Is preinfarction angina related to the presence or absence of coronary plaque rupture?

Abstract

Objective: To analyse the prodrome of acute myocardial infarction in relation to the plaque morphology underlying the infarct.

Design: A retrospective investigation of the relation between rupture and erosion of coronary atheromatous plaques and the clinical characteristics of acute myocardial infarction. The coronary arteries of 100 patients who died from acute myocardial infarction were cut transversely at 3 mm intervals. Segments with a stenosis were examined microscopically at 5 micrometer intervals. The clinical features of the infarction were obtained from the medical records.

Results: A deep intimal rupture was encountered in 81 plaques, whereas 19 had superficial erosions only. There were no differences in the location of infarction, the incidence of hypertension, diabetes mellitus, or hyperlipidaemia, diameter stenosis of the infarcted related artery, Killip class, Forrester's haemodynamic subset, or peak creatine kinase between plaque rupture and plaque erosion groups. The presence of plaque rupture was associated with significantly greater incidences of leucocytosis, current smoking, and sudden or unstable onset of acute coronary syndrome. In patients with unstable preinfarction angina, new onset rest angina rather than worsening angina tended to develop more often in the plaque rupture group than in the plaque erosion group (p = 0.08).

Conclusions: Plaque rupture causes the sudden onset of acute myocardial infarction or unstable preinfarction angina, which may be aggravated by smoking and inflammation.

Figure 1

(A) A coronary plaque rupture was found in a patient who died one week after the onset of acute myocardial infarction. At lower magnification the rupture site (arrow) is seen at the shoulder lesion, which is considered to have had a thin fibrous cap. An occlusive thrombus (T) was present (haematoxylin and eosin stain). (B) A coronary plaque erosion was found in a patient who died two weeks after the onset of acute myocardial infarction. At lower magnification, a concentric hard plaque (HP) which includes focal calcification was present. The luminal (L) plaque surface was in contact with non-occlusive thrombus (arrows) (haematoxylin and eosin stain).

Figure 2

Pie charts showing the status of preinfarction angina. The patients with plaque rupture had a significantly higher incidence of sudden onset and unstable angina than those with plaque erosion.

Figure 3

Pie charts showing the status of unstable angina. The patients with plaque rupture had a higher incidence of new onset of rest angina than those with plaque erosion, but the difference was not significant.

Figure 4

White blood cell count within six hours of the onset of acute myocardial infarction. Error bars = SEM.