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Titolo:
Coronary plaques calling for action - why, where and how many?
Autore:
Bentzon, JF; Falk, E;
Indirizzi:
Aarhus Univ Hosp Skejby, Dept Cardiol, Res Unit, DK-8200 Aarhus N, DenmarkAarhus Univ Hosp Skejby Aarhus Denmark N Unit, DK-8200 Aarhus N, Denmark
Titolo Testata:
EUROPEAN HEART JOURNAL SUPPLEMENTS
fascicolo: I, volume: 3, anno: 2001,
pagine: I3 - I9
SICI:
1520-765X(200108)3:I<I3:CPCFA->2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
C-REACTIVE PROTEIN; HUMAN ATHEROSCLEROTIC PLAQUES; ACUTE MYOCARDIAL-INFARCTION; UNSTABLE ANGINA; ARTERY DISEASE; CARDIOVASCULAR-DISEASE; COLLAGEN CONTENT; SUDDEN-DEATH; LIPID CORE; TROPONIN-T;
Keywords:
atherosclerosis; fibrosis; inflammation; local factors; plaque rupture; systemic factors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Falk, E Aarhus Univ Hosp Skejby, Dept Cardiol, Res Unit, DK-8200 Aarhus N,Denmark Aarhus Univ Hosp Skejby Aarhus Denmark N -8200 Aarhus N, Denmark
Citazione:
J.F. Bentzon e E. Falk, "Coronary plaques calling for action - why, where and how many?", EUR H J SUP, 3(I), 2001, pp. I3-I9

Abstract

Aims Most adults of the Western World harbour advanced atherosclerotic plaques in their coronary arteries, and many will eventually suffer an acute coronary syndrome. The majority, however, will not. This overview sets out to answer the question: Why do some plaques rupture and become the culprit of an acute coronary syndrome whereas most do not? Methods and Results At least part of the answer has been elucidated through meticulous autopsy studies. The risk of plaque rupture appears to depend on plaque morphology rather than plaque size or severity of stenosis. Fibrosis with smooth muscle cell proliferation and collagen synthesis hardens the plaque, stabilizing it against rupture, while inflammation leading to degradation of the fibrous cap and growth of the soft core predisposes the plaque to rupture. Conclusions Traditionally, plaque vulnerability has been viewed as a focaldisorder calling for a target-lesion based approach. However, accumulatingdata indicate that multiple ruptured plaques are the rule rather than the exception in patients who die from atherosclerosis, and that multiple luminal thrombi are not rare. If plaque vulnerability changes for the entire arterial tree as a whole, rather than focally. this calls for systemic treatment modalities. (C) 2001 The European Society of Cardiology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 09:32:05