Noninvasive Cardiac Imaging in Formerly Preeclamptic Women for Early Detection of Subclinical Myocardial Abnormalities: A 2022 Update

Abstract

Preeclampsia is a maternal hypertensive disease, complicating 2-8% of all pregnancies. It has been linked to a 2-7-fold increased risk for the development of cardiovascular disease, including heart failure, later in life. A total of 40% of formerly preeclamptic women develop preclinical heart failure, which may further deteriorate into clinical heart failure. Noninvasive cardiac imaging could assist in the early detection of myocardial abnormalities, especially in the preclinical stage, when these changes are likely to be reversible. Moreover, imaging studies can improve our insights into the relationship between preeclampsia and heart failure and can be used for monitoring. Cardiac ultrasound is used to assess quantitative changes, including the left ventricular cavity volume and wall thickness, myocardial mass, systolic and diastolic function, and strain. Cardiac magnetic resonance imaging may be of additional diagnostic value to assess diffuse and focal fibrosis and perfusion. After preeclampsia, sustained elevated myocardial mass along with reduced myocardial circumferential and longitudinal strain and decreased diastolic function is reported. These findings are consistent with the early phases of heart failure, referred to as preclinical (asymptomatic) or B-stage heart failure. In this review, we will provide an up-to-date overview of the potential of cardiac magnetic resonance imaging and echocardiography in identifying formerly preeclamptic women who are at high risk for developing heart failure. The potential contribution to early cardiac screening of women with a history of preeclampsia and the pros and cons of these imaging modalities are outlined. Finally, recommendations for future research are presented.

Keywords: CMR; cardiac imaging; cardiac strain; cardiac ultrasound; cardiovascular; echocardiography; preeclampsia; tissue mapping.

Figure 1

Left ventricular short-axis view of cine MRI. The left ventricle in the (A) end-diastolic and (B) end-systolic phase. The blue and red lines denote the outer and inner walls of the left ventricle, respectively. Papillary muscles may or may not be included, depending on the individual choice of the researcher/clinician. In this example, they are excluded [21].

Figure 2

A typical example of a native T₁ map. (A) Anatomical reference image of a left ventricle short-axis view. (B) Superimposed heat map showing the different T₁ relaxation times for different tissues. (C) Regions of interest drawn in the mid-septal region and ventricular cavity. (D) Global myocardial T₁ relaxation times can be determined by denotation of the entire left ventricular wall. (E) Superimposition of the drawn contours from image D on the T₁ map. (F) Heat map scale with T₁ relaxation times ranging from 0 to 2000 ms [21].

Figure 3

A graphical representation of the principal strain directions. The black lines represent the distance between two hypothetical features (the red dots). 1a and 1b demonstrate circumferential shortening, 2a and 2b demonstrate radial thickening, and 3a and 3b demonstrate longitudinal shortening.

Figure 4

Typical example of calculation of myocardial strain with MRI feature tracking. (A–C): Anatomical cine MR images of the left ventricular short axis, long-axis 2-chamber, and long-axis 4-chamber view, respectively. (D–F) Delineation of the inner (red) and outer (blue) left ventricular wall in these image planes. (G–I) Feature tracking employed over the entire cardiac cycle, with pathing (the motion of myocardial features over time) made visible by the light-blue lines [21].

Figure 5

First-pass perfusion. (A) shows the contoured mid-height-level myocardium before the first pass of the contrast bolus, though it is already visible in the right ventricle. (B) shows the first pass of the bolus as it enters the left ventricle. (C) shows the second pass of the bolus, also showing the uptake of contrast agent in the myocardium. (D) shows the resulting graphs where signal intensities of the myocardium (green line) and blood pool (red line) are visible. The phases of (A–C) are also visible on the graph with their corresponding letters. Line I shows the upslope of the blood pool, and line II shows the upslope of the myocardium, from which the relative upslope is calculated. Time is measured in seconds (s).