seem unrelated even though they are on the same bar graph. But are they? Or are we just looking at another example of Weinstein's reference to occult TB finding an expanded niche in the cardiovascular system in one of its quests to become "a greater mimic than syphilis ever was"?
In Tuberculosis In Disguise, Rab and Rahman document cases of congestive heart failure and IHD (Ischemic Heart Disease) with chest pain, raised erythocyte sedimentation rate, leukocytosis and inverted T-waves across the chest leads otherwise indistinguishable from the real thing, which turned out to be miliary (systemic) tuberculosis [47]. Rab and Rahman again warned "confusion may occur because tuberculosis can mimic so many other conditions".
Certainly with tuberculosis and for some time now, we have a human population affected that dwarfs syphilis in its prime. At least a staggering 1.7 million around the globe die of tuberculosis each year, while another 1.9 billion are infected with M. tuberculosis and are at risk for active disease[14].The World Health Organization (WHO) estimates that 1/3 of the planet has contracted TB.
It would take such a disease to adequately explain the scope of cardiovascular disease, which affects about 61 million people, or almost one-forth of the population in the US alone. Almost 6 million US hospitalizations each year are due to cardiovascular disease. (www.cdc.gov/nccdphp/aag/aag_cvd.htm)
The linkage of tuberculosis to acute myocardial infarction and resulting heart attacks is nothing new [16,30,55]; yet serious clinical trials have never been undertaken. And one is left wondering whether the present flurry of trials designed to simply label the markers in the blood that TB and the mycobacteria throw our way is ever really going to quell the near epidemic cardiovascular disease that is presently in our midst.
[1] Afek A, George J. Immunization of low-density lipoprotein receptor deficient (LDL-RD) mice with heat shock protein 65 (HSP-65) promotes early atherosclerosis. J Autoimmun 2000;14(2):115­21.
[2] AHA Similarity of tuberculosis and heart disease. Bull Am Heart Assoc 1927;2(5):22.
[3] Anestad G, Hoel T. Atherosclerosis and tuberculosis: are they both chronic infectious diseases. Scand J Infect Dis 2001;33:797.
[4] Av-Gay Y, Sobouti R. Cholesterol is accumulated by mycobacteria but its degradation is limited to non-pathogenic Heart disease: the greatest 'risk' factor of them all 777 fast growing mycobacteria. Can J Microbiol 2000;46(9):826­31.
[5] Bajaj G, Rattan A. Prognostic value of 'C' reactive protein in tuberculosis. Indian Pediatr 1989;26(10):1010­3.
[6] Benditt EP, Benditt JM. Evidence for a monoclonal origin of human atherosclerotic plaques. Proc Natl Acad Sci 1973;70(6):1753­6.
[7] Benson RL, Smith KG. Experimental arteritis and arteriosclerosis associated with streptococcal inoculations. Arch Pathol 1931;12:924­40.
[8] Bruade VI. Cardiovascular diseases in conjunction with pulmonary tuberculosis (pathological-anatomical findings). Sov Med 1966;29(12): 104­7.
[9] CDC Map: TB case rates, United States, 2001. Atlanta Georgia: US Department of Health, Education and Welfare CDC; 2001.
[10] CDC Map total cardiovascular disease ­ 1995 death rate. Atlanta Georgia: US Department of Health, Education Welfare CDC; 1995.
[11] Chun T. Induction of M3-restricted T lymphocyte responses by N- formulated peptides derived from Mycobacterium tuberculosis. J Exp Med 2001;193(10):1213­20.
[12] Collins R, Armitage J. MRC/BHF heart protection study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomized placebo-controlled trial. Lancet 2003;361(9374):2005­16.
[13] David HL. Bacteriology of the mycobacterioses. Atlanta Georgia: Center for disease control, Mycobacteriolgy branch; 1976.
[14] Dye C, Scheele S. Global burden of tuberculosis: estimated incidence, prevalence, and mortality by country. JAMA 1999;282:677­86.
[15] Ellis JG. Plague tuberculosis and plague atherosclerosis. The New England J Med 1977;296(12):695.
