Atheroma.pdf

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Atheroma

An atheroma is an accumulation of degenerative ma-terial in the tunica intima (inner layer) of artery walls.The material consists of (mostly) macrophage cells , ordebris, containing lipids (cholesterol and fatty acids), cal-cium and a variable amount of brous connective tissue .The accumulated material forms a swelling in the arterywall, which may intrude into the channel of the artery,narrowing it and restricting blood ow. Atheroma occursin atherosclerosis , which is one of the three subtypes ofarteriosclerosis (which are atherosclerosis, Monckebergs

arteriosclerosis and arteriolosclerosis ).[1]

In the context of heart or artery matters, atheromata arecommonly referred to as atheromatous plaques . It is anunhealthy condition, but is found in most humans. [2]

Veins do not develop atheromata, unless surgically movedto function as an artery, as in bypass surgery. The ac-cumulation (swelling) is always in the tunica intima, be-tween the endothelium lining and the smooth muscletunica media (middle layer) of the artery wall. While theearly stages, based on gross appearance, have tradition-ally been termed fatty streaks bypathologists, they arenotcomposed of fat cells, i.e. adipose cells, but of accumu-lations of white blood cells, especially macrophages , thathave taken up oxidized low-density lipoprotein (LDL).After they accumulate large amounts of cytoplasmicmembranes (with associated high cholesterol content)they are called foam cells. When foam cells die, theircontents are released, which attracts more macrophagesand creates an extracellular lipid core near the center toinner surface of each atherosclerotic plaque. Conversely,the outer, older portions of the plaque become more cal-cied, less metabolically active and more physically stiffover time.

1 Difficulty of tracking and re-searching atheroma

For most people, the rst clinical symptoms result fromatheromaprogressionwithin the heart arteries , most com-monly resulting in a heart attack and ensuing debility.However, the heart arteries, because (a) they are small(from about5 mm down to microscopic), (b) they arehid-den deep within the chest and (c) they never stop moving,have been a difficult target organ to track, especially clin-

ically in individuals who are still asymptomatic . Addi-tionally, all mass-applied clinical strategies focus on both(a) minimal cost and (b) the overall safety of the pro-

cedure. Therefore, existing diagnostic strategies for de-tecting atheroma and tracking response to treatment havebeen extremely limited. The methods most commonlyrelied upon, patient symptoms and cardiac stress testing ,do not detect any symptoms of the problem until athero-matous disease is very advanced.

2 History of research

In developed countries , with improved public health, in-fection control and increasing life spans, atheroma pro-cesses have become an increasingly important problemand burden for society. Atheromata continue to be theprimary underlying basis for disability and death, despitea trend for gradual improvement since the early 1960s(adjusted for patient age). Thus, increasing efforts to-wards better understanding, treating and preventing theproblem are continuing to evolve.

According to United States data, 2004, for about 65% ofmen and 47% of women, the rst symptom of cardio-

vascular disease is myocardial infarction (heart attack) orsudden death (death within one hour of symptom onset.)

Most artery ow-disrupting events occur at locations withless than 50% lumen narrowing. From clinical stud-ies published in the late 1990s to IVUS (in-the-artery-ultrasound) to visualizedisease status, thetypical heart at-tack occurs at locations with about 20% stenosis (narrow-ing), prior to sudden lumen closure and resulting myocar-dial infarction. Cardiac stress testing , traditionally themost commonly performed noninvasive testing methodfor blood ow limitations, generally only detects lumennarrowing of ~75% or greater, although some physicians

advocate nuclear stress methods that can sometimes de-tect as little as 50%.

3 Artery and atheroma behavior

The healthy epicardial coronary artery consists of threelayers, the intima, media, and adventitia. [3][4] Atheromaand changes in the artery wall usually result in smallaneurysms (enlargements) just large enough to compen-sate for the extra wall thickness with no change in thelumen diameter. However, eventually, typically as a re-

sult of rupture of vulnerable plaques and clots within thelumen over the plaque, stenosis (narrowing) of the vesseldevelops in some areas. Less frequently, the artery en-

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2 4 INTIMA-MEDIA THICKNESS MEASUREMENTS IN THE CAROTID ARTERY

larges so much that a gross aneurysmal enlargement ofthe artery results. All three results are often observed, atdifferent locations, within the same individual.

