Literature DB >> 18239992

Near simultaneous atherothrombotic occlusion of two coronary arteries challenges the theory of the single vulnerable plaque.

Thomas Bartel1, Renate Hiemetzberger, Silvana Müller, Otmar Pachinger.   

Abstract

BACKGROUND: It is unlikely that mechanical stress altering a single vulnerable plaque leads to myocardial infarction from almost simultaneous proximal atherothrombotic closure of the right coronary artery and the left anterior descending coronary artery. ACUTE MANAGEMENT: Immediate catheter diagnosis and revascularization including stent deployment restored TIMI III flow in both coronary arteries. After an initial bolus, abciximab was continuously infused to optimize myocardial perfusion. LABORATORY TESTS ON ADMISSION: The patient's white blood cell count was markedly elevated and the level of C-reactive protein slightly so. After interventional recanalization, C-reactive protein rose steeply before falling again after two days. FOLLOW-UP: Thirty days after acute myocardial infarction, the patient was fully recovered and asymptomatic. Echocardiography revealed only mild-to-moderate global left ventricular hypokinesia.
CONCLUSION: Widespread inflammation associated with multifocal plaque rupture and subsequent two-vessel acute myocardial infarction is a rare phenomenon, usually associated with sudden cardiac death. Widespread inflammation is one of the reasons why the widely accepted theory of the single vulnerable plaque for such events can be contradicted.

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Year:  2008        PMID: 18239992     DOI: 10.1007/s00508-007-0901-5

Source DB:  PubMed          Journal:  Wien Klin Wochenschr        ISSN: 0043-5325            Impact factor:   1.704


  18 in total

1.  Healed plaque ruptures and sudden coronary death: evidence that subclinical rupture has a role in plaque progression.

Authors:  A P Burke; F D Kolodgie; A Farb; D K Weber; G T Malcom; J Smialek; R Virmani
Journal:  Circulation       Date:  2001-02-20       Impact factor: 29.690

2.  Inflammation of the coronary arteries in patients with unstable angina.

Authors:  E Wallsh; G S Weinstein; A Franzone; A Clavel; P A Rossi; E Kreps
Journal:  Tex Heart Inst J       Date:  1986-03

3.  Successful percutaneous coronary intervention for acute myocardial infarction caused by simultaneous occlusion of two major coronary arteries in patients with diabetes mellitus. A report of two cases.

Authors:  Yasumasa Ikeda; Hiroyuki Fujinaga; Toshiharu Niki
Journal:  Acta Cardiol       Date:  2005-04       Impact factor: 1.718

4.  Persistent systemic inflammation in unstable angina is largely unrelated to the atherothrombotic burden.

Authors:  Claudia Monaco; Elisabetta Rossi; Diego Milazzo; Franco Citterio; Francesca Ginnetti; Giuseppe D'Onofrio; Domenico Cianflone; Filippo Crea; Luigi M Biasucci; Attilio Maseri
Journal:  J Am Coll Cardiol       Date:  2005-01-18       Impact factor: 24.094

Review 5.  Coronary plaque disruption.

Authors:  E Falk; P K Shah; V Fuster
Journal:  Circulation       Date:  1995-08-01       Impact factor: 29.690

6.  Impaired coronary blood flow in nonculprit arteries in the setting of acute myocardial infarction. The TIMI Study Group. Thrombolysis in myocardial infarction.

Authors:  C M Gibson; K A Ryan; S A Murphy; R Mesley; S J Marble; R P Giugliano; C P Cannon; E M Antman; E Braunwald
Journal:  J Am Coll Cardiol       Date:  1999-10       Impact factor: 24.094

7.  Elevated levels of C-reactive protein at discharge in patients with unstable angina predict recurrent instability.

Authors:  L M Biasucci; G Liuzzo; R L Grillo; G Caligiuri; A G Rebuzzi; A Buffon; F Summaria; F Ginnetti; G Fadda; A Maseri
Journal:  Circulation       Date:  1999-02-23       Impact factor: 29.690

8.  Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study.

Authors:  G Rioufol; G Finet; I Ginon; X André-Fouët; R Rossi; E Vialle; E Desjoyaux; G Convert; J F Huret; A Tabib
Journal:  Circulation       Date:  2002-08-13       Impact factor: 29.690

9.  Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes.

Authors:  P Avanzas; R Arroyo-Espliguero; J Cosín-Sales; G Aldama; C Pizzi; J Quiles; J C Kaski
Journal:  Heart       Date:  2004-08       Impact factor: 5.994

10.  Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture.

Authors:  P K Shah; E Falk; J J Badimon; A Fernandez-Ortiz; A Mailhac; G Villareal-Levy; J T Fallon; J Regnstrom; V Fuster
Journal:  Circulation       Date:  1995-09-15       Impact factor: 29.690

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