- Poster presentation
- Open Access
CMR features of peri-partum cardiomyopathy
© Cannan et al; licensee BioMed Central Ltd. 2010
- Published: 21 January 2010
- Cardiac Magnetic Resonance
- Pericardial Effusion
- Myocardial Edema
- Vessel Coronary Artery Disease
- Vessel Coronary Artery
The Cardiac Magnetic Resonance (CMR) features of peri-partum cardiomyopathy (PPC) are not well defined. The addition of tissue characterization to structural assessment by CMR may allow more insight into this rare disease.
Describe the CMR features of newly diagnosed PPC with particular attention to tissue characterization.
A retrospective review of the CMR database was performed to identify patients diagnosed with PPC. All patient were within 5 months of delivery with either signs or symptoms of heart failure or abnormal left ventricular function with no other cause for heart failure identified.
Out of a total of 6823 patients, 16 were initially diagnosed with PPC. Two of these were excluded (one patient had her scan one year following delivery and a second patient was found to have severe 3 vessel coronary artery disease). The remaining 14 patients were 30 ± 5.6 years of age. CMR was performed 15 ± 16.7 (range 3 to 54) days post partum. Mean systolic blood pressure was 119 ± 23 mmHg and heart rate was 80 ± 21 beats per minute. Pertinent measures of left ventricular function included an ejection fraction of 36 ± 12% and cardiac index of 3.4 ± 0.8 L/min/m2. 12/14 (86%) had an increased left ventricular end diastolic volume index (range 101-192; normal 55-103 ml/m). Left ventricular mass index was within normal limits in 11/14 (79%) patients. Left ventricular end systolic wall stress index was abnormal in all but one patient (70 ± 18.5 103 N/m2, normal <45 103 N/m2).
Pericardial effusion was seen in 7/14 (50%) and pleural effusion in 10/14 (71%) of patients.
T2 weighted images showed myocardial edema (either global or regional) in 11/14 (79%), with early contrast enhancement seen in 10/11 (91%) in whom this was assessed. Late contrast enhancement was seen in 6/12 (50%) with all having a non-ischemic pattern of distribution.
Besides structural abnormalities, patients with PPC have a high incidence of acute inflammation as evidenced by myocardial edema and hyperemia. Furthermore, half have late myocardial enhancement present suggesting the presence of fibrosis or necrosis.
This article is published under license to BioMed Central Ltd.