3.1 Stenosis and closure

Over time, atheromata usually progress in size and thick-ness and induce the surrounding muscular central region(the media) of the artery to stretch out, termed remod-eling, typically just enough to compensate for their sizesuch that the caliber of the artery opening (lumen) re-mains unchanged until typically over 50% of the arterywall cross-sectional area consists of atheromatous tissue(see: Glagov, below).

If the muscular wall enlargement eventually fails to keepup with the enlargement of the atheroma volume, or aclot forms and organizes over the plaque, then the lumen

of the artery begins to narrow, commonly as a result ofrepeated ruptures of the covering tissues separating theatheroma from the blood stream. This becomes a morecommon event after decades of living, increasingly morecommon after people are in their 30s to 40s.

The endothelium (the cell monolayer on the inside of thevessel) and covering tissue, termed brous cap, separateatheroma from the blood in the lumen. If a rupture oc-curs of the endothelium and brous cap, then a plateletand clotting response over the rupture rapidly develops.Additionally, the rupture may result in a shower of de-bris. Platelet and clot accumulation over the rupture may

produce narrowing/closure of the lumen, and tissue dam-age may occur due to either closure of the lumen result-ing in loss of blood ow beyond the ruptured atheromaand/or by occlusion of smaller downstream vessels by de-bris. See vulnerable plaque. This is the principal mech-anism of myocardial infarction , stroke or other relatedcardiovascular disease problems. As research has shown,thisprocess is not a result of stenosis . Prior to the rupture,there may have been no lumen narrowing, even aneurys-mal enlargement, at the atheroma. On average, by clin-ical research using IVUS, a minor stenosis, about 20%,is present over those unstable atheroma which ruptureand result in major disability or death. Comparatively,stenoses of about 75% are required to produce detectableabnormalities during cardiac stress tests.

3.2 Artery enlargement

If the muscular wall enlargement is overdone over time,then a gross enlargement of the artery results, usuallyover decades of living. This is a less common out-come. Atheroma within aneurysmal enlargement (vesselbulging) can also rupture and shower debris of atheromaand clot downstream. If the arterial enlargement con-

tinues to 2 to 3 times the usual diameter, the walls of-ten become weak enough that with just the stress of thepulse, a loss of wall integrity may occur leading to sud-

den hemorrhage (bleeding), major symptoms and debil-ity; often rapid death. The main stimulus for aneurysmformation is pressure atrophy of the structural supportof the muscle layers. The main structural proteins arecollagen and elastin. This causes thinning and the wallballoons allowing gross enlargement to occur, as is com-mon in the abdominal region of the aorta.

4 Intima-media thickness mea-surements in the carotid artery

Since the 1990s, both small clinical and several larger-scale pharmaceutical trials have used carotid intima-media thickness (IMT) as a surrogate endpoint for evalu-ating the regression and/or progression of atheroscleroticcardiovascular disease. Many studies have documentedthe relationship between the carotid intima-media thick-ness and the presence and severity of atherosclerosis . In2003, the European Society of Hypertension-EuropeanSociety of Cardiology recommended the use of IMTmeasurements in high-risk patients to help identify tar-get organ damage not revealed by other exams such asthe electrocardiogram.

Though carotid intima-media thickness seems to bestrongly associated with atherosclerosis, not all of theprocesses of thickening of the intima-media are due toatherosclerosis. Intimal thickening is in fact a complexprocess, depending on a variety of factors, not necessar-ily related to atherosclerosis. Local hemodynamics playan important role, higher blood pressure and changes inshear stress being potential causes of intimal thickening.Changes in shear stress and blood pressure may cause alocal delay in lumen transportation of potentially athero-genic particles, which favors the penetration of particlesinto the arterial wall and consequent plaque formation.However non-atherosclerotic reactions may also exist, asin intimal hyperplasia and intimal brocellular hypertro-phy, two different compensatory reactions of the arterialwall to changes in shearstress, whichalso consist in thick-ening of the arterial wall. In some cases, more than one

of these reactions may be present, and indeed as all ofthese are associated to particular ow conditions, theyare often found in common areas, such as the inow sideof branches, the inner curvature at bends and oppositethe ow divider at bifurcations. However, changes in theIMT above thresholds of around 900 m almost certainlyare indicative of an atherosclerotic pathology.

