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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.

Left ventricular false tendons (LFTs) have been extensively described and recognized by gross anatomic studies. However, there is very little information available regarding right ventricular false tendons (RFTs). The aim of our study, therefore, was to explore and delineate the morphology, topography and morphometry of the RFTs, and provide a comprehensive picture of their anatomy across a broad range of specimens. We identified 35/100 heart specimens containing right ventricular RFTs and classified them into five types. In Type I (21, 47.7%) the RFTs, was located between the ventricular septum and the anterior papillary muscle; in Type II (11, 22.9%) between ventricular septum and the posterior papillary muscle; in Type III (7, 14.5%) between the anterior leaflet of the tricuspid valve and the right ventricular free wall; in Type IV (5, 10.4%) between the posterior papillary muscle and the ventricular free wall; and lastly, in Type V (4, 8.3%) between the anterior papillary muscle and ventricular free wall. The mean length of the RFTs was 18 +/- 7 mm with a mean diameter of 1.4 +/- 05 mm. Histologic examination with Masson trichrome and PAS revealed that 20 (41.6%) of the 48 RFTs carried conduction tissue fibers. The presence of conduction tissue fibers within the RFTs was limited to Types I, III, and IV. In Types II and V the RFTs resembled fibrous structures in contrast with Type I, II and IV, which were composed more of muscular fibers, including conduction tissue fibers. RFTs containing conduction tissue fibers were identified, which may implicate them in the appearance of arrhythmias.

False tendons (FTs) have been extensively described and recognized by gross anatomic studies. However, in the clinical setting the recognition of FTs is limited to the use of echocardiography. We examined 200 formalin fixed adult hearts, with gross dissections. In addition, 90 of these specimens were also examined with ultrasonographic and endoscopic techniques. Gross examination was able to identify FTs in 128 (62%) specimens. The total number of FTs observed, was 248 and was classified into five types according to their location. In Type I (92, 37.1%) the FT was located between the posteromedial papillary muscle and the ventricular septum. In Type II (55, 22.1%) the FT was located between the two papillary muscles. Type III (41, 16.5%) was classified as an FT between the anterolateral papillary muscle and the ventricular septum. The FT in Type IV (31, 12.5%) was observed to connect between the ventricular septum and the free wall and lastly in Type V (29, 11.6%) the FTs were found to be weblike with three or more points of insertion. When using all three techniques (n = 90), gross dissection and endoscopy were able to identify FTs in 62.2% of specimens while echocardiographic imaging was only able to identify FTs in 27.7% of specimens. Of the 114 FTs detected grossly and endoscopically, echocardiography was only able to identify 46 (40.3%). Therefore, the overall sensitivity of echocardiography for detecting left ventricular FTs was only 40.3%, compared to 100% for endoscopy. Based upon the ability or lack thereof of echocardiography to detect certain topographical patterns, we have created a small series of subtypes for the FTs. Histologically, in 30% of the FTs, conduction tissue fiber was observed to be present, which may implicate them in the appearance of arrhythmias.