Ultrasound evaluation of left ventricular and aortic fibrosis after HELLP syndrome.

Abstract

By means of integrated backscatter (IBS), we described recently the presence of left ventricular (LV) and aortic fibrosis in women with a previous pregnancy complicated by early- or late-onset pre-eclampsia (PE), finding that early-onset PE is characterized by persistent LV fibrosis, which correlates with cardiac structural and functional abnormalities, and a non-statistically significant trend towards aortic fibrosis1. Calibrated IBS (cIBS) provides information on myocardial reflectivity of ultrasound, assessed at the interventricular septum (IVS), LV posterior wall (PW) and ascending aorta (AO), measured in decibels (dB), conventionally as negative numbers, and averaged and calibrated to the reflectivity of the pericardium1. The same echocardiographic evaluation was performed in the population of two other previous studies published in this Journal, involving 49 women with a history of HELLP syndrome and 60 with a previous pregnancy complicated by PE, compared with 60 healthy controls, evaluated between 6 months and 4 years after delivery2,3. Demographic and clinical characteristics of the study cohort are reported elsewhere2–4. We found that HELLP syndrome has a similar, or even stronger, association with persistent LV and aortic fibrosis than does PE (Table 1). In particular, the extent of fibrosis was greater in women with a history of early-onset PE and/or fetal growth restriction (FGR) compared to those with a history of late-onset PE (cIBSIVS, −17.6 ± 6.7 vs −26.2 ± 2.9 dB (P = 0.008); cIBSPW, −19.9 ± 6.1 vs −26.1 ± 3.8 dB (P = 0.031); cIBSAO, −9.3 ± 12.8 vs −21.4 ± 7.6 (P = 0.136)). These data are consistent with our previous finding in the same population that HELLP syndrome and PE share similar cardiovascular sequelae, namely biventricular systolic and diastolic preclinical alteration2, arterial stiffness3, endothelial dysfunction3, altered ventriculoarterial coupling and aortic elastic properties4. This significant overlap suggests a common pathophysiological pathway between the two conditions. As such, a history of HELLP syndrome, FGR or early-onset PE seems to identify a subgroup of women with a higher risk for future development of cardiovascular alterations, as suggested previously2-4. Although little is known about HELLP syndrome and its pathophysiology is not completely understood, its pathognomonic alterations likely reflect a disturbance in the microcirculation. Microvascular alterations of the myocardium and the aortic vasa vasorum may further increase tissue damage and fibrin deposition, combined with the oxidative stress and proinflammatory state typical of HELLP syndrome and PE. Of note, Masci et al. investigated recently, using cardiac magnetic resonance imaging (i.e. the gold standard for fibrosis detection), the prognostic value of myocardial fibrosis in asymptomatic patients with non-ischemic cardiomyopathy and no history of heart failure. They concluded that the presence, and also the extent, of myocardial fibrosis influenced the clinical outcome5. It is well known that the aorta plays a key role in LV performance and remodeling, thus affecting afterload and coronary artery perfusion in diastole. Arterial stiffness is widely considered an independent predictor of cardiovascular morbidity and it is also able to anticipate hypertension in previously normotensive women, providing additional value in cardiovascular risk-profile definition. As highlighted previously1, our findings try to provide another possible explanation for the higher risk of cardiovascular events later in life in these women than in the general female population of the same age. Currently, fibrosis is considered both a dynamic marker of cardiovascular disease severity and a determinant of future LV remodeling. Although no currently known treatment is able to counteract this process, the role of the myocardial interstitium is emerging. Our findings need confirmation in a larger population. The study limitations are outlined elsewhere, including the lack of data on the relationship between cIBS and cardiac magnetic resonance imaging; however, both techniques have been validated against histology on endomyocardial biopsy1.