Mechanisms such as these may explain, at least in part,why the carotid artery seems to be a preferential sitefor analyzing the relation between wall thickness andatherosclerosis. In general, wall thickening may be inthe intimal layer or in the muscular medial layer. As the

carotid artery is an elastic artery, the muscular media isrelatively small. Hence, thickening of the carotid arterialwall is due essentially to intimal thickening. In muscu-
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lar arteries wall thickening may imply instead (or also) athickening of the medial wall. Whether or not wall thick-ening in thecarotid arteryand thefemoral artery (or othermuscular arteries) have the same meaning is as yet uncer-tain. Several studies seem to suggest that the mechanismsunderlying their evolution may at least in part differ, withconsequently possibly different clinical implications.Another issue to consider, once the choice to examine thecarotid artery has been dened, is on which segment ofthe carotid artery to perform the measurement. Often,the measurement of the IMT is measured in three tracts:in the common carotid, at one or two cm from the ow di-vider, at the bifurcation and in the internal carotid artery.

From an academic standpoint, the region to select forIMT measurement is still an object of study. IMT mea-surements of the deep wall by ultrasound are generallymore reliable than measurements performed on the outer

wall. This difference in the accuracy of near and far wallmeasurements may be a problem, as some studies haveused both measurements to quantify the IMT.

A practical approach to tracking disease presence andprogression on any given individual is to select and trackthose regions with the greatest thickness, i.e. greatest dis-ease burden, as opposed to arbitrarily selecting a partic-ular segment in which the individual may not have muchpathology.

5 Evolution of strategies andchanging focus

The sudden nature of the complications of pre-existingatheroma, vulnerable plaque (non-occlusive or softplaque), have led, since the 1950s, to the development ofintensive care units and complex medical and surgical in-terventions. Angiography and later cardiac stress testingwas begun to either visualize or indirectly detect stenosis.Next came bypass surgery, to plumb transplanted veins,sometimes arteries , around the stenoses and more re-cently angioplasty, now including stents, most recently

drug coated stents, to stretch the stenoses more open.Yet despite these medical advances, with success in re-ducing the symptoms of angina and reduced blood ow,atheroma rupture events remain the major problem andstill sometimes result in sudden disability and death de-spiteeven themost rapid, massive andskilled medical andsurgical intervention available anywhere today. Accord-ing to some clinical trials, bypass surgery and angioplastyprocedures have had at best a minimal effect, if any, onimproving overall survival. Typically mortality of bypassoperations is between 1 and 4%, of angioplasty between1 and 1.5%.

Additionally, these vascular interventions are often doneonly after an individual is symptomatic, often alreadypartially disabled, as a result of the disease. It is also

clear that both angioplasty and bypass interventions donot prevent future heart attack .

The older methods for understanding atheroma, datingto before World War II, relied on autopsy data. Au-topsy data has long shown initiation of fatty streaks in

later childhood with slow asymptomatic progression overdecades.

One way to see atheroma is the very invasive and costlyIVUS ultrasound technology; it gives us the precise vol-ume of the inside intima plus the central media layers ofabout 2.5 cm (1 in) of artery length. Unfortunately, itgives no information about the structural strength of theartery. Angiography does not visualize atheroma; it onlymakes the blood ow within blood vessels visible. Alter-native methods that arenonor less physically invasive andless expensive per individual test have been used and arecontinuing to be developed, such as those using computed

tomography (CT; led by the electron beam tomographyform, given its greater speed) and magnetic resonanceimaging (MRI).Themost promisingsince theearly 1990shas beenEBT, detecting calcication within the atheromabefore most individuals start having clinically recognizedsymptoms and debility. Interestingly, statin therapy (tolower cholesterol) does not slow the speed of calcica-tion as determined by CT scan. MRI coronary vesselwall imaging, although currently limited to research stud-ies, has demonstrated the ability to detect vessel wallthickening in asymptomatic high risk individuals. [5] Asa non-invasive, ionising radiation free technique, MRIbased techniques could have future uses in monitoringdisease progression and regression. Most visualizationtechniques are used in research, they are not widely avail-able to most patients, have signicant technical limita-tions, have not been widely accepted and generally arenot covered by medical insurance carriers.

