CoChat
Sign Up
Cited by 1,447

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Pathogenesis of Atherosclerosis

Falk, Erling·2006·Journal of the American College of Cardiology
DOI 10.1016/j.jacc.2005.09.068
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.jacc.2005.09.068

Cites

3 of 3 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Elevated blood LDL-cholesterol is a major risk factor for cardiovascular disease because LDL-cholesterol promotes atherosclerotic plaque formation.

    “elevated blood LDL-cholesterol (hypercholesterolaemia) is a major risk factor for this because LDL-cholesterol promotes the formation of atherosclerotic plaques on the walls of blood vessels, narrowing and eventually completely occluding blood flow [7].”

    From Post-translational regulation of the low-density lipoprotein receptor provides new targets for cholesterol regulation (2024) · cites this paper as [7]

    The Atherogenic Stimuli section identifies elevated plasma cholesterol as a major driver of atherosclerosis and LDL as an atherogenic lipoprotein. The Cellular Components section says persistent atherogenic stimuli can narrow the lumen and reduce blood flow. The citing sentence’s further claim that plaque formation eventually completely occludes flow is not supported: the paper describes thrombosis superimposed on plaques as the cause of the most severe acute consequences. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 40

  1. Naghavi, 2003, From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies. Part I, Circulation, 108, 1664, 10.1161/01.CIR.0000087480.94275.97 · DOI
  2. Naghavi, 2003, From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies. Part II, Circulation, 108, 1772, 10.1161/01.CIR.0000087481.55887.C9 · DOI
  3. Spagnoli, 2004, Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke, JAMA, 292, 1845, 10.1001/jama.292.15.1845 · DOI
  4. Casscells, 2003, Vulnerable atherosclerotic plaque, Circulation, 107, 2072, 10.1161/01.CIR.0000069329.70061.68 · DOI
  5. Glass, 2001, Atherosclerosis. The road ahead, Cell, 104, 503, 10.1016/S0092-8674(01)00238-0 · DOI
  6. Lewis, 2005, New insights into the regulation of HDL metabolism and reverse cholesterol transport, Circ Res, 96, 1221, 10.1161/01.RES.0000170946.56981.5c · DOI
  7. Nissen, 2003, Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes, JAMA, 290, 2292, 10.1001/jama.290.17.2292 · DOI · Paper page
  8. Wang, 2005, Identifying novel genes for atherosclerosis through mouse-human comparative genetics, Am J Hum Genet, 77, 1, 10.1086/431656 · DOI
  9. Wald, 2003, A strategy to reduce cardiovascular disease by more than 80%, BMJ, 326, 1419, 10.1136/bmj.326.7404.1419 · DOI
  10. Law, 2004, The performance of blood pressure and other cardiovascular risk factors as screening tests for ischaemic heart disease and stroke, J Med Screen, 11, 3, 10.1258/096914104772950673 · DOI
  11. Cunningham, 2005, The role of shear stress in the pathogenesis of atherosclerosis, Lab Invest, 85, 9, 10.1038/labinvest.3700215 · DOI
  12. Libby, 2002, Inflammation in atherosclerosis, Nature, 420, 868, 10.1038/nature01323 · DOI · Paper page
  13. Davies, 1988, Morphology of the endothelium over atherosclerotic plaques in human coronary arteries, Br Heart J, 60, 459, 10.1136/hrt.60.6.459 · DOI
  14. Willerson, 2003, Endothelial dysfunction, Circulation, 108, 2060, 10.1161/01.CIR.0000099580.72044.83 · DOI
  15. Houtkamp, 2001, Adventitial infiltrates associated with advanced atherosclerotic plaques, J Pathol, 193, 263, 10.1002/1096-9896(2000)9999:9999<::AID-PATH774>3.0.CO;2-N · DOI
  16. Kaartinen, 1998, Mast cell infiltration in acute coronary syndromes, J Am Coll Cardiol, 32, 606, 10.1016/S0735-1097(98)00283-6 · DOI
  17. Naruko, 2002, Neutrophil infiltration of culprit lesions in acute coronary syndromes, Circulation, 106, 2894, 10.1161/01.CIR.0000042674.89762.20 · DOI
  18. Nilsson, 2005, Immunomodulation of atherosclerosis, Arterioscler Thromb Vasc Biol, 25, 18, 10.1161/01.ATV.0000149142.42590.a2 · DOI
