Maternal interventricular vein of the heart and fetal growth restriction

Abstract

I read with interest the report of Youssef et al1Youssef L. Miranda J. Paules C. et al.Fetal cardiac remodeling and dysfunction is associated with both preeclampsia and fetal growth restriction.Am J Obstet Gynecol. 2020; 222: 79.e1-79.e9Abstract Full Text Full Text PDF Scopus (19) Google Scholar concerning fetal cardiac remodeling and dysfunction. Atrial natriuretic peptide is stored mainly in the right atrium and released in response to an increase in atrial distending pressure. Brain natriuretic peptide is stored mainly in cardiac ventricular myocardium and may be responsive to changes in ventricular filling pressures.2Colucci W.S. Braunwald E. Pathophysiology of heart failure.in: Braunwald E. Heart Disease. 5th ed. WB Saunders, Philadelphia1997: 414Google Scholar The inside corner between the interventricular septum (IVS) and the right anterior ventricular wall exhibits the deep pits called interventricular sinuses. The opening of the interventricular vein (IV) (kuuselian vessel) is located in the interventricular sinuses. The IV is not a canal or channel or blood vessel but a slit between the fibers of the muscle leading to the central muscular part of the IVS and runs at an angle of approximately 90° through the interventricular sphincter (ISP) and the left IVS into the left ventricle (LV). The IV exhibits 2 to 3 oval 2- × 5-mm openings in the left central muscular part of the IVS surrounded by the ISP. Hypoxia may be the physiological factor that recruits IV of the fetal heart and augments the flow of the oxygenated blood from right to left. The ISP and the IV may become patent by relaxing and widening of the helical heart at the right atrial filling phase at the end of the diastole. The sinoatrial node initially activates the right atrium, followed by activation of the left atrium. Left-to-right communication does not result as the earliest left ventricular activation closes the ISP. Hypoxia may recruit the IV of the maternal heart at the right atrial filling phase and create the venous flow from right to left into the LV. This flow may generate the abnormal fourth heart sound common in hypertrophy of systemic hypertension and in ischemic heart disease. The venous flow moves toward the left outflow tract in the LV.3Kuusela P.J. The heart exhibits right to left communication between the fibres of the muscular part of the interventricular septum.Folia Morphol. 2014; 73: 42-50Crossref PubMed Scopus (3) Google Scholar,4Kuusela P.J. Interventricular vessel of the heart.Cardiol Res. 2018; 9: 111-115Crossref PubMed Google Scholar I do not yet fully understand the anatomy, function, and embryology of the human heart and circulation. The hypertensive patient with secondary polycythemia of the reference 4 suggests an unusually plentiful venous flow at the right atrial filling phase from right to left through the IV. I do not know whether recruitment of the maternal IV by hypoxia or by an increase in right atrial pressure and atrial natriuretic peptide or brain natriuretic peptide also regulates circulation and development of the fetus. Fetal cardiac remodeling and dysfunction is associated with both preeclampsia and fetal growth restrictionAmerican Journal of Obstetrics & GynecologyVol. 222Issue 1PreviewPreeclampsia and fetal growth restriction share some pathophysiologic features and are both associated with placental insufficiency. Fetal cardiac remodeling has been described extensively in fetal growth restriction, whereas little is known about preeclampsia with a normally grown fetus. Full-Text PDF Maternal and fetal cardiovascular adaptations in preeclampsia and/or fetal growth restrictionAmerican Journal of Obstetrics & GynecologyVol. 222Issue 3PreviewWe appreciate the comments and insights by Dr Kuusela regarding our recent study.1 We reported in this study for the first time signs of fetal cardiac remodeling and dysfunction in pregnancies complicated by preeclampsia with a normally grown fetus in a similar way to what has been described previously in fetal growth restriction. These signs included structural and functional echocardiographic parameters together with the assessment of cord blood myocardial biomarkers (B-type natriuretic peptide and troponin I). Full-Text PDF