From human clinical trials, it has become increasinglyevident that a more effective focus of treatment is slow-ing, stopping and even partially reversing the atheromagrowth process. There are several prospective epidemio-logic studies including the Atherosclerosis Risk in Com-munities (ARIC) Study and the Cardiovascular HealthStudy (CHS), which have supported a direct correlationof CIMT with myocardial infarction andstroke risk in pa-tients without cardiovascular disease history. The ARICStudy was conducted in 15,792 individuals between 5and 65 years of age in 4 different regions of the USAbetween 1987 and 1989. The baseline CIMT was mea-sured and measurements were repeated at 47 year in-tervals by carotid B mode ultrasonography in this study.An increase in CIMT was correlated with an increasedrisk for CAD. The CHS was initiated in 1988, and therelationship of CIMT with risk of myocardial infarctionand stroke was investigated in 4,476 subjects 65 yearsof age. At the end of approximately 6 years of follow-up,

CIMT measurementswere correlated withcardiovascularevents.
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4 6 DIAGNOSIS

Paroi artrielle et Risque Cardiovasculaire in AsiaAfrica/Middle East and Latin America (PARC-AALA)is another important large-scale study, in which 79 cen-ters from countries in Asia, Africa, the Middle East, andLatin America participated, andthedistribution of CIMTaccording to different ethnic groups and its associationwith the Framingham cardiovascular score was investi-gated. Multi-linear regression analysis revealed that anincreased Framingham cardiovascular score was associ-ated with CIMT, and carotid plaque independent of geo-graphic differences.

Cahn et al. prospectively followed-up 152 patients withcoronary arterydisease for 611 months by carotid arteryultrasonography and noted 22 vascular events (myocar-dial infarction, transient ischemic attack, stroke, andcoronary angioplasty) within this time period. Theyconcluded that carotid atherosclerosis measured by thisnon-interventional method has prognostic signicance incoronary artery patients.In the Rotterdam Study , Bots et al. followed 7,983 pa-tients >55 years of age for a mean period of 4.6 years, andreported 194 incident myocardial infarctions within thisperiod. CIMT was signicantly higher in the myocardialinfarction group compared to the other group. Demircanet al. found that the CIMT of patients with acute coro-nary syndrome were signicantly increased compared topatients with stable angina pectoris.

It has been reported in another study that a maximalCIMT value of 0.956 mm had 85.7% sensitivity and85.1% specicity to predict angiographic CAD. Thestudy group consisted of patients admitted to the cardi-ology outpatient clinic with symptoms of stable anginapectoris. The study showed CIMT was higher in patientswith signicant CAD than in patients with non-criticalcoronary lesions. Regression analysis revealed that thick-ening of the mean intima-media complex more than 1.0was predictive of signicant CAD our patients. Therewas incremental signicant increase in CIMT with thenumber coronary vessel involved. In accordance withthe literature, it was found that CIMT was signicantlyhigher in the presence of CAD. Furthermore, CIMT wasincreased as thenumber of involved vessels increased andthe highest CIMT values were noted in patients with leftmaincoronary involvement. However, human clinical tri-alshavebeen slowto provide clinical & medical evidence,partly because the asymptomatic nature of atheromatamake them especially difficult to study. Promising resultsare found using carotid intima-media thickness scanning(CIMTcan be measured by B-mode ultrasonography), B-vitamins that reduce a protein corrosive, homocysteineand that reduce neck carotid artery plaque volume andthickness, and stroke, even in late-stage disease.

Additionally, understanding what drives atheroma de-velopment is complex with multiple factors involved,only some of which, such as lipoproteins , more im-portantly lipoprotein subclass analysis, blood sugar lev-

els and hypertension are best known and researched.More recently, some of the complex immune system pat-terns that promote, or inhibit, the inherent inammatorymacrophage triggering processes involved in atheromaprogression are slowly being better elucidated in animalmodels of atherosclerosis.

A 4-minute animation of the atherosclerosis process,entitled Pathogenesis of Acute MI, commissioned byPaul M. Ridker at the Harvard Medical School, canbe viewed at pri-med.com . While the animation con-tains a few technical errors, partly due to the great diffi-culty/complexity of making a truly accurate presentation,it correctly illustrates the principal issues.

6 Diagnosis

Arterial wall xation, staining and thin section: histor-ically this has been the gold standard for detection anddescription of atheroma, though only done after autopsy.With special stains and examination, micro calcicationscan be detected, typically with smooth muscle cells of thearterial media near the fatty streaks within a year or twoof fatty streaks forming.