[16] Ferrari-Sacco A, Ferraro U. Myocardial Infarct and Pulmonary Tuberculosis. Discussion of 2 cases of myocardiocoronary disease appearing during hospitalization in a sanatorium. Minerva Cardioangiol 1966;14(8):465­75.
[17] Gatfield J, Pieters J. Essential role for cholesterol in entry of mycobacteria in macrophages. Science 2000;288:1647­750.
[18] George J, Shoenfeld Y. Enhanced fatty streak formation in C57BL/ 6J Mice by immunization with heat shock protein-65 arteriosclerosis. Thromb Vasc Biol 1999;19:505­10.
[19] Gibbs RG, Sian M. Chlamydia pneumoniae does not influence atherosclerotic plaque behavior in patients with established carotid artery stenosis. Stroke 2000;31:2930­5.
[20] Greenland P, Knoll MD. Major Risk Factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA 2003;290(7):891­7.
[21] Gurfinkel E, Bozovich G. Chlamydia pneumoniae: inflammation and instability of the atherosclerotic plaque. Atherosclerosis 1998;140(Suppl 1):31­5.
[22] Haghighi L, Doust JY. C-Reactive protein in pulmonary tuberculosis. Dis Chest 1966;50(6):624­6.
[23] Hektoen L. The vascular changes of tuberculous meningitis. J Exper Med 1986:112.
[24] Wilson PW. Homocysteine and coronary heart disease: how great is the hazard? JAMA 2002;288(16):2042­3.
[25] Kamyshnikova VS, Kolb VG. Biochemical factors involved in atherogenesis in pulmonary tuberculosis. Probl Tuberk 1984;11:48­52.
[26] Kamyshnikov VS, Kolb VG. Lipid metabolism and atherogenesis in tuberculosis in experimental animals. Probl Tuberk 1993;4:53­5.
[27] Kazykhanov NS. Lung tuberculosis in patients with atherosclerosis. Sov Med 1965;28(8):37­44.
[28] Kazykhanov NS. Arteriosclerosis in patients with pulmonary tuberculosis. Kardiologiia 1967;7(10):137.
[29] Kondo E, Kanai K. Accumulation of cholesterol esters in macrophages incubated with mycobacteria in vitro. Jpn J Med Sci Biol 1976;29(3):123­37.
[30] Kossowsky WA, Rafii S. Letter: acute myocardial infarction in miliary tuberculosis. Ann Intern Med 1975;82(6):813­4.
[31] Lamb DC, Kelly DE. A sterol biosynthetic pathway in mycobacterium. FEBS Lett 1998;437(1-2):142­4.
[32] Livingston V. Cancer: a new breakthough. Los Angeles: Nash Publishing; 1972.
[33] Loehe F, Bittmann I. Chlamydia pneumoniae in atherosclerotic lesions of patients undergoing vascular surgery. Ann Vasc Surg 2002;16(4):467­73.
[34] MacCallum WG. Acute and chronic infections as etiological factors in arteriosclerosis. In: Cowdry EV, editor. Arteriosclerosis A survey of the problem. New York: MacMillan Co; 1933. p. 355­62.
[35] Markkansen T, Levanto A. Folic acid and vitamin B12 in tuberculosis. Scand J Haemat 1967;4:283­91.
[36] Molavi A, Weinstein L. In viro activity of erythromycin against atypical mycobacteria. J Infect Dis 1971;123:216­9.
[37] Mukherjee M. De Benedictis association of antibodies to heat- shock protein-65 with percutaneous transluminal coronary angioplasty and subsequent restenosis. Thromb Haemost 1996;75(2):258­60.
[38] Netter FH HEART The Ciba Collection of Medical Illustrations. West Caldwell New Jersey CIBA-GEIGY Corporation 1992.
[39] Nieto FJ. Infections and atherosclerosis: new clues from an old hypothesis. Am J Epidemiol 1998;148(10):937­48.
[40] Okayama A. Ueshima changes in total serum cholesterol and other risk factors for cardiovascular disease in Japan, 1980­1989. Int J Epidemiol 1993;22:1038­47.
