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ArticleTitle Clinicopathological Characteristics of 10 Patients with Rupture of Both Ventricular Free Wall and Septum (Double Rupture) After Acute Myocardial Infarction
AuthorList Keiji Tanaka1, Naoki Sato1, Masahiro Yasutake1, Shinhiro Takeda1, Teruo Takano2, Masami Ochi3, Shigeo Tanaka3, Koichi Tamura4
Affiliation 1Division of Intensive and Coronary Care Unit, Nippon Medical School Hospital 2First Department of Internal Medicine, Nippon Medical School 3Department of Cardiovascular Surgery, Nippon Medical School 4Division of Surgical Pathology, Nippon Medical School
Language EN
Volume 70
Issue 1
Year 2003
Page 21-27
Received July 3, 2002
Accepted August 30, 2002
Keywords ventricular double rupture, ventricular septal rupture, free wall rupture, acute myocardial infarction
Abstract

Cardiac ruptures after myocardial infarction are classified as ventricular free wall ruptures (FWR), ventricular septal ruptures (VSR), and papillary muscle ruptures (PMR). A combination of any two types of rupture is called "ventricular double rupture;" (VDR) and shows a specific clinical course.
3,284 patients with acute myocardial infarction (AMI) were admitted to the CCU of our hospital between April, 1973 and December, 2001, and 10 patients (8 males and 2 female, aged 54∼82 years) with VDR were clinicopathologically evaluated. All were diagnosed as VDR consisting of FWR and VSR. VDR was observed in 0.30% of all patients with AMI, in 3.0% of those with FWR, and in 16.1% of those with VSR. The infarct site was anteroseptal in 3 patients, anterolateral in 3, inferior in 3, and posterolateral in 1. Two patients with inferior infarction complicated RV infarction and a patient with posterolateral infarction had healed inferior infarction.
The risk factors related to VDR were age, a history of hypertension, increased sympathetic tone to improve hemodynamic aggravation after perforation, cardiotonic agents, thrombolytic agents, delayed reperfusion, right ventricular volume overload by shunt and re-infarction. However, these factors might have played only a subsidiary role. The most important factor in VDR was the pathological findings. The site of septal perforation was the apex close to the septum-free wall junction in 9 patients and the site of rupture was also apical in 8 patients.
Four patients already had VSR on admission to our CCU. FWR developed soon after VSR was demonstrated in 4 patients. FWR and VSR occurred simultaneously in one patient. These results suggest that VSR in the apical region is a precursor of VDR and requires the earliest surgical treatment.
Surgical treatment was carried out in the operating room in 5 patients and 3 (60.0%) of them survived for 4 months or more. Two patients with rupture incidentally detected during operation for VSR were discharged and are still alive, though another one with free wall blow out rupture died 129 days after operation. Bedside thracotomy was performed in 3 patients and all of them died.

Correspondence to Keiji Tanaka, MD, Director of Division of Intensive and Coronary Care Unit, Nippon Medical School Hospital, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan
k-tanaka@nms.ac.jp

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