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CLINICAL RESEARCH: PLAQUE RUPTURE

Diffuse and Active Inflammation Occurs in Both Vulnerable and Stable Plaques of the Entire Coronary Tree

A Histopathologic Study of Patients Dying of Acute Myocardial Infarction

Alessandro Mauriello, MD^_*, Giuseppe Sangiorgi, MD, FESC, Stefano Fratoni, MD^_*, Giampiero Palmieri, MD^_*, Elena Bonanno, MD^_*, Lucia Anemona, MD^_*, Robert S. Schwartz, MD, FACC, FAHA and Luigi Giusto Spagnoli, MD^_*,_*

^_* Department of Pathology, University of Rome Tor Vergata, Rome, Italy
Department of Cardiovascular Diseases, University of Rome Tor Vergata, Rome, Italy
Minnesota Cardiovascular Research Institute, Minneapolis Heart Institute Foundation, Minneapolis, Minnesota

Manuscript received August 12, 2004; revised manuscript received December 20, 2004, accepted January 17, 2005.

^_* Reprint requests and correspondence: Prof. Luigi Giusto Spagnoli, Cattedra di Anatomia ed Istologia Patologica, Dipartimento di Biopatologia e Diagnostica per Immagini, Universita di Roma Tor Vergata, Via Montpellier 1, 00133 Roma, Italy (Email: spagnoli{at}uniroma2.it).

OBJECTIVES: This study was undertaken to define and compare geographic coronary artery inflammation in patients who were dying of acute myocardial infarction (AMI), chronic stable angina (SA), and noncardiac causes (CTRL).

BACKGROUND: Biochemical markers and flow cytometry provide indirect evidence of diffuse coronary inflammation in patients dying of acute coronary syndromes. Yet no histopathologic studies have corroborated these findings. A key unanswered question is whether the inflammatory burden involves the entire coronary tree or is limited to a few plaques.

METHODS: We examined 544 coronary artery segments from 16 patients with AMI, 109 segments from 5 patients with SA, and 304 coronary segments from 9 patients with CTRL.

RESULTS: An average of 6.8 ± 0.5 vulnerable segments per patient were found in the AMI group (in addition to culprit lesions) compared with an average of 0.8 ± 0.3 and 1.4 ± 0.3 vulnerable lesions/patient in the SA and CTRL groups, respectively. The AMI group, independent of the type of plaque observed, showed significantly more inflammatory infiltrates compared with the SA and CTRL groups (121.6 ± 12.4 cell x mm² vs. 37.3 ± 11.9 cell x mm² vs. 26.6 ± 6.8 cell x mm², p = 0.0001). In AMI patients, active inflammation was not only evident within the culprit lesion and vulnerable plaques but also involved stable plaques. These showed a three- to four-fold higher inflammation than vulnerable and stable plaques from the SA and CTRL groups, respectively.

CONCLUSIONS: This histopathologic study found that both vulnerable and stable coronary plaques of patients dying of AMI are diffusely infiltrated by inflammatory cells.

Abbreviations and Acronyms   AMI = acute myocardial infarction   CTRL = controls, death of noncardiac causes   IRA = infarct-related coronary artery   non-IRA = non-infarct-related coronary arteries   SA = chronic stable angina

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