The clinical anatomy of the sinutubular junction

Abstract

Specific sites of atherosclerotic processes due to hemodynamic changes and resultant stress, including how these normal anatomical structures become problematic in certain individuals, have yet to be acknowledged. One of these areas of the cardiovascular system occurs at the sinutubular junction (SJ), causing altercation in an otherwise normal flow status. The anatomy of the SJ was examined in 100 adult human hearts during the gross anatomy course at St George’s University, during the years 2006–2007. All hearts were examined in situ, using a General Electric model 3200S ultrasound machine with a 5 MHz linear probe. The aforementioned cadavers were also examined using a Stryker laparoscopic unit. Serial transverse histological sections were made through the SJ perpendicular to its axis, and stained with eosin-hematoxylin, van Gieson, Masson trichrome, and Orcein methods. In addition, an immunohistochemical analysis was performed for the detection of positive smooth muscle cells stained areas. During gross and endoscopic examination we were able to identify the SJ in all adult heart specimens. Neonatal and fetal hearts did not exhibit any gross evident SJ; however, a SJ was evident histologically. Ultrasonographically we were able to identify the SJ in all adult heart specimens examined, and a sinutubular ridge in 62%. A significant association was present between the thickness of the ridge and the age of the specimens. The SJ was found to exhibit atherosclerotic changes and plaque formation in an age-related manner. In older subjects, the SJ was marked with local calcification and hemorrhages. In contrast, the SJ of neonatal hearts appeared to have intimal thickening with focal fragmentation and absent or duplicate internal elastic lamina. Intuitively speaking, the presence of a sinutubular ridge, an inevitable fate in humans based on the results of this study, provides an irreversible atherosclerotic process as there is no evidence that the promoting ridge regresses. This is an alarming situation in those individuals who will eventually develop cardiovascular risk factors, whether through inevitable genetic manifestations or by means of exogenous environmental causes.