Pregnancy-Related Cardiovascular Diseases: A Radiological Overview

Abstract

Pregnancy induces significant hemodynamic changes, and cardiovascular diseases (CVDs) are one of the leading causes of non-obstetric maternal morbidity and mortality during pregnancy or the postpartum period in developed countries. The effective diagnosis and management of CVDs in pregnant women require a thorough evaluation that considers the health of both the mother and the fetus. Imaging plays a pivotal role in this evaluation, offering essential insights into the most significant pregnancy-related CVDs. However, due to concerns about fetal exposure, the use of contrast agents and radiation exposure must be carefully managed. Following to the principle of "As Low As Reasonably Achievable" (ALARA), strategies to minimize these risks are crucial for ensuring patient safety while maintaining diagnostic accuracy. This review highlights the contribution of cardiovascular imaging techniques, particularly computed tomography (CT) and magnetic resonance imaging (MRI), in the assessment of common pregnancy-related CVDs, and outlines strategies to reduce radiation exposure and limit contrast agent use when feasible, aiming to increase radiologists' awareness of this crucial topic.

Keywords: aortic dissection; cardiovascular diseases; computed tomography (CT); magnetic resonance imaging (MRI); peripartum cardiomyopathy; pregnancy; pulmonary embolism; spontaneous coronary artery dissection.

Figure 1

A 47-year-old woman at week 20 of pregnancy with shortness of breath and D-dimer elevation. Axial SSFP images show left and right main pulmonary artery filling defects (a,b), consistent with acute pulmonary embolism, confirmed by T1-w images with blood and fat saturation (c,d). SSFP: steady-state free precession.

Figure 2

A 47-year-old woman with shortness of breath and D-dimer elevation at week 20 of pregnancy. Short-axis SSFP image (a) shows interventricular septum flattening in mid-systolic phase due to increased intracavitary pressure in the right ventricle. The four-chamber SSFP image (b) demonstrates right ventricular enlargement compared to the left ventricle. SSFP: steady-state free precession.

Figure 3

A 31-year-old woman with Marfan syndrome and a history of ascending aortic dissection, previously treated with a Bentall procedure, presented with chest pain a few days postpartum. CTA revealed an extension of the dissection into the descending thoracic and abdominal aorta (3D volume rendering in (a), and sagittal and coronal views in (b and c), respectively), with simultaneous enhancement of both the true and false lumens due to multiple intimal fenestrations (arrows in (c)). The sagittal view (b) shows a heterogeneous collection into the rectus abdominis muscles following a recent cesarean section. Axial image (d) reveals the left renal artery originating across both the true and false lumens. CTA: computed tomography angiography and 3D-VR: 3D volume rendering.

Figure 4

SSFP breath-hold images in coronal (a) and sagittal (b) views demonstrate an intimal-medial flap involving the entire thoracic aorta, including the ascending aorta, consistent with a Stanford Type A dissection. Multiple intimal tears are visible within the flap (arrow in (a)), and massive circumferential pericardial fluid is associated. An axial SE-BB image (c) shows a hypointense true lumen and increased signal intensity in the false lumen due to slow flow. SSFP: steady-state free precession and SE-BB: spin echo-black blood.

Figure 5

A 36-year-old woman at week 36 of pregnancy presented with chest pain and anterior ST-segment elevation on ECG. Urgent ICA (a) and CCTA performed one week later (3D-VR, (b) and curved-MPR, (c,d)) revealed a tapered luminal stenosis in the mid-LAD (white arrow), consistent with mid-LAD dissection. In (e), unenhanced CT shows high-density thickening of the mid-LAD wall, suggestive of IMH (arrowhead). ICA: invasive coronary angiography; CCTA: coronary computed tomography angiography; 3D-VR: three-dimensional volume rendering; MPR: multiplanar reconstruction; LAD: left anterior descending artery; and IMH: intramural hematoma.

Figure 6

A 36-year-old woman at week 36 of pregnancy presented with chest pain and anterior ST-segment elevation on ECG. CMR detected edema in the LAD territory in STIR sequence (a), confirmed by increased T2 mapping values in the same territory, with maximum values in the mid-ventricular anterior and anteroseptal segments (b,d), consistent with recent infarction-related changes. LGE with ischemic subendocardial pattern in LAD territory is depicted in delayed-enhancement sequence (c). CMR: cardiac magnetic resonance; LAD: left anterior descending artery; STIR: short tau inversion recovery; and LGE: late gadolinium enhancement.

Figure 7

A 38-year-old woman presented with chest oppression and hypertension eight days after delivery. TTE (a) showed decreased LVEF (45%) and global left ventricle hypokinesia. CMR confirmed left ventricle disfunction, but no focal delayed enhancement was identified on LGE imaging (b) and STIR images (c) showed faint and diffuse hyperintensity. Quantitative mapping showed high global myocardial native T1, ECV, and T2 values ((d–f): mean value of the basal segments shown in the Figures). TTE: transthoracic echocardiogram; LVEF: left ventricular ejection fraction; CMR: cardiac magnetic resonance; LGE: late gadolinium enhancement; STIR: short tau inversion recovery; and ECV: extracellular volume.