Author + information
- Pier Paolo Bassareo, MD, PhD, MSc∗ (, )
- Vinod Namana, MD,
- Vassilios Fanos, MD and
- Giuseppe Mercuro, MD
- ↵∗Department of Medical Sciences and Public Health, University of Cagliari, Policlinico Universitario, S.S. 554 bivio di Sestu, 09042 Monserrato, Italy
We have read with close attention the recent, excellent paper by Carr et al. (1) reporting the exaggerated number of formerly preterm subjects who develop heart failure without experiencing structural cardiac diseases.
Much evidence has been cited by Carr et al. (1) to explain the reason of this association: altered myocytes development with hypertrophy and raised interstitial fibrosis, with consequent increased left ventricular mass and reduced systolic and diastolic functions. All these issues would be caused by the interrupted myocardial growth due to the early delivery (1).
As a research group focusing on the relationship among preterm birth or intrauterine growth restriction and increased cardiovascular morbidity and mortality, we think that other factors should be considered as well (2). In fact, it is noteworthy that the majority of preterm newborns, particularly those born with a very low gestational age (<28 weeks), were, until the early 1990s, extensively treated with corticosteroids to prevent or reduce the incidence and severity of chronic lung disease. This wide use was justified mainly by the therapeutic effect of corticosteroids in improving respiratory function, reducing the need for both mechanical ventilation and oxygen administration, and producing a decrease in mortality (3). In the short term, corticosteroids administration usually leads to the development of an apparently transient hypertrophic cardiomyopathy, which disappears after their discontinuation. However, recent studies have suggested that neonatal corticosteroids treatment may also have detrimental long-term effects on the heart, possibly initiated by inhibiting the cardiomyocyte mitosis, and resulting in a reduced number of cardiac muscle cells in adulthood. These changes appear to elicit a late systolic dysfunction, due to compensatory cardiac dilation. The damage may lead to a reduction in life expectancy, as observed in rats treated with corticosteroids in the neonatal period (3).
A left ventricular remodeling in humans born preterm has been confirmed by both echocardiography and magnetic resonance imaging, demonstrating that they share dilated left ventricles, thickened walls, and displaced apexes (4). Again, as pioneers in this field, we have already demonstrated the presence, in these apparently healthy young adults, of an electromechanical interaction, resulting in a prolonged QT tract at basal electrocardiography. From a practical point of view, these findings underline a potential risk for patients to develop ventricular arrhythmias when using common drugs capable of prolonging QT interval (i.e., diuretics, proton pump inhibitors, antidepressants, anxiolytics, antihistamines, and some forms of antibiotics) (5).
In conclusion, it is an undoubted fact that preterm birth, intrauterine growth restriction, and the “perinatal environment” in general represent novel and still poorly understood risk factors whose influence should be taken into account by clinical and scientist cardiologists.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation
- Carr H.,
- Cnattingius S.,
- Granatah F.,
- Ludvigsson J.F.,
- Edstedt Bonamy A.K.
- Bassareo P.P.,
- Abella R.,
- Fanos V.,
- Mercuro G.
- Lewandowski A.J.,
- Augustine D.,
- Lamata P.,
- et al.