  19. Kragel, 1989, Morphometric analysis of the composition of atherosclerotic plaques in the four major epicardial coronary arteries in acute myocardial infarction and in sudden coronary death, Circulation, 80, 1747, 10.1161/01.CIR.80.6.1747 · DOI
  20. Schwartz, 2000, The good smooth muscle cells in atherosclerosis, Curr Atheroscler Rep, 2, 422, 10.1007/s11883-000-0081-5 · DOI
  21. Geng, 2002, Progression of atheroma, Arterioscler Thromb Vasc Biol, 22, 1370, 10.1161/01.ATV.0000031341.84618.A4 · DOI
  22. Kolodgie, 2003, Targeting of apoptotic macrophages and experimental atheroma with radiolabeled annexin V, Circulation, 108, 3134, 10.1161/01.CIR.0000105761.00573.50 · DOI
  23. Guyton, 2001, Phospholipid hydrolytic enzymes in a ’cesspool’ of arterial intimal lipoproteins, Arterioscler Thromb Vasc Biol, 21, 884, 10.1161/01.ATV.21.6.884 · DOI
  24. Tedgui, 2001, Apoptosis as a determinant of atherothrombosis, Thromb Haemost, 86, 420, 10.1055/s-0037-1616240 · DOI
  25. Llodrá, 2004, Emigration of monocyte-derived cells from atherosclerotic lesions characterizes regressive, but not progressive, plaques, Proc Natl Acad Sci USA, 101, 11779, 10.1073/pnas.0403259101 · DOI
  26. Hoffmann, 2003, Cardiology patient page. Use of new imaging techniques to screen for coronary artery disease, Circulation, 108, e50, 10.1161/01.CIR.0000085363.88377.F2 · DOI
  27. Pletcher, 2004, Using the coronary artery calcium score to predict coronary heart disease events, Arch Intern Med, 164, 1285, 10.1001/archinte.164.12.1285 · DOI
  28. Beckman, 2001, Relationship of clinical presentation and calcification of culprit coronary artery stenoses, Arterioscler Thromb Vasc Biol, 21, 1618, 10.1161/hq0901.095554 · DOI
  29. Ehara, 2004, Spotty calcification typifies the culprit plaque in patients with acute myocardial infarction, Circulation, 110, 3424, 10.1161/01.CIR.0000148131.41425.E9 · DOI
  30. Barger, 1984, Hypothesis: vasa vasorum and neovascularization of human coronary arteries. A possible role in the pathophysiology of atherosclerosis, N Engl J Med, 310, 175, 10.1056/NEJM198401193100307 · DOI
  31. Kolodgie, 2003, Intraplaque hemorrhage and progression of coronary atheroma, N Engl J Med, 349, 2316, 10.1056/NEJMoa035655 · DOI
  32. Virmani, 2005, Atherosclerotic plaque progression and vulnerability to rupture angiogenesis as a source of intraplaque hemorrhage, Arterioscler Thromb Vasc Biol, 25, 2054, 10.1161/01.ATV.0000178991.71605.18 · DOI
  33. Casscells, 2003, Plaque blush, branch location, and calcification are angiographic predictors of progression of mild to moderate coronary stenoses, Am Heart J, 145, 813, 10.1016/S0002-8703(02)94727-7 · DOI
  34. Vink, 2001, Plaque burden, arterial remodeling and plaque vulnerability, J Am Coll Cardiol, 38, 718, 10.1016/S0735-1097(01)01444-9 · DOI
  35. Schaar, 2004, Terminology for high-risk and vulnerable coronary artery plaques, Eur Heart J, 25, 1077, 10.1016/j.ehj.2004.01.002 · DOI
  36. Falk, 2000, Multiple culprits in acute coronary syndromes, Ital Heart J, 1, 835
  37. Mann, 1999, Mechanisms of progression in native coronary artery disease, Heart, 82, 265, 10.1136/hrt.82.3.265 · DOI
  38. Burke, 2001, Healed plaque ruptures and sudden coronary death, Circulation, 103, 934, 10.1161/01.CIR.103.7.934 · DOI
  39. Sata, 2003, Circulating vascular progenitor cells contribute to vascular repair, remodeling, and lesion formation, Trends Cardiovasc Med, 13, 249, 10.1016/S1050-1738(03)00106-3 · DOI
  40. Caplice, 2003, Smooth muscle cells in human coronary atherosclerosis can originate from cells administered at marrow transplantation, Proc Natl Acad Sci USA, 100, 4754, 10.1073/pnas.0730743100 · DOI

Cited by

Sorted by citations

Metadata

Authors
Falk, E.
Venue
Journal of the American College of Cardiology
Publisher
Elsevier BV
Published
2006-04
Volume
47
Issue
8
Pages
C7-C12
ISSN
0735-1097
DOI
10.1016/j.jacc.2005.09.068
Cited by
1,447
References
3
Language
en
Licence

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review