[41] Orfila JJ. Seroepidemiological evidence for an association between Chlamydia pneumoniae and atherosclerosis. Atherosclerosis 1998;140(Suppl 1):11­5.
[42] Osler W. Diseases of the arteries. In: Osler W, MacCrae T, editors. Modern medicine Its theory and practice in original contributions by Americans and foreign authors, vol. 4. Philadelphia, PA: Lea & Fabiger; 1908. p. 426­47.
[43] Pearson TA, Wang BA. Clonal characteristics of fibrous plaques and fatty streaks from human aortas. Am J Pathol 1975;81:379­87.
[44] Pearson TA, Dillma JM. Clonal characteristics of cutaneous scars and implications for atherogenesis. Am J Pathol 1981;102:49­54.
[45] Purwantini E, Gillis TP. Presence of F420-dependent glucose-6- phosphate dehydogenase in Mycobacterium and Nocardia species, but absence from Streptomyces and Corynebacterium species and methanogenic Archaea. FEMS Microbiol Lett 1997;146(1):129­34.
[46] Qureshi GA, Baig SM. The neurochemical markers in cerebrospinal fluid to differentiate between aseptic and tuberculous meningitis. Neurochem Int 1998;32(2):197­203.
[47] Rab SM, Rahman M. Tuberculosis in disguise. Brit J Dis Chest 1967;61:90­4.
[48] Rifai N, Ridker PM. Inflammatory markers and coronary heart disease. Curr Opin Lipidol 2002;13(4):383­9.
[49] Russel DG. Sturgill-Koszycki S why intracellular parasitism need not be a degrading experience for Mycobacterium. Phil Trans R Soc Lond B 1997;352:1303­10.
[50] Saikku P, Leinonen M. Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. Lancet 1988;2:983­6.
[51] Smith CB, Friedewald WT. Shedding of Mycoplasma pneumonia after tetracycline and erythromycin therapy. New Eng J Med 1967;276:1172­5.
[52] Stille W, Dittmann R. Arteriosclerosis as a sequela of chronic Chlamydia pneumoniae infection. Herz 1998;23(3):185­92.
[53] Sutter MC. Lessons for atherosclerosis research from tuberculosis and peptic ulcer. Can Med Assoc J 1995;152(5):667­70.
[54] Tang S, Xiao H. Changes of proinflammatory cytokines and their receptors in serum from patients with pulmonary tuberculosis. Zhonghua Jie He He Hu Xi Za Zhi 2002;25(6):325­9.
[55] Tarakanova KN, Terent'eva GM. Myocardial infarct in patients with pulmonary tuberculosis. Probl Tuberk 1972;50(4):90­1.
[56] Thom DH, Grayston JT. Association of prior infection with Chlamydia pneumoniae and angiographically demonstrated coronary artery disease. JAMA 1992;268:68­72.
[57] Thomas M, Wong Y. Relation between direct detechion of Chlamydia pneumoniae DNA in human coronary arteries at postmortem examination and histological severity (Stary garding) of associated atherosclerotic plaque. Circulation 1999;99:2733­6.
[58] Tsao TC, Hong J. Increased TNF-alpha, IL-1 beta and IL-6levels in the bronchoalveolar lavage fluid with the upregulation of their mRNA in macrophages lavaged from patients with active pulmonary tuberculosis. Tub Lung Dis 1999;79(5):279­85.
[59] Schwartz P. Amyloid degeneration and tuberculosis in the aged. Gerontologia 1972;18(5-6):321­62.
[60] Weinstein L. Bacterial endocarditis, TB changing presentation. Internal Med News 1982;15(11):2.
[61] Xu Q. Dietrich Induction of arteriosclerosis in normocholesterolemic mice and rabbits by immunization with heat shock protein 65. Arterioscler Thromb 1992;12:789­99.
[62] Xu Q, Kleindienst R. Increased expression of heat shock protein 65 coincides with a population of infiltrating T lymphocytes in atherosclerotic lesions of rabbits specifically responding to heat shock protein 65. J Clin Invest 1993;91:2693­702.
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