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Angiology
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Features of Coronary Artery Lesions Related to Left Ventricular Aneurysm Formation in Anterior Myocardial Infarction

Teruo Inoue

Department of Cardiology, Koshigaya Hospital, Dokkyo University of Medicine, Saitama, Japan

Shigenori Morooka

Department of Cardiology, Koshigaya Hospital, Dokkyo University of Medicine, Saitama, Japan

Terumi Hayashi

Department of Cardiology, Koshigaya Hospital, Dokkyo University of Medicine, Saitama, Japan

Kan Takayanagi

Department of Cardiology, Koshigaya Hospital, Dokkyo University of Medicine, Saitama, Japan

Yoshihiko Sakai

Department of Cardiology, Koshigaya Hospital, Dokkyo University of Medicine, Saitama, Japan

Tsuneo Fujito

Department of Cardiology, Koshigaya Hospital, Dokkyo University of Medicine, Saitama, Japan

Yutaka Takabatake

Department of Cardiology, Koshigaya Hospital, Dokkyo University of Medicine, Saitama, Japan

To determine the factors of left ventricular aneurysm formation in acute myocardial infarction, the authors studied the distribution of coronary artery lesions and the left ventricular wall motion of 43 patients with anterior myocar dial infarction.

Of 15 patients with aneurysm, 9 (60%) showed a single-vessel disease with severe stenosis of the proximal left anterior descending artery. Of 9 patients with triple-vessel disease, 8 (89%) had no aneurysm. In patients with the aneu rysm, the Gensini score of the culprit lesion was significantly higher (p<0.05) and the score except for the culprit lesion was less ({chi} 2=5.7, p<0.05). In 23 patients with single-vessel disease, the collateral score was significantly less (p < 0.05) in patients with the aneurysm.

The systolic wall motion on the ventriculogram appeared more impaired in the anterior infarct area but well maintained in the posterior noninfarct area in patients with the aneurysm.

In conclusion, the important factors of left ventricular aneurysm formation were as follows: (1) A culprit lesion of the myocardial infarction was severe, but other coronary artery lesions were mild. (2) Collateral vessels were poor. (3) The left ventricular wall motion of the infarct area was impaired, but that of the noninfarct area was relatively good.

Angiology, Vol. 44, No. 8, 593-598 (1993)
DOI: 10.1177/000331979304400801
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