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Division of Cardiovascular Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Cardiac Center, King Chulalongkorn Memorial Hospital, Bangkok, Thailand
Division of Cardiovascular Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Cardiac Center, King Chulalongkorn Memorial Hospital, Bangkok, Thailand
Corresponding author at: Division of Cardiovascular Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Division of Cardiovascular Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Cardiac Center, King Chulalongkorn Memorial Hospital, Bangkok, Thailand
A 72-year-old woman with well-controlled hypertension presented to our hospital due
to worsening symptoms of heart failure. She had a history of acute anterior wall ST-elevation
myocardial infarction (MI) diagnosed 2 weeks previously, when she received clinically
successful fibrinolytic therapy at another regional hospital 4 hours after symptom
onset. Four (4) days after hospital discharge, she gradually developed dyspnoea on
exertion and orthopnoea. No recurrent chest pain was reported. On examination, her
blood pressure was 120/65 mmHg with a regular pulse rate at 90/minute. There was a
fine crackle at both lower lungs with a grade 3/6 parasternal pansystolic murmur.
An electrocardiogram showed QS waves at V1-4. Transthoracic echocardiography revealed
a left ventricular (LV) ejection fraction of 50% with akinesis of the mid-anterior
segment and the whole apex. There was a high-velocity flow crossing the ventricular
septum (Figure 1A, asterisk) from the LV to the right ventricle (RV), compatible with ventricular
septal rupture (VSR). The estimated RV systolic pressure was 30 mmHg.
Figure 1An echocardiography shows a high velocity flow crossing the ventricular septum (asterisk,
A) from LV to RV. Cardiac magnetic resonance confirms the 3-mm septal rupture at regional
wall thinning of apical anteroseptal area (asterisks, B and C). There is a nearly
complete intramyocardial tear (dash lines, D and F) covered by pericardium detected
at apical inferior wall. The blood clot is evident in pericardial space adjacent to
the ruptured site from the delayed enhancement (arrow, E) and long inversion time
images (arrow, F).
Clinicopathological characteristics of 10 patients with rupture of both ventricular free wall and septum (double rupture) after acute myocardial infarction.