CIMT (carotid IMT) as mentioned in the Evolution ofStrategies and Changing Focus section, Interventionaland non-interventional methods to detect atherosclero-sis, specically vulnerable plaque (non-occlusive or softplaque), are widely used in research and clinical practice

today; Carotid Intima-media thickness Scan (CIMT canbe measured by B-mode ultrasonography) measurementhas been recommended by the American Heart Associa-tion as the most useful method to identify atherosclerosisand may now very well be the gold standard for detection.

IVUS is the current most sensitive method detecting andmeasuring more advanced atheroma within living indi-viduals, though it is typically not used until decades afteratheroma begin forming due to cost and body invasive-ness.

CT scans using state of the art higher resolution spi-ral, or the higher speed EBT, machines have been the

most effective method for detecting calcication presentin plaque. However, the atheroma have to be ad-vanced enough to have relatively large areas of calci-cation within them to create large enough regions of~130 Hounseld units which a CT scanners software canrecognize as distinct from the other surrounding tissues.Typically, such regions start occurringwithin theheart ar-teries about 23 decades after atheroma start developing.Hence the detection of much smaller plaques than pre-viously possible is being developed by some companies,such as Image Analysis. The presence of smaller, spottyplaques may actually be more dangerous for progressing

to acute myocardial infarction .[6]

Arterial ultrasound,especiallyof the carotid arteries, withmeasurement of the thickness of the artery wall, offers a
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way to partially track thedisease progression. As of 2006,the thickness, commonly referred to as IMT for intimal-medial thickness, is not measured clinically though ithas been used by some researchers since the mid-1990sto track changes in arterial walls. Traditionally, clini-cal carotid ultrasounds have only estimated the degreeof blood lumen restriction, stenosis, a result of very ad-vanced disease. The National Institute of Health did aveyear $5 million study, headed by medical researcherKenneth Ouriel , to study intravascular ultrasound tech-niques regarding atherosclerotic plaque. [7] More progres-sive clinicians have begun using IMT measurement as away to quantify and track disease progression or stabilitywithin individual patients.

Angiography , since the 1960s, has been the traditionalway of evaluating for atheroma. However, angiography isonly motion or still images of dye mixed with the bloodwith the arterial lumen andnever show atheroma; the wallof arteries, including atheroma with the arterial wall re-main invisible. The limited exception to this rule is thatwith very advanced atheroma, with extensive calcica-tion within the wall, a halo-like ring of radiodensity canbe seen in most older humans, especially when arteriallumens are visualized end-on. On cine-oro, cardiolo-gists and radiologists typically look for these calcica-tion shadows to recognize arteries before they inject anycontrast agent during angiograms.

7 Classication of lesions

Type I: Isolated macrophage foam cells [3][8]

Type II: Multiple foam cell layers [3][8]

Type III: Preatheroma, intermediate lesion [3][8]

Type IV: Atheroma [3][8]

Type V: Fibroatheroma [3][8]

Type VI: Fissured, ulcerated, hemorrhagic, throm-botic lesion [3][8]

Type VII: Calcic lesion [3][8]

Type VIII: Fibrotic lesion [3][8]

8 Treatment

Many approaches have been promoted as methods to re-duce atheroma progression:

reducing or eliminating consumption of foods thatcontain saturated fat and cholesterol;

eating a diet of raw fruits, vegetables, nuts, beans,berries, and grains;

consuming foods containing omega-3 fatty acidssuch as sh, sh-derived supplements, as well asax seed oil, borage oil, andother non-animal-basedoils;

abdominal fat reduction;

aerobic exercise;

inhibitorsof cholesterol synthesis (known as statins);

low normal blood glucose levels (glycosylatedhemoglobin , also called HbA1c);

micronutrient (vitamins, potassium, andmagnesium ) consumption;

maintaining normal, or healthy, blood pressure lev-els;

aspirin supplement

9 Additional images

Illustration comparing a normal blood vessel andpartiallyblocked vesseldue to atheroscleroticplaquebuild-up

10 See also

Angiogram

ApoA-1 Milano

Atherosclerosis

Atherothrombosis

Coronary circulation

Coronary catheterization

EBT

Hemorheologic-Hemodynamic Theory ofAtherosclerosis

Lipoprotein

LDL, HDL, IDL and VLDL

11 References

[1] http://www.mercksource.com[]

[2] Lusis AJ (September 2000). Atherosclerosis . Nature407 (6801): 23341. doi:10.1038/35025203 . PMC2826222 . PMID 11001066 .

