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Multicenter Study
. 2017 Apr 3;6(4):e005472.
doi: 10.1161/JAHA.117.005472.

Myocardial Damage Detected by Late Gadolinium Enhancement Cardiac Magnetic Resonance Is Uncommon in Peripartum Cardiomyopathy

Affiliations
Multicenter Study

Myocardial Damage Detected by Late Gadolinium Enhancement Cardiac Magnetic Resonance Is Uncommon in Peripartum Cardiomyopathy

Erik B Schelbert et al. J Am Heart Assoc. .

Abstract

Background: In peripartum cardiomyopathy, the prevalence of focal myocardial damage detected by late gadolinium enhancement (LGE) cardiovascular magnetic resonance is important to elucidate mechanisms of myocardial injury and cardiac dysfunction. LGE equates irreversible myocardial injury, but LGE prevalence in peripartum cardiomyopathy is uncertain.

Methods and results: Among 100 women enrolled within the Investigations of Pregnancy Associated Cardiomyopathy cohort, we recruited 40 women at 13 centers to undergo LGE cardiovascular magnetic resonance, enrolled within the first 13 weeks postpartum. Follow-up scans occurred at 6 months postpartum, and death/transplant rates at 12 months. Baseline characteristics did not differ significantly in the parent cohort according to cardiovascular magnetic resonance enrollment except for mechanical circulatory support. LGE was noted only in 2 women (5%) at baseline. While left ventricular dysfunction with enlargement was prevalent at baseline cardiovascular magnetic resonance scans (eg, ejection fraction 38% [Q1-Q3 31-50%], end diastolic volume index=108 mL/m2 [Q1-Q3 83-134 mL/m2]), most women demonstrated significant improvements at 6 months, consistent with a low prevalence of LGE. LGE was not related to baseline clinical variables, ejection fraction, New York Heart Association heart failure class, or mortality. Neither of the 2 women who died exhibited LGE. LGE was inversely associated with persistent left ventricular ejection fraction at 6 months (P=0.006).

Conclusions: Factors other than focal myocardial damage detectable by LGE explain the initial transient depressions in baseline left ventricular ejection fraction, yet focal myocardial damage may contribute to persistent myocardial dysfunction and hinder recovery in a small minority. Most women exhibit favorable changes in ventricular function over 6 months.

Clinical trial registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01085955.

Keywords: cardiovascular magnetic resonance; heart failure; myocardial fibrosis; peripartum cardiomyopathy; pregnancy and postpartum.

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Figures

Figure 1
Figure 1
Left ventricular ejection fraction improved over time in most participants (A), resulting from decreased end diastolic volumes (B) and end systolic volumes (C) at 6 months compared to baseline. Since cardiovascular magnetic resonance (CMR) occurred 31±24 days postpartum, some women exhibited significant recovery by the time they were scanned. The 2 women with the worst ejection fraction at 6 months exhibited evidence of pathology distinct from the others (A, adjacent thumbnail insets). One woman exhibited marked trabeculations on cine images suggesting left ventricular noncompaction cardiomyopathy (arrow), and the other woman exhibited focal myocardial scar on late gadolinium enhancement (LGE) images indicating irreversible myocardial injury (arrow) also shown in Figure 2C. Alternate pathologies may exist given the nonspecific diagnostic criteria of peripartum cardiomyopathy.
Figure 2
Figure 2
Examples of focal myocardial damage detected by late gadolinium enhancement (LGE, arrows) in 3 participants. In (C), the 2‐chamber orientation is rotated, rendering the LGE not clearly visible. None of these participants exhibited extensive myocardial damage, and none experienced adverse events. The LGE pattern in patient in (A) resembles the injury pattern in myocarditis. The 6‐month left ventricular ejection fractions were 53%, 41%, and 19% for the participants in (A through C), respectively. Coronary artery disease in the patients in (B and C) could not be excluded definitively. Given: (1) the low pretest probability of coronary disease in younger premenopausal women, and (2) the limited involvement in the long‐axis direction (ie, base to apex) that is unusual for coronary disease, we believed the probability of coronary artery disease was low. Still, we could not exclude vasospasm, embolization, cocaine, or recanalized myocardial infarction as potential etiologies.
Figure 3
Figure 3
No late gadolinium enhancement (LGE) was detected for the 2 individuals who died (A and B). The woman in (A) had a measured left ventricular ejection fraction of 15%, and died after left ventricular assist device implantation and eventual orthotopic heart transplantation. The woman in (B) had a measured left ventricular ejection fraction of 17% and died prior to surgical interventions.

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