[3] Coronary Artery Atherosclerosis at eMedicine
https://en.wikipedia.org/wiki/EMedicinehttp://emedicine.medscape.com/article/153647-overviewhttps://www.ncbi.nlm.nih.gov/pubmed/11001066https://en.wikipedia.org/wiki/PubMed_Identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826222https://en.wikipedia.org/wiki/PubMed_Centralhttps://dx.doi.org/10.1038%252F35025203https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826222http://www.mercksource.com/%5B%5Dhttps://en.wikipedia.org/wiki/VLDLhttps://en.wikipedia.org/wiki/Intermediate_density_lipoproteinhttps://en.wikipedia.org/wiki/High_density_lipoproteinhttps://en.wikipedia.org/wiki/LDLhttps://en.wikipedia.org/wiki/Lipoproteinhttps://en.wikipedia.org/wiki/Hemorheologic-Hemodynamic_Theory_of_Atherosclerosishttps://en.wikipedia.org/wiki/Hemorheologic-Hemodynamic_Theory_of_Atherosclerosishttps://en.wikipedia.org/wiki/Electron_beam_tomographyhttps://en.wikipedia.org/wiki/Coronary_catheterizationhttps://en.wikipedia.org/wiki/Coronary_circulationhttps://en.wikipedia.org/wiki/Atherothrombosishttps://en.wikipedia.org/wiki/Atherosclerosishttps://en.wikipedia.org/wiki/ApoA-1_Milanohttps://en.wikipedia.org/wiki/Angiogramhttps://en.wikipedia.org/wiki/Magnesiumhttps://en.wikipedia.org/wiki/Potassiumhttps://en.wikipedia.org/wiki/HbA1chttps://en.wikipedia.org/wiki/Glycosylated_hemoglobinhttps://en.wikipedia.org/wiki/Glycosylated_hemoglobinhttps://en.wikipedia.org/wiki/Blood_glucosehttps://en.wikipedia.org/wiki/Statinshttps://en.wikipedia.org/wiki/Cholesterolhttps://en.wikipedia.org/wiki/Omega-3https://en.wikipedia.org/wiki/Contrast_agenthttps://en.wikipedia.org/wiki/Angiographyhttps://en.wikipedia.org/wiki/Kenneth_Ourielhttps://en.wikipedia.org/wiki/Medical_researchhttps://en.wikipedia.org/wiki/National_Institute_of_Healthhttps://en.wikipedia.org/wiki/Stenosis


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6 12 FURTHER READING

[4] Waller BF, Orr CM, Slack JD, Pinkerton CA, Van Tas-sel J, Peters T (June 1992). Anatomy, histology, andpathology of coronary arteries: a review relevant to newinterventional and imaging techniquesPart I. Clin Car-diol 15 (6): 4517. doi:10.1002/clc.4960150613 . PMID1617826 .

[5] Kim 2002, Circulation

[6] Ehara S, Kobayashi Y, Yoshiyama M, et al. (Novem-ber 2004). Spotty calcication typies the culprit plaquein patients with acute myocardial infarction: an intravas-cular ultrasound study. Circulation 110 (22): 34249. doi:10.1161/01.CIR.0000148131.41425.E9 . PMID15557374 .

[7] Dr. Kenneth Ouriel (biography)" . New York-Presbyterian Hospital. 2009-09-22. Retrieved 2009-09-22.

[8] Stary, Herbert C. (2003). Atlas of atherosclerosis: pro-

gression and regression . Parthenon Pub. p. 16. ISBN978-1-84214-153-3 .

12 Further reading

Ornish D, Brown SE, Scherwitz LW, et al. (July1990). Can lifestyle changes reverse coro-nary heart disease? The Lifestyle Heart Trial.Lancet 336 (8708): 12933. doi:10.1016/0140-6736(90)91656-U . PMID 1973470 .

Gould KL, Ornish D, Scherwitz L, et al.(September 1995). Changes in myocardialperfusion abnormalities by positron emissiontomography after long-term, intense risk fac-tor modication. JAMA 274 (11): 894901.doi:10.1001/jama.1995.03530110056036 . PMID7674504 .

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